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New research is connecting genetic variations to schizophrenia and other mental illnesses

The conversation Article

We know that changes in our genetic code can be associated with an increased risk for psychiatric illnesses such as schizophrenia and bipolar disorder. But how can a genetic mutation lead to complex psychiatric symptoms such as vivid hallucinations, manic episodes and bizarre delusions?

To find out, researchers are trying to fill in the blanks between the genetic blueprint (genotype) and psychiatric disorder (psychiatric phenotype). Phenotypes are a set of observable characteristics that result when a particular genotype interacts with its environment. The phenotype is the eventual outcome of a specific genotype.

But between genotype and psychiatric phenotype lie many measurable traits that together are called endophenotypes. This is an aspect of genetics that scientists are just starting to understand.

The National Institute of Mental Health has recently begun an initiative to push researchers to study endophenotypes with a program called Research Domain Criterion (RDoC), described as an effort to study basic dimensions of functioning that underlie human behavior.

So what exactly are endophenotypes, and how might they contribute to psychiatric illnesses?

Endophenotypes lie between genes and psychiatric phenotypes

An endophenotype can refer to anything from the size and shape of brain cells, to changes in brain structure, to impairments in working memory. The term can refer to a physical trait or a functional one.

An endophenotype must be associated with a specific psychiatric illness, such as schizophrenia, and it must be heritable. It must also be present even if the illness is not active. Within families, the endophenotype must be more common in ill family members than in healthy family members. But the endophenotype must be more common among nonaffected relatives of people with the associated illness than among the general population.

Certain endophenotypes are thought to precede behavioral symptoms. For instance, in several conditions, such as schizophrenia and Alzheimer’s disease, changes in brain structure have been found years before the onset of symptoms.

Currently doctors diagnose a psychiatric disorder based on the patient’s symptoms. The underlying neurobiology isn’t usually considered, because we lack the data to really use it.

In the future, endophenotypes might let us detect who is susceptible to psychiatric illness before clinical symptoms develop. That means we could try to combat, or at least appease, the symptoms of the disorder before they start. And knowing how endophenotypes contribute to these disorders could lead to precision medicine treatments.

How do you study endophenotypes?

One way to study the endophenotypes is to focus on a specific genetic alteration that is associated with a psychiatric disorder. This way we can get a sense of what brain changes the genetic change causes.

The links leading from genetic alterations to psychiatric illness in 22q11.2 Deletion Syndrome. Rachel Jonas, CC BY

For instance, I study a genetic disorder called 22q11.2 Deletion Syndrome (also called 22q11DS). The syndrome is due to a deletion of up to 60 genes, many of which are linked to brain function. About 30 percent of individualswith 22q11DS will develop schizophrenia (the rate in the U.S. population overall is about one percent).

Studying 22q11DS lets us draw a line from a genetic alteration to a psychiatric phenotype, such as decreased neural function, brain structure changes or fewer neurons in certain parts of the brain, and to a psychiatric phenotype, such as schizophrenia.

Let’s go through some concrete examples of how this can be done.

22q11DS: a model syndrome to study endophenotypes

In one study researchers looked at a group of 70 children and adolescents with 22q11DS, and found deficits in executive function (which encompasses cognitive processes such as motivation, working memory and attention) in patients with 22q11DS.

In fact, researchers were actually able to predict subsequent development of psychotic symptoms in individuals with 22q11DS. This study shows that cognitive endophenotypes may underlie psychiatric phenotypes and demonstrates their predictive power. And, like all endophenotypes, it is invisible to the naked eye, but measurable in the lab.

Another study, using functional magnetic resonance imaging (fMRI), found reduced neural activity in patients with 22q11DS when they performed a working memory task compared to a group of healthy control subjects. What’s more, the magnitude of the decrease correlated with the severity of their psychotic symptoms. This suggests abnormalities in neural activity might underlie symptoms associated with schizophrenia.

Other studies have found an association between psychiatric illnesses such as schizophreniaand abnormalities in the size and shape of different brain regions. For instance, a recent study found that certain parts of the brain were thicker in patients with 22q11DS. What’s more, the degree of thickness was related to psychotic symptoms. Changes in brain structure have also been associated with psychiatric disorders, such as obsessive compulsive disorder.

Researchers can you use mice models to learn about endophenotypes. Mouse via www.shutterstock.com.

In order to gain a more in-depth understanding of the underlying physiology in 22q11DS, researchers can breed mice with the deletion syndrome by “knocking out” genes in the mouse genome.

Researchers have found that mice with 22q11DS had fewer neurons in a part of the brain associated with cognition compared to unaffected mice.

