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Schizophrenia and Toxoplasmosis

 

 

Parasite May Play Role in Some Schizophrenia Cases

A parasite responsible for toxoplasmosis – Toxoplasma gondii – may be involved in the cause of around a fifth of schizophrenia cases in the US. This is according to a new study published in the journal Preventive Veterinary Medicine.

Definition of schizophrenia

University of Pennsylvania researcher Greg Smith calculated that around a fifth of schizophrenia cases may be attributable toT. gondiiinfection.

The Centers for Disease Control and Prevention (CDC) estimate that around 60 million people in the US may be infected with T. gondii. Infection most commonly occurs through eating undercooked, contaminated meat, drinking contaminated water and coming into contact with cat feces that contain T. gondii.

Most people with T. gondii infection are unaware they have it; people with healthy immune systems are usually able to stop the parasite causing illness. But for those with weaker immune systems, such as older people, pregnant women and those with immune system disorders, the parasite can cause toxoplasmosis.

Toxoplasmosis a disease characterized by flu-like symptoms, including swollen lymph glands and muscle aches and pains. In severe cases, toxoplasmosis can cause damage to the eyes, brain and other organs.

Some studies, however, have linked T. gondii infection to mental health conditions. In 2012, for example, Medical News Today reported on a study linking T. gondi to increased risk of self-harm or suicide among new mothers.

More recently, studies have linked T. gondii infection to schizophrenia, and some have found that antipsychotic medication may even stop the parasite from replicating. But such research has been met with much criticism.

In this latest study, Gary Smith, of the School of Veterinary Medicine at the University of Pennsylvania, wanted to gain a better understanding of the link between T. gondii infection and schizophrenia.

Link between T. gondii and schizophrenia ‘should be considered, not ridiculed’

Smith wanted to determine the proportion of schizophrenia cases that could be attributable to T.gondii infection. He did this by calculating the population attributable fraction (PAF) – a measure used by epidemiologists to understand the importance of a risk factor.

“In other words,” explains Smith, “we ask, if you could stop infections with this parasite, how many [schizophrenia] cases could you prevent?”

Smith calculated the PAF fraction throughout an average lifetime to be 21.4%, meaning that a fifth of all schizophrenia cases over a lifetime could be prevented by stopping T. gondiiinfections from occurring. “That, to me, is significant,” says Smith.

He notes that many countries have a much higher prevalence of T. gondii infections than the US, and such countries also have a higher prevalence of schizophrenia.

Schizophrenia is one of the leading causes of disability in the US, affecting more than 3.5 million people.

Smith believes that his findings indicate the importance of gaining a better understanding of the link between T. gondii infection and schizophrenia. He adds:

By finding out how important a factor T. gondii infection is, this work might inform our attitude to researching the subject.

Instead of ridiculing the idea of a connection between T. gondiiand schizophrenia because it seems so extraordinary, we can sit down and consider the evidence. Perhaps then we might be persuaded to look for more ways to reduce the number of people infected with toxoplasma.”

Common food preservative may help to treat schizophrenia

A new randomized trial from Taiwan shows that a common food preservative could enhance the effect of a schizophrenia drug, even in the case of people normally resistant to treatment.
older man taking pillsNew research suggests that a common food preservative could be the answer for treatment-resistant people with schizophrenia.

Schizophrenia is a chronic, sometimes disabling mental disorder characterized by delusions, flat affect, agitated movements, and a difficulty in sustaining activities.

Treatments include antipsychotic medication — such as brexpiprazole, clozapine, or risperidone — and psychosocial treatments.

Studies have shown that “one fifth to one half of [people with schizophrenia] are classified as refractory to pharmacological treatment,” meaning that they do not respond to antipsychotics.

Researchers from China Medical University in Taiwan may now have found a way of boosting the effectiveness of certain drugs, which may help some people living with schizophrenia to respond better to treatment.

The answer, says the study’s lead investigator Dr. Hsien-Yuan Lane, may be found in a common food preservative: sodium benzoate. Dr. Lane and team conducted a randomized, double-blind, placebo-controlled trial showing that this preservative could enhance the effects of the antipsychotic drug clozapine.

“Clozapine,” he explains, “is considered the last-line antipsychotic agent for patients with refractory schizophrenia.” Despite this, a significant number of people living with schizophrenia are resistant to this drug.

The new trial seems to confirm for the first time that sodium benzoate — which has successfully been used as an add-on to other antipsychotics — can be added to clozapine to improve the symptoms of drug-resistant patients.

Dr. Lane and colleagues’ findings were recently published in the journal Biological Psychiatry. “If the finding can be confirmed, this approach may bring hope for treating patients with the most refractory schizophrenia,” he suggests.

Sodium Benzoate, a D-Amino Acid Oxidase Inhibitor, Added to Clozapine for the Treatment of Schizophrenia_ A Randomized, Double-Blind, Placebo-Controlled Trial

D-Amino Acid Oxidase Inhibition A New Glutamate Twist for Clozapine Augmentation in Schizophrenia

A series of clinical trials
found that currently available NMDA-enhancing agents
including glycine, D-cycloserine, D-serine, and sarcosine were
efficacious in improving the overall psychopathology of
schizophrenia without side effect or safety concern.

16. Lin CH, Lane HY, Tsai GE (2012): Glutamate signaling in the pathophysiology and therapy of schizophrenia. Pharmacol Biochem Behav 100:665–677.
17. Heresco-Levy U (2005): Glutamatergic neurotransmission modulators as emerging new drugs for schizophrenia. Expert Opin Emerg Drugs 10:827–844.
18. Coyle JT (2012): NMDA receptor and schizophrenia: A brief history. Schizophr Bull 38:920–926.
19. Javitt DC, Schoepp D, Kalivas PW, Volkow ND, Zarate C, Merchant K, et al. (2011): Translating glutamate: From pathophysiology to treatment.Sci Transl Med 3:102mr102.

Cat ownership in childhood linked to greater risk of later-life mental illness

They are cute, fluffy and have that wide-eyed glare that few of us can resist; it is no wonder more than 95 million of us own a cat. But there may be a darker side to our four-legged friends. New research claims the animals could increase our risk of mental illnesses, including schizophrenia and bipolar disorder.
Cat using litter boxHumans can become infected with Toxoplasma gondii by accidentally swallowing the parasite after coming into contact with a cat’s feces.

Two studies published in the journals Schizophrenia Research and Acta Psychiatrica Scandinavica attribute this association to Toxoplasma gondii – a parasite found in the intestines of cats. Humans can become infected with the parasite by accidentally swallowing it after coming into contact with the animal’s feces.

T. gondii is the cause of a disease known as toxoplasmosis. According to the Centers for Disease Control and Prevention (CDC), more than 60 million people in the US are infected with the parasite, though the majority of people are not aware of it.

People with a healthy immune system often stave off T. gondii infection, so it does not present any symptoms. However, pregnant women and people with weakened immune systems are more susceptible to infection and may experience flu-like symptoms – such as muscle aches and pains and swollen lymph nodes – as a result, while more severe infection may cause blindness and even death.

Previous studies have also linked T. gondii infection to greater risk of mental disorders. In November 2014, for example, Medical News Today reported on a study claiming the parasite is responsible for around a fifth of schizophrenia cases. Now, new research provides further evidence of this association.

Link between T. gondii and schizophrenia ‘should be considered, not ridiculed’

Smith wanted to determine the proportion of schizophrenia cases that could be attributable to T.gondii infection. He did this by calculating the population attributable fraction (PAF) – a measure used by epidemiologists to understand the importance of a risk factor.

“In other words,” explains Smith, “we ask, if you could stop infections with this parasite, how many [schizophrenia] cases could you prevent?”

Smith calculated the PAF fraction throughout an average lifetime to be 21.4%, meaning that a fifth of all schizophrenia cases over a lifetime could be prevented by stopping T. gondiiinfections from occurring. “That, to me, is significant,” says Smith.

He notes that many countries have a much higher prevalence of T. gondii infections than the US, and such countries also have a higher prevalence of schizophrenia.

Schizophrenia is one of the leading causes of disability in the US, affecting more than 3.5 million people.

Smith believes that his findings indicate the importance of gaining a better understanding of the link between T. gondii infection and schizophrenia. He adds:

By finding out how important a factor T. gondii infection is, this work might inform our attitude to researching the subject.

Instead of ridiculing the idea of a connection between T. gondiiand schizophrenia because it seems so extraordinary, we can sit down and consider the evidence. Perhaps then we might be persuaded to look for more ways to reduce the number of people infected with toxoplasma.”

People with ‘rage’ disorder twice as likely to have toxoplasmosis

A disorder that causes the individual to fly off the handle unexpectedly, as in road rage, has been significantly linked with toxoplasmosis, a parasite commonly associated with cat feces, according to the Journal of Clinical Psychiatry.

[road rage]

People with IED are prone to sudden anger.

Intermittent explosive disorder (IED) has been defined as “recurrent, impulsive, problematic outbursts of verbal or physical aggression that are disproportionate to the situations that trigger them.”

Up to 16 million Americans are thought to have IED, more than the total number for bipolar disorder and schizophrenia combined.

Toxoplasmosis is a common and generally harmless parasitic infection that is passed on through the feces of infected cats, contaminated water or undercooked meat.

 

It affects around 30% of all humans but is normally latent1.

Research has revealed that the parasite is found in brain tissue, and it has been linked to a number of psychiatric conditions, including schizophrenia, bipolar disorder and suicidal behavior.

Researchers from the University of Chicago, led by Dr. Emil Coccaro, have been looking for more effective ways to diagnose and treat IED and impulsive aggression.

 

This is a scanning electron micrograph of the protozoan parasite Toxoplasma gondii, tissue cyst in brain of an infected mouse.
Credit: David Ferguson

Individuals with a psychiatric disorder involving recurrent bouts of extreme, impulsive anger–road rage, for example–are more than twice as likely to have been exposed to a common parasite than healthy individuals with no psychiatric diagnosis.

In a study involving 358 adult subjects, a team led by researchers from the University of Chicago found that toxoplasmosis, a relatively harmless parasitic infection carried by an estimated 30 percent of all humans, is associated with intermittent explosive disorder and increased aggression.

The findings are published in the Journal of Clinical Psychiatry on March 23, 2016.

“Our work suggests that latent infection with the toxoplasma gondiiparasite may change brain chemistry in a fashion that increases the risk of aggressive behavior,” said senior study author Emil Coccaro, MD, Ellen. C. Manning Professor and Chair of Psychiatry and Behavioral Neuroscience at the University of Chicago.

“However, we do not know if this relationship is causal, and not everyone that tests positive for toxoplasmosis will have aggression issues,” Coccaro said, adding that additional studies are needed.

Intermittent explosive disorder (IED) is defined by the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, as recurrent, impulsive, problematic outbursts of verbal or physical aggression that are disproportionate to the situations that trigger them. IED is thought to affect as many as 16 million Americans, more than bipolar disorder and schizophrenia combined.

As part of their pioneering research to improve diagnosis and treatment for IED and impulsive aggression, Coccaro and his colleagues examined possible connections to toxoplasmosis, an extremely common parasitic infection. Transmitted through the feces of infected cats, undercooked meat or contaminated water, toxoplasmosis is typically latent and harmless for healthy adults. However, it is known to reside in brain tissue, and has been linked to several psychiatric diseases, including schizophrenia, bipolar disorder and suicidal behavior.

The research team recruited 358 adult subjects from the U.S., who were evaluated for IED, personality disorder, depression and other psychiatric disorders. Study participants were also scored on traits including anger, aggression and impulsivity. Participants fell into one of three groups. Roughly one third had IED. One third were healthy controls with no psychiatric history. The remaining third were individuals diagnosed with some psychiatric disorder, but not IED. This last group served as a control to distinguish IED from possible confounding psychiatric factors.

Hold your cats

The research team found that IED-diagnosed group was more than twice as likely to test positive for toxoplasmosis exposure (22 percent) as measured by a blood test, compared to the healthy control group (9 percent).

Around 16 percent of the psychiatric control group tested positive for toxoplasmosis, but had similar aggression and impulsivity scores to the healthy control group. IED-diagnosed subjects scored much higher on both measures than either control group.

Across all study subjects, toxoplasmosis-positive individuals scored significantly higher on scores of anger and aggression. The team noted a link between toxoplasmosis and increased impulsivity, but when adjusted for aggression scores, this link became non-significant. This finding suggests toxoplasmosis and aggression are most strongly correlated.

However, the authors caution that the study results do not address whether toxoplasmosis infection may cause increased aggression or IED.

“Correlation is not causation, and this is definitely not a sign that people should get rid of their cats,” said study co-author Royce Lee, MD, Associate Professor of Psychiatry and Behavioral Neuroscience at the University of Chicago. “We don’t yet understand the mechanisms involved–it could be an increased inflammatory response, direct brain modulation by the parasite, or even reverse causation where aggressive individuals tend to have more cats or eat more undercooked meat. Our study signals the need for more research and more evidence in humans.”

Coccaro and his team are now further examining the relationship between toxoplasmosis, aggression and IED. If better understood, this connection may inform new strategies to diagnose or treat IED in the future.

“It will take experimental studies to see if treating a latent toxoplasmosis infection with medication reduces aggressiveness,” Coccaro said. “If we can learn more, it could provide rational to treat IED in toxoplasmosis-positive patients by first treating the latent infection.”

People with rage disorder twice as likely to have latent toxoplasmosis parasite infection

Adjunctive Use of a Standardized Extract of Withania somnifera (Ashwagandha) to Treat Symptom Exacerbation in Schizophrenia

22% of subjects with IED tested positive for the parasite

In the current study, the authors evaluated 358 adult Americans for IED, personality disorderdepression and other psychiatric disorders and gave them scores for traits such as anger, aggression and impulsivity. They also screened for toxoplasmosis using blood tests.

Fast facts about toxoplasmosis

  • Around 60 million Americans are thought to have toxoplasmosis
  • If a woman catches it just before or during pregnancy, it can be dangerous for the baby
  • For those with a weakened immune system, there are medications to treat it.

They then classified the participants into three groups: approximately one third had IED, one third were healthy controls with no psychiatric history, and one third had received a diagnosis for a psychiatric disorder but not IED.

The purpose of the last group was to enable the team to distinguish IED from other psychiatric factors.

Findings showed that 22% of those with IED tested positive for toxoplasmosis exposure, compared with 9% of the healthy control group and 16% of the psychiatric control group.

The psychiatric group and the healthy group had similar scores for aggression and impulsivity, but the group with IED scored far higher on both counts than either of the other two groups.

An association emerged between toxoplasmosis and impulsivity. However, when the team adjusted for aggression scores, this association became non-significant, indicating a strong correlation between toxoplasmosis and aggression.

The authors point out that the findings do not mean that toxoplasmosis causes IED, or that people with cats are more likely to have the condition. It simply reveals a relationship.

T. gondii infection ‘may double schizophrenia risk’

For one study, Dr. Robert H. Yolken, of the Stanley Laboratory of Developmental Neurovirology at Johns Hopkins University School of Medicine in Baltimore, MD, and colleagues assessed the results of two previous studies.

These studies had identified a link between cat ownership in childhood and development of later-life schizophrenia and other mental disorders, comparing them with the results of a 1982 National Alliance for the Mentally Ill (NAMI) questionnaire.

The NAMI questionnaire – conducted around a decade before any data was published on cat ownership and mental illness – revealed that around 50% of individuals who had a cat as a family pet during childhood were diagnosed with schizophrenia or other mental illnesses later in life, compared with 42% who did not have a cat during childhood.

The questionnaire, the researchers say, produced similar results to those of the two previous studies, suggesting that “cat ownership in childhood is significantly more common in families in which the child later becomes seriously mentally ill.”

“If true,” the authors add, “an explanatory mechanism may be T. gondii. We urge our colleagues to try and replicate these findings to clarify whether childhood cat ownership is truly a risk factor for later schizophrenia.”

In another study, A. L. Sutterland, of the Academic Medical Centre in Amsterdam, the Netherlands, and colleagues conducted a meta-analysis of more than 50 studies that established a link between T. gondii and increased risk of schizophrenia.

They found that people infected with T. gondii are at more than double the risk of developing schizophrenia than those not infected with the parasite.

The team also identified a link between T. gondii infection and greater risk of bipolar disorderobsessive-compulsive disorder (OCD) and addiction.

“These findings suggest that T. gondii infection is associated with several psychiatric disorders and that in schizophrenia, reactivation of latent T. gondii infection may occur,” note the authors.

The CDC recommend changing a cat’s litter box every day to reduce the risk of T. gondii infection, noting that the parasite does not become infectious until 1-5 days after it has been shed in the animal’s feces.

They also recommend feeding cats only canned or dried commercial foods or well-cooked meats; feeding them raw or undercooked meats can increase the presence of T. gondii in a cat’s feces.

It is important to note that cat feces are not the only source of T. gondii infection. Humans can contract the parasite through consuming undercooked or contaminated meats and by drinking contaminated water.

How a cat parasite can change your personality

A new study suggests that infection with the cat-borne parasite Toxoplasma gondii could make people more risk-prone and likely to start their own business.
cute kitten

Your cute cat may host a parasite that could influence your behavior in surprising ways.

As humans who still inherit Enlightenment’s worship of rationality, we like to think that our decisions are autonomous and driven by reason alone.

However, science seems to contradict this popular belief. More and more research is showing that microorganisms such as bacteria and viruses influence our behavior and emotional states.

For instance, the bacteria in our guts may be responsible for states of anxiety and depression. Conversely, other studies have shown that some probiotic bacteria may relieve the effects of stress.

Now, a new study suggests that infection with the cat-borne parasite Toxoplasma gondii could make people change their behavior so that they become more prone to business and entrepreneurial ventures.

Stefanie K. Johnson, an associate professor at the University of Colorado (CU) Boulder’s Leeds School of Business, co-led the research in collaboration with Pieter Johnson, a professor in CU Boulder’s Department of Ecology and Evolutionary Biology.

The findings were published in the journal Proceedings of the Royal Society B.

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Multiple Chemical Sensitivity

Add multiple chemical sensitivity to the long list of chronic diseases that have been written off as psychosomatic for far too long. Chronic diseases are inherently complex and confusing for patients and doctors alike.

Fortunately, we live in a time where awareness for ‘invisible illnesses’ are on the rise. Hopefully, we can continue to spread awareness and get quality information into the hands of those that need it.

Today, I want to talk about multiple chemical sensitivity and dive deep into the science behind it.

 

What is Multiple Chemical Sensitivity?

Multiple chemical sensitivity is a condition that is activated by specific classes of chemicals which act along different pathways in the body and cause an increase in N-methyl-D-aspartate (NMDA) activity. NMDA receptors are critical in neuroplasticity, which affects your memory and brain function. NMDA is an amino acid that mimics glutamate, which is the neurotransmitter that normally binds to NMDA receptors.

Another way of saying this is: instead of glutamate acting on the NMDA receptors (which helps with normal brain function), multiple chemical sensitivity causes a higher level of NMDA to replace the glutamate, which can cause brain dysfunction.

These reactions in the body are lowered by NMDA antagonists, which suggests that it’s our body’s way of dealing with these toxic chemicals. But when that’s not enough and the body can’t properly detox, it can initiate multiple chemical sensitivity.

Genetically, there are certain genes that have been associated with the metabolism of these chemicals, and they can indicate whether or not a person will be susceptible to developing multiple chemical sensitivity.

 

Symptoms of Multiple Chemical Sensitivity

When the NO/ONOO (nitric oxide and peroxynitrite) cycle is thrown off due to the elevated NMDA activity, it can cause:

  • Energy metabolism dysfunction
  • Blood-brain barrier breakdown
  • Increased chemical sensitivity
  • Increased TRVP1 activity
  • Increased NMDA activity
  • Oxidative stress
  • Increased nitric oxide
  • Increased peroxynitrite
  • Increase inflammatory cytokines
  • Increased levels of intracellular calcium
  • Neurogenic inflammation
  • Airway sensitivity

These can cause a wide variety of symptoms in individuals and may include:

  • Headaches
  • Extreme
  • Nausea
  • Dizziness
  • Chest
  • Heart palpitations
  • Muscle pain
  • Brain fog
  • Constipation
  • Diarrhea
  • Memory problems
  • Mood changes
  • Congestion
  • Sneezing
  • Sore throat
  • Chest pain
  • Rashes
  • Breathing problems

 

What Types of Chemicals Trigger Multiple Chemical Sensitivity?

Because we are surrounded by tens of thousands of chemicals each day, it’s difficult to identify exactly where the chemicals that trigger multiple chemical sensitivity come from. The sheer number of chemicals combined with everybody’s unique body chemistry create an infinite number of combinations and potential reactions.

For a long time, researchers even argued that the diversity of chemicals made it unlikely that there would be a common response. So, defining multiple chemical sensitivity has been challenging.

That being said there are number of chemicals and toxins that have been identified in multiple chemical sensitivity, including:

  • Organic solvents
  • Organophosphorus pesticide (like glyphosate)
  • Carbamate pesticides
  • Organochlorine pesticides
  • Pyrethroid Pesticides
  • Mercury
  • Hydrogen sulfide
  • Carbon monoxide

You might look at this list and think, “what the heck are these?”

Unfortunately, most of these are pesticides and herbicides that end up in our food and water. These chemicals produce common toxic responses in the body and cause an elevation of NMDA activity, which result in perplexing symptoms.

Finally, there are lawsuits being waged against Monsanto for it’s misleading claims about glyphosate, hopefully something will come of it. I recently wrote about this and glyphosate, you can read that here:  We Can No Longer Ignore Glyphosate.

 

Diagnosing and Treating Multiple Chemical Sensitivity

Similar to other chronic diseases, multiple chemical sensitivity causes widespread systemic responses that vary from person to person – therefore it’s not an obvious diagnosis.

There are 5 principles of multiple chemical sensitivity that set it apart from other chronic toxin related illnesses.

  1. Short-term stressors trigger multi-system responses by raising nitric oxide and other cycles.
  2. This trigger is converted into a chronic illness through long-term elevation of peroxynitrite and other cycle elements.
  3. Symptoms and signs of these illnesses include other mechanisms. Such as elevated levels of peroxynitrite, inflammatory cytokines, oxidative stress, elevated NMDA, TRPV1 receptor activity, ATP depletion, and BH4 depletion.
  4. The influence of these mechanisms occur on a local level via individual cells and biological tissues.
  5.  Therapy should focus on down-regulating NO/ONOO (nitric oxide and peroxynitrite) cycle biochemistry.

 

When MCS is Mistaken for CFS/ME and Fibromyalgia

Multiple chemical sensitivity differs from chronic fatigue syndrome/myalgic encephalomyelitis and fibromyalgia because it’s specifically triggered by the chemicals listed above. Though multiple chemical sensitivity might be mistaken for these conditions. Especially since they are also associated with increased nitric acid level oxide levels. The important distinction here is the mechanism that causes increased nitric acid level oxide levels in multiple chemical sensitivity is the increased NMDA activity.

So, if you’ve ever received a chronic fatigue syndrome/myalgic encephalomyelitis or fibromyalgia diagnosis, it’s important that you make sure your doctor is aware of the growing research on multiple chemical sensitivity. These conditions are often mistaken for one another.

 

Work to Reduce Your Toxic Burden

I realize this is one of my more technical articles, but I wanted to include as much information as possible since there is a general lack of quality articles on multiple chemical sensitivity available online.

If you suspect you have multiple chemical sensitivity, remember you are your best advocate. It is possible that your doctor is not aware of this condition because it is a very complex illness involving multiple systems in the body. Researchers are still working to define its parameters and diagnostic procedures.

Just like so many other chronic illnesses, when it comes to multiple chemical sensitivity the name of the game is to reduce your overall toxic burden.

I have written extensively on reducing toxic burden and you can find my blog on this here as well as my free guide on how to reduce your daily toxin exposure here.

 

Resources:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181613/  NMDA receptor function, memory, and brain aging

https://www.ncbi.nlm.nih.gov/pubmed/15256524 Case-control study of genotypes in multiple chemical sensitivity CYP2D6, NAT1, NAT2, PON 1, MTHFR

http://emerge.org.au/wp-content/uploads/2015/02/Pall-M.-L.-2009.-Multiple-chemical-sensitivity-toxicological-questions-and-mechanisms-John-Wiley-Sons-Ltd.pdf

Toxic Burden

I believe environmental toxicity is one of the biggest contributors to the rise in chronic illness today. And yet, because doctors don’t really learn about chronic toxic burden in medical school,  it’s now become somewhat of an elephant in the room.

The fact of the matter is when it comes to toxicity we mostly understand when it’s acute – when it causes sudden and definitive symptoms. However, most toxin exposures are chronic, involve more than one toxin, and happen after years, even decades of accumulation. This accumulation overloads the body’s detox mechanisms and causes symptoms such as:

  • Fatigue
  • Memory disturbance
  • Sleep issues
  • Headaches

Over time, if the environmental toxicity and detox pathways aren’t addressed, the toxic burden can lead to conditions like:

  • Cancer
  • Autoimmune disease
  • Neurodegenerative diseases

In a 2015 review in the prestigious journal Carcinogenesis, researchers found that lifestyle factors are responsible for a considerable portion of cancers worldwide. Concluding that 7-19% of all cancers are attributable to toxic environmental exposures. On top of this, they examined 85 chemicals and found 59% of them exerted low-dose effects.

In my personal practice, I’ve seen the devastating effects of environmental toxin exposure.  Because the symptoms are chronic and multisystem it can lead to a perplexing situation for both the patient and the practitioner. I found the best method for helping a patient with a chronic condition is to reduce their levels of toxin exposure and improve detoxification to bring down their toxic burden.

So today I want to talk about different types of toxins, other factors that add to your burden, symptoms and conditions of suspected environmental toxicity, and detoxification.

 

17 Possible Environmental Toxins

Toxins can either be introduced to the body through external exposure or internal exposure.  I break different exposures down into exotoxins (external) and endotoxins (internal). A huge part of reducing your toxic burden is being aware of different sources of toxins so that you can avoid potential exposures. With that in mind the list below is meant to be a resource for different areas of your life that should be considered when you work to reduce your toxic burden.

Exotoxins:

  1. Heavy metals – Can come from cookware, tap water, personal care products, and home furnishings.
  2. Solvents/VOCs – Can come from cleaning products or off gas from new furniture or carpet. Oftentimes are indoor air is more toxic than the air outside.
  3. Pesticides – As an exotoxin, pesticides affect people when they work with them either at their job or in their personal garden or lawn.
  4. BPA – BPA is an endocrine disruptor and also found in plastics.
  5. Phthalates – Can be found in personal care products, home cleaning products, and makeup.
  6. Parabens – Also found in personal care products, home cleaning products, and makeup.
  7. EMF radiation – This comes from electronics and Wi-Fi sources, so cell phones, smart TVs, microwaves, fitness trackers, routers, cell phone towers, and airplanes.
  8. Heterocyclic amines – These are chemicals that are released from animal products when they are cooked at high temperatures.
  9. Mold – Look Below

 

Endotoxins:

  1. Intestinal bacteria – Such as endotoxemia from LPS.
  2. Yeast/candida – Candida produce the toxin acetaldehyde.
  3. Other infectious diseases – Common ones include Epstein-Barr and Lyme disease.
  4. Food – Standard American Diet contributes to total toxic burden. Chemicals, food additives, and glyphosate all cause problems. When it comes to food your best bet is to eat as organic as possible.
  5. Insulin resistance – When insulin resistance climbs in your body it causes stress. Work to promote insulin sensitivity instead.
  6. Medications – Medications generally contribute to overall toxic burden.
  7. Stress – Stress is an extremely powerful influence in your overall health and yet it’s often not taken into consideration.
  8. Emotions – Emotions cause biochemical reactions in the body and are often overlooked.

 

What Else Can Add to Your Total Toxic Burden?

Besides toxins there are other things that can contribute to your total toxic burden that you might not have considered. This is because your total toxic burden includes all stressors on the body, which means things like emotional and psychological stress.

I mentioned stress and emotions above but it’s worth taking the time to dig a little deeper on each because they are all too commonly overlooked. They don’t fit our traditional idea of a toxin. A few potential stressors that are outright “toxins” include:

  • Age
  • Sex
  • Financial stress
  • Sedentary lifestyle
  • Career stress
  • Toxic personal relationships
  • Significant life events, such as a death in the family or divorce
  • Unresolved emotional trauma

 

25 Symptoms of Environmental Toxicity

Over the years I’ve noticed there are some symptoms that are more commonly seen in patients with environmental toxicity. If someone comes into my office with a few of any of the following symptoms I immediately start checking for sources of toxins and for ways to reduce their overall toxic burden.

Here are 25 symptoms of environmental toxicity:

  1. Fatigue
  2. Muscle aches
  3. Joint pain
  4. Sinus congestion
  5. Postnasal drip
  6. Headaches
  7. Gas/Bloating
  8. Constipation
  9. Diarrhea
  10. Foul-smelling stools
  11. Heartburn
  12. Insomnia
  13. Difficulty concentrating
  14. Food cravings
  15. Water retention
  16. Trouble losing weight
  17. Rashes
  18. Skin problems
  19. Eczema
  20. Psoriasis
  21. Acne
  22. Canker sores
  23. Dark circles under the eyes
  24. Premenstrual syndrome
  25. Bad breath

In addition to these symptoms there are a few conditions that are major red flags to me. These include:

  • Immune system dysfunction
  • Chronic infection
  • Autoimmune diseases
  • Endocrine disorders
  • Multiple chemical sensitivity
  • Infertility
  • Adverse reactions to medications
  • Allergies and asthma
  • Obvious industrial or agricultural exposure
  • Poor caffeine tolerance

 

5 Methods of Detoxification Support

Here’s the deal, we all need detoxification support. This is because we live in a time when we are constantly bombarded with toxins unlike any other point in human history. Tens of thousands of chemicals are introduced via our products each day and there’s very little oversight. Basically, we’re all human guinea pigs and we need to take steps to reduce our routes of exposure and support our detoxification organs.

  • Glutathione – A master antioxidant which can be taken orally or intravenously. Glutathione reduces oxidative stress, is an intracellular antioxidant, and helps with detoxification of environmental toxins.
  • Reducing medication use – Genexa Health has come up with a line of natural products for various ailments. I recommend most of my patients do what they can to address the root causes of their conditions so they can limit the amount of medications they’re on. Genexa Health is a great way to get people off of over-the-counter medications such as Advil, which only contribute to leaky gut and inflammation.
  • Make sure you’re going to the bathroom regularly – To properly eliminate toxins in the body you need to be sure you are not constipated. Consider using an Elimination Diet to find any food sensitivities.
  • Use detox binders – I recommend using detox binders like activated charcoal and GI detox. These bind to toxins and help your body eliminate them more readily.
  • Take detox supporting nutrients:
    • Chlorophyll
    • Green Tea
    • Quercetin
    • Active B complex
    • Milk Thistle
    • Calcium D-glucarate
    • Curcumin
    • Probiotics 50 billion CFUs

I’ve put together a thorough guideline with more detail to help you through the process of reducing your toxin exposure. You can find that here: Reduce Your Daily Toxin Exposure.