The number of neurons correlated with how well the mice performed on tasks measuring executive function. These results suggest that individuals with psychiatric illnesses might actually have microscopic changes in their brain cells. This is a significant finding, because we can’t study these effects directly in humans.

These are just some examples of how we can experimentally determine endophenotypes that underlie schizophrenia in 22q11DS. And while 22q11DS is a risk factor for schizophrenia, what we learn from studying this syndrome could help us understand the endophenotypes behind other illnesses.

Of course defining endophenotypes for psychiatric illness is just the first step. After that, researchers and scientists need to find ways to use these results to inform diagnosis, treatment and prevention strategies.

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New research, which features in the journal Neuron, shows that primates lose excitement in anticipation of a reward when a specific area of their brain becomes overactive. The study also shows that ketamine affects this brain region and prevents the loss of pleasure.

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A loss of interest or pleasure in activities that were once exciting is one of the hallmarks of depression.

Depression is “the leading cause of disabilityworldwide” and one of the most commonmental health problems in the United States.

The symptoms of major depression include depressed mood and loss of interest or pleasure in daily activities. Some people may also experience difficulty sleeping, eating, and focusing or have intrusive thoughts of death or taking their own life.

The loss of interest, pleasure, or excitement in anticipation of activities that the individual once perceived as enjoyable is called anhedonia.

The brain mechanisms that underpin anhedonia in depression have remained unclear until now, and this lack of knowledge has hindered the success of many antidepressant treatments.

Now, a new study casts much-needed light on this symptom. Leading a team of researchers, professor Angela Roberts from the Department of Physiology, Development, and Neuroscience at the University of Cambridge, United Kingdom, and doctoral researcher and medical student Laith Alexander set out to study this phenomenon in marmosets.

Marmosets are a type of nonhuman primate with frontal lobes that are very similar to those of humans. This physical similarity means that the findings are more easily translatable to humans than they would be if the study involved rodents instead.

Prof. Roberts and colleagues tested the effects of ketamine, a hallucinogenic drug that has recently garnered interest as a potential treatment for depression, and found that it had a positive effect on the primates.

Studying anhedonia in primates

Prof. Roberts explains the motivation behind the study, saying, “Imaging studies of [people with depression] have given us a clue about some of the brain regions that may be involved in anhedonia, but we still don’t know which of these regions is causally responsible.”

“A second important issue,” she adds, “is that anhedonia is multi-faceted — it goes beyond a loss of pleasure and can involve a lack of anticipation and motivation, and it’s possible that these different aspects may have distinct underlying causes.”

To find out more about the brain mechanisms behind anhedonia, Prof. Roberts and her team devised an experiment in which they trained primates to react to two sounds. Sound A indicated that the marmosets would receive marshmallows as a treat while no treat followed sound B.

After the training, blood pressure measurements and head movements showed that the marmosets would get excited on hearing sound A but would not respond in this way to sound B.

Next, the scientists surgically implanted very thin metal tubes into the marmosets’ heads, through which they injected either a drug or a placebo into the brains of the primates.

The researchers targeted a specific brain region called “area 25,” which the drug made temporarily hyperactive. They used PET scans to study the primates’ brain activity.

Brain’s area 25 is key in anhedonia

The primates that received the drug showed increased activity in area 25 in the brain and also displayed significantly lower excitement in anticipation of the marshmallows.

In contrast, there was no change in either the brain activity or behavior of the primates that received the placebo.

In a second experiment, the primates had to work for their rewards. At first, they received a treat after touching a colored shape on a screen just once.

However, over the course of the experiment, the primates had to press the shape an increasing number of times before they received the marshmallow. Eventually, the animals would give up because the treat was no longer worth the effort.

The researchers found that the marmosets with a hyperactive area 25 gave up much more quickly. PET scans also revealed that abnormal activity in this brain area overflowed into other brain areas, which also became overactive when the anticipatory excitement dwindled.

How ketamine prevents the loss of pleasure

Finally, the researchers tested the effect that ketamine had on the primates. They gave the marmosets ketamine 24 hours before repeating the same experiments as before.

This time, ketamine blocked the activity of the drug that overactivated area 25. The brain activity of the primates that received ketamine looked normal in PET scans, and the primates continued to exhibit just as much excitement in anticipation of the marshmallow treats.

“Understanding the brain circuits that underlie specific aspects of anhedonia is of major importance,” says first author Laith Alexander, “not only because anhedonia is a core feature of depression but also because it is one of the most treatment-resistant symptoms.”

Studies show that as many as 30 percent of people living with depression have a form of the condition that does not respond to treatment.

“By revealing the specific symptoms and brain circuits that are sensitive to antidepressants like ketamine, this study moves us one step closer to understanding how and why patients may benefit from different treatments.”

Laith Alexander

Fractionating Blunted Reward ProcessingCharacteristic of Anhedonia by Over-ActivatingPrimate Subgenual Anterior Cingulate Cortex

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5 Common Signs of Drug Misuse in Its Early Stages

There is a point between casual drug usage and troubling drug misuse that happens before addiction fully sets in that needs to be addressed. Recreational drug use has been a facet of society for as long as history has existed. Drugs of all kinds, from opioids to alcohol, have always found their way into the lifestyles of the upper-class, as well as those who are stricken by poverty. Just like addiction, drug misuse doesn’t belong to a particular “type” of person or demographic, even though some people may be predisposed to addiction or drug use based on genetics and their surrounding environment. The focus of drug misuse is the bridge between experimentation and continued use into eventual dependency and addiction. Recognizing troublesome misuse early on can potentially stop cases of addiction in their tracks which is why it’s important to be aware of the signs.

 What Is Drug Misuse?

There are many different phrases when talking about the use of drugs but what is “misuse”?

  • The use of illicit drugs: Experimentation can quickly go from a one-time use to habitual use, even if it doesn’t occur every day. The recreational use of illicit substances is always a risk since there is no way to fully know what a person is ingesting when a drug is acquired “off the street.”
  • Incorrect use of medication: Even legal, prescription drugs can be a part of drug misuse, especially when the person taking these drugs is using them outside of medical reasons without a doctor’s discretion or in dosage amounts that exceed the doctor’s instruction. This also occurs when someone is taking medication that does not belong to them.
  • Overuse of legal drugs: For example, just because caffeine and alcohol are legal doesn’t mean they cannot be misused. Regular or binge use of these substances can pose serious health concerns and result in potentially fatal consequences once a level of dependency is reached.

Drug misuse is a willful act which, when done continuously, can lead directly to dependency and unintended addiction. When someone habitually disregards the negative effects of drug misuse it’s likely they have crossed from misuse into addiction. The following are signs that someone has reached the stage of drug misuse:

1) Making Drugs A Priority

When someone starts planning their days, evenings, or entire weekends about obtaining and consuming drugs, misuse is likely a factor. Typically this begins shortly after the first or second experimental experiences they’ve had with a drug and become curious to try more. This can also become somewhat of a ritual. Leisure time is no longer to relax; it begins to focus solely on using the drug of choice in excess until there is no more left or more needs to be acquired. When social outings or gatherings seem to be exclusively dependent on having the drug available, misuse is in play.

2) Drastic Changes in Social Circle

Sometimes people are exposed to drugs and begin to experiment as a way to get acquainted with new friends. Usually, this involves someone new entering a social circle that opens members to a particular drug where its use becomes more and more prevalent. When someone drastically changes their social habits and social circle to include only other people who participate in the use of that drug, it’s more than likely they are misusing the drug regularly. They are most likely associating with people who can give them access to more of the drug.

3) Decline in Health or Appearance

When someone misuses drugs, their body typically experiences neglect or  mistreatment. If someone is showing signs of:

  • constant fatigue
  • confusion
  • lethargy
  • Other unusual outward behavior due to their excessive “partying”

it’s likely they are misusing drugs in their free time. People who are usually ‘put together’ may come stumbling into work or class looking disheveled or ill to hide a hangover or may be struggling through the “come down” from a high from the night before. Mysterious “illnesses” will also be a common excuse as to why they are frequently feeling sick from the misuse of drugs, or the effects that follow after a large dose.

4) Normalizing Drug Use

While some circles may treat recreational drug use lightly, the complete normalization of drug use every time someone goes out or socializes could be a sure sign of drug use. When people no longer attempt to hide the frequency of their consumption of drugs and begin to use them freely around other people, they have completely normalized the misuse of these drugs. Speaking fondly of the drug and their many adventures while using the drug can also be a sign that their use is has moved past the experimental or recreational phase into more serious use. If someone grew up in a household where drug misuse was frequent, this puts them at a much higher risk of drug misuse.

5) Facing Negative Consequences

When wild, drug-fueled events or nights out start leading to unwanted ramifications like constantly being late for work, receiving bad grades, or ruining close relationships, misuse is likely at the source. When people begin to take bigger and bigger risks to consume their drug of choice, it’s likely that their misuse has become full-fledged and they are now starting to see consequences of their decision-making. When someone starts dealing with constant social problems that are a direct result of their drug use, it may lead them to rethink their actions, but those who are misusing drugs at a constant rate may be lacking the self-awareness to correct their behavior.