 

Resources:

https://www.ncbi.nlm.nih.gov/pubmed/26106142 Overview of air pollution and endocrine disorders  |  Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment

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detox binders

You might be wondering, why would you want to detox in the first place?

Our bodies are exposed to more chemicals now than ever before. Every day new chemicals are added to our personal environments via food, pollution, plastics, furniture, food containers, cookware, carpets, electronics, personal care products, and more.

Some of these chemicals are newly created and their effects on the human body are entirely unknown. Others are only a few decades or even a couple of years old and we are still learning about their impacts.

Possibly the most concerning factor behind all these chemicals is that there are few to no barriers in the process which allows chemicals to be used in everyday items. Meaning your body is slowly taking in small amounts of new chemicals and toxic buildup over time.

It’s a war of attrition.

This constant chemical bombardment your body is fighting each day just to keep you healthy is why you should be interested in detox.

I’m not talking about a harsh detox that can sometimes put the body under more pressure and stress than necessary. Juice cleanses and powerful liver detoxes can backfire because they deprive your body of nutrients or place overwhelming stress on detox pathways.

We need to reduce our toxic burden wherever possible, support our body’s natural detox pathways, and incorporate detox binders into our health routine.

I want to focus on this last strategy – using binders for detox – because I’ve seen binders work well in my personal practice and I want to share them with you. Binders work by:

 

Detoxing to support your health

There are some toxins we should be worried about more than others. Some of the worst offenders are mold toxins, heavy metals, and bisphenol-A (BPA). When it comes to ridding our bodies of these chemicals, I’ve found there are two binders work particularly well:

GI Detox and Upgraded Coconut Charcoal are two effective binders that help you with daily detox from mold, heavy metals, and other toxins. They are also strong enough to use in more targeted therapies such as mold exposure treatments.

 

GI Detox

GI Detox is made from two binders – it consists of 75 percent Pyrophyllite clay and 25 percent activated charcoal.

Pyrophyllite clay a very rare clay that has been used medicinally for thousands of years. It’s richer in silica and quartz than other clays (such as bentonite) and works through both adsorbing (to bind to) and absorbing (to ‘swallow’ up) chemicals.

Phyrophyllite clay is negatively charged and binds readily to endotoxins from Gram negative bacteria, by-products of yeast and bacteria, and heavy metals. This process assists in restoring gut microbial balance and is recommended as an effective detox strategy that is also gentle enough to use daily.

Activated charcoal is one of the most effective binders known to man. Considered more effective than stomach pumping in poisoned patients, charcoal effectively rids the body of unwanted toxins. This is why I recommend using is on its own as well as in the GI Detox.

For normal use, I recommend taking one to two capsule of GI Detox once a day on an empty stomach – an hour before eating or two hours after.

 

Upgraded Coconut Charcoal

Activated charcoal works by binding to toxins through adsorption. Adsorption is different from absorption because the chemicals are trapped in the little holes of this porous substance rather than being soaked up. The charcoal isn’t absorbable by your body so it passes through the GI tract while taking unwanted toxins with it.

You can order Upgraded Coconut Charcoal here. For normal use, take Upgraded Coconut Charcoal with other binders on an empty stomach. You can also take your activated charcoal with food you know to be low quality.

 

Using Binders for Mold Detox

You can use both GI Detox and Upgraded Coconut Charcoal to fight daily toxins or in a mold treatment protocol. The toxins produced by toxic mold are called mycotoxins and ridding your body of these takes a comprehensive plan that lasts between six months to a year.

GI Detox – Take one to two capsules twice daily with Upgraded Coconut Charcoal.

Upgraded Coconut Charcoal – Take 1000 to 1500 mg (2-3 capsules) twice daily with water, GI Detox, and on an empty stomach.

For more specifics on mold detox protocol, you can read a Mold Exposure Treatment Guide.  Your_Complete_Mold_Exposure_Guide and SURVIVING MOLD LINK

 and Do binders interfere with nutrient absorption?

Because of the effectiveness of binders in their absorption and adsorption of chemicals, it’s a completely logical concern to think they would also bind with beneficial nutrients. In general, we need more research on this subject but preliminary animal studies have found that adding charcoal to sheep’s diets did not decrease their nutrient levels. Also, toxins are predominantly positively charged, which is how the negatively charged binders are readily attracted to them.

You can reduce the chance your binders will work on the wrong particles through taking them on an empty stomach. All binders should be taken at the same time and either one hour before or two hours after medications and supplements.

 

Other Detox Strategies Worth Considering

We live in a time where we are exposed to more chemicals than ever before. Learning about detox strategies is now as important as learning to eat a healthy and balanced diet. Other detox strategies worth learning more about include:

  1. Infrared saunas ( See Below)
  2. Exercise
  3. Glutathione – Love this brand…. Bulletproof Liposomal Gluathione Force
  4. Calcium D-Glucarate

Each of these can be used on their own or together for a compounding effect. Also, each of these are included in  A Mold Exposure Treatment Guide. Your_Complete_Mold_Exposure_Guide

 

Add Detox to Your Daily Routine

Toxins are a part of our daily lives. Fortunately, there steps you can take to reduce their overall impact on your health. I recommend incorporating GI Detox and activated charcoal into your daily health routine.

If you’re healthy, take both the GI Detox and Upgraded Coconut Charcoal to deal with daily toxins.

If you’ve been exposed to mold, you can take GI Detox and Upgraded Coconut Charcoal to help with a comprehensive Mold Exposure Treatment. Remember, these two binders are only part of a mold treatment protocol.

I recommend adding detox strategies to your daily routine to combat the unprecedented number of chemicals that bombard us each day.

 

Resources:

http://www.cnn.com/2016/07/01/health/everyday-chemicals-we-need-to-reduce-exposure-to/index.html

https://www.ncbi.nlm.nih.gov/pubmed/3521259

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1676641/pdf/bmj00002-0006.pdf

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1306980/

https://www.ncbi.nlm.nih.gov/pubmed/6499964

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Infrared Saunas

The term sauna is typically used to refer to a Finnish sauna, which is a deeply ingrained part of the culture in Finland. In the United States very few people use saunas, though they are making somewhat of a stir in the health and wellness community due to their benefits. Infrared saunas have numerous health benefits including helping your body rid itself of toxins, reduce inflammation, and increase blood flow.

Plus, infrared saunas feel pretty amazing.

 

Infrared saunas versus saunas – what’s the difference?

In all saunas your body temperature is raised which induces sweating. With traditional wet or dry saunas the air is heated and you warm from the outside in. Infrared saunas cause your body temperature to rise, but the surrounding air remains the same – your body temperature rises from the inside out.

Two major benefits of infrared saunas are their cost and portability – they can be used in most homes and there are even some that pack down very small for easy storage. Infrared saunas also allow people to withstand the heating effects longer than a traditional sauna would and are therefore a good option for people sensitive to excess heat.

Infrared heat penetrates the body more deeply than heated air, which results in a more vigorous sweating at a lower temperature. The way your body sweats in infrared saunas compared to traditional saunas is believed to be more effective for delivering benefits to your body.

 

7 Benefits of Infrared Saunas

1. Flushes toxins

If you do a quick Google search you’ll find a lot of people knocking the ability of saunas to flush toxins, but we’ve known for a long time that sweating helps the body rid itself of toxins.

Studies have found that increased sweating, as experienced in a sauna, can help you excrete toxic metals like arsenic, cadmium, lead, and mercury. One study found “that body stores of trace metals may be depleted during prolonged exposure to heat.”

Another study found that “induced sweating in saunas can mobilize BPA in adipose tissue thus leading to enhanced excretion in sweat.” The science is there – sweating helps you eliminate toxins and infrared saunas can help you sweat at a much faster rate.

2. Fights dementia & Alzheimer’s disease

Saunas have been shown to improve vascular function, blood pressure, reduce inflammation, and boost cognition. One study found that Finnish men who frequently used saunas had a significant reduction in dementia and Alzheimer’s risk. With Alzheimer’s now clocking in as the third most common cause of death in the United States, any technique that can help resist the impacts of dementia onset adds hope.

3. Burns calories

The calorie burning effect of infrared saunas is one of the most sought after benefits. Infrared saunas are able to increase your body’s core temperature in a manner similar to working out. You can burn between 400 to 600 calories in a 30-minute session, which has led to the use of infrared saunas in weight loss programs.

4. Speeds up recovery

Studies have found that infrared saunas help your neuromuscular system recover faster. Athletes have found they are able to recover from endurance training more quickly while enjoying the pleasurable effects of an infrared sauna.

In most infrared sauna studies, researchers comment on the enjoyable and relaxing effects which are experienced on top of the healing outcomes.

5. Improves athletic performance

On top of the added recovery benefits infrared saunas can help improve overall athletic performance. Athletes who used saunas post-workout saw an improvement in plasma, red blood cell volumes, and an improvement in overall performance.

One study found that post-exercise sauna use produced a “worthwhile enhancement of endurance running performance” and researchers suggested it was due to an overall increase in blood volume.

6. Improves cardiovascular function

Using a sauna is often compared to working out because of the raised body temperature, sweating, released endorphins, and other similarities. Studies on the effects of infrared saunas on cardiovascular health typically find similar benefits.

One study that examined heart health and sauna use found that saunas reduce the risk of sudden cardiac death, coronary heart disease, fatal cardiovascular disease, and all-cause mortality.

7. Pain reduction

This is one of my favorite benefits of the infrared sauna.

Though it may sound counterintuitive, infrared saunas appear to help with inflammation and pain. Numerous studies have found that infrared saunas reduce pain caused by inflammation.

One study found infrared saunas reduced the pain experienced by fibromyalgia patients by half. Another study examining the impacts of infrared saunas on cardiovascular health found they were effective in reducing chronic pain. Infrared saunas have shown to be an effective treatment for those suffering from chronic lower back pain.

With the opioid crisis claiming more and more lives, it’s important that we explore all non-pharmaceutical pain relief options seriously. Though infrared saunas may require a steep initial investment, if used regularly they could quickly become a very worthwhile purchase. This is especially true for those suffering with chronic pain because infrared saunas are a potential pain solution that prevents the need for addictive substances such as opioids.

 

Why quality matters with infrared saunas

Infrared saunas are generally seen as a more convenient option for consumers. They are typically cheaper and easier to move than their wet and dry Finnish counterparts. You can even find one on Amazon for around $200, but I have concerns surrounding these cheaper models.

Electromagnetic fields are often radiated directly from electrical infrared saunas and can literally bathe you in harmful electromagnetic radiation. This is why I recommend High Tech Health International’s infrared saunas. They’ve addressed the EMF concern and more.

Next week, we will be digging deeper into the concerns behind EMF and why you should consider unplugging your Wi-Fi at night.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Thinking of getting your own sauna?!  

Here are two brands I highly recommend:

1. TR2 Infrared Detox Sauna from High Tech Health in Boulder, CO

  • Lowest total EMF from our in-house designed, patent-pending heaters
  • Healthy materials, very low-toxicity

2.  Sunlighten M-Pulse 3 in 1 Sauna –

  • Full-spectrum IR technology
  • Customizable heaters
  • Preset health programs
  • LCD touch-screen control panel
  • Five mPulse Infrared Sauna Models Available

 

Resources:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2718593/

https://www.hindawi.com/journals/jeph/2012/184745/

https://pdfs.semanticscholar.org/6b45/e199b8720aa23b09d1537e6bd7d8469a601d.pdf

https://www.hindawi.com/journals/jeph/2012/185731/

https://www.ncbi.nlm.nih.gov/pubmed/27932366

https://jamanetwork.com/journals/jama/article-abstract/360118

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4493260/

https://www.ncbi.nlm.nih.gov/pubmed/25705824

https://www.ncbi.nlm.nih.gov/pubmed/16877041

https://www.jstage.jst.go.jp/article/internalmedicine/47/16/47_16_1473/_pdf

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2718593/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2539004/

https://www.jstage.jst.go.jp/article/internalmedicine/47/16/47_16_1473/_pdf

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2539004/

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Is Toxic Mold Exposure the Cause of Your Symptoms?

Is Toxic Mold Exposure the Cause of Your Symptoms?

Are you one of the many people unknowingly living or working in water damaged building?  Did you know it may be dramatically affecting your health?  It’s estimated that indoor air pollutants, including mold and mycotoxins may be contributing to more than 50% of our patient’s illnesses.  Typically we think of smog, smoke, and outdoor pollution as detrimental to our health but indoor air quality may be an even bigger risk to your health.  Many patients are unaware that a toxic home or workplace is contributing to their symptoms.

Exposure to water-damaged indoor environments is associated with exposure to molds.  The most common types of mold that are found indoors include CladosporiumPenicilliumAlternaria, and AspergillusStachybotrys chartarum (sometimes referred to as “toxic black mold”) is a greenish-black mold, which grows on household surfaces that have high cellulose content, such as wood, fiberboard, gypsum board, paper, dust, and lint and is usually an indicator that there has been elevated moisture present or previous water damage.

Some molds secrete mycotoxins, that can be measured in the urine, such as ochratoxin, aflatoxin, and trichothecenes.  Exposure to mold and mold components is well known to trigger inflammation, allergies and asthma, oxidative stress, and immune dysfunction in both human and animal studies.  Mold spores, fungal fragments, and mycotoxins can be measured in the indoor environments of moldy buildings and in humans who are exposed to these environments.  Most of the time, we are exposed to molds, like stachybotrys, through the skin contact, through ingestion, and by inhalation.  Most common are reports of exposure involve water-damaged homes, schools, office buildings, court houses, hospitals, and hotels.  It’s estimated that as many as 25% of buildings in the US have had some sort of water damage.  Molds have the ability to produce various symptoms, such as skin rashes, respiratory distress, various types of inflammation,  cognitive issues, neurological symptoms, and immune suppression. The most common symptoms associated with mold exposure are allergic rhinitis and new onset asthma.

How do you know if you’ve been exposed to mold or a water damaged building?

Top Symptoms Associated with Mold-Associated Illness:

  1. Fatigue and weakness
  2. Headache, light sensitivity
  3. Poor memory, difficult word finding
  4. Difficulty concentration
  5. Morning stiffness, joint pain
  6. Unusual skin sensations, tingling and numbness
  7. Shortness of breath, sinus congestion or chronic cough
  8. Appetite swings, body temperature regulation,
  9. Increased urinary frequency or increased thirst
  10. Red eyes, blurred vision, sweats, mood swings, sharp pains
  11. Abdominal pain, diarrhea, bloating
  12. Tearing, disorientation, metallic taste in mouth
  13. Static shocks
  14. Vertigo, feeling lightheaded

Checklist that might indicate mold exposure or mold sensitivity (from ECH website)

  • Do musty odors bother you?
  • Have you worked or lived in a building where the air vents or ceiling tiles were discolored?
  • Have you noticed water damage or discoloration elsewhere?
  • Has your home been flooded?
  • Have you had leaks in the roof?
  • Do you experience unusual shortness of breath?
  • Do you experience recurring sinus infections?
  • Do you experience recurring respiratory infections and coughing?
  • Do you have frequent flu-like symptoms?
  • Do your symptoms worsen on rainy days?
  • Do you have frequent headaches?
  • Are you fatigued and have a skin rash?

How do I Treat Mold/mycotoxin Exposure?

  1. Remove yourself from the contaminated environment first. (don’t even think about going on to other treatments until you get out of the contaminated environment)
  2. Avoid exposure to porous items (paper, clothing, etc) from the moldy environment.
  3. Use clay, charcoal, cholestyramine or other binders to bind internal mycotoxins
    1. The Shoemaker protocol has proven effectiveness for cholestyramine powder or prescription Welchol as off-label bile sequestering agents to decrease total toxic load of mold and other toxins from water damaged buildings.
    2. I also recommend Upgraded Coconut Charcoal or GI Detox to bind toxins in the gastrointestinal tract and Glutathione Force to support glutathione, which is often depleted in toxin-related illness.
  4. While you are using binders, you must maintain normal bowel function and avoid constipation.  You can add magnesium citrate, buffered C powder, or even gentle laxatives if needed but constipation is the enemy of detoxification!
  5. Treat colonizing molds/fungal or bacterial infections in the body
    • Common locations of colonization include sinuses, gut, bladder, vagina, lungs
    • Test and treat for candida overgrowth – living in an environment with mold leads to immune dysregulation that allows candida to overgrow in the body in some immunocompromised patients
  6. Enhance detoxification support
    • Some common supplements used to aid detox are liposomal glutathione, milk thistle, n-acetylcysteine, alpha lipoid acid, glycine, glutamine, and taurine.  Methylation support is also key and involves optimal levels of methylcobalamin (B12), methyl-folate, B6, riboflavin, and minerals
  7. Invest in a high quality air filter and home and at work, like Austin Air Healthmate Plus
  8. Avoid common mycotoxin containing foods:
    • Corn, wheat, barley, rye, peanuts, sorghum, cottonseed, some cheeses, and alcoholic beverages such as wine and beer.  Others include oats, rice, tree nuts pistachios, brazil nuts, chiles, oil seeds, spices, black pepper, dried fruits, figs, coffee, cocoa, beans, bread.

Other Treatment Options

  • Follow A Low Mold Diet – many patients to well on a paleo, grain-free diet since grains are often contaminated with mycotoxins and molds
  • The Low Mold Diet

    THE LOW MOLD DIET

    The Low Mold Diet. Use this guide to shift your diet away from high sugar and starchy foods to more fresh, whole foods.  If you suspect you’ve been exposed to mold or mycotoxins,  read on below.

    Foods that must be avoided

    Avoid sugar  and sugar containing foods: Table sugar and all other simple, fast releasing sugars such as fructose, lactose, maltose, glucose, mannitol and sorbitol.  This includes honey and natural sugar syrup type products such as maple syrup and molasses. This also includes all candies, sweets, cakes, cookies, and baked goods.

    Sweetleaf whole leaf stevia concentrate may be used in moderation

    High sugar fruits:

    • Avoid pineapple, mango, banana, melons, oranges, and grapes
    • Organic berries, apples and lemon/lime are ok

    Packaged and processed foods:

    • Avoid canned, bottled, boxed and otherwise processed and pre-packaged foods as they more often than not contain sugar of one type or another.
    • Canned – Baked beans, soups, ready-made sauces.
    • Bottled – Soft drinks, fruit juices, all condiments and sauces.
    • Boxed/Packaged – Ready-made meals, breakfast cereals, chocolate/candy, ice cream, frozen foods.

    Mold and yeast containing foods:

    • Cheeses: all cheese, especially moldy cheeses like stilton are the worst, buttermilk, sour cream               and sour milk products.
    • Alcoholic drinks: beer, wine, cider, whiskey, brandy, gin and rum.
    • Condiments: vinegar and foods containing vinegar, mayonnaise, pickles, soy sauce, mustard, relishes.
    • Edible fungi: including all types of mushrooms and truffles.
    • Processed and smoked meats: sausages, hot dogs, corned beef, pastrami, smoked fish, ham, bacon.
    • Fruit juices: All packaged fruit juices may potentially contain molds.
    • Dried fruits: raisins, apricots, prunes, figs, dates, etc.

    Foods ok to be eaten in small amounts

    1. Gluten-free grains: brown rice, quinoa, buckwheat, millet, teff, certified gluten-free oats
    2. High starch vegetables and legumes: sweet corn, potatoes, beans and peas, lentils, sweet potatoes, squashes, turnips, parsnips.
    3. Fruits: low sugar types such as berries, apples, pears and peaches.

    Foods to be eaten freely

    1. Organic pastured animal products: beef, bison, veal, lamb buffalo, wild-caught seafood, poultry, pastured eggs
    2. Low carbohydrate vegetables: broccoli, spinach, cauliflower, kale, cabbage, arugula, chard, cucumber, peppers, tomato (fresh only), onion, leek, asparagus, garlic, artichokes,
    3. Raw nuts and seeds: sunflower seeds, pumpkin seeds, flax seeds, chia seeds, almonds, low mold nuts (No peanuts, walnuts, pecans,cashews, brazil nuts, )
    4. Healthy Fats: Extra virgin olive oil, coconut oil, coconut milk, ghee, avocado, organic butter
    5. Other: Tempeh, Miso, Apple Cider Vinegar
    6. Beverages: Filtered Water, non-fruity herbal teas, mineral water, fresh veggie juice
  • Sublingual immunotherapy (SLIT)
  • Anti-fungal herbs and medications
  • Infared sauna
  • Detoxification support – oral and IV
  • Remediation procedures for environment and belongings
  • Create a “safe” place, with little potential for mold/allergens and great filtration system – this could be a bedroom or other room that is mold and chemical free
  • Some patients benefit from IV immunoglobulin therapy (IVIg)

Here is a chart from article in Townsend Letter July 2014 that explains sources and binders for common mycotoxins: Townsend-Letter-Mold-Article-1

Screen Shot 2015-02-07 at 8.45.26 PM

 

PODCASTS:

More Helpful Resources:

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BROCCOLI SPROUT BEVERAGE HELPS DETOXIFY AIR POLLUTANTS

antioxidant-green-drink John Groopman, Ph.D.
Johns Hopkins Bloomberg School of Public Health
NIEHS Grant P01ES006052, P30ES003819

Research funded in part by NIEHS has shown that drinking a broccoli sprout beverage daily can enhance the detoxification of some airborne pollutants. This inexpensive food-based intervention may provide a way to decrease the long-term health risks of air pollution.

The researchers conducted a clinical trial that included 291 men and women living in a rural farming community in Jiangsu Province, China, an area that experiences high levels of air pollution due to its proximity to Shanghai. Broccoli sprouts provide a good source of glucoraphanin, which is converted to sulforaphane when consumed. Sulforaphane has been shown to increase levels of enzymes involved in detoxification. During the 12-week trial, the researchers asked one group of study participants to drink a broccoli sprout-derived beverage that provided daily doses of 600 micromol glucoraphanin and 40 micromol sulforaphane while a control group of participants consumed a drink that did not contain broccoli sprouts.

For participants receiving the broccoli sprout beverage, the rate of excretion of the carcinogen benzene increased 61 percent on the first day and was maintained throughout the 12 weeks. The rate of excretion of the irritant acrolein rapidly increased 23 percent during the 12-week trial. Additional analyses indicated that sulforaphane might activate the signaling molecule NRF2, which increases the capacity to adapt to and survive a broad range of environmental toxins.

Citation: Egner PA, Chen JG, Zarth AT, Ng D, Wang J, Kensler KH, Jacobson LP, Munoz A, Johnson JL, Groopman JD, Fahey JW, Talalay P, Zhu J, Chen TY, Qian GS, Carmella SG, Hecht SS, Kensler TW. 2014. Rapid and Sustainable Detoxication of Airborne Pollutants by Broccoli Sprout Beverage: Results of a Randomized Clinical Trial in China. Cancer Prev Res (Phila); doi: 10.1158/1940-6207.CAPR-14-0103 [Online 9 June 2014].

The Mastocytosis Society, Inc.
www.tmsforacure.org

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Mold and Biotixins Resources – Local and California

*Inclusion on this list does not necessarily mean that we endorse the organization, group, or business. Before making any changes in your treatment, always be sure to consult your physician.

Mold and Biotixins Resources – National

*Inclusion on this list does not necessarily mean that we endorse the organization, group, or business. Before making any changes in your treatment, always be sure to consult your physician.

  • Mast

    WAIT! Before you get started, make sure to access your FREE guide to mold exposure HERE.

    Mast cells are an important part of your immune system, without them you would never heal from an injury. However, there is a condition where they become overactive and cause serious problems in the body – this condition is called mast cell activation syndrome (MCAS).

    Mast cell activation syndrome is different from mastocytosis because mast cells aren’t accumulating in various organs. With mastocytosis, there is a proliferation or growth of mast cells, like a cancer. Mastocytosis is also very rare and not usually triggered by an irritant.

    On the other hand, MCAS is characterized by overactive mast cells. MCAS can be imagined as though something rubbed up against your mast cells wrong, causing them to become aggravated. Another important difference between MCAS and mastocytosis is that MCAS patients will often come up normal during lab work.

    Many things can trigger MCAS, including:

    • Mold
    • Chemicals
    • Allergens
    • Viruses
    • Heavy metals
    • Toxins

    From what I’ve seen in my practice and have heard from my colleagues, mold is probably the number one trigger of MCAS, followed by infections. Once these cells are activated they start pouring out all sorts of inflammatory agents, such as histamine, and cytokines.

     

    Beyond Histamine

    Up until recently, when anything to do with mast cells where mentioned, histamine was the main inflammatory mediator that came to mind. However, we’ve come to realize that histamine is a very small part of the story.

    Hundreds of chemicals have been associated with mast cells and they all have different actions in the body. Mediators include:

    • Histamine
    • Cytokines
    • Interleukins
    • Prostaglandins
    • Chemokines

     

    Symptoms of MCAS

    Currently, the most common illness associated with mold is chronic inflammatory response syndrome (CIRS) but we are finding MCAS is another disease often triggered by mold exposure. Similar to CIRS, MCAS has widespread symptoms that affect nearly every system of the body. This adds to the difficult nature of diagnosing MCAS properly.

    Here some of the most common symptoms of MCAS:

    • Fatigue
    • Poor memory
    • Brain fog
    • Inability to focus
    • Mood disorders
    • Migraines
    • Rashes
    • Hives
    • Low blood pressure
    • Heart racing
    • Becomes lightheaded when they stand up quickly
    • Diarrhea
    • Abdominal pain
    • Constipation
    • Nausea
    • Bloating
    • Strong PMS symptoms
    • Allergy-like symptoms
    • Asthma
    • Wheezing
    • Shortness of breath

    It’s a common misconception that patients with MCAS have skin problems as the primary symptom. The number one sign of MCAS are neurological symptoms. However, they may also have skin reactions especially if there are a mold patient. Most of my mold patients have hives, flushing, and other skin reactions. This is especially true if they are coming in direct contact with mold or if they are detoxing from mold.

    It is possible for a patient with CIRS to also have MCAS. You can tell this is happening when CIRS is correctly and systematically treated, yet the patient doesn’t get well. This is when doctors tend to notice things like flushing and rashes, which are all signs of classical histamine reactions.

    Histamine is problematic because it causes blood-brain barrier permeability and gut permeability. Usually, this is accompanied by food allergies and sensitivities. Chronic conditions such as MCAS are inherently complex, this makes diagnosis a process of elimination.

    When I see suspected MCAS patients, we have to systematically work through multiple potential diagnoses until we rule out each disease individually. Ultimately, we come to the conclusion that they are struggling with MCAS by ruling out other possibilities.

     

    My Personal Experience with Mold and Mast Cells

    In 2014, my office flooded and we had massive mold issues which I didn’t realize for several months. When I realized, I implemented the Shoemaker Protocol immediately. I started taking binders, used other detox methods, and removed myself from the mold exposure.

    Shortly after, my body broke out in very severe hives. I took an anti-histamine to deal with the hives but realized what was happening was a massive mast cell activation in detox. My body was detoxing from mold through my treatments and by removing myself from the exposure, but it was causing mast cell activation symptoms. I experiences brain fog, respiratory issues, gastrointestinal distress, and my skin was covered in hives.

    I’ve experienced firsthand mast cell activation – it can be very scary. What this means for me is that my body is going to continue to be more sensitive to environmental changes and toxin exposures than the average person. I am more prone to getting hives to exposures like VOCs and other triggers. While this is somewhat unfortunate, there is a lot that can be done for MCAS. Though MCAS treatment does require vigilance, it is possible to live a relatively normal life.

     

    Biomarkers for MCAS

    Though there is no definitive test for MCAS there are numerous tests you can combine to  support your diagnosis. In the figure below, you’ll find the most common biomarker testing recommended for those suspected of having MCAS. There’s no one lab that does all of these tests, you’ll need to use both LabCorp and Quest.

    When it comes to MCAS that’s triggered by mold, there are few biomarkers that are more common than others. These include:

    • MMP – 9
    • C4a (C4b is usually seen  bacterial trigger)
    • TGF beta
    • VEGF

    Also, you need to be sure that your doctor and the lab both know how to carefully handle samples for accurate results. Ultimately, blood test can’t really confirm or deny the presence of an illness. The best way to know if you have MCAS or not, is by ruling out other illnesses through a comprehensive process of elimination. Lab testing helps this process but it’s not the full solution.

    Slide credit to Dr. Sandeep Gupta with Mold Illness Made Simple

     

    MTHFR status and MCAS

    When people have MTHFR, A1298C and C677T, They have impaired methylation.  If they don’t have enough active methylfolate or active methyl B12 or P5P or Riboflavin they’re prone to have problems with methylation. This is especially important with anyone suspected of having MCAS,

    Because methylation is one of the most important pathways our body uses to break down histamine.

    In the situation where a patient has impaired methylation, deficiencies and B vitamins, and the MTHFR genetic mutation,  this can complicate problems with excess histamine in the body. This is because the body is unable to break down histamine  well. If I find a patient is positive for the MTHFR status, we can add methyl B12 and methylfolate.

    Other ways the body breaks down histamine include the DAO and  MAO enzymes.

     

    Reducing mold exposure is the name of the game

    If you suspect you have CIRS or MCAS,  it’s important to check for mold exposure.  without identifying mold exposure symptoms will only continue to get worse and treatments will be ineffective.  this may mean removing yourself from the water damage building.

    However, even when you fully remove yourself from a mold exposure your mass cells still might remain active. This is because they need assistance to detox and to return to a stable state.

     

    Treating MCAS

    When it comes to treating MCAS  that’s been triggered by mold, you must eliminate mold exposure. Imagine your MCAS like a bucket, the more factors you have contributing to your activated mast cells, the worse your symptoms are.

    You need to reduce the number of factors contributing to your MCAS. This is what I mean when I say you need to reduce your toxin burden. You might be surprised at how big of a difference it can make to get yourself into clean air and eating clean food. I always recommend eating as organic as possible, using a water filter, and an air purifier.

    At first I can feel overwhelming, but if you change a little at a time, eventually you can make the overhaul necessary to live a full and healthy life. My patients often asked me if everything needs to be done with a hundred percent accuracy. When it comes to mold you really do need to remove yourself completely from the mold filled environment. In other areas of your life you might not necessarily need to be as strict after a while. However, it pays to be as strict as possible when you’re working to stabilize your mast cells initially.

    There are a number of supplements you can take to help MCAS, these include natural antihistamines and mast cell stabilizers.

      • Ascorbic acid
      • Quercetin
      • Omega 3s
      • Vitamin B6
      • Vitamin B12
      • Vitamin C
      • Glutathione
      • Turmeric
      • P5P
      • Diamine Oxidase enzymes (DAO)
      • Resveratrol
      • Methylfolate
      • Umbrellux DAO
      • Lactobacillus rhamnosus
      • Bifidobacterium spp

    If you suspect you have mast cell activation syndrome, I recommend you find an experiences functional medicine doctor who you like working with and trust. Because working to get a chronic condition under control takes time and patience. The good news is – it is possible to live a full and healthy live with MCAS.