Without addressing misuse, we cannot effectively make efforts stop addiction in its early phases. There is a period between experimentation and addiction that is the cornerstone of how people develop a substance use disorder. No matter what drug is being misused, the behaviors and subsequent consequences that result in misuse are what can turn a healthy, vibrant person into a shell of their former selves. We cannot ignore the fact that the attitude towards recreational drug misuse in society is troubling and sending the wrong message. While we fail to address misuse, people who fall victim to substance use disorders that once started as occasional misuse will still have to deal with the awful stigma attached to addiction. We can’t ignore something until it becomes an uncontrollable problem while blaming those who have succumbed to it. Prevention can and will help many if the message is clear. Discussing topics like misuse could potentially save many lives before they ever begin to experiment with addictive substances.

Explore the links below for more information, resources and support:
Addiction Forum Treatment
Methadone Pregnancy Information
Narcotics Anonymous
NAMA Resource
National Institute on Drug Abuse
Substance Abuse and Mental Health Services Administration
American Association for the Treatment of Opioid Dependence
Faces and Voices of Recovery
Decisions in Recovery: Treatment for Opioid Use Disorder
Make the Connection: Resources for Veterans
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What Makes Recreational Drug Use Dangerous?

According to SAMHSA, in 2016, 28.6 million people aged 12 or older used an illicit drug in the past 30 days, which corresponds to about 1 in 10 Americans overall (10.6%) but ranges as high as 1 in 4 for young adults aged 18 to 25. An estimated 11.8 million people misused opioids in the past year, including 11.5 million pain reliever misusers and 948,000 heroin users. Additional information is gathered in NSDUH for the misuse of pain relievers in the past year. Among people aged 12 or older who misused pain relievers in the past year, about 6 out of 10 people indicated that the main reason they misused pain relievers the last time was to relieve physical pain (62.3%), and about half (53.%) indicated that they obtained the last pain relievers they misused from a friend or relative.

With recreational drug use in America on the rise, it’s important to understand the risks involved with drugs that can lead to addiction. There is a very short amount of time between the experimental phase of recreational drug use and the next steps towards losing control. Based on statistics, recreational drug use is common among a wide range of ages and socioeconomic classes because addiction does not discriminate. Knowing the potential dangers of drug misuse can help educate others to prevent them from using drugs that could lead them down a dark path.

Drug Use that Leads to Addiction

While growing up, many of us are exposed to scare tactics that are used by school programs to help steer us away from drugs and alcohol. While their intentions are good, curiosity, peer pressure, and underlying risk factors that make people prone to addiction tend to override these measures.  According to the National Institute on Drug Abuse (NIDA), about 24% of 12th graders have used illicit drugs in the last month. While the general attitude towards teenagers is that we expect them to rebel, drug misuse at an early age can severely affect young developing brains. The prefrontal cortex controls the flow of dopamine in their brains, helping with logical decision making. This area doesn’t fully develop until mid-to-late 20s. When a young person has access to drugs during these developmental stages, it can acutely increase their risk of drug use disorder. The most common drugs teenagers are using that can quickly lead to addiction are opioids, methamphetamines, cocaine, and various forms of ecstasy.

From Recreational Use to Addiction

Most commonly, people who consume drugs recreationally do so when they want to let loose and party, whether it be at special events, concerts, or other social situations. Under these circumstances, it’s important to closely consider when use has become a problem, like when they can no longer enjoy themselves if they are not under the influence. Red flags are raised when they begin to consume much more than their friends or even begin to use when alone, outside of social situations. When personal responsibilities fall by the wayside, and drug use becomes the focus, it’s time to seek treatment. Once the line has been crossed, and the addiction has taken over, it’s very difficult to successfully recover without the help of a drug treatment program that can help assist with many different levels of care.

Phases of Misuse

Typically, the steps from recreational use to addiction are gradual. The typical process stems from early curiosity and can potentially lead to something much more serious.

  1. Experimental: Usually this step occurs while still young. Peer pressure builds, and they want to fit in with friends who are doing it too. It can affect adults too. Some people experiment with drugs for a change of pace. It can also appear to help ease social anxiety or negative emotions surrounding an event or incident.
  2. Recreational: Consumption of drugs becomes more frequent during this phase. Every month there’s an occasion where drugs are consumed socially. Usually, there is thrill-seeking involved. There usually aren’t many negative consequences at this phase other than feeling worn out and depleted after using.
  3. Regular Misuse: Drugs have become commonplace every weekend and sometimes on weekdays. Things are dull when not experienced while high and using and obtaining more of the drug becomes a focus. Their social circle begins to mostly include people who use as well, and former friends have slowly pushed
  4. Risky Use: Higher doses become the norm. There are consequences at stake, yet drug use trumps them all. Financial problems start to set in as most funds are used towards obtaining drugs. Usually, run-ins with the law like DWIs or worse are involved at this level.
  5. Dependence: Drugs have taken control over their life, and most relationships have deteriorated with loved ones and close friends. Their body has become physically dependent and needs a constant stream of drugs to function normally.
  6. Addiction: A high is no longer achievable, but the main purpose of ingesting drugs is to simply ward off withdrawal symptoms. Most significant areas of life have been heavily impacted by drug use, and they are holding onto life by a single thread, whether it is blatantly obvious or not from the outside.

Taking drugs recreationally may seem harmless, but it’s one step towards addiction. While some people can experiment with substances without losing control, there are many other factors involved in what makes someone more prone to addiction. Once the wheels towards addiction are set in motion, it’s hard to stop them.

If you find yourself questioning whether or not your drug use is truly recreational, or whether or not you have reached the level of addiction with your drug use, consider taking an assessment at a treatment center to help stop addiction in its tracks with the help of trained professionals.

Medmark

 

 

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Can We stop Suicides?

The link above attached to the New York Times article opinion section that discusses Ketamine and its transforming ability for depression and related mood  disorders. Below is the excerpt:

In May of 2017, Louise decided that her life was just too difficult, so she’d end it. In the previous four years, three siblings and a half-sibling had died, two from disease, one from fire and one from choking. Close friends had moved away. She felt painfully, unbearably alone. It would be the fourth time Louise (I’m using her middle name to protect her privacy), then 68, would attempt suicide, and she was determined to get it right.

She wrote a letter with instructions on where to find important documents and who should inherit what. She packed up her jewelry and artwork, addressing each box to particular friends and family members. Then she checked into a motel — homes where people have committed suicide lose value and she didn’t want hers to sell below market — put a plastic sheet on the bed, lay down and swallowed what she figured was an overdose of prescription pills with champagne.

A few days later, she woke up in a psychiatric ward in Albuquerque. The motel maid had found her. “I was very upset I had failed,” she told me recently. So she tried to cut her wrists with a bracelet she was wearing — unsuccessfully.

The suicide rate has been rising in the United States since the beginning of the century, and is now the 10th leading cause of death, according to the Centers for Disease Control and Prevention. It’s often called a public health crisis. And yet no new classes of drugs have been developed to treat depression (and by extension suicidality) in about 30 years, since the advent of selective serotonin reuptake inhibitors like Prozac.

The trend most likely has social causes — lack of access to mental health care, economic stress, loneliness and despair, the opioid epidemic, and the unique difficulties facing small-town America. These are serious problems that need long-term solutions. But in the meantime, the field of psychiatry desperately needs new treatment options for patients who show up with a stomach full of pills.

Now, scientists think that they may have found one — an old anesthetic called ketamine that, at low doses, can halt suicidal thoughts almost immediately

Depression ran in Louise’s family. It had afflicted all her siblings, both of her parents and her grandmother. Prozac had helped Louise for a time, but stopped working for her in the late 2000s, as it sometimes does. No other drug seemed able to lift her dark moods.

After her suicide attempt, Louise’s psychiatrist suggested she try ketamine. She agreed, and received an infusion intravenously. Within hours, her sense of well-being improved. The hospital discharged her. Back home, she discovered that going to the market was no longer a “herculean task.” Getting her car washed wasn’t an insurmountable chore. “Life was better,” she said. “Life was doable.”

Using ketamine to treat depression and suicidality is somewhat controversial. Numerous small studies suggest that it holds great promise, but it’s only now being tested in placebo-controlled trials with hundreds of patients. It is also popular as a club drug in some circles. Like morphine, it may operate on the opioid system, and it can induce feelings of euphoria. Occasionally ketamine abusers develop severe symptoms, including brain damage, persistent hallucinations and a painful inflammation of the bladder called cystitis.

Nonetheless, if proven safe and effective in small doses, ketamine stands to transform how doctors deal with suicidal patients and depression generally.

The drug seems to address a longstanding problem in emergency psychiatry. Sedation and physical restraint aside, doctors have few ways to quickly stop suicidal ideation, or thoughts of killing oneself. The current crop of anti-depressants can take weeks and sometimes months to work, if they work at all. They may also, paradoxically, increase suicidality in some patients. Talk therapy takes time to help as well (assuming it does). Here’s a sobering fact: Some studies indicate that suicide risk peaks soon after patients have been discharged from a medical facility.