     

    Resources:

    https://www.ncbi.nlm.nih.gov/pubmed/24784142

    https://www.ncbi.nlm.nih.gov/pubmed/28262205

    https://www.ncbi.nlm.nih.gov/pubmed/23179866

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3753019/

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3069946/

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Old Club Drug Is Repurposed Into Depression Treatment

A North Texas woman said a popular club drug and animal tranquilizer saved her from a life of depression and suicidal thoughts.

You may have heard of the drug before, as Special K on the street. it was designed as a horse tranquilizer, but Ketamine is gaining popularity as a treatment for depression.

Some doctors believe the controversial drug will become a game-changer in slowing the nation’s suicide epidemic.

Tiffany McCombie, a 40-year-old mother of one, knows what depression feels like in its darkest moments.

“I definitely was feeling what I would consider suicidal, not really wanting to live, not really wanting to die, just numb. That’s not a healthy place for me,” McCombie said.

She said she has lived with depression and Bipolar disorder for 30 years, has tried dozens of medications and supplements to combat it, but nothing, she said, has worked as well as the Ketamine infusions she gets at Rise Wellness Center.

She’s had six of them in ten months.”I had the right attitude and wanted to be healed and believing that it was going to happen for me and my brain. It happened. It cut down the mood stabilizers and antidepressants I had been on for years. I don’t take them at all,” she said.

More studies,like this one, are finding that Ketamine may be more effective and work faster than traditional antidepressants.

A local team of anesthesiologists had used the drug before, as an anaesthetic inside the operating room, but after seeing its potential to treat depression, they opened Rise Wellness Center, which specializes in Ketamine infusions.

“We get people that are so far down and so dark that we need this to get them out, to get them up, to get them moving. No drug does that like Ketamine,” said Dr.  Renaud Rodrigue, a pain management physician at Rise Wellness Center.

Experts say Ketamine can be dangerous, even deadly, if abused or taken in large doses.

Even though it’s not FDA-approved to treat depression, Dr. Rodrigue said, when given in small doses and in a clinical setting, 90 percent of his patients with severe depression reported long-term benefits.

Researchers at the University of Illinois published this study about how Ketamine may trigger a depression-fighting protein in the brain.

“This protein changed the game for us. We know now there’s something that is created just by the drug itself, which is staying in the central nervous system and is exerting this affect way beyond the duration of the drug,” said Dr. Rodrigue.

McCombie said Ketamine saved her life.

Could Ketamine conquer Treatment resistant depression?

A notorious drug that can cause dangerous hallucinations and even death when abused may be the key to treating severely depressed patients when used under proper physician care. UT Southwestern’s Dr. Lisa Monteggia has uncovered how the drug Ketamine works so rapidly and why patients are seeing success when other treatments have failed.

Transcript

{Video opens with music and pictures of UTSW patient Megan Joyce along with her mother and with her husband.}

Megan Joyce: Everything in my life seems great.

Narrator: Megan Joyce’s life may look picture perfect.

Megan: I graduated college. I got married. He’s an amazing person. He is incredibly supportive.

Narrator: But what these happy photos hide is a relentless inner struggle.

Megan: This is not something that I love to admit, but I fight for my life every single day.

Narrator: The 27-year-old has spent more than a decade battling severe depression. It triggers for no obvious reason.

Megan: They have defined my bipolar illness as treatment resistant.

Narrator: She says she tried every medication in the books … as well as checking into inpatient and outpatient treatment centers. Nothing worked. Until doctors at UT Southwestern Medical Center tried something bold. Ketamine infusion therapy.

Megan: I don’t know if I would be here without the Ketamine treatment. I drive from Austin every 10 days, and I come for treatment, and I’m in the hospital for about 5 hours, and then I go home the same day.

Narrator: Several studies show ketamine can quickly stabilize severely depressed patients. But it does come with risks.

Dr. Madhukar Trivedi: There is a risk for addiction so that if people start taking Ketamine on their own on the black market, then that can be very dangerous. There are toxic effects in the brain if you overdose. On the other hand, for patients who do well on this and are getting the right dose under the guidance of a physician, it can be life saving.

Megan: When I have the IV in, it’s for 40 minutes, and then I stay for 2 hours after because it is an anesthetic so they want to make sure you don’t have adverse side effects.

Narrator: Dr. Madukhar Trivedi is closely monitoring Joyce … as well as the work his colleagues are doing at the bench.

Dr. Trivedi: At UT Southwestern, we have the whole breadth of work being done. There are people working like Dr. Monteggia in basic research. Understanding the exact mechanism of how Ketamine changes molecularly and changes the mechanism of action.

Dr. Lisa Monteggia: We got involved with how Ketamine triggers an anti-depressant effect because of the real need. Some of the recent clinical data has really shown that about a third of all patients don’t respond to anti-depressants. So, what do you do for treatment for those individuals?

Narrator: UT Southwestern’s Dr. Lisa Monteggia is a neuroscientist whose lab pinpointed a key protein that helps tigger Ketamine’s rapid antidepressent effects in the brain. Whereas traditional antidepressents can take up to 8 weeks to work, the effects of ketamine are seen within 60 to 90 minutes.

Dr. Monteggia: The idea of trying to understand how you generate a rapid anti-depressant response in patients … it’s really the first time we’ve been able to study it.

Narrator: Her study, published in the prestigious journal Nature, shows that ketamine blocks a protein responsible for a range of normal brain functions.

Dr. Monteggia: How we think Ketamine triggers an anti-depressant effect, this blocking the NMDA receptor, we think may also be causing the side effects associated with Ketamine. One of the things we’re working on is to try and see if we can identify compounds, slight derivatives perhaps, that may have the beneficial effects of Ketamine, in terms of triggering anti-depressant effects, without the side effects.

Narrator: In the meantime, Joyce remains optimistic for her future and the millions of others trying to defeat depression.

Megan: That’s why I really sought out Ketamine is I really wanted to give back and just have a chance at a semi-normal life.

Depression Patients Turning to Local Doctor’s Ketamine Therapy

The deaths of designer Kate Spade on Tuesday and TV Chef Anthony Bourdain Friday morning are bringing new attention to depression and suicide.

A new Center for Disease Control and Prevention report reveals suicide rates have risen 30 percent across much of the country since 1999.

But right here in San Diego, there is hope for a category of patients some doctors call “the untreatable.”

This patient, we’ll call Lisa, is composing a letter to the editor about her 20-year fight to stay alive.

“I know how tall the bridge is. I know how many seconds it takes to land,” Lisa said.

Lisa is an attorney with severe depression. Conventional medicines could not suppress her suicidal thoughts.

“It’s awful,” she said. “The day starts with waking up thinking ‘Can I even get out of bed?’ You just fight it to exhaustion every single day.”

She was referred to Dr. David Feifel who NBC 7 first also spoke to three years ago. Patients travel from as far away as Canada to undergo his Ketamine therapy.

“Sort of a psychedelic experience. It’s also been termed dissociative experience because it is sort of an out-of-body feeling,” Dr. Feifel said of his therapy.

Dr. Feifel says low doses of Ketamine have an almost immediate effect on his patients, unlike conventional anti-depressants that can take weeks to build up a therapeutic level.

While Ketamine doesn’t stay in the body more than a day, its effects can last for months.

“It seems to be able to vaporize people’s sense of wanting to take their life.” Dr. Feifel said.

Lisa has received some 35 treatments over the last four months.

“I walk in here crappy, I’ll leave happy. It is a remarkable, remarkable experience that in 20 years nothing has ever come close” Lisa said.

Her goal is to need fewer treatments and experience longer-lasting effects.

Lisa’s hope for the so-called “untreatable community” of depressed people is they find help.

Ketamine-Associated Brain Changes – A Review of the Neuroimaging Literature

KEY POINTS:

                  Ketamine-Associated Brain Changes: A Review of the Neuroimaging Literature

Subanesthetic doses of ketamine have rapid (within hours), robust (across a variety of symptoms), and relatively sustained (typically up to one week) antidepressant effects—even in patients with TRD (treatment resistant depression). Clinical studies show that about 50% of patients with TRD have a significant decrease in symptoms within 24 hours of a single intravenous subanesthetic ketamine dose.

Animal models show that ketamine’s antidepressant effects are likely mediated by its antagonism of N-methyl-D-aspartate (NMDA) receptors through increased α-amino-3-hydroxy-5- methyl-4-isoxazolepropionic acid (AMPA)–mediated glutamatergic signaling. This triggers activation of intracellular synaptogenic pathways, most notably in the mechanistic target of rapamycin (mTOR)–signaling pathway, which also has implications in many other psychiatric disorders.

With regard to MDD patients, decreased glutamate has been noted in various prefrontal regions, including the dorsolateral prefrontal cortex (dlPFC), dorsomedial PFC (dmPFC), and anterior cingulate cortex (ACC), when compared to controls.8–10 This shortage of glutamate makes ketamine an ideal treatment for MDD; by creating a surge in glutamate levels in regions of the brain that suffer from a glutamate deficit, ketamine may provide some normalization of glutamate levels in patients with MDD. This “glutamate surge” hypothesis has dominated as the primary theory of ketamine’s antidepressant mechanism.

Ketamine may work through additional receptors, as it is known to have effects on several opioid receptors, adrenergic receptors, and several serotonin and norepinephrine transporters.17–19 It is also possible that acute dissociative side effects of ketamine may be mediating antidepressant response.

One salient biological metric that may provide insight into ketamine’s mechanism of action is related to dissociation. Dissociative side effects begin from infusion, reach a peak typically within an hour of infusion, and are completely diminished 230 minutes after infusion.20 The same study has shown that increased dissociation and psychotomimetic symptoms immediately following infusion may predict antidepressant response. (Luckenbaugh DA, Niciu MJ, Ionescu DF, et al. Do the dissociative side effects of ketamine mediate its antidepressant effects? J Affect Disord 2014;159:56–61Do the dissociative side effects of ketamine mediate its antidepressant effects.)

Certain themes have emerged with Ketamine. First are our findings of convergent brain regions implicated in MDD and how ketamine modulates those areas. Specifically, the subgenual ACC has been a region of interest in many previous studies. In relation to emotion and cognition, ketamine appears to reduce brain activation in regions associated with self-monitoring, to increase neural regions associated with emotional blunting, and to increase neural activity in reward processing.

Overall, ketamine’s effects were most notably found in the subgenual ACC, PCC, PFC, and hippocampus. Abnormalities in overlapping regions (specifically, the dorsal and subgenual ACC, amygdala, hippocampus, and ventral striatum) have been implicated, via a growing body of neuroimaging literature, in the pathophysiology of depression.  The subgenual ACC, in particular, has been a frequently studied area of interest concerning ketamine and MDD.

FMRI found significant reductions in subgenual ACC coupling with hippocampus, retrosplenial cortex, and thalamus. Immediate reductions in subgenual ACC blood flow and focal reductions in OFC blood flow strongly predicted dissociation.

NIMH studies using PET 120 minutes postinfusion found that increased metabolism in the subgenual ACC was positively correlated with improvements in depression scores post-ketamine. (Neural correlates of rapid antidepressant response to ketamine in bipolar disorder..)

Analysis of resting-state scans in healthy volunteers further suggests that dissociation may be responsible for ketamine’s antidepressant effects because it may disconnect the “excessive effects of an aversive visceromotor state on cognition and the self”—a hallmark of depression.40(p 163) Related, one study found that ketamine may dampen brain regions involved in rumination (the repetitive focusing of attention on negative feelings and thoughts in response to negative mood) by reducing the functional connectivity between the pregenual ACC and the dorsal PCC, and decreasing connectivity between the left and right executive-control networks.  (. Lehmann M, Seifritz E, Henning A, et al. Differential effects of rumination and distraction on ketamine induced modulation of resting state functional connectivity and reactivity of regions within the default-mode network. Soc Cogn Affect Neurosci 2016;11:1227–35 .Differential effects of rumination and distraction on ketamine induced modulation of resting state functional connectivity and reactivity of regions within the default-mode network.)

Taken together, these studies suggest that ketamine may cause a “disconnect” in several circuits related to affective processing, perhaps by shifting focus of attention away from the internal states of anxiety, depression, and somatization, and more toward the perceptual changes (e.g., hallucinations, visual distortions, derealization) induced by ketamine. Similarly, during an emotion task, ketamine attenuated responses to negative pictures, suggesting that the processing of negative information is specifically altered in response to ketamine. (Scheidegger M, Henning A, Walter M, et al. Ketamine administration reduces amygdalo-hippocampal reactivity to emotional stimulation. Hum Brain Mapp 2016;37:1941–52.Ketamine administration reduces amygdalo‐hippocampal reactivity to emotional stimulation)

By taking the focus off “oneself” and placing it on other stimuli, it is possible that ketamine decreases awareness of negative experiences and consequently improves mood.

Perhaps most interesting are ketamine’s effects on brain connectivity as it relates to self-monitoring behaviors. Reduced connectivity between the pregenual ACC and dorsal PCC was associated with increased dissociation during infusion, and reduced activation in the left superior temporalcortex was associated with impaired self-monitoring56,65—which is disruptive to patients with psychotic illness—especially those with chronic symptoms of psychosis. By contrast, the transient dissociation experienced by depressed patients during a ketamine infusion may have the effect of dampening what the hyperactive self-monitoring associated with depressive illness (Lehmann M, Seifritz E, Henning A, et al. Differential effects of rumination and distraction on ketamine induced modulation of resting state functional connectivity and reactivity of regions within the default-mode network. Soc Cogn Affect Neurosci 2016;11:1227–35Differential effects of rumination and distraction on ketamine induced modulation of resting state functional connectivity and reactivity of regions within the default-mode network. b)

During ketamine administration, subjects experience emotional blunting, which may be associated with reduced limbic responses to emotional stimuli.54,55 It is possible that by decreasing the activity of deep limbic structures (thought to be involved in the pathophysiology of depression, such as the amygdala), ketamine acutely disables the emotional resources required to perpetuate the symptoms of depression. (Abel KM, Allin MP, Kucharska-Pietura K, et al. Ketamine and fMRI BOLD signal: distinguishing between effects mediated by change in blood flow versus change in cognitive state. Hum Brain Mapp 2003;18:135–45. Ketamine and fMRI BOLD signal Distinguishing between effects mediated by change in blood flow versus change in cognitive state|||| Abel KM, Allin MP, Kucharska-Pietura K, et al. Ketamine alters neural processing of facial emotion recognition in healthy men: an fMRI study. Neuroreport 2003;14:387–91 Ketamine alters neural processing of facial emotion recognition in healthy men an fMRI study.)

Ketamine may play a role in reactivating reward areas of the brain in patients with MDD. This reactivation may be especially important, as reward areas in MDD have been characterized by decreased subcortical and limbic activity and by an increased cortical response to reward paradigms. (Zhang WN, Chang SH, Guo LY, Zhang KL, Wang J. The neural correlates of reward-related processing in major depressive disorder: a meta-analysis of functional magnetic resonance imaging studies. J Affect Disord 2013;151:531–9.)

In resting-state scans, BOLD activation in the cingulate gyrus, hippocampus, insula, thalamus, and midbrain increased after ketamine.( Stone J, Kotoula V, Dietrich C, De Simoni S, Krystal JH, Mehta MA. Perceptual distortions and delusional thinking following ketamine administration are related to increased pharmacological MRI signal changes in the parietal lobe. J Psychopharmacol 2015;29:1025–8.Perceptual distortions and delusional thinking following ketamine administration are related to increased pharmacological MRI signal changes in the parietal lobe)

In addition, ketamine increases neural activation in the bilateral MCC, ACC, and insula, as well as the right thalamus.  Activation of these areas is consistent with activation of reward-processing areas, suggesting that ketamine may play a role in activating reward neurocircuitry. (Hoflich A, Hahn A, Kublbock M, et al. Ketamine-dependent neuronal activation in healthy volunteers. Brain Struct Funct 2017;222:1533–42.)

Though no single brain area has been singled out as the locus of depression, ketamine affects different areas of the brain in various ways, which may contribute to overall mood improvements. For example, at baseline, patients with MDD, compared to healthy volunteers, had reduced global connectivity in the PFC and increased connectivity in the posterior cingulate, precuneus, lingual gyrus, and cerebellum; postketamine, responders had increased connectivity in the lateral PFC, caudate, and insula. (Abdallah CG, Averill LA, Collins KA, et al. Ketamine treatment and global brain connectivity in major depression. Neuropsychopharmacology 2017;42:1210–9.Ketamine Treatment and Global Brain Connectivity in Major Depression.)

These findings may reflect ketamine’s ability to reclaim frontal control over deeper limbic structures, thus strengthening the cognitive control of emotions and decreasing depressive symptoms. Similarly, TRD patients, compared to healthy volunteers, had reduced insula and caudate responses to positive emotions at baseline, which normalized in the caudate post-ketamine. (Murrough JW, Collins KA, Fields J, et al. Regulation of neural responses to emotion perception by ketamine in individuals with treatment-resistant major depressive disorder. Transl Psychiatry 2015;5:e509 Regulation of neural responses to emotion perception by ketamine in individuals with treatment-resistant major depressive disorder.)

Improvements are correlated with increased metabolism in the hippocampus, dorsal ACC, and decreased metabolism in the OFC. (Lally N, Nugent AC, Luckenbaugh DA, Niciu MJ, Roiser JP, Zarate CA Jr. Neural correlates of change in major depressive disorder anhedonia following open-label ketamine. J Psychopharmacol 2015;29:596–607 Neural correlates of change in major depressive disorder anhedonia following open-label ketamine.)

Specifically, based on this review, future studies should likely focus on ketamine’s action in the subgenual ACC, PCC, PFC, and hippocampus. Another promising direction for research builds on the view that depression is the product of underactive prefrontal and limbic mood-regulation networks and overreactive subcortical limbic networks, which are involved in emotional and visceral responses. (Drevets WC, Price JL, Furey ML. Brain structural and functional abnormalities in mood disorders: implications for neurocircuitry models of depression. Brain Struct Funct 2008; 213:93–118 Brain structural and functional abnormalities in mood disorders.)

Ketamine’s potential use in both research and treatment is promising indeed.

 

Neural correlates of exercise training in individuals with schizophrenia and in healthy individuals A systematic review.

Mechanisms of Ketamine Action as an Antidepressant

Ketamine and Ketamine Metabolite Pharmacology Insights into Therapeutic Mechanisms.

Ketamine and other N-methyl-D-aspartate receptor antagonists in the treatment of depression a perspective review

THE NEUROBIOLOGY OF ketamine and addiction

Psychedelic-Assisted Psychotherapy – A Paradigm Shift in Psychiatric Research and Development

KETAMINE FOR TREATMENT-RESISTANT UNIPOLAR AND BIPOLAR MAJOR DEPRESSION – CRITICAL REVIEW AND IMPLICATIONS FOR CLINICAL PRACTICE.

Ketamine for the treatment of addiction Evidence and potential mechanisms  <<<<<<<<<<<<<<<<<<<<<<<<<<<

REVIEW OF KETAMINE ABUSE AND DIVERSION

Cognitive behavior therapy may sustain antidepressant effects of intravenous ketamine in treatment-resistant depression

The Effect of a Single Dose of Intravenous Ketamine on suicidal ideation – systemic review and meta-analysis

Rapid-Acting Antidepressants Mechanistic Insights and Future Directions.

Ketamine and rapid-acting antidepressants a new era in the battle against depression and suicide.

Molecular and Cellular Mechanisms of Rapid-Acting Antidepressants Ketamine and Scopolamine

A Circadian Genomic Signature Common to Ketamine and Sleep Deprivation in the Anterior Cingulate Cortex

New Targets for Rapid Antidepressant Action

Role of copper in depression. Relationship with ketamine treatment

Ketamine normalizes brain activity during emotionally valenced attentional processing in depression.

Glutamate and Gamma-Aminobutyric Acid Systems in the Pathophysiology of Major Depression and Antidepressant Response to Ketamine.

Recognizing Depression from the Microbiota⁻Gut⁻Brain Axis. b

Psychobiotics and the gut–brain axis in the pursuit of happines

Symptomatology and predictors of antidepressant efficacy in extended responders to a single ketamine infusion

Default Mode Connectivity in Major Depressive diosrder measured up to 10 days after Ketamine administration

S-Adenosyl Methionine and Transmethylation Pathways in Neuropsychiatric Diseases Throughout Life

S-Adenosyl Methionine in the Therapy of Depression and Other Psychiatric Disorders.

Ketamine for Depression, 2 Diagnostic and Contextual Indications.

Ketamine’s antidepressant efficacy is extended for at least four weeks in subjects with a family history of an alcohol use disorder

Predictors of Response to Ketamine in Treatment Resistant Major Depressive Disorder and Bipolar Disorder

The role of adipokines in the rapid antidepressant effects of ketamine.

response to ketamine and prediction of treatment outcome

What is the mechanism of Ketamine’s rapid‐onset antidepressant effect A concise overview of the surprisingly large number of possibilities

Medical comorbidity in bipolar disorder The link with metabolic-inflammatory systems.

Sterile Inflammation of Brain, due to Activation of Innate Immunity, as a Culprit in Psychiatric Disorders

Sterile Inflammation of Brain, due to Activation of Innate Immunity, as a Culprit in Psychiatric Disorders

Role of neuro-immunological factors in the pathophysiology of mood disorders.

Anti-inflammatory agents in the treatment of bipolar depression a systematic review and meta-analysis

The role of tryptophan metabolism and food craving in the relation between obesity and bipolar disorder

Immune-based strategies for mood disorders facts and challenges

Metabolic syndrome in psychiatric patients implications

Genetic Studies on the Tripartite Glutamate Synapse in the Pathophysiology and Therapeutics of Mood Disorders

The Impact of a Single Nucleotide Polymorphism in SIGMAR1 on Depressive Symptoms in Major Depressive Disorder and Bipolar Disorder.

Case–control association study of 14 variants of CREB1, CREBBP and CREM on MDD and bipolar

Metabolic syndrome in psychiatric patients overview, mechanisms, and implications.

Peripheral inflammation, Physical Activity and Cognition in Bipolar Disorder

The putative role of oxidative stress and inflammation in the pathophysiology of sleep dysfunction across neuropsychiatruc disorders – chronic fatigue bipolar MS

Bipolar Disorder and Inflammation.

Pharmacologic implications of inflammatory comorbidity in bipolar disorder.

Minding the brain- the role of pharmacotherapy in substance-use disorder treatment

Molecular and Cellular Effects of Traumatic Stress Implications for PTSD

Synaptic Loss and the Pathophysiology of PTSD Implications for Ketamine as a Prototype Novel Therapeutic

__________________________

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Blocking microglial pannexin-1 channels alleviates morphine withdrawal symptoms

Opiates are essential for treating pain, but termination of
opiate therapy can cause a debilitating withdrawal syndrome
in chronic users. To alleviate or avoid the aversive symptoms
of withdrawal, many of these individuals continue to use
opiates1–4. Withdrawal is therefore a key determinant of opiate
use in dependent individuals, yet its underlying mechanisms
are poorly understood and effective therapies are lacking. Here,
we identify the pannexin-1 (Panx1) channel as a therapeutic
target in opiate withdrawal. We show that withdrawal from
morphine induces long-term synaptic facilitation in lamina I
and II neurons within the rodent spinal dorsal horn, a principal
site of action for opiate analgesia. Genetic ablation of Panx1
in microglia abolished the spinal synaptic facilitation and
ameliorated the sequelae of morphine withdrawal. Panx1
is unique in its permeability to molecules up to 1 kDa in size
and its release of ATP5,6. We show that Panx1 activation
drives ATP release from microglia during morphine withdrawal
and that degrading endogenous spinal ATP by administering
apyrase produces a reduction in withdrawal behaviors.
Conversely, we found that pharmacological inhibition of
ATP breakdown exacerbates withdrawal. Treatment with
a Panx1-blocking peptide (10panx) or the clinically used
broad-spectrum Panx1 blockers, mefloquine or probenecid,
suppressed ATP release and reduced withdrawal severity.
Our results demonstrate that Panx1-mediated ATP release
from microglia is required for morphine withdrawal in rodents
and that blocking Panx1 alleviates the severity of withdrawal
without affecting opiate analgesia. 

Could This Inexpensive Medication Reduce Your Withdrawal Symptoms?

Could This Inexpensive Medication Reduce Your Withdrawal Symptoms?

Withdrawal. It’s a huge hurdle on the path to recovery.

Those struggling to leave opioids behind know they’ll eventually have to face the intimidating mental and physical effects of withdrawal. It’s a powerful and frightening thought.

Some of the most common withdrawal symptoms include:

  • Muscle aches and cramps
  • Nausea, vomiting, and diarrhea
  • Anxiety, profuse sweating, and restlessness
  • Blurry vision
  • High blood pressure

Help Where It’s Needed Most

Even though millions of Americans are in the midst of this battle, few medications are available to effectively manage their symptoms. This unavailability – and the onset of painful withdrawal symptoms – are often enough to make many people give up and return to opioids for relief.

But this could soon change…

According to the results of a recent study, help for intense withdrawal symptoms might be on the horizon, thanks to the discovery of a new drug.

“Opioid withdrawal is aversive, debilitating, and can compel individuals to continue using the drug in order to prevent these symptoms,” explains lead researcher Tuan Trang, PhD.

“In our study, we effectively alleviated withdrawal symptoms in rodents, which could have important implications for patients that may wish to decrease or stop their use of these medications.”

The Study

Researchers from the University of Calgary’s Faculty of Veterinary Medicine and Hotchkiss Brain Institute investigated the process of withdrawal and its’ possible causes. The study involved rats which had been given two potent opioids, morphine and fentanyl. The team identified the glycoprotein, pannexin-1, as the source of withdrawal symptoms in rodents. Pannexin-1 is also located throughout the human body, including the brain and spinal cord.

After identifying the cause of these symptoms, the team tested a drug already proven to block the effects of pannexin-1 called, Probenecid. It’s an anti-gout medication that’s fairly cheap and has few side effects.

The results showed this medicine was “effective in reducing the severity of withdrawal symptoms in opioid-dependent rodents.” Another encouraging aspect about their findings: the medication didn’t affect an opioids’ ability to relieve pain.

Previous research hadn’t explored this avenue, and this investigation has provided a better understanding of opioid withdrawal at the cellular level.

The Implications

Canadian pain researcher, Dr. Michael Salter, notes, “This is an exciting study which reveals a new mechanism and a potential therapeutic target for managing opioid withdrawal. The findings of Dr. Trang and his team could have important implications for people on opioid therapy and those attempting to stop opioid use.”

The team behind the study plan to continue their work and hope this new insight will lead to the creation of a more effective treatment method for the symptoms of withdrawal. Dr. Trang says their next steps will be to determine the drug effectiveness in humans and to ensure its’ safety. Their goal is to develop an effective method to treat the millions struggling with pain management and opioid dependency across the nation and around the world.

These results have already lead to the development of a clinical trial at the Calgary Pain Clinic.

 

FDA approves first medication to reduce opioid withdrawal symptoms

Announcement

May 16, 2018

LofexidineCourtesy of US WorldMeds, LLC.

The National Institute on Drug Abuse (NIDA), part of the National Institutes of Health, is pleased to announce that lofexidine, the first medication for use in reducing symptoms associated with opioid withdrawal in adults, has been approved by the U.S. Food and Drug Administration. Lofexidine, an oral tablet, is designed to manage the symptoms patients often experience during opioid discontinuation. Opioid withdrawal symptoms, which can begin as early as a few hours after the drug was last taken, may include aches and pains, muscle spasms/twitching, stomach cramps, muscular tension, heart pounding, insomnia/problems sleeping, feelings of coldness, runny eyes, yawning, and feeling sick, among others. The product will be marketed under the brand name LUCEMYRATM.

In 2016, more than 42,000 people died from an opioid overdose, or approximately 115 people per day. Although effective treatments exist for opioid addiction, painful and difficult withdrawal is one of the reasons treatment fails, and relapse occurs. By alleviating symptoms associated with opioid withdrawal, LUCEMYRA could help patients complete their discontinuation of opioids and facilitate successful treatment. To date, no other medications have been approved to treat opioid withdrawal symptoms.

LUCEMYRA will be marketed by US WorldMeds, a specialty pharmaceutical company that acquired a license for lofexidine from Britannia Pharmaceuticals in 2003. NIDA provided funding to US WorldMeds to support clinical trials to document the clinical pharmacokinetics of lofexidine and to test medical safety and efficacy of the medication, as compared to a placebo, among patients undergoing medically supervised opioid discontinuation. LUCEMYRA is expected to be commercially available in the United States in August 2018.

Read FDA press release: FDA approves the first non-opioid treatment for management of opioid withdrawal symptoms in adults

Read NIDA Director Dr. Nora Volkow’s blog: NIDA-Supported Science Leads to First FDA-Approved Medication for Opioid Withdrawal

For more information about opioids, go to the Opioids webpage. For information about treatment approaches for drug addiction, go to Treatment Approaches for Drug Addiction.

Medication for Opioid Withdrawal

 

May 16, 2018

Image of drug Lucemyra (Lofexidine)Courtesy of US WorldMeds, LLC

In 2016, 115 Americans died every day from an overdose involving prescription or illicit opioids. Addiction to any drug has multiple components—altered functioning of the reward system, learned associations with drug cues that promote preoccupation and craving, and changes to prefrontal circuits necessary for proper exertion of self-control. But physiological and psychological withdrawal symptoms play a major role in driving users repeatedly back to the drug, despite efforts to stop using.

Withdrawal is notoriously hard to endure for people addicted to opioids. Physical symptoms can start a few hours after last taking the drug and may include stomach cramps, aches and pains, coldness, muscle spasms or tension, pounding heart, insomnia, and many others. These symptoms, along with mood changes, like depression and anxiety, are a major reason people with opioid addiction may relapse. Yet until now, no medication has been approved to treat withdrawal.

This week, the Food and Drug Administration (FDA) approved lofexidine, the first medication targeted specifically to treat the physical symptoms associated with opioid withdrawal. NIDA’s medications development program helped fund the science leading to the drug’s approval. Lofexidine could benefit the thousands of Americans seeking medical help for their opioid addiction, by helping them stick to their detoxification or treatment regimens.

Two of the three FDA-approved medications to treat opioid use disorder, methadone and buprenorphine, can be initiated while a person is experiencing withdrawal symptoms, and can help curb craving. However, these medications are not always easy to access, and at this point are only received by a minority of people with opioid use disorder. The third FDA-approved drug, extended-release naltrexone, has also been found effective, but only after people have been fully detoxified.  The need to detox first—and endure those symptoms—prevents many patients from being treated with naltrexone. Lofexidine could make a big difference in making the latter treatment option more widely used.