Antidepressants and Suicide Risk A Comprehensive Overview

Antidepressants and Suicide Risk A Comprehensive Overview

Suicide risk peaks in first week of psychiatric hospitalisation and post discharge  <, See commentary excerpt at bottom of this page

 

Researchers at Yale discovered ketamine’s potential as an antidepressant in the late 1990s and scientists at the National Institute of Mental Health confirmed it the mid 2000s. Numerous studies followed suggesting that the drug helps precisely with that subset of depressive patients — about a third — for whom nothing else works. It doesn’t work for everyone in this group, but when it does, it works within hours, not weeks.

A Randomized Trial of an N-methyl-D-aspartate Antagonist in Treatment-Resistant Major Depression<<<Carlos Zarate

Suicidality doesn’t perfectly overlap with depression. Many people attempt suicide not because they’re clinically depressed, but rather impulsively, because they’ve been fired or they’ve broken up with girl- and boyfriends, or sometimes because they’re just really drunk. I’ve heard people who show up in the hospital in this state — despondent, angry and uninhibited more than depressed — described as “drunkicidal.”

Many are fine once they sober up. For those who aren’t, ketamine may help independent of its effect on depression. And because ketamine is already approved by the Food and Drug Administration, doctors can prescribe it off-label. Meaning that not only does a drug exist right now that could help with depression and suicidality, it’s theoretically available to patients.

I kept thinking about this during the recent spate of high-profile suicides: the chef Anthony Bourdain, the designer Kate Spade, the actress Margot Kidder. Could ketamine have saved any of them? Did they know about it? Did their psychiatrists?

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One more reason to treat your depression rapidly with Ketamine:

 

Depression Linked to Increased Risk of Developing Atrial Fibrillation

NEW YORK—Depression appears to be a risk factor for atrial fibrillation, the most common arrhythmia in the U.S., according to new observational data from the national Multi-Ethnic Study of Atherosclerosis (MESA) study.

Considering that 20% of U.S. adults report depressive symptoms, “our findings identify a large portion of the U.S. population that is potentially at an increased risk of developing atrial fibrillation and who may benefit from more targeted efforts to prevent atrial fibrillation,” Dr. Parveen Garg, from the Keck School of Medicine at the University of Southern California in Los Angeles, told Reuters Health by email.

He presented the study March 22 at the American Heart Association’s Epidemiology and Prevention/Lifestyle and Cardiometabolic Health Scientific Sessions in New Orleans.

The analysis included 6,644 adults (mean age, 62; 53% women, 38% white, 28% black, 22% Hispanic, 12% Chinese-American) with no known heart disease at baseline who were followed for a median of 13 years as part of the MESA study.

In the fully adjusted model, individuals with a Centers for Epidemiologic Studies Depression Scale (CES-D) score of 16 or higher (indicating clinically relevant depressive symptoms) had a 34% (P=0.039) higher risk of developing atrial fibrillation during follow-up compared with those with a CES-D score of less than 2. Similarly, individuals reporting antidepressant use had a significant 36% increase in their risk of developing atrial fibrillation compared with those not on the drugs.

“An important next step is to confirm these results in other studies, especially those with more comprehensive and clinically validated assessments of depression. If confirmed, then it will be important to determine if treating individuals with depression actually reduces their risk of atrial fibrillation,” Dr. Garg said.

Several mechanisms have been proposed to explain a possible link between depression and atrial fibrillation, Dr. Garg explained. Depression can increase systemic inflammation and activate the autonomic nervous system, which increases catecholamine levels, and the hypothalamic-pituitary-adrenal axis, which increases cortisol levels. Depression may also activate the renin-angiotensin-aldosterone system.

“Taken together, these changes may induce atrial fibrillation susceptibility either directly by disrupting the electrophysiologic properties of the atria or indirectly by promoting atrial fibrosis, increasing the atrial pressure,” Dr. Garg said, adding that further research is needed to fully understand the mechanisms involved.

Dr. Gordon Tomaselli, a spokesman for the American Heart Association, said this study “affirms the association between depression and atrial fibrillation in a population that I think is important because it’s a mixed population and not just the standard Caucasian population.”

“There are some associated risk factors in people with depression that might increase their risk of atrial fibrillation, including an increased incidence of hypertension in some patients who have depression as well as other disorders that might be driven by activation of the sympathetic nervous system like anxiety disorder. So there are several reasons why people might have depression and atrial fibrillation,” Dr. Tomaselli, who was not involved in the research, told Reuters Health by phone.

“One question is what should we do about it, and I’m not sure we have an answer from this study except to make sure that we are looking for symptoms of depression,” he said. “We don’t know whether treatment of depression will reduce the incidence of atrial fibrillation. There is some reason to think that it might, but there are other reasons to think that antidepressant drugs actually have some effects on the heart, the ion channels that determine the rhythm of the heart.”

The study had no commercial funding and the authors have no relevant disclosures.

SOURCE: https://bit.ly/2pCdkOA

AHA Epidemiology and Prevention – Lifestyle and Cardiometabolic Health Scientific Sessions 2018.

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Image result for intranasal ketamine
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At NOVA Health recovery [703-844-0184 | Fairfax, Va 22306 ] we offer our patients cutting-edge treatment options for their depression, and one of our main stars is IV (intravenous) ketamine. But why does it have to be IV? “I don’t like needles, why can’t I just take this as a pill or as that nasal spray everyone is talking about?” you may be thinking. IV is the best route for your brain to receive ketamine because of something called bioavailability. In addition, it is also more effective, more precise, and safer for you.

What is bioavailability? It is the amount of medication that your body and brain is actually able to use, which is sometimes different than the amount of medication that your body receives. When you take any medication, parts of the active ingredients in them don’t go to your bloodstream; they get digested, altered into an unusable form, metabolized and excreted into your body. This is particularly prevalent in oral and intranasal medications. In fact, receiving a medication intravenously is the only way to have 100% bioavailability. Let’s take a look at the different bioavailability percentages based on what route you receive ketamine:

Intravenous: 100%

Intramuscular: 93%
Intranasal: 25-50%
Sublingual (under the tongue): 30%
Orally (by mouth): 16-24%

When we give ketamine intravenously, we know exactly where your entire dose is going: straight to your brain. The same cannot be said for other forms of ketamine. Intranasal ketamine has to bypass several layers of tissue before it can reach your brain, and too many things can happen that could cause you to lose some or most of your dose: sneezing, dripping, running down the back of your throat, etc. The same can be said for an oral pill and an intramuscular injection; these routes are just too unpredictable, and when it comes to treating your depression, we don’t want the results to be unpredictable.

When you receive IV ketamine in our office setting, it is given slowly over one hour. By doing this, we are able to monitor you closely, and if you experience any unpleasant side effects and want to stop the infusion, we are able to do that. By contrast, a dose of ketamine via intranasal spray would be done at home with no physician or nursing supervision, so side effects cannot be immediately addressed if they arise. The same is true for intramuscular or oral dosing – after you take the pill, or receive a shot of ketamine into your muscle, there is no way to stop the absorption of the medication into your bloodstream as the full dose is administered within seconds.

IV ketamine is by far the safest and most effective approach in using ketamine to treat depression. You are in a comfortable setting with healthcare providers with you the whole time, the potential for side effects is low, and you are certain that the dose you receive is the dose that is going to your brain, maximizing the benefits of this cutting-edge treatment.

However, we do offer the other routes of administration and take – home prescriptions for Ketamine therapies for those who are in our program. Contact us today at 703-844-0184 to get started on your treatment.

 

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Ketamine Nasal Sprays for Depression

What is ketamine?

Ketamine Nasal Spray
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Ketamine is a drug currently approved by the FDA for use as a general anesthetic during minor surgical procedures such as biopsies. It is widely known as a recreational drug because of its ability to induce cognitive-dissociative, hallucinogenic, and euphoric states in humans. Recently, it has been implicated in research as a potential therapeutic agent in depression especially in patients who have failed previous standard therapies.

Why ketamine?

Standard pharmacologic therapies for depression take several weeks of treatment before patients experience relief. Ketamine is different in that it has been shown to reduce depression symptoms and suicidal ideation in as little as forty minutes. This is considered a potentially lifesaving breakthrough in the treatment of depression because ketamine can rapidly reduce symptoms especially in emergency situations.

How does it work?

The most common medications used in depression affect serotonin in the brain. Ketamine works by a different mechanism. It has been shown to block the glutamate receptors in the brain resulting in its famous hallucinogenic effects. Ketamine has been shown to act on several other receptors, but it is theorized that at low doses, blocking glutamate receptors in the brain may be the reason for its anti-depressive effects.

Who should (and shouldn’t) take ketamine?

Ketamine has not been approved by the FDA for treatment of depression. Although, because of new studies, psychiatrists have been prescribing ketamine “off-label” for patients who did not respond to selective serotonin reuptake inhibitors (SSRIs) such has Celexa (citalopram), Zoloft (sertraline), or Prozac (fluoxetine) for immediate treatment of symptoms.

Ketamine has been shown to transiently yet significantly increase blood pressure following administration. Patients with high blood pressure should use caution when using ketamine. Ketamine has also been shown to be associated with increases in psychosis or dissociative properties.