New Nonopioid Med Blunts Drug Withdrawal Symptoms  < Medscape

Lofexidine is not an opioid. It acts to inhibit the release of norepinephrine in the brain and elsewhere in the nervous system. It was originally developed as a medication for hypertension, but has mainly been used for opioid withdrawal in the United Kingdom since the early 1990s. US WorldMeds acquired a license for lofexidine from Britannia Pharmaceuticals in 2003 and will market it in the US under the brand name LUCEMYRATM beginning this summer. NIDA helped fund the clinical trials to test lofexidine’s pharmacological properties, safety, and efficacy in patients who were discontinuing opioid use under medical supervision.

Lofexidine cannot address the psychological symptoms of opioid withdrawal; further research is needed to develop medications that could address mood problems during detoxification and after. But approval of the first medication to treat the physical symptoms of opioid withdrawal is a major milestone, one that could improve the lives and treatment success of thousands of people living with opioid addiction. And by helping prevent relapse, it could save lives. The approval of lofexidine is also a welcome example of the power of public-private collaborations in developing new treatments.

MIAMI — Lofexidine (Lucemyra, US Worldmeds), which has been in use in the United Kingdom for more than 20 years, is now
available in the United States. The drug is used in the management of symptoms of severe opioid withdrawal.
Dr Danesh Alam
In a double-blind, placebo-controlled, multicenter trial in opioid-dependent patients, lofexidine significantly improved opioid
withdrawal symptoms and significantly increased completion of a 7-day opioid discontinuation treatment program compared with
placebo.
“We desperately need something to address the opioid crisis, where we are losing about 100 Americans every day, with some
16 million on opioids,” Danesh Alam, MD, Northwestern Medicine Central Dupage Hospital, Winfield, Illinois, told Medscape
Medical News.
“Now we have a drug that actually enables us to achieve a rapid withdrawal from opioids. When we use lofexidine, we can
literally bring in someone using opioids, give them this drug, and they can immediately stop using opioids,” said Alam.
The study was presented at the American Society for Clinical Psychopharmacology (ASCP) 2018.
A Better Alternative
Currently, the standard of care for the treatment of opioid withdrawl is medication-assisted therapy with buprenorphine (multiple
brands), but many patients wish to stop using opioids completely, Alam said.
“Buprenorphine is essentially another opioid, albeit a designer opioid, but a number of patients object to clinicians saying that
the best evidence is to switch them over to buprenorphine and do buprenorphine for the rest of their life,” he said.
Lofexidine, a selective alpha-2-adrenergic agonist, acts on the central nervous system. Through its effect on the brain stem, it
reduces the symptoms of withdrawal to a point at which they become very tolerable.
“We found in our study that you could basically give patients the lofexidine and stop the opiate. In the majority of cases, the
withdrawal symptoms at that point were mild,” Alam said.
The researchers enrolled 602 men and women aged 18 years or older who sought treatment for dependence on short-acting
opioids. Most were men (71%); the mean age of the patients was 35 years (±11 years).
Most patients (83%) were dependent on heroin.
Participants were randomly assigned to receive placebo, lofexidine 0.6 mg qid (2.4 mg/day), or lofexidine 0.8 mg qid (3.2
mg/day) for 7 days after abrupt opioid discontinuation.
The study assessed the benefit of lofexidine with the Short Opiate Withdrawal Scale–Gossop (SOWS-G), a 10-item inventory of
common opioid withdrawal symptoms in which higher scores indicate worse symptoms; by the percentage of participants who
completed the study; and by use of the Clinical Opiate Withdrawal Scale (COWS), an 11-item inventory of opioid withdrawal
signs and symptoms in which higher scores indicate worse symptoms.

Scores on the SOWS-G were lower for patients treated with lofexidine at both doses compared to patients given placebo (-0.21
for lofexidine 2.4 mg, P = .02; and -0.26 for lofexidine 3.2 mg, P = .003). More patients in the lofexidine-treated group completed
the 7-day trial than in the placebo group (41.5% in the 2.4-mg group (odds ratio [OR], 1.85, P = .007), and 39.6% in the 3.2-mg
group (OR, 1.71; P = .02), vs 27.8% for placebo.
Mean COWS scores were significantly lower on days 1 to 5 for patients in the lofexidine groups than for patients who received
placebo (P < .01).
Good Timing
The most common side effects seen with lofexidine were hypotension, orthostatic hypotension, and bradycardia, but they
resulted in few study discontinuations.
The US debut of lofexidine comes at a crucial time. It was recently granted approval by the US Food and Drug Administration
(FDA), as reported by Medscape Medical News.
This approval came after 17 years of hard work on the part of the National Institute on Drug Abuse (NIDA).

Ketamine for Depression | NOVA Health Recovery 703-844-0184 | Ketamine treatment for Bipolar, PTSD, Anxiety disorders

CAll 703-844-0184 for an immediate appointment to evaluate you for a Ketamine infusion:

Ketaminealexandria.com    703-844-0184 Call for an infusion to treat your depression. PTSD, Anxiety, CRPS, or other pain disorder today.

email@novahealthrecovery.com

Ketamine center in Fairfax, Virginia    << Ketamine infusions

Ketamine – NOVA Ketamine facebook page – ketamine treatment for depression

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NOVA Health Recovery  << Ketamine clinic Fairfax, Va  – Call 703-844-0184 for an appointment – Fairfax, Virginia

Ketamine Consultants Blog

 

 

__________________________________________________________________________________________________________

Ketamine has been around for a long time and offers successful opportunities to treat individuals with very resistant depression, PTSD and anxiety. It is also rapid acting. Look at the following links below,

Useful in depression,anxiety, Bipolar, PTSD, pain, migraines, Bipolar, post partum depression, fibromyalgia, and multiple other hard-to-treat disorders. Here are some links and information below to popular press articles on Ketamine!

 

Ketamine For Severe Depression: ‘How Do You Not Offer This Drug To People?’

and

 

ketamine-a-miracle-drug-for-depression/   <<< Link to article

 

Ketamine Relieves Depression By Restoring Brain Connections

Chris Stephens, 28, has been battling depression all of his life. At times he wouldn’t get out of bed for weeks. In January, he said his depression hadn’t returned since he started taking ketamine.

Lianne Milton/For NPR

Scientists say they have figured out how an experimental drug called ketamine is able to relieve major depression in hours instead of weeks.

Researchers from Yale and the National Institute of Mental Health say ketamine seems to cause a burst of new connections to form between nerve cells in parts of the brain involved in emotion and mood.

The discovery, described in Science, should speed development of the first truly new depression drugs since the 1970s, the researchers say.

“It’s exciting,” says Ron Duman, a a psychiatarist and neurobiologist at Yale University. “The hope is that this new information about ketamine is really going to provide a whole array of new targets that can be developed that ultimately provide a much better way of treating depression.”

Ketamine is an FDA-approved anesthetic. It’s also a popular club drug that can produce out-of-body experiences. Not exactly the resume you’d expect for a depression drug.

But a few years ago, researchers discovered that ketamine could help people with major depression who hadn’t responded to other treatments. What’s more, the relief came almost instantly.

The discovery “represents maybe one of the biggest findings in the field over the last 50 years,” Duman says.

A rat neuron before (top) and after (bottom) ketamine treatment. The increased number of orange nodes are restored connections in the rat’s brain.

Ronald Duman/Yale University

Depression is associated with a loss of so-called synaptic connections between nerve cells, Duman says. So he and other scientists began to study mice exposed to stresses that produce symptoms a lot like those of human depression.

The stressed mice lost connections in certain parts of the brain. But a dose of ketamine was able to “rapidly increase these connections and also to rapidly reverse the deficits that are caused by stress,” Duman says.

A team at the National Institute of Mental Health also has found evidence that ketamine works by encouraging synaptic connections.

It’s possible to see the change just by studying rodent brain cells with a microscope, says Carlos Zarate from the Mood and Anxiety Disorders Program at NIMH.

A healthy neuron looks like a tree in spring, he says, with lots of branches and leaves extending toward synaptic connections with other neurons. “What happens in depression is there’s a shriveling of these branches and these leaves and It looks like a tree in winter. And a drug like ketamine does make the tree look like one back in spring.”

And there’s also indirect evidence that ketamine is restoring synaptic connections in people, Zarate says.

His team studied 30 depressed patients who got ketamine. And they found changes in brainwave activity that indicated the drug had strengthened connections between neurons in areas of the brain involved in depression.

All of this research is intended to produce drugs that will work like ketamine, but without the hallucinations. And several of these alternative drugs are already being tried in people.

Preliminary results suggest that “some of these compounds do have rapid antidepressant effects without the side effects that occur with ketamine,” Zarate says.

One of these drugs, called GLYX-13, has already been tested in two large groups of people — a key step toward FDA approval. The company that makes the drug, Naurex, says it will tell scientists how well GLYX-13 works at a meeting in December.

From Chaos To Calm: A Life Changed By Ketamine

 

Clinical experience using intranasal ketamine in the longitudinal treatment of juvenile bipolar disorder with fear of harm phenotype.

Clinical experience using intranasal ketamine in the longitudinal treatment of juvenile bipolar disorder with fear of harm phenotype.

 2018 Jan 1;225:545-551. doi: 10.1016/j.jad.2017.08.081. Epub 2017 Aug 30.

Clinical experience using intranasal ketamine in the longitudinal treatment of juvenile bipolar disorder with fear of harm phenotype.

Abstract

OBJECTIVES:

Fear of Harm (FOH) is a pediatric onset phenotype of bipolar disorder (BD) characterized by BD plus treatment resistance, separation anxiety, aggressive obsessions, parasomnias, and thermal dysregulation. Intranasal ketamine (InK) in 12 youths with BD-FOH produced marked improvement during a two-week trial. Here we report on the open effectiveness and safety of InK in maintenance treatment of BD-FOH from the private practice of one author.

METHODS:

As part of a chart review, patients 18 years or older and parents of younger children responded to a clinical effectiveness and safety survey. Effectiveness was assessed from analysis of responses to 49 questions on symptomatology plus qualitative content analyses of written reports and chart review. Adverse events (AEs) were analyzed by frequency, duration and severity. Peak InK doses ranged from 20 to 360mg per administration.

RESULTS:

Surveys were completed on 45 patients treated with InK for 3 months to 6.5 years. Almost all patients were “much” to “very much” improved clinically and in ratings of social function and academic performance. Significant reductions were reported in all symptom categories. There were 13 reports of persistent AEs, none of which resulted in discontinuation. Acute emergence reactions were sporadically observed in up to 75%, but were mild and of brief duration.

LIMITATIONS:

Retrospective review from a single practice without placebo control with potential for response and recall bias.

CONCLUSIONS:

InK every 3-4 days at sub-anesthetic doses appeared to be a beneficial and well-tolerated treatment. Use of InK may be considered as a tertiary alternative in treatment refractory cases. Randomized control trials are warranted.

___________________________________________________________________________________

Low-dose ketamine for treatment resistant depression in an academic clinical practice setting. <<< ARTICLE link

BACKGROUND:

Recent studies demonstrating a rapid, robust improvement in treatment resistant depression (TRD) following a single sub-anesthetic infusion of ketamine have generated much excitement. However, these studies are limited in their generalizability to the broader TRD population due to their subject exclusion criteria which typically limit psychiatric comorbidity, concurrent medication, and level of suicide risk. This paper describes the safety and efficacy of sub-anesthetic ketamine infusions in a naturalistic TRD patient sample participating in a real-world TRD treatment program within a major university health system.

METHODS:

The effects of a sub-anesthetic dose (0.5mg/kg) of ketamine infused IV over forty minutes on TRD patients participating in a treatment program at the University of California, San Diego was investigated by retrospectively analyzing the medical charts of 41 adult TRD patients with a diagnosis of Major Depressive Disorder (MDD) or Bipolar Disorder (BD).

RESULTS:

Subjects were aged 48.6, 78% white, 36.6% female, and 82.9% had MDD. Significant psychiatric comorbidity existed in 73%. Average pre-infusion BDI score was 32.6 ± 8.4 (S.D) and dropped to 16.8 ± 3.1 at 24-h post-infusion (p < 0.001). The 24-h response (≥ 50% reduction from pre-infusion) and remission (BDI <13) rates were 53.7% and 41.5%, respectively. Three quarters of responders maintained responder status at 7-days. Ketamine infusions were well tolerated with occasional nausea or anxiety and mild hemodynamic effects during the infusion.

LIMITATIONS:

Retrospective nature of this study, lack of control group and use of self-report depression ratings scales.

CONCLUSIONS:

This is the first published study of sub-anesthetic ketamine infusions in a real-world TRD population. The results suggest that this treatment is effective and well tolerated in this population.

 

BACKGROUND:

Recent studies demonstrating a rapid, robust improvement in treatment resistant depression (TRD) following a single sub-anesthetic infusion of ketamine have generated much excitement. However, these studies are limited in their generalizability to the broader TRD population due to their subject exclusion criteria which typically limit psychiatric comorbidity, concurrent medication, and level of suicide risk. This paper describes the safety and efficacy of sub-anesthetic ketamine infusions in a naturalistic TRD patient sample participating in a real-world TRD treatment program within a major university health system.

METHODS:

The effects of a sub-anesthetic dose (0.5mg/kg) of ketamine infused IV over forty minutes on TRD patients participating in a treatment program at the University of California, San Diego was investigated by retrospectively analyzing the medical charts of 41 adult TRD patients with a diagnosis of Major Depressive Disorder (MDD) or Bipolar Disorder (BD).

RESULTS:

Subjects were aged 48.6, 78% white, 36.6% female, and 82.9% had MDD. Significant psychiatric comorbidity existed in 73%. Average pre-infusion BDI score was 32.6 ± 8.4 (S.D) and dropped to 16.8 ± 3.1 at 24-h post-infusion (p < 0.001). The 24-h response (≥ 50% reduction from pre-infusion) and remission (BDI <13) rates were 53.7% and 41.5%, respectively. Three quarters of responders maintained responder status at 7-days. Ketamine infusions were well tolerated with occasional nausea or anxiety and mild hemodynamic effects during the infusion.

LIMITATIONS:

Retrospective nature of this study, lack of control group and use of self-report depression ratings scales.

CONCLUSIONS:

This is the first published study of sub-anesthetic ketamine infusions in a real-world TRD population. The results suggest that this treatment is effective and well tolerated in this population.

 

NOVA Health Recovery

Call 703-844-0184 if you are interested in options for Ketamine treatment for Depression, Anxiety, PTSD, fibromyalgia, Lyme disease, CRPS, or other disorders.

Population scale data reveals the antidepressant effects of ketamine and other therapeutics approved for non-psychiatric indications    << ARTICLE LINK

Population scale data reveals the antidepressant effects of Ketamine  << PDF copy

 

This article looked at the adverse event reporting system, evaluating the ‘side effects’ of Ketamine, which demonstrated LOWER depression rates in patients using Ketamine for pain. These same patients had fewer side effects from those pain medicines as well when they used Ketamine. In numerous settings, we have utilized Ketamine as an adjunct to control pain when opioids have failed (i.e.morphine) with excellent results.

Depression affects 8-12 % of the population at any one time and steals away quality of life as well as productivity. Depression is listed as the 4th leading cause of disease burden on the population by the World Health Organization.
Standard medications, such as SSRI antidepressants, may be ineffective or take several weeks to begin to have any effect. Ketamine has been shown to result in immediate (12-24 hours) improvement of depressive symptoms in a large percentage of patients. We see the same in many of our office infusions.

There is an inflammatory component to depression. This same article points out that Diclofenac, minocycline (an antibiotic), and Botox, also have some antidepressant effect as a result of their anti-inflammatory effects.

The bottom line is that Ketamine showed effectiveness for treatment-resistant depression in this article.

Has anyone had Botox with a Ketamine infusion? Just curious…

FACEBOOK NOVAKetamine LINK

Population scale data reveals the antidepressant effects of ketamine and other therapeutics approved for non-psychiatric indications

  • Scientific Reportsvolume 7, Article number: 1450

Current therapeutic approaches to depression fail for millions of patients due to lag in clinical response and non-adherence. Here we provide new support for the antidepressant effect of an anesthetic drug, ketamine, by Inverse-Frequency Analysis of eight million reports from the FDA Adverse Effect Reporting System. The results of the examination of population scale data revealed that patients who received ketamine had significantly lower frequency of reports of depression than patients who took any other combination of drugs for pain. The analysis also revealed that patients who took ketamine had significantly lower frequency of reports of pain and opioid induced side effects, implying ketamine’s potential to act as a beneficial adjunct agent in pain management pharmacotherapy. Further, the Inverse-Frequency Analysis methodology provides robust statistical support for the antidepressant action of other currently approved therapeutics including diclofenac and minocycline.

 

The World Health Organization estimates depression as the 4th highest disease burden in the world1. In majority of the countries lifetime depression prevalence ranges 8–12%2,3,4. Current standard of practice of depression treatment consists of five main classes of antidepressants, serotonin reuptake inhibitors (SSRIs) being the most common. Nearly half of psychiatric and primary care patients discontinue their antidepressant therapy prematurely5. The main reasons for the discontinuation of therapy include late onset of beneficial outcomes, lack of efficacy for a fraction of patients, adverse reactions, fear of drug dependence, and lack of mechanisms to enforce adherence5. The initial therapeutic effect of antidepressants is delayed by 2–3 weeks after the first dose and the optimal effect is delayed by 6–10 weeks6. The long lag period renders the standard of care antidepressants ineffective for suicidal patients who can’t afford to wait 2–6 weeks. Aside from the lag in antidepressant effects, there is insufficient evidence that antidepressants prevent suicide during long-term treatment7, and in many cases the antidepressant increases the risk of suicidal thoughts and actions8. Efficacy is another issue affecting depression treatment. In the STAR*D protocol study depression remission is 67% after every drug class and drug class combination is tried9.

Because of these problems, some clinicians have been driven to utilize other drugs, such as ketamine, for treatment resistant depression (TRD) patients10,11,12. Ketamine is a drug used illicitly as a hallucinogen and clinically as an anesthetic since 1970’s. It is given intravenously, almost exclusively, due to a lack of an approved oral formulation. There have been some clinical trials where ketamine shows acute efficacy in treating TRD10,11, bipolar depression12 and major depressive disorder with suicidal ideation13, but the number of subjects in these trials ranges from 20 to 57 patients. There are financial and ethical obstacles for a larger scale clinical trial. Here we sought larger scale statistical evidence of ketamine antidepressant action in the FDA Adverse Event Reporting System (FAERS) postmarketing database containing over eight million patient records. Although FAERS was originally intended to track frequent adverse events, with sufficient amount of data, it can also be used to track the beneficial outcomes indirectly through monitoring reductions of related complaint frequencies. Here we apply Inverse-Frequency Analysis (IFA), which looks for statistically significant values of the negative log odds ratio (LogOR).

We found that patients listed in the FAERS database who received ketamine in addition to other therapeutics had significantly lower frequency of reports of depression than patients who took any other combination of drugs for pain (LogOR −0.67 ± 0.034) (Fig. 1c). This reduction in depression is specific to ketamine and is known to be much more rapid than current antidepressants, making this observed effect very promising for treatment of patients with acute depressive or suicidal episodes11. These patients cannot afford to wait up to six weeks for reductions in their depressive symptoms. Pain reports were also significantly lower for ketamine patients (LogOR −0.41 ± 0.019) (Fig. 1c)

Figure 1

Legend: (a) Frequencies of adverse events in patients on FAERS who took ketamine. Adverse events above 2.5% were reported. (b) Odds ratios were calculated comparing adverse event rates of ketamine patients (n = 41,337) and pain patients (n = 238,516). (c) LogOR of pain and depression event rates were calculated from the ketamine and pain patient cohorts. Negative values showing protective effect of ketamine. (d) LogOR of constipation, vomiting, and nausea were calculated from the ketamine and pain patient cohorts. Negative values showing protective effect of ketamine.

The analysis of the whole FAERS database revealed several other unintentional depression reducing drugs among antibiotics, cosmeceuticals and NSAIDS (Fig. 2). Our data supported previous studies that observed the psychiatric polypharmacology of minocycline, a tetracycline antibiotic14 (Fig. 2). The NSAID, diclofenac, was also observed to have some antidepressant properties (Fig. 2). It is theorized that both of these drugs may accomplish antidepressant effects through an anti-inflammatory mechanism15. Because of the antidepressant activity of several NSAIDs, we further separated the non-ketamine pain cohort. Ketamine patients were then compared to patients who received any other combination of drugs for pain excluding NSAIDs. It was observed that depression event rates remained low (LogOR −0.56 ± 0.035) (Fig. 2).

Figure 2

LogOR of psychiatric events were calculated from FAERS patients who used botox, diclofenac or minocycline. FAERS patients who took any drugs for the indication of depression were used as the control cohort. Negative values showing protective effect

The reduction of depression rates in ketamine patient records makes a case for study of ketamine as a psychiatric drug. These results imply that ketamine may be further explored as a monotherapy or adjunct therapy for depression. It should also be noted that FAERS data revealed that ketamine use lead to renal side effects and awareness and caution in patients with renal or hepatic impairment may be warranted (Fig. 1a and b).

As an important side note, we also evaluated efficacy and side effects with the use of ketamine for pain management. We found that patients who were on ketamine had reduced opioid induced side effects including constipation (LogOR −0.17 ± 0.023), vomiting (LogOR −0.16 ± 0.025), and nausea (LogOR −0.45 ± 0.034) than patients who received any other combination of drugs for pain indications (Fig. 1d). Our data supports ketamine’s opioid-sparing properties and alludes to the fact that patients may receive benefits of improved pain, reduced requirement of opioids, and ultimately less opioid reduced side effects.

The results of this study support previous small scale studies’ conclusions that ketamine is a good monotherapy or adjunct therapy for depression. In clinical practice ketamine would be especially useful for depression because of the quick onset of its action compared to existing first line therapies10,11,12,13. Regardless of the causative mechanism ketamine appears to have therapeutic potential for TRD. Further, the potential to reduce many of the most complained side effects of opioid treatment makes ketamine adjunct therapy for pain seem desirable.

Overall, this study demonstrates that the therapeutic potential of ketamine can be derived from appropriate statistical analysis of existing population scale data. This study also outlines a methodology for discovering off label pharmacology of existing approved drugs. This method can be applied to other indications and may reveal new important uses of already approved drugs, providing reliable justification for new indications without large investments in additional clinical trials.

 

The rest of the article can be easily accessed from the above Link.

 

Botox and ketamine could help treat depression, study finds

Call 703-844-0184 to schedule a Ketamine evaluation or infusion.

 

The ketamine infusion for depression experience is not as scary as some people think. Read on to learn about what the ketamine infusion protocol feels like.
Ketamine Fairfax, Va |22308|703-844-0184 | Alexandria, Va | Ketamine for depression

Before getting ketamine infusions for depression, you’ll likely want to know what a ketamine infusion experience is like. While the ketamine infusion experience is different from person to person, the protocol for ketamine infusions for depression is similar for everyone. Read on to learn what it’s really like to receive intravenous ketamine infusions.

What Is a Ketamine Infusion?

A ketamine infusion is a dose of ketamine that is given via the intravenous (IV) route of administration. Ketamine infusions are typically used to treat major depression or depression in bipolar disorder but can be used to treat chronic pain conditions as well.

Before Getting a Ketamine Infusion

Before getting a ketamine infusion, you should expect thorough medical and psychiatric evaluations as well as medical tests to make sure you are healthy enough for the treatment. These assessments and tests are very important as ketamine infusions can be challenging both mentally and physically and only a doctor who is well-acquainted with your health can make good decisions for you.

Ketamine Infusion Procedure

You will likely be shown to a room with a comfortable reclining chair or bed. You will not need to disrobe or wear a hospital gown for treatment. The Ketamine Advocacy Network suggests that you always request a single-person room as a ketamine infusion is a very personal experience. A loved one is usually allowed to stay with you during the ketamine infusion treatment if you want. You’ll then be connected to vital sign monitors such as pulse and oxygen saturation monitors.

It is at this point that you’ll have an IV inserted. A tiny needle is used to insert a tube into a vein in your hand or arm and many find this to be painless. The tube will be connected to a bag held a couple of feet above you. The bag contains the specific dose of ketamine you will require and it will be delivered directly into your bloodstream at a controlled rate. The rate may be adjusted during your treatment to maximize its benefit. It takes approximately 45 minutes for a ketamine infusion and you may need to be under observation after that for an hour or occasionally more. You cannot drive yourself home after an infusion.

People, typically, initially receive six infusions over the course of two-three weeks.

What Does Getting an IV Ketamine Infusion for Depression Feel Like?

Once the ketamine enters your system, it will reach your brain within seconds and you will quickly be able to feel its effects. You won’t be able to stand or converse normally and you’ll feel extremely relaxed but you will still be awake. While others may view a person that seems almost asleep, your brain will still fully be engaged. While this sensation is often found to be “weird”, most people do find it pleasant.

Experience of Side Effects of the Ketamine Infusion

During the infusion, you may experience dissociation, where the mind and body seem to separate. This side effect of the ketamine infusion can often be minimized simply by opening your eyes.

As stated, your mind will be very active during the IV infusion so it may wander to thoughts of trauma or anxiety, but unlike your usual feelings around those thoughts, you will view it matter-of-factly. One patient described his ketamine infusion experience like this:

“. . . you start disassociating with everything, like you’re observing, not participating in anything. It’s really weird . . . As far as the mind goes, you start going through these weird levels, kind of like in the movies Inception or The Matrix, where you don’t know what’s real.

“You start thinking about all kinds of stuff. Whatever races through your mind—and usually when you’re depressed it’s negative sh*t—when you’re on ketamine, it’s just like: ‘Well, nothing I can do about that.’ You feel like, ‘I’m not in control, and that’s fine; you’re going to die someday and that’s just life.’ You kind of learn to just accept it, I guess.”

Although most patients do experience relaxation during a ketamine infusion, there can be moments of fright, particularly if you go into the experience with very high anxiety. Listening to calming music or watching a calming image may help with this, however.

Feeling Better After the Ketamine Infusion Procedure

It varies as to how long it will take for the ketamine to kick in. Some find relief within only an hour or two while others need multiple infusions to feel the benefit. Unfortunately, 20-40% of people do not experience a positive response to ketamine treatment (Reviews on Ketamine for Depression).

What’s important to remember is that no matter what you experience during a ketamine infusion, it’s the changes that the ketamine makes to your brain that relieve depression and not the infusion experience itself.

 

 

Ketamine treatment for depression reviews are scant but some are available. Read about ketamine for depression reviews from patients and doctors.

Ketamine is a relatively new treatment for depression so people are often looking for ketamine treatment for depression reviews to help guide their choices. This is understandable as ketamine treatment cost falls between $400-800 per intravenous (IV) infusion and more than six infusions may be needed. Read on for real patients’ ketamine for depression reviews.

Ketamine Treatment for Depression Reviews

It’s important to note that reviews for any type of treatment are personal and individual. This means that any one person may or may not have the same experience as you. This is why it’s important to work with your doctor to decide if ketamine is a good treatment option for your depression.

That being said, there are ketamine treatment for depression reviews available.

A site like PatientsLikeMe can be valuable as individual patients can report their experiences with a treatment. As of August 2017, four patients who took ketamine for major depressive disorder and two patients who took ketamine for bipolar depression have left reviews. Of the six, three indicated that ketamine had “major effectiveness” on their condition. Two patients noted moderate effectiveness and one noted no effectiveness. Side effects to ketamine included: dissociation, dizziness, nausea, memory problems, cognition problems and drowsiness. Two of the patients noted no side effects although one of those also reported no useful effect either.

When looking at these ketamine infusion reviews, most people were happy with the treatment, with one patient saying, “Very effective. I would do it again in a heartbeat.”

However, most patients noted the cost of ketamine infusions as being burdensome.

When looking at the reviews that all patients left, regardless as to the reason the ketamine was prescribed, two out of 24 noted severe side effects and nine out of 24 noted no side effects.

Ketamine Review Article

In 2015, Vice.com published a ketamine review article called, I Used Ketamine to Treat My Depression. In it, one person with bipolar depression discusses his experience with receiving ketamine infusion for depression. Brent Miles, a 41-year-old songwriter and journalist from Phoenix, Arizona, regularly got ketamine infusion treatments at a clinic in North Scottsdale in 2013 and shares his story.

Miles’ experiences are quite positive although he notes that he could not continue the ketamine depression treatment due to cost.

You can read Miles’ experience here.

 

Ketamine Treatment for Depression Reviews by Doctors

As with many treatments, some doctors are wary of this new depression treatment while others forge ahead with cautious optimism.

“A really important part of these recommendations is to make sure people fully understand what the risks and benefits are to treatment so that they are able to make an informed decision based on knowing what the risk-benefit ratio is,” said Gerard Sanacora, MD, PhD, professor of psychiatry and director of the Yale Depression Research Program.

Dr. Sanacora also added:

“The reality is that this is a unique situation where we have a tremendously promising treatment. We use it a lot, and I believe this really is a transformative change in the field, but we do have to appreciate the limits of the knowledge that we are working with right now.”

Ketamine side effects range from mild to severe. Get complete details on side effects of ketamine for depression on HealthyPlace.

The side effects of ketamine for depression are typically mild but can range in severity. Understanding the ketamine infusion therapy for depression side effects before starting treatment is a good idea so that you know what to look for and aren’t surprised by the more common ketamine side effects.

Side Effects of Ketamine

It’s important to remember that the doses of ketamine for depression treatment are far smaller than any dose that would be used recreationally or as an anesthetic (Can You Get Addicted to Ketamine?). Thus, if you read about the side effects of ketamine in general, you will likely see more severe and different side effects listed than those experienced by those being treated for depression.

Some of the common side effects experienced when larger dosages are used include:

  • High blood pressure
  • Increased cardiac output
  • Pressure inside the skull (intracranial pressure)
  • Irregular heart rhythm
  • Seizure-type movements (tonic-clonic movements)
  • Hallucinations
  • Vivid dreams

Side Effects of Ketamine for Depression

As mentioned, dosages of ketamine when used to treat depression are very small. However, ketamine infusion therapy side effects still exist.

According to a small 2012 study wherein patients received up to six ketamine infusion treatments for treatment-resistant depression, the following were the commonly-reported side effects:

  • The presence of psychotic symptoms (delusions and/or experiences of things that don’t exist such as hallucinations)
  • Dissociative symptoms (feeling “out of body,” disconnected, etc.)
  • Feeling “strange” or “unreal”
  • Abnormal sensations
  • Blurred vision
  • Feeling drowsy or sleepy
  • Elevated heart rate or blood pressure

Notably, only four people in the study (16.7%) reported any side effect that impaired functioning at any time.

That said, the majority of people who were given ketamine infusion therapy for depression did experience some side effects, most remitting within two hours after the infusion.

Those who responded positively to the ketamine treatment experienced the same level and type of side effects that those who did not respond experienced.

Positive Effects of Ketamine for Depression

In a small, recent study, it was found that within two hours of the first dose of ketamine, each individual item on a depression scale known as the Montgomery– Asberg Depression Rating Scale (MADRS), was reduced with the exception of appetite and sleep items which couldn’t be assessed at that time.

The following positive effects of ketamine for depression were seen as reductions in:

  • Suicidal thoughts
  • Pessimistic thoughts
  • Inability to feel
  • Feelings of weariness, diminished energy or listlessness (lassitude)
  • Concentration difficulties
  • Inner tension
  • Reported sadness
  • Apparent sadness

The largest positive changes were seen in lassitude, concentration difficulties, and apparent sadness.

It’s important to remember that while these positive ketamine health effects will be seen by many, not everyone responds to ketamine treatment in this way. In the above-mentioned study, 71% of people had a positive response to ketamine treatment for depression and it is known that those receiving more treatments have a better chance at a positive response.

Ketamine is both a legitimate medical treatment as well as a street drug. But can you get addicted to ketamine? Find out on HealthyPlace.

Ketamine isn’t just a drug used to treat depression, chronic pain or as an anesthesia, ketamine is also a street drug of abuse. Often called “special k,” ketamine is used in large doses by some in the party scene. It’s important to remember, however, that recreationally, people take much larger doses of ketamine than are used in depression treatment (How Does Ketamine Work for Depression?). This means that recreational users are more likely to experience increasing tolerance to the drug’s effects, seek greater doses and become addicted.

Ketamine Addiction

Ketamine is the number one drug of abuse in Asia, particularly Hong Kong. Some of the ketamine found on the street is diverted from pharmaceutical supplies but there is also increasing evidence of ketamine production specifically for street use, particularly in India and China. Ketamine may also be found in ecstasy in Asia.

Ketamine is also a drug of abuse in the United States. The reason why people abuse ketamine is its desirable acute effects on the person. If a person takes a street dose of ketamine, he or she may experience:

  • Reduced sensations in the body / a lack of pain
  • A floating or detached feeling
  • A feeling of being incapable of moving
  • A change in how the person sees and hears things, possibly causing hallucinations

Some people find these effects desirable. However, ketamine can also cause:

  • Confusion
  • Agitation
  • Panic attacks
  • Impairment in short- and long-term memory impairment
  • Attention problems
  • Difficulty in cognition
  • Impaired reaction time

Death from acute ketamine use is rare but does occur.

If a person continues to abuse ketamine, over time even worse effects can be felt. Someone who is addicted to ketamine or who consistently abuses ketamine may experience:

  • Depression
  • Very serious bladder problems possibly leading to the bladder needing removal
  • Serious damage to the urinary tract
  • Liver dysfunction
  • Impaired gallbladder activity
  • Kidney failure
  • Extreme pain, particularly during urination

You may not experience a physical addiction to ketamine but you can become addicted to ketamine psychologically. Being addicted to ketamine is no joke and anyone who abuses ketamine or who is addicted to ketamine needs to seek help immediately.

How to Get Off Ketamine

Getting off ketamine involves the same thing as getting off of other drugs: going through withdrawal. Withdrawal effects make it difficult for someone trying to get off ketamine to stay sober, but withdrawal effects can be managed.
If you’re trying to get off of ketamine, symptoms of withdrawal that you might experience include:

  • Double vision
  • Hearing loss
  • Increased heart beat
  • Rapid breathing
  • Loss of motor skills
  • Loss of coordination
  • Depression

These effects are not typically medically dangerous although if they get out of hand, medical intervention may be needed in the short-term. While these withdrawal effects may sound awful, it’s important to remember that these effects are short-lived and day-by-day, you will start to feel better.

 

I attached a youtube video on SAD – seasonal Affective Disorder

www.ubcsad.ca   <<  SAD website
https://youtu.be/pUYOxnuzRHU?t=1

 

 

 

https://www.healthyplace.com/depression/depression-treatment/can-you-get-addicted-to-ketamine/

Ketamine in the NEWS April 2018

http://sltbr.org/ Biological rhythms – depression  << Website

Medical Express Article regarding Ketamine for Depression <<<<

Ketamine, notorious club drug, shows promise as a treatment for depression, studies indicate

April 20, 2018 by John Keilman, Chicago Tribune

Sabrina Misra suffered from depression for most of her life, but last summer, it became almost too heavy to bear.

Despite years of therapy and many medications, Misra, 36, had become so despondent that she started planning her suicide. But then her psychiatrist introduced her to a new treatment with an unusual back story.

The treatment was ketamine, an anesthetic used to sedate both people and animals before surgery. It’s also a notorious street drug, abused by clubgoers seeking a trancelike, hallucinatory high.

But in recent years, numerous studies have found that ketamine can be an effective and speedy treatment for people with depression—particularly those who, like Misra, have found little relief from other medications.

“After the first couple of treatments it didn’t seem to work, but after I hit my fourth one, everything started to change,” said Misra, a therapist and college instructor who lives in Lisle, Ill. “I went from actively wanting to kill myself to being fine.”

Though some researchers have found that ketamine can be a valuable antidepressant, no one has performed the large-scale clinical trials necessary to get U.S. Food and Drug Administration approval to use it a psychiatric medication.

Consequently, most insurance plans won’t pay for it, leaving patients to pay thousands of dollars out of pocket for a series of intravenous infusions.

Some warn that questions remain about ketamine’s long-term safety and effectiveness. Dr. James Murrough, a psychiatrist at the Icahn School of Medicine at Mount Sinai in New York, said people who misuse the drug have developed cognitive problems, and high doses have proved toxic in rats.

And because ketamine has a history of abuse, he said, doctors and patients must consider the threat of addiction.

“We think the risk is low, but it’s probably not zero, particularly if it gets scaled up,” he said. “There’s excitement but also a justified caution.”

Nonetheless, demand for the drug is so great that dozens of specialty clinics are popping up around the country. The doctors who run them say ketamine has helped most of their patients.

“It’s much better than anything we’ve had before,” said Dr. Abid Nazeer, the psychiatrist who treated Misra at his Oak Brook clinic, Advanced Psychiatric Solutions. “I’ve seen it work so quickly that one infusion gets rid of suicidal thoughts that had been there for 20 years.”

Ketamine was created as an anesthetic, and doctors including veterinarians and battlefield medics embraced it for its fast-acting properties and relative safety. But because it produces strong out-of-body sensations in high doses, it became a club drug, potent enough to send hundreds of people to emergency rooms each year.

In the 1990s, researchers discovered another use for ketamine: A small dose, they found, limits the concentration of a neurotransmitter called glutamate in the brain, and with startling speed, lifts the mood of many depression sufferers who haven’t been helped by medications like Prozac or Lexapro.

“Our standard antidepressants can take six to eight weeks to be effective—ketamine can take just one hour,” said Dr. Carlos Zarate of the National Institute of Mental Health, whose studies in the 2000s accelerated interest in the drug.

Over the past few years, doctors have opened specialty clinics that offer ketamine to patients who have depression or, to a lesser extent, chronic pain. Though the FDA has not approved those uses, the agency allows doctors to dispense drugs for “off-label” purposes if they believe it is medically appropriate.

The basic regimen calls for the intravenous infusion of a small dose—0.5 mg per kilogram of body weight, far less than someone would use to get high—six times over two weeks. After that, patients return every few weeks or months for booster doses.

Clinic operators say they screen clients to focus on those who have not improved with standard antidepressants.

“This is a last resort for those that are treatment-resistant,” said Dr. June Lee of Lombard’s Optimum Ketamine Center. “Most of the patients we’ve seen here have tried everything.”

Zarate said research has shown ketamine to be effective for about 60 percent of people with treatment-resistant depression, though some local clinics say their results have been better.

“We’ve had about a 70 percent response rate, but it really works for them,” said Dr. Vikas Patel, an emergency room physician who runs the Midwest Ketamine Center in Arlington Heights. “For the 30 percent it doesn’t work for, there’s no benefit at all. I would say there isn’t a big in-between.”

He charges $500 per infusion. Insurance typically won’t cover ketamine treatments, though Patel said he expects that to change. A pharmaceutical company is seeking FDA approval for a nasal spray, he said, and other companies are testing their own versions.

But for now, the out-of-pocket cost limits the number of people who can afford the treatment. Misra said that while she put the infusions on her credit card, seeing them as a life-or-death investment, others aren’t so fortunate.

“I have patients who are struggling right now, and they actually can’t swing it,” she said. “I think that’s a horrible thing. No one should have to die because they can’t pay for treatment.”

Dominic Sisti, who directs the Scattergood Program for Applied Ethics of Behavioral Health Care at the University of Pennsylvania, co-wrote a paper three years ago warning about the possible risks of using for depression.

The research that has come out since then has persuaded him that it is appropriate for many people, he said, but he still believes doctors should share data on their results to further knowledge of the drug and improve the protocols for using it.

“In a sense, each patient they treat is an experiment of one,” he said. “It would be really helpful if all these clinics got together and figured out a way to report those outcomes. Without those data, I worry that someone’s going to get hurt.”

Antidepressant response within hours? Experts weigh evidence on ketamine as fast-acting treatment for depression

antidepressant-response-hours-experts-evidence << Article

Recent studies suggest that ketamine, a widely used anesthetic agent, could offer a wholly new approach to treating severe depression—producing an antidepressant response in hours rather than weeks. Two reviews of recent evidence on ketamine and related drugs for treating depression appear in the Harvard Review of Psychiatry.

Ketamine and related drugs may represent a “paradigm shift” in the treatment of  (MDD) and bipolar depression—especially in patients who do not respond to other treatments, according to a review by Carlos A. Zarate, Jr, MD and colleagues at the National Institute of Mental Health. A second article explores evidence on the mechanisms behind ‘s rapid antidepressant effects.

Growing Evidence, Clinical Caution about Ketamine for Severe Depression

Current treatments for MDD and bipolar depression have major limitations. Many patients with severe depressive symptoms don’t respond to available antidepressant drugs. Even for those who do respond, it may take several weeks before symptoms improve.

Ketamine, an anesthetic, is one of several glutamatergic drugs affecting neurotransmitters in the central nervous system. Over the past decade, several studies have reported “rapid, robust, and relatively sustained antidepressant response” to ketamine, injected intravenously at low, subanesthetic doses.

Dr. Zarate and colleagues review the research on ketamine and other glutamatergic drugs for depression. Ketamine, by far the best-studied of these medications, is notable for its very rapid antidepressant effects. In patients with treatment-resistant MDD, ketamine has produced initial reductions in depressive symptoms within two hours, with peak effects at 24 hours.

Ketamine may also rapidly reduce suicidal thoughts. Combined with other medications, ketamine has also produced rapid antidepressant effects in patients with treatment-resistant bipolar depression.

Prompted by these studies, some doctors are already using ketamine in patients with severe or treatment-resistant depression. However, since it is FDA-approved only as an anesthetic, use of ketamine in depressive disorders is “off-label,” unregulated, and not standardized. Many questions remain about its short- and long-term side effects and potential for abuse.

“Efforts are underway to bring ketamine to market, standardize its use, and determine its real-world effectiveness,” Dr. Zarate and coauthors write. They also present evidence on several other glutamatergic drugs. One , esketamine, has been given “breakthrough therapy” status by the FDA for  at imminent risk of suicide.

Cristina Cusin, MD of Massachusetts General Hospital and colleagues review neuroimaging studies evaluating ketamine’s effects in the brain. The studies show ketamine-induced changes in several brain areas involved in the development of depression. Ketamine may exert its antidepressant effects by “acutely disabl[ing] the emotional resources required to perpetuate the symptoms of depression,” as well as by increasing emotional blunting and increasing activity in reward processing.

Independent of how ketamine works or its ultimate role in clinical treatment, antidepressant response to glutamatergic drugs points to an exciting conclusion: “that rapid antidepressant effects are indeed achievable in humans,” Dr. Zarate and coauthors write. “This paradigm shift lends additional urgency to the development of novel treatments for MDD and bipolar , particularly for patient subgroups that do not respond to currently available therapies.”

Glutamatergic Modulators in Depression

Ketamine-Associated Brain Changes A Review of the Neuroimaging Literature bb

Brain-Derived Neurotrophic Factor and Major Depressive Disorder Evidence from Meta-Analyses

Suicidal thoughts rapidly reduced with ketamine, finds study

Suicidal thoughts rapidly reduced with ketamine, finds study

December 14, 2017, Columbia University Medical Center
Ketamine
3-D model of Ketamine. Credit: Wikipedia

Ketamine was significantly more effective than a commonly used sedative in reducing suicidal thoughts in depressed patients, according to researchers at Columbia University Medical Center (CUMC). They also found that ketamine’s anti-suicidal effects occurred within hours after its administration.

The findings were published online last week in the American Journal of Psychiatry.

According to the Centers for Disease Control and Prevention, suicide rates in the U.S. increased by 26.5 percent between 1999 and 2015.

“There is a critical window in which  who are suicidal need rapid relief to prevent self-harm,” said Michael Grunebaum, MD, a research psychiatrist at CUMC, who led the study. “Currently available antidepressants can be effective in reducing  in with depression, but they can take weeks to have an effect. Suicidal, depressed patients need treatments that are rapidly effective in reducing suicidal thoughts when they are at highest risk. Currently, there is no such treatment for rapid relief of suicidal thoughts in depressed patients.”

Most antidepressant trials have excluded patients with suicidal thoughts and behavior, limiting data on the effectiveness of antidepressants in this population. However, previous studies have shown that low doses of ketamine, an anesthetic drug, causes a rapid reduction in depression symptoms and may be accompanied by a decrease in suicidal thoughts.

The 80 depressed adults with clinically significant suicidal thoughts who enrolled in this study were randomly assigned to receive an infusion of low-dose ketamine or midazolam, a sedative. Within 24 hours, the ketamine group had a clinically significant reduction in suicidal thoughts that was greater than with the midazolam group. The improvement in suicidal thoughts and depression in the ketamine group appeared to persist for up to six weeks.

Those in the ketamine group also had greater improvement in overall mood, depression, and fatigue compared with the midazolam group. Ketamine’s effect on depression accounted for approximately one-third of its effect on suicidal thoughts, suggesting the treatment has a specific anti-suicidal effect.

Side effects, mainly dissociation (feeling spacey) and an increase in blood pressure during the infusion, were mild to moderate and typically resolved within minutes to hours after receiving ketamine.

“This study shows that ketamine offers promise as a rapidly acting  for reducing suicidal thoughts in patients with ,” said Dr. Grunebaum. “Additional research to evaluate ‘s antidepressant and anti-suicidal effects may pave the way for the development of new antidepressant medications that are faster acting and have the potential to help individuals who do not respond to currently available treatments.”

The study is titled, “Ketamine for Rapid Reduction of Suicidal Thoughts in Major Depression: A Midazolam-Controlled Randomized Clinical Trial.”

https://ajp.psychiatryonline.org/doi/10.1176/appi.ajp.2018.17060720

Intravenous ketamine may rapidly reduce suicidal thinking in depressed patients

Repeat intravenous treatment with low doses of the anesthetic drug ketamine quickly reduced suicidal thoughts in a small group of patients with treatment-resistant depression. In their report receiving Online First publication in the Journal of Clinical Psychiatry, a team of Massachusetts General Hospital (MGH) investigators report the results of their study in depressed outpatients who had been experiencing suicidal thought for three months or longer.

“Our finding that low doses of , when added on to current antidepressant medications, quickly decreased suicidal thinking in depressed patients is critically important because we don’t have many safe, effective, and easily available treatments for these patients,” says Dawn Ionescu, MD, of the Depression Clinical and Research Program in the MGH Department of Psychiatry, lead and corresponding author of the paper. “While several previous studies have shown that ketamine quickly decreases symptoms of depression in patients with treatment-resistant depression, many of them excluded patients with current suicidal thinking.”

It is well known that having suicidal thoughts increases the risk that patients will attempt suicide, and the risk for suicide attempts is 20 times higher in patients with depression than the general population. The medications currently used to treat patients with suicidal thinking—including lithium and clozapine—can have serious , requiring careful monitoring of blood levels; and while electroconvulsive therapy also can reduce suicidal thinking, its availability is limited and it can have significant side effects, including memory loss.

Primarily used as a general anesthetic, ketamine has been shown in several studies to provide rapid relief of symptoms of depression. In addition to excluding patients who reported current suicidal thinking, many of those studies involved only a single ketamine dose. The current study was designed not only to examine the antidepressant and antisuicidal effects of repeat, low-dose ketamine infusions in depressed outpatients with suicidal thinking that persisted in spite of antidepressant treatment, but also to examine the safety of increased ketamine dosage.

The study enrolled 14 patients with moderate to severe treatment-resistant depression who had suicidal thoughts for three months or longer. After meeting with the research team three times to insure that they met study criteria and were receiving stable antidepressant treatment, participants received two weekly ketamine infusions over a three-week period. The initial dosage administered was 0.5 mg/kg over a 45 minute period—about five times less than a typical anesthetic dose—and after the first three doses, it was increased to 0.75 mg/kg. During the three-month follow-up phase after the ketamine infusions, participants were assessed every other week.

The same assessment tools were used at each visit before, during and after the active treatment phase. At the treatment visits they were administered about 4 hours after the infusions were completed. The assessments included validated measures of suicidal thinking, in which patients were directly asked to rank whether they had specific suicide-related thoughts, their frequency and intensity.

While only 12 of the 14 enrolled participants completed all treatment visits—one dropped out because of ketamine side effects and one had a scheduling conflict—most of them experienced a decrease in suicidal thinking, and seven achieved complete remission of  at the end of the treatment period. Of those seven participants, two maintained remission from both suicidal thinking and depression symptoms throughout the follow-up period. While there were no serious adverse events at either dose and no major differences in side effects between the two dosage levels, additional studies in larger groups of patients are required before any conclusions can be drawn.

“In order to qualify for this study, patients had to have suicidal thinking for at least three months, along with persistent depression, so the fact that they experienced any reduction in suicidal thinking, let alone remission, is very exciting,” says Ionescu, who is an instructor in Psychiatry at Harvard Medical School. “We only studied intravenous ketamine, but this result opens the possibility for studying oral and intranasal doses, which may ease administration for  in suicidal crises.”

She adds, “One main limitation of our study was that all participants knew they were receiving ketamine. We are now finishing up a placebo-controlled study that we hope to have results for soon. Looking towards the future, studies that aim to understand the mechanism by which ketamine and its metabolites work for people with suicidal thinking and  may help us discover areas of the brain to target with new, even better therapeutic drugs.”

Dawn F. Ionescu et al, Rapid and Sustained Reductions in Current Suicidal Ideation Following Repeated Doses of Intravenous Ketamine, The Journal of Clinical Psychiatry (2016). DOI: 10.4088/JCP.15m10056

Rapid and Sustained Reductions in Current Suicidal Ideation Following Repeated Doses of Intravenous Ketamine: Secondary Analysis of an Open-Label Study

Background: Ketamine rapidly reduces thoughts of suicide in patients with treatment-resistant depression who are at low risk for suicide. However, the extent to which ketamine reduces thoughts of suicide in depressed patients with current suicidal ideation remains unknown.

Methods: Between April 2012 and October 2013, 14 outpatients with DSM-IV–diagnosed major depressive disorder were recruited for the presence of current, stable (≥ 3 months) suicidal thoughts. They received open-label ketamine infusions over 3 weeks (0.5 mg/kg over 45 minutes for the first 3 infusions; 0.75 mg/kg over 45 minutes for the last 3). In this secondary analysis, the primary outcome measures of suicidal ideation (Columbia-Suicide Severity Rating Scale [C-SSRS] and the Suicide Item of the 28-item Hamilton Depression Rating Scale [HDRS28-SI]) were assessed at 240 minutes postinfusion and for 3 months thereafter in a naturalistic follow-up.

Results: Over the course of the infusions (acute treatment phase), 7 of 14 patients (50%) showed remission of suicidal ideation on the C-SSRS Ideation scale (even among patients whose depression did not remit). There was a significant linear decrease in this score over time (P < .001), which approached significance even after controlling for severity of 6-item Hamilton Depression Rating Scale (HDRS6) core depression items (P = .05). Similarly, there were significant decreases in the C-SSRS Intensity (P < .01) and HDRS28-SI (P < .001) scores during the acute treatment phase. Two of the 7 patients who achieved remission during the acute treatment phase (29%) maintained their remission throughout a 3-month naturalistic follow-up.

Conclusions: In this preliminary study, repeated doses of open-label ketamine rapidly and robustly decreased suicidal ideation in pharmacologically treated outpatients with treatment-resistant depression with stable suicidal thoughts; this decrease was maintained for at least 3 months following the final ketamine infusion in 2 patients.

Ketamine improved bipolar depression within minutes

May 30, 2012, Elsevier

Bipolar disorder is a serious and debilitating condition where individuals experience severe swings in mood between mania and depression. The episodes of low or elevated mood can last days or months, and the risk of suicide is high.

Antidepressants are commonly prescribed to treat or prevent the , but they are not universally effective. Many patients still continue to experience periods of depression even while being treated, and many patients must try several different types of  before finding one that works for them. In addition, it may take several weeks of treatment before a patient begins to feel relief from the drug’s effects.

For these reasons, better treatments for depression are desperately needed. A new study in  this week confirms that scientists may have found one in a drug called ketamine.

A group of researchers at the National Institute of Mental Health, led by Dr. Carlos Zarate, previously found that a single dose of ketamine produced rapid antidepressant effects in  with . They have now replicated that finding in an independent group of depressed patients, also with bipolar disorder. Replication is an important component of the scientific method, as it helps ensure that the initial finding wasn’t accidental and can be repeated.

In this new study, they administered a single dose of ketamine and a single dose of placebo to a group of patients on two different days, two weeks apart. The patients were then carefully monitored and repeatedly completed ratings to ‘score’ their  and suicidal thoughts.

When the patients received ketamine, their  significantly improved within 40 minutes, and remained improved over 3 days. Overall, 79% of the patients improved with ketamine, but 0% reported improvement when they received placebo.

Importantly, and for the first time in a group of patients with bipolar depression, they also found that ketamine significantly reduced . These antisuicidal effects also occurred within one hour. Considering that bipolar disorder is one of the most lethal of all psychiatric disorders, these study findings could have a major impact on public health.

“Our finding that a single infusion of ketamine produces rapid antidepressant and antisuicidal effects within one hour and that is fairly sustained is truly exciting,” Dr. Zarate commented. “We think that these findings are of true importance given that we only have a few treatments approved for acute bipolar depression, and none of them have this rapid onset of action; they usually take weeks or longer to have comparable antidepressant effects as ketamine does.”

Ketamine is an N-methyl-D-aspartate (NMDA) receptor antagonist, which means that it works by blocking the actions of NMDA. Dr. Zarate added, “Importantly, confirmation that blocking the NMDA receptor complex is involved in generating rapid antidepressant and antisuicidal effects offers an avenue for developing the next generation of treatments for depression that are radically different than existing ones.”

The article is “Replication of Ketamine’s Antidepressant Efficacy in Bipolar Depression: A Randomized Controlled Add-On Trial” by Carlos A. Zarate Jr., Nancy E. Brutsche, Lobna Ibrahim, Jose Franco-Chaves, Nancy Diazgranados, Anibal Cravchik, Jessica Selter, Craig A. Marquardt, Victoria Liberty, and David A. Luckenbaugh (doi: 10.1016/j.biopsych.2011.12.010). The article appears in Biological Psychiatry, Volume 71, Issue 11 (June 1, 2012)

Replication of Ketamine’s Antidepressant Efficacy in bipolar depression

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Areas served by NOVA Health Recovery:

Maryland (MD):
Bethesda 20814 – Bethesda 20816 – Bethesda 20817 – Chevy Chase 20815 – Colesville 20904 – Cabin John 20815 – Glen Echo 20812 – Gaithersburg 20855 – Gaithersburg 20877- Gaithersburg 20878 – Gaithersburg 20879 – Garrett Park 20896 – Kensington 20895 – Montgomery Village 20886 – Olney 20830 – Olney 20832 – Potomac 20854 – Potomac 20859 – Rockville 20850 – Rockville 20852 – Rockville 20853 – Silver Spring 20903 – Silver Spring 20905 – Silver Spring 20906 – Silver Spring 20910 – Takoma Park 20912 – Wheaton 20902

Washington DC:
Crestwood 20011- North Capitol Hill 20002 – Cathedral Heights 20016 – American University Park 20016 – Columbia Heights 20010 – Mount Pleasant 20010 – Downtown 20036 – Dupont Circle 20009 – Logan Circle 20005- Adams Morgan 20009 – Chevy Chase 20015 – Georgetown 20007 – Cleveland Park 20008 – Foggy Bottom 20037 – Rock Creek Park – Woodley Park 20008 – Tenleytown 20016

Northern Virginia:
McLean 22101- McLean 22102 – McLean 22106 – Great Falls 22066 – Arlington 22201 – Arlington 22202 – Arlington 22203 – Arlington 22205 – Falls Church 22041 – Vienna 22181 – Alexandria 22314 – 22308 -22306 -22305 -22304 Fairfax – 20191 – Reston – 22009 – Springfield – 22152 22015 Lorton 22199
Fairfax, Va
2303 – 22307 – 22306 – 22309 – 22308 22311 – 22310 – 22312
22315 -22003 – 20120 – 22015 – 22027 20121 – 22031 – 20124
22030 – 22033 – 22032 – 22035 – 22039 22041 – 22043
22042 – 22046 – 22044 – 22060 – 22066 20151 – 22079 – 20153 – 22101
22102 – 20171 – 20170 – 22124 – 22151 22150 – 22153
22152 – 20191 – 20190 – 22181- 20192 22180 – 20194 – 22182
Woodbridge – 22191 – 22192 -22193 -22194 – 22195
Springfield – 22150 – 22151 -22152-22153-22154-22155 -22156 – 22157 -22158 -22159 -22160 – 22161
Front Royal 22630
Warren County 22610 22630 22642 22649
Fredericksburg Va 22401 22402 – 22403 – 22404 -22405 -22406 -22407 -22408 – 22412
Zip Code City County Zip Code Map 20101 Dulles Loudoun – 20102 Dulles Loudoun – 20103 Dulles Loudoun – 20104 Dulles Loudoun – 20105 Aldie Loudoun – 20106 Amissville Culpeper – 20107 Arcola Loudoun – 20108 Manassas Manassas City – 20109 Manassas Prince William – 20110 Manassas Manassas City – 20111 Manassas Prince William – 20112 Manassas Prince William – 20113 Manassas Manassas Park City – 20115 Marshall Fauquier – 20116 Marshall Fauquier – 20117 Middleburg Loudoun – 20118 Middleburg Loudoun – 20119 Catlett Fauquier View
Map 20120 Centreville Fairfax – 20121 Centreville Fairfax – 20122 Centreville Fairfax – 20124 Clifton Fairfax – 20128 Orlean Fauquier – 20129 Paeonian Springs Loudoun – 20130 Paris Clarke – 20131 Philomont Loudoun – 20132 Purcellville Loudoun – 20134 Purcellville Loudoun – 20135 Bluemont Clarke – 20136 Bristow Prince William – 20137 Broad Run Fauquier – 20138 Calverton Fauquier – 20139 Casanova Fauquier – 20140 Rectortown Fauquier – 20141 Round Hill Loudoun – 20142 Round Hill Loudoun – 20143 Catharpin Prince William View
Map 20144 Delaplane Fauquier – 20146 Ashburn Loudoun – 20147 Ashburn Loudoun – 20148 Ashburn Loudoun – 20149 Ashburn Loudoun – 20151 Chantilly Fairfax – 20152 Chantilly Loudoun – 20153 Chantilly Fairfax – 20155 Gainesville Prince William – 20156 Gainesville Prince William – 20158 Hamilton Loudoun – 20159 Hamilton Loudoun – 20160 Lincoln Loudoun – 20163 Sterling Loudoun – 20164 Sterling Loudoun – 20165 Sterling Loudoun – 20166 Sterling Loudoun – 20167 Sterling Loudoun – 20168 Haymarket Prince William View
Map 20169 Haymarket Prince William – 20170 Herndon Fairfax – 20171 Herndon Fairfax – 20172 Herndon Fairfax – 20175 Leesburg Loudoun – 20176 Leesburg Loudoun – 20177 Leesburg Loudoun – 20178 Leesburg Loudoun – 20180 Lovettsville Loudoun – 20181 Nokesville Prince William – 20182 Nokesville Prince William – 20184 Upperville Fauquier – 20185 Upperville Fauquier – 20186 Warrenton Fauquier – 20187 Warrenton Fauquier – 20188 Warrenton Fauquier – 20189 Dulles Loudoun – 20190 Reston Fairfax – 20191 Reston Fairfax View
Map 20192 Herndon Fairfax – 20193 Reston Fairfax – 20194 Reston Fairfax – 20195 Reston Fairfax – 20196 Reston Fairfax – 20197 Waterford Loudoun – 20198 The Plains Fauquier – 20199 Dulles Loudoun – 22003 Annandale Fairfax – 22009 Burke Fairfax – 22015 Burke Fairfax – 22025 Dumfries Prince William – 22026 Dumfries Prince William – 22027 Dunn Loring Fairfax – 22030 Fairfax Fairfax City – 22031 Fairfax Fairfax – 22032 Fairfax Fairfax – 22033 Fairfax Fairfax – 22034 Fairfax Fairfax View
Map 22035 Fairfax Fairfax – 22036 Fairfax Fairfax – 22037 Fairfax Fairfax – 22038 Fairfax Fairfax City – 22039 Fairfax Station Fairfax – 22040 Falls Church Falls Church City – 22041 Falls Church Fairfax – 22042 Falls Church Fairfax – 22043 Falls Church Fairfax – 22044 Falls Church Fairfax – 22046 Falls Church Falls Church City – 22047 Falls Church Fairfax – 22060 Fort Belvoir Fairfax – 22066 Great Falls Fairfax – 22067 Greenway Fairfax – 22079 Lorton Fairfax – 22081 Merrifield Fairfax – 22082 Merrifield Fairfax – 22092 Herndon Fairfax View
Map 22093 Ashburn Loudoun – 22095 Herndon Fairfax – 22096 Reston Fairfax – 22101 Mc Lean Fairfax – 22102 Mc Lean Fairfax – 22103 West Mclean Fairfax – 22106 Mc Lean Fairfax – 22107 Mc Lean Fairfax – 22108 Mc Lean Fairfax – 22109 Mc Lean Fairfax – 22116 Merrifield Fairfax – 22118 Merrifield Fairfax – 22119 Merrifield Fairfax – 22120 Merrifield Fairfax – 22121 Mount Vernon Fairfax – 22122 Newington Fairfax – 22124 Oakton Fairfax – 22125 Occoquan Prince William – 22134 Quantico Prince William View
Map 22135 Quantico Stafford – 22150 Springfield Fairfax – 22151 Springfield Fairfax – 22152 Springfield Fairfax – 22153 Springfield Fairfax – 22156 Springfield Fairfax – 22158 Springfield Fairfax – 22159 Springfield Fairfax – 22160 Springfield Fairfax – 22161 Springfield Fairfax – 22172 Triangle Prince William – 22180 Vienna Fairfax – 22181 Vienna Fairfax – 22182 Vienna Fairfax – 22183 Vienna Fairfax – 22184 Vienna Fairfax – 22185 Vienna Fairfax – 22191 Woodbridge Prince William – 22192 Woodbridge Prince William View
Map 22193 Woodbridge Prince William – 22194 Woodbridge Prince William – 22195 Woodbridge Prince William – 22199 Lorton Fairfax – 22201 Arlington Arlington – 22202 Arlington Arlington – 22203 Arlington Arlington – 22204 Arlington Arlington – 22205 Arlington Arlington – 22206 Arlington Arlington – 22207 Arlington Arlington – 22209 Arlington Arlington – 22210 Arlington Arlington – 22211 Ft Myer Arlington – 22212 Arlington Arlington – 22213 Arlington Arlington – 22214 Arlington Arlington – 22215 Arlington Arlington – 22216 Arlington Arlington View
Map 22217 Arlington Arlington – 22218 Arlington Arlington – 22219 Arlington Arlington – 22222 Arlington Arlington – 22223 Arlington Arlington – 22225 Arlington Arlington – 22226 Arlington Arlington – 22227 Arlington Arlington – 22229 Arlington Arlington – 22230 Arlington Arlington – 22234 Arlington Arlington – 22240 Arlington Arlington – 22241 Arlington Arlington – 22242 Arlington Arlington – 22243 Arlington Arlington – 22244 Arlington Arlington – 22245 Arlington Arlington – 22246 Arlington Arlington – 22301 Alexandria Alexandria City View
Map 22302 Alexandria Alexandria City – 22303 Alexandria Fairfax – 22304 Alexandria Alexandria City – 22305 Alexandria Alexandria City – 22306 Alexandria Fairfax – 22307 Alexandria Fairfax – 22308 Alexandria Fairfax – 22309 Alexandria Fairfax – 22310 Alexandria Fairfax – 22311 Alexandria Alexandria City – 22312 Alexandria Fairfax – 22313 Alexandria Alexandria City – 22314 Alexandria Alexandria City – 22315 Alexandria Fairfax – 22320 Alexandria Alexandria City – 22321 Alexandria Fairfax – 22331 Alexandria Alexandria City – 22332 Alexandria Alexandria City – 22333 Alexandria Alexandria City View
Map 22334 Alexandria Alexandria City – 22336 Alexandria Alexandria City – 22401 Fredericksburg Fredericksburg City – 22402 Fredericksburg Fredericksburg City – 22403 Fredericksburg Stafford – 22404 Fredericksburg Fredericksburg City – 22405 Fredericksburg Stafford – 22406 Fredericksburg Stafford – 22407 Fredericksburg Spotsylvania – 22408 Fredericksburg Spotsylvania – 22412 Fredericksburg Stafford – 22427 Bowling Green Caroline – 22428 Bowling Green Caroline – 22430 Brooke Stafford – 22432 Burgess Northumberland – 22433 Burr Hill Orange – 22435 Callao Northumberland – 22436 Caret Essex – 22437 Center Cross Essex View
Map 22438 Champlain Essex – 22442 Coles Point Westmoreland – 22443 Colonial Beach Westmoreland – 22446 Corbin Caroline – 22448 Dahlgren King George – 22451 Dogue King George – 22454 Dunnsville Essex – 22456 Edwardsville Northumberland – 22460 Farnham Richmond – 22463 Garrisonville Stafford – 22469 Hague Westmoreland – 22471 Hartwood Stafford – 22472 Haynesville Richmond – 22473 Heathsville Northumberland – 22476 Hustle Essex – 22480 Irvington Lancaster – 22481 Jersey King George – 22482 Kilmarnock Lancaster – 22485 King George King George View
Map 22488 Kinsale Westmoreland – 22501 Ladysmith Caroline – 22503 Lancaster Lancaster – 22504 Laneview Essex – 22507 Lively Lancaster – 22508 Locust Grove Orange – 22509 Loretto Essex – 22511 Lottsburg Northumberland – 22513 Merry Point Lancaster – 22514 Milford Caroline – 22517 Mollusk Lancaster – 22520 Montross Westmoreland – 22523 Morattico Lancaster – 22524 Mount Holly Westmoreland – 22526 Ninde King George – 22528 Nuttsville Lancaster – 22529 Oldhams Westmoreland – 22530 Ophelia Northumberland – 22534 Partlow Spotsylvania View
Map 22535 Port Royal Caroline – 22538 Rappahannock Academy Caroline – 22539 Reedville Northumberland – 22542 Rhoadesville Orange – 22544 Rollins Fork King George – 22545 Ruby Stafford – 22546 Ruther Glen Caroline – 22547 Sealston King George – 22548 Sharps Richmond – 22552 Sparta Caroline – 22553 Spotsylvania Spotsylvania – 22554 Stafford Stafford – 22555 Stafford Stafford – 22556 Stafford Stafford – 22558 Stratford Westmoreland – 22560 Tappahannock Essex – 22565 Thornburg Spotsylvania – 22567 Unionville Orange – 22570 Village Richmond View
Map 22572 Warsaw Richmond – 22576 Weems Lancaster – 22577 Sandy Point Westmoreland – 22578 White Stone Lancaster – 22579 Wicomico Church Northumberland – 22580 Woodford Caroline – 22581 Zacata Westmoreland – 22601 Winchester Winchester City – 22602 Winchester Frederick – 22603 Winchester Frederick – 22604 Winchester Winchester City – 22610 Bentonville Warren – 22611 Berryville Clarke – 22620 Boyce Clarke – 22622 Brucetown Frederick – 22623 Chester Gap Rappahannock – 22624 Clear Brook Frederick – 22625 Cross Junction Frederick – 22626 Fishers Hill Shenandoah View
Map 22627 Flint Hill Rappahannock – 22630 Front Royal Warren – 22637 Gore Frederick – 22638 Winchester Frederick – 22639 Hume Fauquier – 22640 Huntly Rappahannock – 22641 Strasburg Shenandoah – 22642 Linden Warren – 22643 Markham Fauquier – 22644 Maurertown Shenandoah – 22645 Middletown Frederick – 22646 Millwood Clarke – 22649 Middletown Warren – 22650 Rileyville Page – 22652 Fort Valley Shenandoah – 22654 Star Tannery Frederick – 22655 Stephens City Frederick – 22656 Stephenson Frederick – 22657 Strasburg Shenandoah View
Map 22660 Toms Brook Shenandoah – 22663 White Post Clarke – 22664 Woodstock Shenandoah – 22701 Culpeper Culpeper – 22709 Aroda Madison – 22711 Banco Madison – 22712 Bealeton Fauquier – 22713 Boston Culpeper – 22714 Brandy Station Culpeper – 22715 Brightwood Madison – 22716 Castleton Rappahannock – 22718 Elkwood Culpeper – 22719 Etlan Madison – 22720 Goldvein Fauquier – 22721 Graves Mill Madison – 22722 Haywood Madison – 22723 Hood Madison – 22724 Jeffersonton Culpeper – 22725 Leon Madison View
Map 22726 Lignum Culpeper – 22727 Madison Madison – 22728 Midland Fauquier – 22729 Mitchells Culpeper – 22730 Oakpark Madison – 22731 Pratts Madison – 22732 Radiant Madison – 22733 Rapidan Culpeper – 22734 Remington Fauquier – 22735 Reva Madison – 22736 Richardsville Culpeper – 22737 Rixeyville Culpeper – 22738 Rochelle Madison – 22739 Somerville Fauquier – 22740 Sperryville Rappahannock – 22741 Stevensburg Culpeper – 22742 Sumerduck Fauquier – 22743 Syria Madison – 22746 Viewtown Culpeper View
Map 22747 Washington Rappahannock – 22748 Wolftown Madison – 22749 Woodville Rappahannock – 22801 Harrisonburg Harrisonburg City – 22802 Harrisonburg Harrisonburg City – 22803 Harrisonburg Harrisonburg City – 22807 Harrisonburg Harrisonburg City – 22810 Basye Shenandoah – 22811 Bergton Rockingham – 22812 Bridgewater Rockingham – 22815 Broadway Rockingham – 22820 Criders Rockingham – 22821 Dayton Rockingham – 22824 Edinburg Shenandoah – 22827 Elkton Rockingham – 22830 Fulks Run Rockingham – 22831 Hinton Rockingham – 22832 Keezletown Rockingham – 22833 Lacey Spring Rockingham View
Map 22834 Linville Rockingham – 22835 Luray Page – 22840 Mc Gaheysville Rockingham – 22841 Mount Crawford Rockingham – 22842 Mount Jackson Shenandoah – 22843 Mount Solon Augusta – 22844 New Market Shenandoah – 22845 Orkney Springs Shenandoah – 22846 Penn Laird Rockingham – 22847 Quicksburg Shenandoah – 22848 Pleasant Valley Rockingham – 22849 Shenandoah Page – 22850 Singers Glen Rockingham – 22851 Stanley Page – 22853 Timberville Rockingham – 22901 Charlottesville Albemarle – 22902 Charlottesville Charlottesville City – 22903 Charlottesville Charlottesville City – 22904 Charlottesville Charlottesville City View
Map 22905 Charlottesville Charlottesville City – 22906 Charlottesville Charlottesville City – 22907 Charlottesville Charlottesville City – 22908 Charlottesville Charlottesville City – 22909 Charlottesville Albemarle – 22910 Charlottesville Charlottesville City – 22911 Charlottesville Albemarle – 22920 Afton Nelson – 22922 Arrington Nelson – 22923 Barboursville Orange – 22924 Batesville Albemarle – 22931 Covesville Albemarle – 22932 Crozet Albemarle – 22935 Dyke Greene – 22936 Earlysville Albemarle – 22937 Esmont Albemarle – 22938 Faber Nelson – 22939 Fishersville Augusta – 22940 Free Union Albemarle View
Map 22942 Gordonsville Orange – 22943 Greenwood Albemarle – 22945 Ivy Albemarle – 22946 Keene Albemarle – 22947 Keswick Albemarle – 22948 Locust Dale Madison – 22949 Lovingston Nelson – 22952 Lyndhurst Augusta – 22957 Montpelier Station Orange – 22958 Nellysford Nelson – 22959 North Garden Albemarle – 22960 Orange Orange – 22963 Palmyra Fluvanna – 22964 Piney River Nelson – 22965 Quinque Greene – 22967 Roseland Nelson – 22968 Ruckersville Greene – 22969 Schuyler Nelson – 22971 Shipman Nelson View
Map 22972 Somerset Orange – 22973 Stanardsville Greene – 22974 Troy Fluvanna – 22976 Tyro Nelson – 22980 Waynesboro Waynesboro City – 22987 White Hall Albemarle – 22989 Woodberry Forest Madison – 23001 Achilles Gloucester – 23002 Amelia Court House Amelia – 23003 Ark Gloucester – 23004 Arvonia Buckingham – 23005 Ashland Hanover – 23009 Aylett King William – 23011 Barhamsville New Kent – 23014 Beaumont Goochland – 23015 Beaverdam Hanover – 23018 Bena Gloucester – 23021 Bohannon Mathews – 23022 Bremo Bluff Fluvanna View
Map 23023 Bruington King And Queen – 23024 Bumpass Louisa – 23025 Cardinal Mathews – 23027 Cartersville Cumberland – 23030 Charles City Charles City – 23031 Christchurch Middlesex – 23032 Church View Middlesex – 23035 Cobbs Creek Mathews – 23038 Columbia Goochland – 23039 Crozier Goochland – 23040 Cumberland Cumberland – 23043 Deltaville Middlesex – 23045 Diggs Mathews – 23047 Doswell Hanover – 23050 Dutton Gloucester – 23055 Fork Union Fluvanna – 23056 Foster Mathews – 23058 Glen Allen Henrico – 23059 Glen Allen Henrico View
Map 23060 Glen Allen Henrico – 23061 Gloucester Gloucester – 23062 Gloucester Point Gloucester – 23063 Goochland Goochland – 23064 Grimstead Mathews – 23065 Gum Spring Goochland – 23066 Gwynn Mathews – 23067 Hadensville Goochland – 23068 Hallieford Mathews – 23069 Hanover Hanover – 23070 Hardyville Middlesex – 23071 Hartfield Middlesex – 23072 Hayes Gloucester – 23075 Highland Springs Henrico – 23076 Hudgins Mathews – 23079 Jamaica Middlesex – 23081 Jamestown James City – 23083 Jetersville Amelia – 23084 Kents Store Fluvanna View
Map 23085 King And Queen Court House King And Queen – 23086 King William King William – 23089 Lanexa New Kent – 23090 Lightfoot York – 23091 Little Plymouth King And Queen – 23092 Locust Hill Middlesex – 23093 Louisa Louisa – 23101 Macon Powhatan – 23102 Maidens Goochland – 23103 Manakin Sabot Goochland – 23105 Mannboro Amelia – 23106 Manquin King William – 23107 Maryus Gloucester – 23108 Mascot King And Queen – 23109 Mathews Mathews – 23110 Mattaponi King And Queen – 23111 Mechanicsville Hanover – 23112 Midlothian Chesterfield – 23113 Midlothian Chesterfield View
Map 23114 Midlothian Chesterfield – 23115 Millers Tavern Essex – 23116 Mechanicsville Hanover – 23117 Mineral Louisa – 23119 Moon Mathews – 23120 Moseley Chesterfield – 23123 New Canton Buckingham – 23124 New Kent New Kent – 23125 New Point Mathews – 23126 Newtown King And Queen – 23127 Norge James City – 23128 North Mathews – 23129 Oilville Goochland – 23130 Onemo Mathews – 23131 Ordinary Gloucester – 23138 Port Haywood Mathews – 23139 Powhatan Powhatan – 23140 Providence Forge New Kent – 23141 Quinton New Kent View
Map 23146 Rockville Hanover – 23147 Ruthville Charles City – 23148 Saint Stephens Church King And Queen – 23149 Saluda Middlesex – 23150 Sandston Henrico – 23153 Sandy Hook Goochland – 23154 Schley Gloucester – 23155 Severn Gloucester – 23156 Shacklefords King And Queen – 23160 State Farm Goochland – 23161 Stevensville King And Queen – 23162 Studley Hanover – 23163 Susan Mathews – 23168 Toano James City – 23169 Topping Middlesex – 23170 Trevilians Louisa – 23173 University Of Richmond Richmond City – 23175 Urbanna Middlesex – 23176 Wake Middlesex View
Map 23177 Walkerton King And Queen – 23178 Ware Neck Gloucester – 23180 Water View Middlesex – 23181 West Point King William – 23183 White Marsh Gloucester – 23184 Wicomico Gloucester – 23185 Williamsburg James City – 23186 Williamsburg Williamsburg City – 23187 Williamsburg Williamsburg City – 23188 Williamsburg James City – 23190 Woods Cross Roads Gloucester – 23192 Montpelier Hanover – 23218 Richmond Richmond City – 23219 Richmond Richmond City – 23220 Richmond Richmond City – 23221 Richmond Richmond City – 23222 Richmond Richmond City – 23223 Richmond Richmond City – 23224 Richmond Richmond City View
Map 23225 Richmond Richmond City – 23226 Richmond Henrico – 23227 Richmond Henrico – 23228 Richmond Henrico – 23229 Richmond Henrico – 23230 Richmond Henrico – 23231 Richmond Henrico – 23232 Richmond Richmond City – 23233 Richmond Henrico – 23234 Richmond Chesterfield – 23235 Richmond Chesterfield – 23236 Richmond Chesterfield – 23237 Richmond Chesterfield – 23238 Richmond Henrico – 23240 Richmond Richmond City – 23241 Richmond Richmond City – 23242 Richmond Henrico – 23249 Richmond Richmond City – 23250 Richmond Henrico View
Map 23255 Richmond Henrico – 23260 Richmond Richmond City – 23261 Richmond Richmond City – 23269 Richmond Richmond City – 23273 Richmond Richmond City – 23274 Richmond Richmond City – 23276 Richmond Richmond City – 23278 Richmond Richmond City – 23279 Richmond Richmond City – 23282 Richmond Richmond City – 23284 Richmond Richmond City – 23285 Richmond Richmond City – 23286 Richmond Richmond City – 23288 Richmond Henrico – 23289 Richmond Richmond City – 23290 Richmond Richmond City – 23291 Richmond Richmond City – 23292 Richmond Richmond City – 23293 Richmond Richmond City View
Map 23294 Richmond Henrico – 23295 Richmond Richmond City – 23297 Richmond Chesterfield – 23298 Richmond Richmond City – 23301 Accomac Accomack – 23302 Assawoman Accomack – 23303 Atlantic Accomack – 23304 Battery Park Isle Of Wight – 23306 Belle Haven Accomack – 23307 Birdsnest Northampton – 23308 Bloxom Accomack – 23310 Cape Charles Northampton – 23313 Capeville Northampton – 23314 Carrollton Isle Of Wight – 23315 Carrsville Isle Of Wight – 23316 Cheriton Northampton – 23320 Chesapeake Chesapeake City – 23321 Chesapeake Chesapeake City – 23322 Chesapeake Chesapeake City View
Map 23323 Chesapeake Chesapeake City – 23324 Chesapeake Chesapeake City – 23325 Chesapeake Chesapeake City – 23326 Chesapeake Chesapeake City – 23327 Chesapeake Chesapeake City – 23328 Chesapeake Chesapeake City – 23336 Chincoteague Island Accomack – 23337 Wallops Island Accomack – 23341 Craddockville Accomack – 23345 Davis Wharf Accomack – 23347 Eastville Northampton – 23350 Exmore Northampton – 23354 Franktown Northampton – 23356 Greenbackville Accomack – 23357 Greenbush Accomack – 23358 Hacksneck Accomack – 23359 Hallwood Accomack – 23389 Harborton Accomack – 23395 Horntown Accomack View
Map 23396 Oak Hall Accomack – 23397 Isle Of Wight Isle Of Wight – 23398 Jamesville Northampton – 23399 Jenkins Bridge Accomack – 23401 Keller Accomack – 23404 Locustville Accomack – 23405 Machipongo Northampton – 23407 Mappsville Accomack – 23408 Marionville Northampton – 23409 Mears Accomack – 23410 Melfa Accomack – 23412 Modest Town Accomack – 23413 Nassawadox Northampton – 23414 Nelsonia Accomack – 23415 New Church Accomack – 23416 Oak Hall Accomack – 23417 Onancock Accomack – 23418 Onley Accomack – 23419 Oyster Northampton View
Map 23420 Painter Accomack – 23421 Parksley Accomack – 23422 Pungoteague Accomack – 23423 Quinby Accomack – 23424 Rescue Isle Of Wight – 23426 Sanford Accomack – 23427 Saxis Accomack – 23429 Seaview Northampton – 23430 Smithfield Isle Of Wight – 23431 Smithfield Isle Of Wight – 23432 Suffolk Suffolk City – 23433 Suffolk Suffolk City – 23434 Suffolk Suffolk City – 23435 Suffolk Suffolk City – 23436 Suffolk Suffolk City – 23437 Suffolk Suffolk City – 23438 Suffolk Suffolk City – 23439 Suffolk Suffolk City – 23440 Tangier Accomack View
Map 23441 Tasley Accomack – 23442 Temperanceville Accomack – 23443 Townsend Northampton – 23450 Virginia Beach Virginia Beach City – 23451 Virginia Beach Virginia Beach City – 23452 Virginia Beach Virginia Beach City – 23453 Virginia Beach Virginia Beach City – 23454 Virginia Beach Virginia Beach City – 23455 Virginia Beach Virginia Beach City – 23456 Virginia Beach Virginia Beach City – 23457 Virginia Beach Virginia Beach City – 23458 Virginia Beach Virginia Beach City – 23459 Virginia Beach Virginia Beach City – 23460 Virginia Beach Virginia Beach City – 23461 Virginia Beach Virginia Beach City – 23462 Virginia Beach Virginia Beach City – 23463 Virginia Beach Virginia Beach City – 23464 Virginia Beach Virginia Beach City – 23465 Virginia Beach Virginia Beach City View
Map 23466 Virginia Beach Virginia Beach City – 23467 Virginia Beach Virginia Beach City – 23471 Virginia Beach Virginia Beach City – 23479 Virginia Beach Virginia Beach City – 23480 Wachapreague Accomack – 23482 Wardtown Northampton – 23483 Wattsville Accomack – 23486 Willis Wharf Northampton – 23487 Windsor Isle Of Wight – 23488 Withams Accomack – 23501 Norfolk Norfolk City – 23502 Norfolk Norfolk City – 23503 Norfolk Norfolk City – 23504 Norfolk Norfolk City – 23505 Norfolk Norfolk City – 23506 Norfolk Norfolk City – 23507 Norfolk Norfolk City – 23508 Norfolk Norfolk City – 23509 Norfolk Norfolk City View
Map 23510 Norfolk Norfolk City – 23511 Norfolk Norfolk City – 23512 Norfolk Norfolk City – 23513 Norfolk Norfolk City – 23514 Norfolk Norfolk City – 23515 Norfolk Norfolk City – 23517 Norfolk Norfolk City – 23518 Norfolk Norfolk City – 23519 Norfolk Norfolk City – 23520 Norfolk Norfolk City – 23521 Norfolk Norfolk City – 23523 Norfolk Norfolk City – 23529 Norfolk Norfolk City – 23541 Norfolk Norfolk City – 23551 Norfolk Norfolk City – 23601 Newport News Newport News City – 23602 Newport News Newport News City – 23603 Newport News Newport News City – 23604 Fort Eustis Newport News City View
Map 23605 Newport News Newport News City – 23606 Newport News Newport News City – 23607 Newport News Newport News City – 23608 Newport News Newport News City – 23609 Newport News Newport News City – 23612 Newport News Newport News City – 23628 Newport News Newport News City – 23630 Hampton Hampton City – 23651 Fort Monroe Hampton City – 23661 Hampton Hampton City – 23662 Poquoson Poquoson City – 23663 Hampton Hampton City – 23664 Hampton Hampton City – 23665 Hampton York – 23666 Hampton Hampton City – 23667 Hampton Hampton City – 23668 Hampton Hampton City – 23669 Hampton Hampton City – 23670 Hampton Hampton City View
Map 23681 Hampton Hampton City – 23690 Yorktown York – 23691 Yorktown York – 23692 Yorktown York – 23693 Yorktown York – 23694 Lackey York – 23696 Seaford York – 23701 Portsmouth Portsmouth City – 23702 Portsmouth Portsmouth City – 23703 Portsmouth Portsmouth City – 23704 Portsmouth Portsmouth City – 23705 Portsmouth Portsmouth City – 23707 Portsmouth Portsmouth City – 23708 Portsmouth Portsmouth City – 23709 Portsmouth Portsmouth City – 23801 Fort Lee Prince George – 23803 Petersburg Petersburg City – 23804 Petersburg Petersburg City – 23805 Petersburg Petersburg City View
Map 23806 Petersburg Petersburg City – 23821 Alberta Brunswick – 23822 Ammon Dinwiddie – 23824 Blackstone Nottoway – 23825 Blackstone Nottoway – 23827 Boykins Southampton – 23828 Branchville Southampton – 23829 Capron Southampton – 23830 Carson Dinwiddie – 23831 Chester Chesterfield – 23832 Chesterfield Chesterfield – 23833 Church Road Dinwiddie – 23834 Colonial Heights Colonial Heights City – 23836 Chester Chesterfield – 23837 Courtland Southampton – 23838 Chesterfield Chesterfield – 23839 Dendron Surry – 23840 Dewitt Dinwiddie – 23841 Dinwiddie Dinwiddie View
Map 23842 Disputanta Prince George – 23843 Dolphin Brunswick – 23844 Drewryville Southampton – 23845 Ebony Brunswick – 23846 Elberon Surry – 23847 Emporia Greensville – 23850 Ford Dinwiddie – 23851 Franklin Franklin City – 23856 Freeman Brunswick – 23857 Gasburg Brunswick – 23860 Hopewell Hopewell City – 23866 Ivor Southampton – 23867 Jarratt Greensville – 23868 Lawrenceville Brunswick – 23870 Jarratt Greensville – 23872 Mc Kenney Dinwiddie – 23873 Meredithville Brunswick – 23874 Newsoms Southampton – 23875 Prince George Prince George View
Map 23876 Rawlings Brunswick – 23878 Sedley Southampton – 23879 Skippers Greensville – 23881 Spring Grove Surry – 23882 Stony Creek Sussex – 23883 Surry Surry – 23884 Sussex Sussex – 23885 Sutherland Dinwiddie – 23887 Valentines Brunswick – 23888 Wakefield Sussex – 23889 Warfield Brunswick – 23890 Waverly Sussex – 23891 Waverly Sussex – 23893 White Plains Brunswick – 23894 Wilsons Dinwiddie – 23897 Yale Sussex – 23898 Zuni Isle Of Wight – 23899 Claremont Surry – 23901 Farmville Prince Edward View
Map 23909 Farmville Prince Edward – 23915 Baskerville Mecklenburg – 23917 Boydton Mecklenburg – 23919 Bracey Mecklenburg – 23920 Brodnax Brunswick – 23921 Buckingham Buckingham – 23922 Burkeville Nottoway – 23923 Charlotte Court House Charlotte – 23924 Chase City Mecklenburg – 23927 Clarksville Mecklenburg – 23930 Crewe Nottoway – 23934 Cullen Charlotte – 23936 Dillwyn Buckingham – 23937 Drakes Branch Charlotte – 23938 Dundas Lunenburg – 23939 Evergreen Appomattox – 23941 Fort Mitchell Lunenburg – 23942 Green Bay Prince Edward – 23943 Hampden Sydney Prince Edward View
Map 23944 Kenbridge Lunenburg – 23947 Keysville Charlotte – 23950 La Crosse Mecklenburg – 23952 Lunenburg Lunenburg – 23954 Meherrin Prince Edward – 23955 Nottoway Nottoway – 23958 Pamplin Appomattox – 23959 Phenix Charlotte – 23960 Prospect Prince Edward – 23962 Randolph Charlotte – 23963 Red House Charlotte – 23964 Red Oak Charlotte – 23966 Rice Prince Edward – 23967 Saxe Charlotte – 23968 Skipwith Mecklenburg – 23970 South Hill Mecklenburg – 23974 Victoria Lunenburg – 23976 Wylliesburg Charlotte – 24001 Roanoke Roanoke City View
Map 24002 Roanoke Roanoke City – 24003 Roanoke Roanoke City – 24004 Roanoke Roanoke City – 24005 Roanoke Roanoke City – 24006 Roanoke Roanoke City – 24007 Roanoke Roanoke City – 24008 Roanoke Roanoke City – 24009 Roanoke Roanoke City – 24010 Roanoke Roanoke City – 24011 Roanoke Roanoke City – 24012 Roanoke Roanoke City – 24013 Roanoke Roanoke City – 24014 Roanoke Roanoke City – 24015 Roanoke Roanoke City – 24016 Roanoke Roanoke City – 24017 Roanoke Roanoke City – 24018 Roanoke Roanoke – 24019 Roanoke Roanoke – 24020 Roanoke Roanoke View
Map 24022 Roanoke Roanoke City – 24023 Roanoke Roanoke City – 24024 Roanoke Roanoke City – 24025 Roanoke Roanoke City – 24026 Roanoke Roanoke City – 24027 Roanoke Roanoke City – 24028 Roanoke Roanoke City – 24029 Roanoke Roanoke City – 24030 Roanoke Roanoke City – 24031 Roanoke Roanoke City – 24032 Roanoke Roanoke City – 24033 Roanoke Roanoke City – 24034 Roanoke Roanoke City – 24035 Roanoke Roanoke City – 24036 Roanoke Roanoke City – 24037 Roanoke Roanoke City – 24038 Roanoke Roanoke City – 24040 Roanoke Roanoke City – 24042 Roanoke Roanoke City View
Map 24043 Roanoke Roanoke City – 24044 Roanoke Roanoke City – 24045 Roanoke Roanoke City – 24048 Roanoke Roanoke City – 24050 Roanoke Botetourt – 24053 Ararat Patrick – 24054 Axton Henry – 24055 Bassett Henry – 24058 Belspring Pulaski – 24059 Bent Mountain Roanoke – 24060 Blacksburg Montgomery – 24061 Blacksburg Montgomery – 24062 Blacksburg Montgomery – 24063 Blacksburg Montgomery – 24064 Blue Ridge Botetourt – 24065 Boones Mill Franklin – 24066 Buchanan Botetourt – 24067 Callaway Franklin – 24068 Christiansburg Montgomery View
Map 24069 Cascade Pittsylvania – 24070 Catawba Roanoke – 24072 Check Floyd – 24073 Christiansburg Montgomery – 24076 Claudville Patrick – 24077 Cloverdale Botetourt – 24078 Collinsville Henry – 24079 Copper Hill Floyd – 24082 Critz Patrick – 24083 Daleville Botetourt – 24084 Dublin Pulaski – 24085 Eagle Rock Botetourt – 24086 Eggleston Giles – 24087 Elliston Montgomery – 24088 Ferrum Franklin – 24089 Fieldale Henry – 24090 Fincastle Botetourt – 24091 Floyd Floyd – 24092 Glade Hill Franklin View
Map 24093 Glen Lyn Giles – 24095 Goodview Bedford – 24101 Hardy Franklin – 24102 Henry Franklin – 24104 Huddleston Bedford – 24105 Indian Valley Floyd – 24111 Mc Coy Montgomery – 24112 Martinsville Martinsville City – 24113 Martinsville Martinsville City – 24114 Martinsville Martinsville City – 24115 Martinsville Martinsville City – 24120 Meadows Of Dan Patrick – 24121 Moneta Bedford – 24122 Montvale Bedford – 24124 Narrows Giles – 24126 Newbern Pulaski – 24127 New Castle Craig – 24128 Newport Giles – 24129 New River Pulaski View
Map 24130 Oriskany Botetourt – 24131 Paint Bank Craig – 24132 Parrott Pulaski – 24133 Patrick Springs Patrick – 24134 Pearisburg Giles – 24136 Pembroke Giles – 24137 Penhook Franklin – 24138 Pilot Montgomery – 24139 Pittsville Pittsylvania – 24141 Radford Radford – 24142 Radford Radford – 24143 Radford Radford – 24146 Redwood Franklin – 24147 Rich Creek Giles – 24148 Ridgeway Henry – 24149 Riner Montgomery – 24150 Ripplemead Giles – 24151 Rocky Mount Franklin – 24153 Salem Salem View
Map 24155 Roanoke Salem – 24157 Roanoke Salem – 24161 Sandy Level Pittsylvania – 24162 Shawsville Montgomery – 24165 Spencer Henry – 24167 Staffordsville Giles – 24168 Stanleytown Henry – 24171 Stuart Patrick – 24174 Thaxton Bedford – 24175 Troutville Botetourt – 24176 Union Hall Franklin – 24177 Vesta Patrick – 24178 Villamont Bedford – 24179 Vinton Roanoke – 24184 Wirtz Franklin – 24185 Woolwine Patrick – 24201 Bristol Bristol – 24202 Bristol Washington – 24203 Bristol Bristol View
Map 24209 Bristol Bristol – 24210 Abingdon Washington – 24211 Abingdon Washington – 24212 Abingdon Washington – 24215 Andover Wise – 24216 Appalachia Wise – 24217 Bee Dickenson – 24218 Ben Hur Lee – 24219 Big Stone Gap Wise – 24220 Birchleaf Dickenson – 24221 Blackwater Lee – 24224 Castlewood Russell – 24225 Cleveland Russell – 24226 Clinchco Dickenson – 24228 Clintwood Dickenson – 24230 Coeburn Wise – 24236 Damascus Washington – 24237 Dante Russell – 24239 Davenport Buchanan View
Map 24243 Dryden Lee – 24244 Duffield Scott – 24245 Dungannon Scott – 24246 East Stone Gap Wise – 24248 Ewing Lee – 24250 Fort Blackmore Scott – 24251 Gate City Scott – 24256 Haysi Dickenson – 24258 Hiltons Scott – 24260 Honaker Russell – 24263 Jonesville Lee – 24265 Keokee Lee – 24266 Lebanon Russell – 24269 Mc Clure Dickenson – 24270 Mendota Washington – 24271 Nickelsville Scott – 24272 Nora Dickenson – 24273 Norton Norton City – 24277 Pennington Gap Lee View
Map 24279 Pound Wise – 24280 Rosedale Russell – 24281 Rose Hill Lee – 24282 Saint Charles Lee – 24283 Saint Paul Wise – 24290 Weber City Scott – 24292 Whitetop Grayson – 24293 Wise Wise – 24301 Pulaski Pulaski – 24311 Atkins Smyth – 24312 Austinville Wythe – 24313 Barren Springs Wythe – 24314 Bastian Bland – 24315 Bland Bland – 24316 Broadford Tazewell – 24317 Cana Carroll – 24318 Ceres Bland – 24319 Chilhowie Smyth – 24322 Cripple Creek Wythe View
Map 24323 Crockett Wythe – 24324 Draper Pulaski – 24325 Dugspur Carroll – 24326 Elk Creek Grayson – 24327 Emory Washington – 24328 Fancy Gap Carroll – 24330 Fries Grayson – 24333 Galax Galax City – 24340 Glade Spring Washington – 24343 Hillsville Carroll – 24347 Hiwassee Pulaski – 24348 Independence Grayson – 24350 Ivanhoe Wythe – 24351 Lambsburg Carroll – 24352 Laurel Fork Carroll – 24354 Marion Smyth – 24360 Max Meadows Wythe – 24361 Meadowview Washington – 24363 Mouth Of Wilson Grayson View
Map 24366 Rocky Gap Bland – 24368 Rural Retreat Wythe – 24370 Saltville Smyth – 24374 Speedwell Wythe – 24375 Sugar Grove Smyth – 24377 Tannersville Tazewell – 24378 Troutdale Grayson – 24380 Willis Floyd – 24381 Woodlawn Carroll – 24382 Wytheville Wythe – 24401 Staunton Staunton City – 24402 Staunton Staunton City – 24411 Augusta Springs Augusta – 24412 Bacova Bath – 24413 Blue Grass Highland – 24415 Brownsburg Rockbridge – 24416 Buena Vista Buena Vista City – 24421 Churchville Augusta – 24422 Clifton Forge Alleghany View
Map 24426 Covington Covington City – 24430 Craigsville Augusta – 24431 Crimora Augusta – 24432 Deerfield Augusta – 24433 Doe Hill Highland – 24435 Fairfield Rockbridge – 24437 Fort Defiance Augusta – 24438 Glen Wilton Botetourt – 24439 Goshen Rockbridge – 24440 Greenville Augusta – 24441 Grottoes Rockingham – 24442 Head Waters Highland – 24445 Hot Springs Bath – 24448 Iron Gate Alleghany – 24450 Lexington Lexington City – 24457 Low Moor Alleghany – 24458 Mc Dowell Highland – 24459 Middlebrook Augusta – 24460 Millboro Bath View
Map 24463 Mint Spring Augusta – 24464 Montebello Nelson – 24465 Monterey Highland – 24467 Mount Sidney Augusta – 24468 Mustoe Highland – 24469 New Hope Augusta – 24471 Port Republic Rockingham – 24472 Raphine Rockbridge – 24473 Rockbridge Baths Rockbridge – 24474 Selma Alleghany – 24476 Steeles Tavern Augusta – 24477 Stuarts Draft Augusta – 24479 Swoope Augusta – 24482 Verona Augusta – 24483 Vesuvius Rockbridge – 24484 Warm Springs Bath – 24485 West Augusta Augusta – 24486 Weyers Cave Augusta – 24487 Williamsville Bath View
Map 24501 Lynchburg Lynchburg City – 24502 Lynchburg Lynchburg City – 24503 Lynchburg Lynchburg City – 24504 Lynchburg Lynchburg City – 24505 Lynchburg Lynchburg City – 24506 Lynchburg Lynchburg City – 24512 Lynchburg Lynchburg City – 24513 Lynchburg Lynchburg City – 24514 Lynchburg Lynchburg City – 24515 Lynchburg Lynchburg City – 24517 Altavista Campbell – 24520 Alton Halifax – 24521 Amherst Amherst – 24522 Appomattox Appomattox – 24523 Bedford Bedford – 24526 Big Island Bedford – 24527 Blairs Pittsylvania – 24528 Brookneal Campbell – 24529 Buffalo Junction Mecklenburg View
Map 24530 Callands Pittsylvania – 24531 Chatham Pittsylvania – 24533 Clifford Amherst – 24534 Clover Halifax – 24535 Cluster Springs Halifax – 24536 Coleman Falls Bedford – 24538 Concord Campbell – 24539 Crystal Hill Halifax – 24540 Danville Danville City – 24541 Danville Danville City – 24543 Danville Danville City – 24544 Danville Danville City – 24549 Dry Fork Pittsylvania – 24550 Evington Campbell – 24551 Forest Bedford – 24553 Gladstone Nelson – 24554 Gladys Campbell – 24555 Glasgow Rockbridge – 24556 Goode Bedford View
Map 24557 Gretna Pittsylvania – 24558 Halifax Halifax – 24562 Howardsville Buckingham – 24563 Hurt Pittsylvania – 24565 Java Pittsylvania – 24566 Keeling Pittsylvania – 24569 Long Island Pittsylvania – 24570 Lowry Bedford – 24571 Lynch Station Campbell – 24572 Madison Heights Amherst – 24574 Monroe Amherst – 24576 Naruna Campbell – 24577 Nathalie Halifax – 24578 Natural Bridge Rockbridge – 24579 Natural Bridge Station Rockbridge – 24580 Nelson Mecklenburg – 24581 Norwood Nelson – 24586 Ringgold Pittsylvania – 24588 Rustburg Campbell View
Map 24589 Scottsburg Halifax – 24590 Scottsville Albemarle – 24592 South Boston Halifax – 24593 Spout Spring Appomattox – 24594 Sutherlin Pittsylvania – 24595 Sweet Briar Amherst – 24597 Vernon Hill Halifax – 24598 Virgilina Halifax – 24599 Wingina Buckingham – 24601 Amonate Tazewell – 24602 Bandy Tazewell – 24603 Big Rock Buchanan – 24604 Bishop Tazewell – 24605 Bluefield Tazewell – 24606 Boissevain Tazewell – 24607 Breaks Dickenson – 24608 Burkes Garden Tazewell – 24609 Cedar Bluff Tazewell – 24612 Doran Tazewell View
Map 24613 Falls Mills Tazewell – 24614 Grundy Buchanan – 24619 Horsepen Tazewell – 24620 Hurley Buchanan – 24622 Jewell Ridge Tazewell – 24624 Keen Mountain Buchanan – 24627 Mavisdale Buchanan – 24628 Maxie Buchanan – 24630 North Tazewell Tazewell – 24631 Oakwood Buchanan – 24634 Pilgrims Knob Buchanan – 24635 Pocahontas Tazewell – 24637 Pounding Mill Tazewell – 24639 Raven Buchanan – 24640 Red Ash Tazewell – 24641 Richlands Tazewell – 24646 Rowe Buchanan – 24647 Shortt Gap Buchanan – 24649 Swords Creek Russell View
Map 24651 Tazewell Tazewell – 24656 Vansant Buchanan – 24657 Whitewood Buchanan – 24658 Wolford Buchanan – 24701 Bluefield Mercer – 24712 Athens Mercer – 24714 Beeson Mercer – 24715 Bramwell Mercer – 24716 Bud Wyoming – 24719 Covel Wyoming – 24724 Freeman Mercer – 24726 Herndon Wyoming – 24729 Hiawatha Mercer – 24731 Kegley Mercer – 24732 Kellysville Mercer – 24733 Lashmeet Mercer – 24736 Matoaka Mercer – 24737 Montcalm Mercer – 24738 Nemours Mercer View
Map 24739 Oakvale Mercer – 24740 Princeton Mercer – 24747 Rock Mercer – 24751 Wolfe Mercer – 24801 Welch Mcdowell – 24808 Anawalt Mcdowell – 24811 Avondale Mcdowell – 24813 Bartley Mcdowell – 24815 Berwind Mcdowell – 24816 Big Sandy Mcdowell – 24817 Bradshaw Mcdowell – 24818 Brenton Wyoming – 24822 Clear Fork Wyoming – 24823 Coal Mountain Wyoming – 24824 Coalwood Mcdowell – 24826 Cucumber Mcdowell – 24827 Cyclone Wyoming – 24828 Davy Mcdowell – 24829 Eckman Mcdowell View
Map 24830 Elbert Mcdowell – 24831 Elkhorn Mcdowell – 24834 Fanrock Wyoming – 24836 Gary Mcdowell – 24839 Hanover Wyoming – 24842 Hemphill Mcdowell – 24843 Hensley Mcdowell – 24844 Iaeger Mcdowell – 24845 Ikes Fork Wyoming – 24846 Isaban Mcdowell – 24847 Itmann Wyoming – 24848 Jenkinjones Mcdowell – 24849 Jesse Wyoming – 24850 Jolo Mcdowell – 24851 Justice Mingo – 24853 Kimball Mcdowell – 24854 Kopperston Wyoming – 24855 Kyle Mcdowell – 24857 Lynco Wyoming View
Map 24859 Marianna Wyoming – 24860 Matheny Wyoming – 24861 Maybeury Mcdowell – 24862 Mohawk Mcdowell – 24866 Newhall Mcdowell – 24867 New Richmond Wyoming – 24868 Northfork Mcdowell – 24869 North Spring Wyoming – 24870 Oceana Wyoming – 24871 Pageton Mcdowell – 24872 Panther Mcdowell – 24873 Paynesville Mcdowell – 24874 Pineville Wyoming – 24878 Premier Mcdowell – 24879 Raysal Mcdowell – 24880 Rock View Wyoming – 24881 Roderfield Mcdowell – 24882 Simon Wyoming – 24884 Squire Mcdowell View
Map 24887 Switchback Mcdowell – 24888 Thorpe Mcdowell – 24892 War Mcdowell – 24894 Warriormine Mcdowell – 24895 Wilcoe Mcdowell – 24898 Wyoming Wyoming – 24901 Lewisburg Greenbrier – 24902 Fairlea Greenbrier – 24910 Alderson Greenbrier – 24915 Arbovale Pocahontas – 24916 Asbury Greenbrier – 24918 Ballard Monroe – 24920 Bartow Pocahontas – 24924 Buckeye Pocahontas – 24925 Caldwell Greenbrier – 24927 Cass Pocahontas – 24931 Crawley Greenbrier – 24934 Dunmore Pocahontas – 24935 Forest Hill Summers View
Map 24938 Frankford Greenbrier – 24941 Gap Mills Monroe – 24943 Grassy Meadows Greenbrier – 24944 Green Bank Pocahontas – 24945 Greenville Monroe – 24946 Hillsboro Pocahontas – 24951 Lindside Monroe – 24954 Marlinton Pocahontas – 24957 Maxwelton Greenbrier – 24961 Neola Greenbrier – 24962 Pence Springs Summers – 24963 Peterstown Monroe – 24966 Renick Greenbrier – 24970 Ronceverte Greenbrier – 24974 Secondcreek Monroe – 24976 Sinks Grove Monroe – 24977 Smoot Greenbrier – 24981 Talcott Summers – 24983 Union Monroe View
Map 24984 Waiteville Monroe – 24985 Wayside Monroe – 24986 White Sulphur Springs Greenbrier – 24991 Williamsburg Greenbrier – 24993 Wolfcreek Monroe – 25002 Alloy Fayette – 25003 Alum Creek Kanawha – 25005 Amma Roane – 25007 Arnett Raleigh – 25008 Artie Raleigh – 25009 Ashford Boone – 25011 Bancroft Putnam – 25015 Belle Kanawha – 25019 Bickmore Clay – 25021 Bim Boone – 25022 Blair Logan – 25024 Bloomingrose Boone – 25025 Blount Kanawha – 25026 Blue Creek Kanawha View
Map 25028 Bob White Boone – 25030 Bomont Clay – 25031 Boomer Fayette – 25033 Buffalo Putnam – 25035 Cabin Creek Kanawha – 25036 Cannelton Fayette – 25039 Cedar Grove Kanawha – 25040 Charlton Heights Fayette – 25043 Clay Clay – 25044 Clear Creek Raleigh – 25045 Clendenin Kanawha – 25047 Clothier Logan – 25048 Colcord Raleigh – 25049 Comfort Boone – 25051 Costa Boone – 25053 Danville Boone – 25054 Dawes Kanawha – 25057 Deep Water Fayette – 25059 Dixie Nicholas View
Map 25060 Dorothy Raleigh – 25061 Drybranch Kanawha – 25062 Dry Creek Raleigh – 25063 Duck Clay – 25064 Dunbar Kanawha – 25067 East Bank Kanawha – 25070 Eleanor Putnam – 25071 Elkview Kanawha – 25075 Eskdale Kanawha – 25076 Ethel Logan – 25079 Falling Rock Kanawha – 25081 Foster Boone – 25082 Fraziers Bottom Putnam – 25083 Gallagher Kanawha – 25085 Gauley Bridge Fayette – 25086 Glasgow Kanawha – 25088 Glen Clay – 25090 Glen Ferris Fayette – 25093 Gordon Boone View
Map 25102 Handley Kanawha – 25103 Hansford Kanawha – 25106 Henderson Mason – 25107 Hernshaw Kanawha – 25108 Hewett Boone – 25109 Hometown Putnam – 25110 Hugheston Kanawha – 25111 Indore Clay – 25112 Institute Kanawha – 25113 Ivydale Clay – 25114 Jeffrey Boone – 25115 Kanawha Falls Fayette – 25118 Kimberly Fayette – 25119 Kincaid Fayette – 25121 Lake Logan – 25123 Leon Mason – 25124 Liberty Putnam – 25125 Lizemores Clay – 25126 London Kanawha View
Map 25130 Madison Boone – 25132 Mammoth Kanawha – 25133 Maysel Clay – 25134 Miami Kanawha – 25136 Montgomery Fayette – 25139 Mount Carbon Fayette – 25140 Naoma Raleigh – 25141 Nebo Clay – 25142 Nellis Boone – 25143 Nitro Kanawha – 25148 Orgas Boone – 25149 Ottawa Boone – 25152 Page Fayette – 25154 Peytona Boone – 25156 Pinch Kanawha – 25159 Poca Putnam – 25160 Pond Gap Kanawha – 25161 Powellton Fayette – 25162 Pratt Kanawha View
Map 25164 Procious Clay – 25165 Racine Boone – 25168 Red House Putnam – 25169 Ridgeview Boone – 25173 Robson Fayette – 25174 Rock Creek Raleigh – 25177 Saint Albans Kanawha – 25180 Saxon Boone – 25181 Seth Boone – 25183 Sharples Logan – 25185 Mount Olive Fayette – 25186 Smithers Fayette – 25187 Southside Mason – 25193 Sylvester Boone – 25201 Tad Kanawha – 25202 Tornado Kanawha – 25203 Turtle Creek Boone – 25204 Twilight Boone – 25205 Uneeda Boone View
Map 25206 Van Boone – 25208 Wharton Boone – 25209 Whitesville Boone – 25211 Widen Clay – 25213 Winfield Putnam – 25214 Winifrede Kanawha – 25231 Advent Jackson – 25234 Arnoldsburg Calhoun – 25235 Chloe Calhoun – 25239 Cottageville Jackson – 25241 Evans Jackson – 25243 Gandeeville Roane – 25244 Gay Jackson – 25245 Given Jackson – 25247 Hartford Mason – 25248 Kenna Jackson – 25251 Left Hand Roane – 25252 Le Roy Jackson – 25253 Letart Mason View
Map 25259 Looneyville Roane – 25260 Mason Mason – 25261 Millstone Calhoun – 25262 Millwood Jackson – 25264 Mount Alto Mason – 25265 New Haven Mason – 25266 Newton Roane – 25267 Normantown Gilmer – 25268 Orma Calhoun – 25270 Reedy Roane – 25271 Ripley Jackson – 25275 Sandyville Jackson – 25276 Spencer Roane – 25285 Wallback Clay – 25286 Walton Roane – 25287 West Columbia Mason – 25301 Charleston Kanawha – 25302 Charleston Kanawha – 25303 Charleston Kanawha View
Map 25304 Charleston Kanawha – 25305 Charleston Kanawha – 25306 Charleston Kanawha – 25309 Charleston Kanawha – 25311 Charleston Kanawha – 25312 Charleston Kanawha – 25313 Charleston Kanawha – 25314 Charleston Kanawha – 25315 Charleston Kanawha – 25317 Charleston Kanawha – 25320 Charleston Kanawha – 25321 Charleston Kanawha – 25322 Charleston Kanawha – 25323 Charleston Kanawha – 25324 Charleston Kanawha – 25325 Charleston Kanawha – 25326 Charleston Kanawha – 25327 Charleston Kanawha – 25328 Charleston Kanawha View
Map 25329 Charleston Kanawha – 25330 Charleston Kanawha – 25331 Charleston Kanawha – 25332 Charleston Kanawha – 25333 Charleston Kanawha – 25334 Charleston Kanawha – 25335 Charleston Kanawha – 25336 Charleston Kanawha – 25337 Charleston Kanawha – 25338 Charleston Kanawha – 25339 Charleston Kanawha – 25350 Charleston Kanawha – 25356 Charleston Kanawha – 25357 Charleston Kanawha – 25358 Charleston Kanawha – 25360 Charleston Kanawha – 25361 Charleston Kanawha – 25362 Charleston Kanawha – 25364 Charleston Kanawha View
Map 25365 Charleston Kanawha – 25375 Charleston Kanawha – 25387 Charleston Kanawha – 25389 Charleston Kanawha – 25392 Charleston Kanawha – 25396 Charleston Kanawha – 25401 Martinsburg Berkeley – 25402 Martinsburg Berkeley – 25403 Martinsburg Berkeley – 25404 Martinsburg Berkeley – 25405 Martinsburg Berkeley – 25410 Bakerton Jefferson – 25411 Berkeley Springs Morgan – 25413 Bunker Hill Berkeley – 25414 Charles Town Jefferson – 25419 Falling Waters Berkeley – 25420 Gerrardstown Berkeley – 25421 Glengary Berkeley – 25422 Great Cacapon Morgan View
Map 25423 Halltown Jefferson – 25425 Harpers Ferry Jefferson – 25427 Hedgesville Berkeley – 25428 Inwood Berkeley – 25429 Martinsburg Berkeley – 25430 Kearneysville Jefferson – 25431 Levels Hampshire – 25432 Millville Jefferson – 25434 Paw Paw Morgan – 25437 Points Hampshire – 25438 Ranson Jefferson – 25440 Ridgeway Berkeley – 25441 Rippon Jefferson – 25442 Shenandoah Junction Jefferson – 25443 Shepherdstown Jefferson – 25444 Slanesville Hampshire – 25446 Summit Point Jefferson – 25501 Alkol Lincoln – 25502 Apple Grove Mason View
Map 25503 Ashton Mason – 25504 Barboursville Cabell – 25505 Big Creek Logan – 25506 Branchland Lincoln – 25507 Ceredo Wayne – 25508 Chapmanville Logan – 25510 Culloden Cabell – 25511 Dunlow Wayne – 25512 East Lynn Wayne – 25514 Fort Gay Wayne – 25515 Gallipolis Ferry Mason – 25517 Genoa Wayne – 25520 Glenwood Mason – 25521 Griffithsville Lincoln – 25523 Hamlin Lincoln – 25524 Harts Lincoln – 25526 Hurricane Putnam – 25529 Julian Boone – 25530 Kenova Wayne View
Map 25534 Kiahsville Wayne – 25535 Lavalette Wayne – 25537 Lesage Cabell – 25540 Midkiff Lincoln – 25541 Milton Cabell – 25544 Myra Lincoln – 25545 Ona Cabell – 25547 Pecks Mill Logan – 25550 Point Pleasant Mason – 25555 Prichard Wayne – 25557 Ranger Lincoln – 25559 Salt Rock Cabell – 25560 Scott Depot Putnam – 25562 Shoals Wayne – 25564 Sod Lincoln – 25565 Spurlockville Lincoln – 25567 Sumerco Lincoln – 25569 Teays Putnam – 25570 Wayne Wayne View
Map 25571 West Hamlin Lincoln – 25572 Woodville Boone – 25573 Yawkey Lincoln – 25601 Logan Logan – 25606 Accoville Logan – 25607 Amherstdale Logan – 25608 Baisden Mingo – 25611 Bruno Logan – 25612 Chauncey Logan – 25614 Cora Logan – 25617 Davin Logan – 25621 Gilbert Mingo – 25624 Henlawson Logan – 25625 Holden Logan – 25628 Kistler Logan – 25630 Lorado Logan – 25632 Lyburn Logan – 25634 Mallory Logan – 25635 Man Logan View
Map 25637 Mount Gay Logan – 25638 Omar Logan – 25639 Peach Creek Logan – 25644 Sarah Ann Logan – 25646 Stollings Logan – 25647 Switzer Logan – 25649 Verdunville Logan – 25650 Verner Mingo – 25651 Wharncliffe Mingo – 25652 Whitman Logan – 25653 Wilkinson Logan – 25654 Yolyn Logan – 25661 Williamson Mingo – 25665 Borderland Mingo – 25666 Breeden Mingo – 25667 Chattaroy Mingo – 25669 Crum Wayne – 25670 Delbarton Mingo – 25671 Dingess Mingo View
Map 25672 Edgarton Mingo – 25674 Kermit Mingo – 25676 Lenore Mingo – 25678 Matewan Mingo – 25685 Naugatuck Mingo – 25686 Newtown Mingo – 25688 North Matewan Mingo – 25690 Ragland Mingo – 25691 Rawl Mingo – 25692 Red Jacket Mingo – 25696 Varney Mingo – 25697 Vulcan Mingo – 25699 Wilsondale Wayne – 25701 Huntington Cabell – 25702 Huntington Cabell – 25703 Huntington Cabell – 25704 Huntington Wayne – 25705 Huntington Cabell – 25706 Huntington Cabell View
Map 25707 Huntington Cabell – 25708 Huntington Cabell – 25709 Huntington Cabell – 25710 Huntington Cabell – 25711 Huntington Cabell – 25712 Huntington Cabell – 25713 Huntington Cabell – 25714 Huntington Cabell – 25715 Huntington Cabell – 25716 Huntington Cabell – 25717 Huntington Cabell – 25718 Huntington Cabell – 25719 Huntington Cabell – 25720 Huntington Cabell – 25721 Huntington Cabell – 25722 Huntington Cabell – 25723 Huntington Cabell – 25724 Huntington Cabell – 25725 Huntington Cabell View
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Map 26104 Parkersburg Wood – 26105 Vienna Wood – 26106 Parkersburg Wood – 26120 Mineral Wells Wood – 26121 Mineral Wells Wood – 26133 Belleville Wood – 26134 Belmont Pleasants – 26136 Big Bend Calhoun – 26137 Big Springs Calhoun – 26138 Brohard Wirt – 26141 Creston Wirt – 26142 Davisville Wood – 26143 Elizabeth Wirt – 26146 Friendly Tyler – 26147 Grantsville Calhoun – 26148 Macfarlan Ritchie – 26149 Middlebourne Tyler – 26150 Mineral Wells Wood – 26151 Mount Zion Calhoun View
Map 26152 Munday Calhoun – 26155 New Martinsville Wetzel – 26159 Paden City Wetzel – 26160 Palestine Wirt – 26161 Petroleum Ritchie – 26162 Porters Falls Wetzel – 26164 Ravenswood Jackson – 26167 Reader Wetzel – 26169 Rockport Wood – 26170 Saint Marys Pleasants – 26175 Sistersville Tyler – 26178 Smithville Ritchie – 26180 Walker Wood – 26181 Washington Wood – 26184 Waverly Wood – 26186 Wileyville Wetzel – 26187 Williamstown Wood – 26201 Buckhannon Upshur – 26202 Fenwick Nicholas View
Map 26203 Erbacon Webster – 26205 Craigsville Nicholas – 26206 Cowen Webster – 26208 Camden On Gauley Webster – 26209 Snowshoe Pocahontas – 26210 Adrian Upshur – 26215 Cleveland Upshur – 26217 Diana Webster – 26218 French Creek Upshur – 26219 Frenchton Upshur – 26222 Hacker Valley Webster – 26224 Helvetia Randolph – 26228 Kanawha Head Upshur – 26229 Lorentz Upshur – 26230 Pickens Randolph – 26234 Rock Cave Upshur – 26236 Selbyville Upshur – 26237 Tallmansville Upshur – 26238 Volga Barbour View
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Map 26278 Mabie Randolph – 26280 Mill Creek Randolph – 26282 Monterville Randolph – 26283 Montrose Randolph – 26285 Norton Randolph – 26287 Parsons Tucker – 26288 Webster Springs Webster – 26289 Red Creek Tucker – 26291 Slatyfork Pocahontas – 26292 Thomas Tucker – 26293 Valley Bend Randolph – 26294 Valley Head Randolph – 26296 Whitmer Randolph – 26298 Bergoo Webster – 26301 Clarksburg Harrison – 26302 Clarksburg Harrison – 26306 Clarksburg Harrison – 26320 Alma Tyler – 26321 Alum Bridge Lewis View
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Map 26369 Hepzibah Harrison – 26372 Horner Lewis – 26374 Independence Preston – 26376 Ireland Lewis – 26377 Jacksonburg Wetzel – 26378 Jane Lew Lewis – 26384 Linn Gilmer – 26385 Lost Creek Harrison – 26386 Lumberport Harrison – 26404 Meadowbrook Harrison – 26405 Moatsville Barbour – 26408 Mount Clare Harrison – 26410 Newburg Preston – 26411 New Milton Doddridge – 26412 Orlando Lewis – 26415 Pennsboro Ritchie – 26416 Philippi Barbour – 26419 Pine Grove Wetzel – 26421 Pullman Ritchie View
Map 26422 Reynoldsville Harrison – 26424 Rosemont Taylor – 26425 Rowlesburg Preston – 26426 Salem Harrison – 26430 Sand Fork Gilmer – 26431 Shinnston Harrison – 26434 Shirley Tyler – 26435 Simpson Taylor – 26436 Smithburg Doddridge – 26437 Smithfield Wetzel – 26438 Spelter Harrison – 26440 Thornton Taylor – 26443 Troy Gilmer – 26444 Tunnelton Preston – 26447 Walkersville Lewis – 26448 Wallace Harrison – 26451 West Milford Harrison – 26452 Weston Lewis – 26456 West Union Doddridge View
Map 26461 Wilsonburg Harrison – 26463 Wyatt Harrison – 26501 Morgantown Monongalia – 26502 Morgantown Monongalia – 26504 Morgantown Monongalia – 26505 Morgantown Monongalia – 26506 Morgantown Monongalia – 26507 Morgantown Monongalia – 26508 Morgantown Monongalia – 26519 Albright Preston – 26520 Arthurdale Preston – 26521 Blacksville Monongalia – 26524 Bretz Preston – 26525 Bruceton Mills Preston – 26527 Cassville Monongalia – 26531 Dellslow Monongalia – 26534 Granville Monongalia – 26537 Kingwood Preston – 26541 Maidsville Monongalia View
Map 26542 Masontown Preston – 26543 Osage Monongalia – 26544 Pentress Monongalia – 26546 Pursglove Monongalia – 26547 Reedsville Preston – 26554 Fairmont Marion – 26555 Fairmont Marion – 26559 Barrackville Marion – 26560 Baxter Marion – 26561 Big Run Wetzel – 26562 Burton Wetzel – 26563 Carolina Marion – 26566 Colfax Marion – 26568 Enterprise Harrison – 26570 Fairview Marion – 26571 Farmington Marion – 26572 Four States Marion – 26574 Grant Town Marion – 26575 Hundred Wetzel View
Map 26576 Idamay Marion – 26578 Kingmont Marion – 26581 Littleton Wetzel – 26582 Mannington Marion – 26585 Metz Marion – 26586 Montana Mines Marion – 26587 Rachel Marion – 26588 Rivesville Marion – 26590 Wana Monongalia – 26591 Worthington Marion – 26601 Sutton Braxton – 26610 Birch River Nicholas – 26611 Cedarville Gilmer – 26615 Copen Braxton – 26617 Dille Clay – 26619 Exchange Braxton – 26621 Flatwoods Braxton – 26623 Frametown Braxton – 26624 Gassaway Braxton View
Map 26627 Heaters Braxton – 26629 Little Birch Braxton – 26631 Napier Braxton – 26636 Rosedale Gilmer – 26638 Shock Gilmer – 26651 Summersville Nicholas – 26656 Belva Nicholas – 26660 Calvin Nicholas – 26662 Canvas Nicholas – 26667 Drennen Nicholas – 26671 Gilboa Nicholas – 26675 Keslers Cross Lanes Nicholas – 26676 Leivasy Nicholas – 26678 Mount Lookout Nicholas – 26679 Mount Nebo Nicholas – 26680 Nallen Fayette – 26681 Nettie Nicholas – 26684 Pool Nicholas – 26690 Swiss Nicholas View
Map 26691 Tioga Nicholas – 26704 Augusta Hampshire – 26705 Aurora Preston – 26707 Bayard Grant – 26710 Burlington Mineral – 26711 Capon Bridge Hampshire – 26714 Delray Hampshire – 26716 Eglon Preston – 26717 Elk Garden Mineral – 26719 Fort Ashby Mineral – 26720 Gormania Grant – 26722 Green Spring Hampshire – 26726 Keyser Mineral – 26731 Lahmansville Grant – 26739 Mount Storm Grant – 26743 New Creek Mineral – 26750 Piedmont Mineral – 26753 Ridgeley Mineral – 26755 Rio Hampshire View
Map 26757 Romney Hampshire – 26761 Shanks Hampshire – 26763 Springfield Hampshire – 26764 Terra Alta Preston – 26767 Wiley Ford Mineral – 26801 Baker Hardy – 26802 Brandywine Pendleton – 26804 Circleville Pendleton – 26807 Franklin Pendleton – 26808 High View Hampshire – 26810 Lost City Hardy – 26812 Mathias Hardy – 26814 Riverton Pendleton – 26815 Sugar Grove Pendleton – 26817 Bloomery Hampshire – 26818 Fisher Hardy – 26823 Capon Springs Hampshire – 26833 Maysville Grant – 26836 Moorefield Hardy View
Map 26838 Milam Hardy – 26845 Old Fields Hardy – 26847 Petersburg Grant – 26851 Wardensville Hardy – 26852 Purgitsville Hampshire – 26855 Cabins Grant – 26865 Yellow Spring Hampshire – 26866 Upper Tract Pendleton – 26884 Seneca Rocks Pendleton – 26886 Onego Pendleton

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Vibrating gloves for osteoarthritis

Osteoarthritis Chronic Hand Pain May Be Improved With Vibrating Gloves

Efficacy of Vibrating Gloves for Chronic Hand Pain due to Osteoarthritis

Vibrating gloves may help reduce hand pain in women with hand osteoarthritis (OA). The findings were presented at the American Pain Society’s 36th Annual Scientific Meeting held May 17-20, 2017 in Pittsburgh, Pennsylvania.1

To study whether gloves that massage the hands via mild compression and light vibration had lasting benefit with periodic use, the researchers randomly assigned 60 women with hand OA pain to either wear the gloves for 20 minutes a day or to be monitored without the gloves, for a period of 3 months.

All participants were assessed at baseline via questionnaires, subjected to a brief quantitative sensory test (QST), and indicated their pain level on a daily basis using a smartphone app. The app reminded participants to complete daily assessments of their pain, sleep, activity interference, mood, and any perceived change. The participants also completed written questionnaires at 6 weeks and 3 months.

The researchers had potential participants try on the gloves to assess whether they would agree to wear them during the 3-month trial; 3 participants (<5%) did not want to participate after trying on the gloves.

The average age of participants was 62.7±7.7. Pain intensity averaged 4.1±1.9 on a scale of 0 to 10, and participants reported having pain for an average of 11.5±9.6 years. Most of the participants were right-handed (88.5%), and 50.0% reported primarily right hand pain.

Over time, the participants wore the gloves less often — an average of 5.2 days a week.

Compared with the control group, patients in the experimental group had reduced pain intensity (P <.05). There were no differences in mood or sleep. Individuals with greater sensitivity on the QST showed most benefit from wearing the gloves (P <.05).

 

 

Transcranial Magnetic Stimulation (TMS) for Knee pain osteoarthritis and other great things

Transcranial Direct Current Stimulation Effective for Knee OA Pain

Transcranial direct current stimulation (tDCS) can effectively alleviate osteoarthritis (OA)-related knee pain, according to results from a double-blind, randomized and sham-controlled pilot clinical study presented at the American Pain Society’s 36th Annual Scientific Meeting in Pittsburgh, Pennsylvania. Upon session completion, participants in the tDCS group showed improved analgesia compared with patients in the sham tDCS group, as indicated by reported pain ratings (on a 0 to 100 numeric scale: 18.50 ± 3.60 vs 6.45 ± 2.26; mean difference 12.05 [P =.007]).

Efficacy of Transcranial Direct Current Stimulation on Clinical Pain Severity in Older Adults with Knee Osteoarthritis Pain A Double-Blind, Randomized, Sham-Controlled Pilot Clinical S

The knee joint is the most affected one in individuals with OA, the most prevalent type of arthritis and itself a major cause of disability in individuals aged ≥45 years. Although OA pain is commonly managed pharmacologically, these treatments (eg, tapentadol, corticosteroids) are often associated with adverse effects.2,3Neuromodulation of central pain pathways therefore represents an attractive alternative for the treatment of chronic pain, including knee OA-related pain. tDCS, a noninvasive technique increasingly used for the treatment of several conditions that include chronic pain, as well as motor and psychiatric disorders, exerts its effects by depolarizing (anodal tDCS) or hyperpolarizing (cathodal tDCS) cortical neurons.4,5

The current study aimed to evaluate the efficacy of tDCS in alleviating knee OA pain. Study participants (n = 40; mean age, 59 years; ages 50 to 70 years; 53% women) were randomly assigned to receive tDCS (2 mA) or sham tDCS for 20 minutes daily over a 5-day period. tDCS electrodes were placed on the primary motor cortex of the side contralateral to the painful knee (anode) and on the supraorbital region ipsilaterally (cathode).

Story from clinical pain adviser.

 

Evidence-based guidelines on the therapeutic use of transcranial direct current stimulation (tDCS).

Abstract

A group of European experts was commissioned by the European Chapter of the International Federation of Clinical Neurophysiology to gather knowledge about the state of the art of the therapeutic use of transcranial direct current stimulation (tDCS) from studies published up until September 2016, regarding pain, Parkinson’s disease, other movement disorders, motor stroke, poststroke aphasia, multiple sclerosis, epilepsy, consciousness disorders, Alzheimer’s disease, tinnitus, depression, schizophrenia, and craving/addiction. The evidence-based analysis included only studies based on repeated tDCS sessions with sham tDCS control procedure; 25 patients or more having received active treatment was required for Class I, while a lower number of 10-24 patients was accepted for Class II studies. Current evidence does not allow making any recommendation of Level A (definite efficacy) for any indication. Level B recommendation (probable efficacy) is proposed for: (i) anodal tDCS of the left primary motor cortex (M1) (with right orbitofrontal cathode) in fibromyalgia; (ii) anodal tDCS of the left dorsolateral prefrontal cortex (DLPFC) (with right orbitofrontal cathode) in major depressive episode without drug resistance; (iii) anodal tDCS of the right DLPFC (with left DLPFC cathode) in addiction/craving. Level C recommendation (possible efficacy) is proposed for anodal tDCS of the left M1 (or contralateral to pain side, with right orbitofrontal cathode) in chronic lower limb neuropathic pain secondary to spinal cord lesion. Conversely, Level B recommendation (probable inefficacy) is conferred on the absence of clinical effects of: (i) anodal tDCS of the left temporal cortex (with right orbitofrontal cathode) in tinnitus; (ii) anodal tDCS of the left DLPFC (with right orbitofrontal cathode) in drug-resistant major depressive episode. It remains to be clarified whether the probable or possible therapeutic effects of tDCS are clinically meaningful and how to optimally perform tDCS in a therapeutic setting. In addition, the easy management and low cost of tDCS devices allow at home use by the patient, but this might raise ethical and legal concerns with regard to potential misuse or overuse. We must be careful to avoid inappropriate applications of this technique by ensuring rigorous training of the professionals and education of the patients.

Efficacy of transcranial direct current stimulation and repetitive transcranial magnetic stimulation for treating fibromyalgia syndrome a systematic review.

 To systematically review the literature to date applying repetitive transcranial magnetic stimulation (rTMS) or transcranial direct current stimulation (tDCS) for patients with fibromyalgia syndrome (FMS).

METHOD:

 Electronic bibliography databases screened included PubMed, Ovid MEDLINE, PsychINFO, CINAHL, and Cochrane Library. The keyword “fibromyalgia” was combined with (“transcranial” and “stimulation”) or “TMS” or “tDCS” or “transcranial magnetic stimulation” or “transcranial direct current stimulation”.

RESULTS:

 Nine of 23 studies were included; brain stimulation sites comprised either the primary motor cortex (M1) or the dorsolateral prefrontal cortex (DLPFC). Five studies used rTMS (high-frequency-M1: 2, low-frequency-DLPFC: 2, high-frequency-DLPFC: 1), while 4 applied tDCS (anodal-M1: 1, anodal-M1/DLPFC: 3). Eight were double-blinded, randomized controlled trials. Most (80%) rTMS studies that measured pain reported significant decreases, while all (100%) tDCS studies with pain measures reported significant decreases. Greater longevity of significant pain reductions was observed for excitatory M1 rTMS/tDCS.

CONCLUSION:

 Studies involving excitatory rTMS/tDCS at M1 showed analogous pain reductions as well as considerably fewer side effects compared to FDA apaproved FMS pharmaceuticals. The most commonly reported side effects were mild, including transient headaches and scalp discomforts at the stimulation site. Yearly use of rTMS/tDCS regimens appears costly ($11,740 to 14,507/year); however, analyses to apapropriately weigh these costs against clinical and quality of life benefits for patients with FMS are lacking. Consequently, rTMS/tDCS should be considered when treating patients with FMS, particularly those who are unable to find adequate symptom relief with other therapies. Further work into optimal stimulation parameters and standardized outcome measures is needed to clarify associated efficacy and effectiveness.

Transcranial Magnetic Stimulation-Mediated Analgesia is Independent of Improvements in Depression

Repetitive transcranial magnetic stimulation of the right secondary somatosensory motor cortex (S2) produces pain relief in patients with chronic neuropathic orofacial pain, an effect that was shown to be direct, and not a result of improvements in psychiatric or sleep disorder comorbidities. These findings were published in November in Medicine

The study participants had been diagnosed by a neurologist and an orofacial pain physician as follows: 7 had trigeminal neuropathic pain, 4 had atypical facial pain, and 5 had burning mouth syndrome. All patients displayed dysfunction of the trigeminal small- (and also large-, in some) fiber system, as well as a score ≥4 on the 0 to 10 numerical rating scale (NRS) for chronic daily neuropathic orofacial pain (daily average, 5.7; mean duration, 10.4 years).

Each study participant received 3 rTMS treatments (one of which was a placebo session), administered 4 weeks apart in a single-blind/within-subject manner. Stimulations (50 pulses at 90% of the resting motor threshold, every 10 s) targeted the facial area within the somatotopic representation of the primary sensorimotor cortex (S1/M1) and S2 in a random order.

Patients were assessed for psychiatric disorders based on the structured clinical interview for axis I disorders.3 Pain, mood, sleep and quality of life were assessed by study participants using the NRS to rate both pain and sleep and collected in study diaries for 4 weeks prior to and following treatment.

In addition, total hours of sleep, intensity, and interference of pain (measured using the Brief Pain Inventory),4 and sleep characteristics (assessed using the Basic Nordic Sleep Questionnaire),5 were all reported.

A more thorough assessment of sleep quality, measuring the 6 dimensions of sleep (ie, sleep disturbance , snoring, awakening with shortness of breath or headache, sleep adequacy, daytime somnolence, and quantity of sleep) was achieved through the Medical Outcomes Study (MOS) Sleep Measure, prior to and 1 month following each rTMS session.6

The authors found that neither sleep nor psychiatric disorders or medications (eg, opioids) had predictive value for rTMS treatment efficacy in study participants. The treatments had no detectable impact on either mood (assessed with the Beck Depression Inventory),7 or sleep quality.

Pain scores specific to neuropathic pain — but not to general pain — were reduced following S2 stimulation, as indicated by lower scores on the Neuropathic Pain Impact on Quality-of-Life questionnaire8 in treated vs sham-stimulated patients (P=.0031).

Six (38%) and 10 (63%) of the patients had a current or lifetime psychiatric disorder (depression or anxiety), respectively.

The authors concluded that “the present results show that the analgesic effect of rTMS given to the right S2 cortex as previously reported is most likely due to a direct action on specific top-down pain modulation networks rather than a result of an indirect action via improvement of comorbid psychiatric or sleep disturbances.”

They also added that “S2 stimulation had no effect on depressive symptoms, sleep diary measures, or the MOS sleep scale index scores, and that “comorbidities such as depression, anxiety disorders, and sleep problems did not predict the rTMS treatment outcome.”

The analgesic effect of therapeutic rTMS is not mediated or predicted by comorbid psychiatric or sleep disorders

Lindholm P, Lamusuo S, Taiminen T, et al. The analgesic effect of therapeutic rTMS is not mediated or predicted by comorbid psychiatric or sleep disorders. Medicine (Baltimore). 2016;95(44)

Lindholm P, Lamusuo S, Taiminen T, et al. Right secondary somatosensory cortex-a promising novel target for the treatment of drug-resistant neuropathic orofacial pain with repetitive transcranial magnetic stimulation. Pain. 2015;156(7):1276-1283

Right secondary somatosensory cortex-a promising novel target for the treatment of drug-resistant neuropathic orofacial pain with repetitive transcranial magnetic stimulation

Transcranial Direct Current Stimulation in Epilepsy

Results: We analyzed 9 articles with different methodologies (3 animals/6 humans) with a total of 174 stimulated individuals; 109 animals and 65 humans. In vivo and in vitro animal studies showed that direct current stimulation can successfully induce suppression of epileptiform activity without neurological injury and 4/6 (67%) clinical studies showed an effective decrease in epileptic seizures and 5/6 (83%) reduction of inter-ictal epileptiform activity. All patients tolerated tDCS well. Conclusions: tDCS trials have demonstrated preliminary safety and efficacy in animals and patients with epilepsy. Further larger studies are needed to define the best stimulation protocols and long-term follow-up.

Beck AT, Rial WY, Rickels K. Short form of depression inventory: crossvalidation. Psychol Rep. 1974;34:1184–1186

 

 

 

Nanoparticles and gut effects – generally recognized as safe?

Models for oral uptake of nanoparticles in consumer products

Titanium dioxide nanoparticle ingestion alters nutrient absorption in an in vitro model of the small intestine

Zhongyuan Guo, Nicole J. Martucci, Fabiola Moreno-Olivas, Elad Tako, Gretchen J. Mahler. Titanium dioxide nanoparticle ingestion alters nutrient absorption in an in vitro model of the small intestine. NanoImpact, 2017; 5: 70 DOI: 10.1016/j.impact.2017.01.002

In the study above, researchers took a meal’s worth of titanium oxide nanoparticles — 30 nanometers across — over four hours (acute exposure), or three meal’s worth over five days (chronic exposure) and determined the effect on the gut. Acute exposure caused no harm,  but chronic exposure diminished the absorptive projections on the surface of intestinal cells called microvilli. With fewer microvilli, the intestinal barrier was weakened, metabolism slowed and some nutrients — iron, zinc, and fatty acids, specifically — were more difficult to absorb. Enzyme functions were negatively affected, while inflammation signals increased. It turns out that nanoparticles are everywhere, especially in food, cosmetics, and pharmaceuticals. It can enter the digestive system through toothpastes, since Titanium dioxide is used to create abrasion needed for cleaning. The oxide is also used in some chocolate to give it a smooth texture; in donuts to provide color; and in skimmed milks for a brighter, more opaque appearance which makes the milk more palatable. Dunkin Donuts stopped using powdered sugar with titanium dioxide nanoparticles in 2015 in response to pressure from the advocacy group As You Sow.

http://www.binghamton.edu/us/story/417/food-additive-found-in-candy-chewing-gum-could-alter-digestive-cell-structu

There is emerging evidence that we have generated strategies to utilise nanoparticles for dietary and physiological benefit evolutionarily.  Thus, nanoparticulate structures are neither inherently toxic nor inherently safe: like all molecules these decisions will rest upon molecular structure, biological environment, degree of exposure and host susceptibility.

Nanoparticues act in a number of wasy internally, especially in the gut lumen, where they are exposed to mucin, proteins, pH changes, and other existing charged particles. There has been described a protein coating of nanoparticle surfaces, referred to as a ‘corona’, this phenomenon has been known for decades and will inevitably happen in the particle’s native environment. In the gastrointestinal tract it is likely that the acidic pH of the stomach, which mainly is maintained even postprandially, and the presence of gastrointestinal enzymes, will serve to denude ingested particles of their surface-adsorbed molecules but then re-adsorption of novel entities will occur in the less acidic small bowel lumen.

There are many exogenous inorganic particles are man-made particles comprising titanium dioxide or silicates/aluminosilicates. Titanium dioxide (designated E171 in Europe) is used for whitening and brightening foods, especially for confectionary, white sauces and dressings, and certain powdered foods.

Titanium dioxide (designated E171 in Europe) is used for whitening and brightening foods, especially for confectionary, white sauces and dressings, and certain powdered foods. It is also used in the pharmaceutical industry as an opacity agent. Titanium dioxide is typically found in gut tissue in the anatase polymorphic form and is a 100-200 nm diameter spherical particle that is resistant to gastrointestinal degradation. Particulate silicates and aluminosilicates (E554, E556 and E559 in Europe) are used in the food industry as anti-caking agents and to allow the flow of powders, and some are present in cheeses, sugars and powdered milks. In the UK, the major five food sources of particulate silicates are salt, drinking powders, chewing gum, instant pot savory snacks and icing sugar.Overall, intake of dietary inorganic microparticles in the UK has been estimated to be about 40 mg/person/day (35 mg for the silicates and 5 mg for titanium dioxide) which equates to a staggering daily exposure of 101214 particles/person.

How are  the partciles taken up in the gut? M-cell-uptake (transcytosis) at the surface of intestinal lymphoid aggregates is the quintessential pathway for gut particle uptake and is very well described, especially for large nanoparticles (20-100 nm) and small microparticles (100-500 nm). Hydrophobic particles appear to be much better taken up than hydrophilic particles,  and  generally, small particles are better taken up than large ones with, perhaps, an optimal size of around 50 nm diameter.

Other sources of nanoparticles (NM) relevant for oral exposure comprise mainly cosmetics (sunscreen, lipsticks, skin creams, toothpaste) and food (packaging, storage life sensors, food additives, juice clarifiers). Whereas NMs in food are intended to be ingested, nanoparticles for instance in cosmetics and ingredients in food packaging may accidently get into the gastrointestinal tract. Major materials used in these products are: silver, and metal oxides of zinc, silica, and titanium. Nanosilver (Ag) is used in food packaging. According to the Woodrow Wilson Nanotechnology Consumer Products Inventory 2011, Ag nanoparticles are the most commonly used new NM in consumer products followed by TiO2, ZnO, platinum (Pt) and silicium oxide NMs (http://www.nanotechproject.org/inventories/consumer/). Although gold NMs are also used in cosmetics, food packaging, beverage and toothpaste their main applications are in the medical field.

Decrease of particle size in the nanoscale has been identified as a main parameter for the increased toxicity of different materials. Polystyrene, for instance, is a very biocompatible polymer used in cell culture. Nanoparticles, however, made from this material are cytotoxic.

Compared to other metal and metal oxide nanoparticles intake of TiO2 by food is relatively high at 5 mg TiO2/person/d .Metal and metal oxide nanoparticles can accumulate in plants  and in animals of the food chain. That is worrisome.

A number of factors effect uptake of particles by the gut. Even in healthy individuals gastrointestinal transit is by far not constant and shows considerable variation through the large intestine . These effects are known to influence oral bioavailability of conventional drugs but are even more important for the effects of NMs because NMs readily adsorb proteins. Mucus represents an efficient acellular barrier. Mucus consists of mucin proteins (highly glycosylated extracellular proteins with characteristic gel-forming properties), antiseptic proteins (lysozyme) and other proteins (lactoferrin), inorganic salts and water. The major functions are the protection and the lubrication of the underlying tissue. The saliva, which is produced by the salivary glands, mainly consists of water (up to 99.5%), inorganic salts, proteins, and mucins. The high molecular weight mucin MG1 can bind to the surface of the epithelium and build the so-called mucus layer, displaying the acellular barrier of the oral cavity The mucus of the following parts, stomach and small and large intestine, is mainly produced by intraepithelial cells, and hickness increases from proximal to distal parts of the small and large intestine . Depending on the method used for the determination, the thickness of the mucus layer shows marked variation..The characteristics facilitating the passage through human mucus are relatively well known: electrostatic repulsion from negatively charged sugar moieties favors the penetration of positively charged hydrophilic molecules; the passage of lipophilic compounds is slow. Viruses, like the Norwalk virus with a size of 38 nm and human papilloma virus with a size of 55 nm diffused in human mucus as rapidly as they do in water These findings suggest that the surface charge plays a crucial role in the transport rates of nanoparticles through a mucus layer

In addition to particle size, dose and duration of the exposure are important for the interpretation of the data. In addition to particle size, dose and duration of the exposure are important. There is  a size-dependent decrease of the uptake from 34% for 50 nm particles to 26% for 100 nm particles , and dose and duration of the exposure are also important for absorption and uptake of NM.

Changes in mucus composition induced by Ag nanoparticles (Jeong et al., 2010), polystyrene particles and diesel exhaust increased mucus permeability and permeation of small molecules by a factor of 5. Thus NM enter more quickly through disease barriers.

The adherence of polystyrene nanoparticles to inflamed colonic mucosa was much higher than to normal mucosa. Inflammation appears to increase uptake and permeation of NMs in vitro and in vivo. Inflammation caused by Yersinia pseudotuberculosis increases the uptake of 100 nm carboxyl polystyrene particles in cell monolayers and in intestinal biopsies. Other factors of absorption include pH and thickness of the mucus layer, the gastrointestinal flora and in gastrointestinal passage time (motility)

Whereas plasma membranes restrict the cellular access for metal ions like silver cations, silver nanoparticles were readily internalized and intracellular silver concentrations were much higher than for silver ions. Studies for uptake and toxicity should, therefore, include AgNO3 for silver nanoparticles (Trojan horse effect) or bulk material.. Absorption may also be altered by a changed metabolization by enterocytes. Polystyrene and silver particles have been shown to inhibit the activity of cytochrome P450 enzymes, of note

To avoid foods rich in titanium oxide nanoparticles you should avoid processed foods, and especially candy. This information may make one question if these NM have any impact on the surge of colitis seen ion the general poplulation? How about autoimmune diseases? How about general inflammation, for if NM damage the intestinal barrier, inflammation results and it’s attendant consequences.

 

http://www.nanotechproject.org/cpi/

MIND diet and complex nutritional interactions

 

Hybrid ‘MIND’ Diet Keeps Aging Brain Sharp

MIND diet slows cognitive decline with aging.

Physical Activity Recommendations for the Aging Brain A Clinician-Patient Guide

Is the Mediterranean diet a feasible approach to preserving cognitive function and reducing risk of dementia

Detoxification reactions Relevance to aging

Dietary patterns, cognitive decline, and dementia a systematic review.

Are Anxiety Disorders Associated with Accelerated Aging A Focus on Neuroprogression.

Mediterranean Diet, Cognitive Function, and Dementia A Systematic Review

Highlights From the Institute for Functional Medicine’s 2014 Annual Conference Functional Perspectives on Food and NutritionThe Ultimate Upstream Medicine.

“MIND” is an acronym for Mediterranean-DASH Diet Intervention for Neurodegenerative Delay. Both the Mediterranean and DASH diets have been found to reduce the risk for hypertension, myocardial infarction, and stroke.

What Are the Components to the MIND Diet

MIND diet associated with reduced incidence of Alzheimer’s disease

The MIND diet has 15 dietary components, including 10 “brain-healthy” food groups and five unhealthy groups (ie, red meat, butter and stick margarine, cheese, pastries and sweets, and fried or fast food). To stick to the MIND diet, a person has to limit intake of the designated unhealthy foods, especially butter (<1 tablespoon/day), sweets and pastries, whole fat cheese, and fried or fast food (<1 serving a week for any of the three). As for the brain-healthy foods, a person would need to eat at least three servings of whole grains, a green leafy vegetable, and one other vegetable each day, along with having a glass of wine. They would also need to snack most days on nuts, have beans every other day or so, and eat poultry and berries at least two times a week (berries are the only fruits allowed in the MIND diet) and fish at least once a week. The overall rate of change in cognitive score was a decline of 0.8 standardized score units per year. In mixed models adjusted for a variety of relevant factors, including age, sex, education, total energy intake, APOE4 carrier status, and participation in cognitive activities, the MIND diet score was “positively and statistically significantly” associated with slower decline in global cognitive score (β = 0.0092; P < .0001) and with five cognitive domains, especially episodic memory, semantic memory, and perceptual speed, the researchers report. If a person is eating in a manner that is heart healthy, that’s probably also going to be brain healthy, because the brain does use so much of the nutrients and the oxygen that are carried in the vascular system, and as you age, if your brain isn’t getting enough nutrients and oxygen, it is going to be less likely to be able to deal with other factors that cause Alzheimer’s disease or other dementias. 

Dietary intakes of berries and flavonoids in relation to cognitive decline  Results: Greater intakes of blueberries and strawberries were associated with slower rates of cognitive decline (eg, for a global score averaging all 6 cognitive tests, for blueberries: p-trend ¼ 0.014 and mean difference ¼ 0.04, 95% confidence interval [CI] ¼ 0.01–0.07, comparing extreme categories of intake; for strawberries: p-trend ¼ 0.022 and mean difference ¼ 0.03, 95% CI ¼ 0.00–0.06, comparing extreme categories of intake), after adjusting for multiple potential confounders. These effect estimates were equivalent to those we found for approximately 1.5 to 2.5 years of age in our cohort, indicating that berry intake appears to delay cognitive aging by up to 2.5 years. Additionally, in further supporting evidence, greater intakes of anthocyanidins and total flavonoids were associated with slower rates of cognitive decline (p-trends ¼ 0.015 and 0.053, respectively, for the global score). Interpretation: Higher intake of flavonoids, particularly from berries, appears to reduce rates of cognitive decline in older adults.

http://www.medscape.com/viewarticle/863839

Diet and Cognitive Decline Untangling the Evidence

When it comes to single or multiple nutrients, the evidence has also exploded. For example, omega-3 fatty acids or E vitamins, curcumin, vitamin D, and caffeinated foods: These are all different dietary components that may or may not play a role in development of Alzheimer disease. Dr Martha Clare Morris and her colleagues from Rush University presented a great paper that studied very specific brain-healthy eating patterns, which she calls the MIND diet, with the results suggesting a reduction in the likelihood of developing cognitive impairment significantly over several years.  omega-3 fatty acids: First of all, not all omega-3’s are created equal. DHA and EPA have the most evidence for reducing a person’s risk of developing cognitive decline. The key here is that certain people with different genes may respond preferentially; people with an ApoE4 gene may respond favorably while people without that gene may respond less. When it comes to Alzheimer’s treatment, those omega-3’s didn’t pan out in terms of randomized studies, but omega-3’s used for Alzheimer’s prevention or risk reduction are something we want to think about. Also, when it comes to personalized medicine based on genes, we can focus on Alzheimer disease in a new area called clinical precision medicine, where we look not only at genetics, but also at people’s individual biologies, nutritional patterns, and lifestyle patterns, and then give a clinically precise approach for treatment or prevention. For example, if a person has high homocysteine levels, then B complex vitamins—folic acid, B12, and B6—in randomized studies have been shown to slow overall brain atrophy as well as increase memory function. The key take-home point here is that B complex therapy only works in patients who have high homocysteine levels and those who have an adequate level of omega-3’s in the blood. When it comes to blueberries, you’ve heard about flavonols. Dark cocoa powder may be effective for boosting memory. You can’t just eat one blueberry and think you’re going to prevent or cure Alzheimer disease—it doesn’t work that way. But in the Nurses’ Health Study,[3] a half a cup of blueberries two to three times a week was shown to delay the onset of cognitive decline.

Cocoa flavanol consumption improves cognitive function, blood pressure control, and metabolic profile in elderly subjects the Cocoa, Cognition, and Aging (CoCoA) Study : This dietary intervention study provides evidence that regular CF consumption can reduce some measures of age-related cognitive dysfunction, possibly through an improvement in insulin sensitivity. These data suggest that the habitual intake of flavanols can support healthy cognitive function with age. Abstract—Flavanol consumption is favorably associated with cognitive function. We tested the hypothesis that dietary flavanols might improve cognitive function in subjects with mild cognitive impairment. We conducted a double-blind, parallel arm study in 90 elderly individuals with mild cognitive impairment randomized to consume once daily for 8 weeks a drink containing 990 mg (high flavanols), 520 mg (intermediate flavanols), or 45 mg (low flavanols) of cocoa flavanols per day. Cognitive function was assessed by Mini Mental State Examination, Trail Making Test A and B, and verbal fluency test. At the end of the follow-up period, Mini Mental State Examination was similar in the 3 treatment groups (P0.13). The time required to complete Trail Making Test A and Trail Making Test B was significantly (P0.05) lower in subjects assigned to high flavanols (38.1010.94 and 104.1028.73 seconds, respectively) and intermediate flavanols (40.2011.35 and 115.9728.35 seconds, respectively) in comparison with those assigned to low flavanols (52.6017.97 and 139.2343.02 seconds, respectively). Similarly, verbal fluency test score was significantly (P0.05) better in subjects assigned to high flavanols in comparison with those assigned to low flavanols (27.506.75 versus 22.308.09 words per 60 seconds). Insulin resistance, blood pressure, and lipid peroxidation also decreased among subjects in the high-flavanol and intermediate-flavanol groups. Changes of insulin resistance explained 40% of composite z score variability through the study period (partial r2 0.4013; P0.0001). To the best of our knowledge, this is the first dietary intervention study demonstrating that the regular consumption of cocoa flavanols might be effective in improving cognitive function in elderly subjects with mild cognitive impairment. This effect appears mediated in part by an improvement in insulin sensitivity. 

Benefits in Cognitive Function, Blood Pressure, and Insulin Resistance Through Cocoa Flavanol Consumption in Elderly Subjects With Mild Cognitive Impairment

9 Brain Boosting Benefits of Dark Chocolate

 

The effect of flavanol-rich cocoa on cerebral perfusion in healthy older adults during conscious resting state

Results Significant increases in regional perfusion across the brain were observed following consumption of the high flavanol drink relative to the low flavanol drink, particularly in the anterior cingulate cortex and the central opercular cortex of the parietal lobe.

The prevention and treatment of cognitive decline and dementia_ An overview of recent research on experimental treatments

Diet and Alzheimer’s disease risk factors or prevention the current evidence

Polyphenol Stilbenes Molecular Mechanisms of Defence against Oxidative Stress and Aging-Related Diseases.

Phytochemical Compounds and Antioxidant Capacity of Tucum-Do-Cerrado (Bactris setosa Mart), Brazil’s Native Fruit.

Polyphenols multipotent therapeutic agents in neurodegenerative diseases.

Pinosylvin-mediated protection against oxidative stress in human retinal pigment epithelial cells.

Mechanisms of Neuroprotection by Quercetin Counteracting Oxidative Stress and More.

Antioxidants inhibit neuronal toxicity in Parkinson’s disease-linked LRRK2.