Ketamine nasal sprays offer a quick and convenient way to administer ketamine for patients who need immediate relief, although they are currently not available commercially, so you will not find them at your local community pharmacy. Compounding pharmacies have the proper experience, equipment, and personnel to safely compound and customize this medication for you.

References

  1. Ketalar [package insert]. Chestnut Ridge, NY 10977: Par pharmaceutical; 2017 https://www.accessdata.fda.gov/drugsatfda_docs/label/2017/016812s043lbl.pdf
  2. Browne CA, Lucki I. Antidepresssant effects of ketamine: mechanisms underlying fast-acting novel antidepressants. Front Pharmacol December 2013.
  3. Lapidus K, Levitch CF, Perez AM, et al. A randomized controlled trial of intranasal ketamine in major depressive disorder. Biol Psychology 2014;76:970–976
  4. Sanacora G, Frye MA, McDonald W, et al. A consensus statement on the use of ketamine in the treatment of mood disorders. JAMA Psychiatry 2017;74(4):399-405.

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Ketamine for Delirium Tremens

This study suggests that ketamine can safely be used to avoid intubation and may decrease length of intensive care unit stay.

Severe alcohol withdrawal, or delirium tremens (DT), is a life-threatening condition that can require massive doses of benzodiazepines or barbiturates (GABA agonists), which can require intubation and prolonged intensive care unit (ICU) care. These authors studied a retrospective sample of adult patients admitted to a single ICU with DT to determine whether adjunctive therapy with ketamine improved outcomes.

They compared outcomes in 29 patients who received symptom-triggered therapy with GABA agonists with outcomes in 34 patients who were treated after initiation of a guideline that added an intravenous ketamine infusion (0.15–0.3 mg/kg/hour) to GABA agonist therapy. Using multivariable modeling that accounted for initial ethanol level and the total amount of GABA agonist required for treatment, patients who received ketamine had significantly lower rates of intubation (29% vs. 76% for patients who did not receive ketamine) and shorter ICU stay (5.7 days vs. 11.2 for patients who did not receive ketamine). There were no reported adverse events.

Adjunct Ketamine Use in the Management of Severe Ethanol Withdrawal

NOVA Health Recovery

 

ON A NORMAL DAY OF WORK, THIS IS WHERE YOU CAN FIND ME:

Wine Crying Desk

BUT AS SOON AS THE CLOCK HITS 5PM ON FRIDAY, OUT COMES THE WINE, AND THE LARGEST GLASS I CAN FIND:

Kitty Wine

BEFORE I HEAD HOME TO START THE NIGHT, I GET A QUICK WORKOUT IN:

Karen Walker Juice Boxes

THEN AFTER MY WORKOUT, IT’S TIME TO START THE NIGHT THE ONLY WAY I KNOW HOW:

Bottle Drinking

SERIOUSLY:

cameron-diaz-wine

WHEN I FINALLY HEAD OUT, IT’S CHAMPAGNE FOR EVERYBODY!

Lucille Ball Wine

AS WELL AS BOTTLES OF WINE FOR EVERYBODY! WHO WANTS THEIR OWN BOTTLE? WE ALL WANT A BOTTLE!

Julia Louis Dreyfus Wine

IF SOMEONE JUDGES, I JUST SHAKE MY HEAD, BECAUSE THERE ARE NO JUDGEMENTS WHEN IT COMES TO WINE:

Bored To Death Wine

THE NEXT DAY, I MAY BE A LITTLE TIRED, BUT IT’S OK, OFF TO BRUNCH!

Wine IV

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Cera-Q – The Anti-Aging Supplement From a Silkworm

Getting old sucks. From the physical standpoint, our metabolism slows down, muscle gain and fat loss become more difficult, and joints stiffen. From the cognition standpoint, our forgetfulness increases, it becomes more difficult to learn new tasks, and our brain physically shrinks in volume.

In the early 2000s, a group of researchers from South Korea began exploring all-natural compounds that could fight brain aging and discovered one of the most unlikely heroes – the silkworm. Specifically, the cocoon of the species Bombyx mori.

As we age, harmful protein called beta-amyloid plaque builds up in the brain. This plaque degrades neuron membrane receptors, blocks cell-to-cell signaling, and increase whole-body inflammation. [1] Researchers currently believe the buildup of beta-amyloid plaques is the primary cause of Alzheimer’s, the most common neurodegenerative disease on the planet.

Cera-Q is a protein hydrolysate extracted from fibroin, the major protein in silkworm cocoons. [2] Traditional Korean medicine has prescribed silkworm fibroin for centuries to improve health and longevity. This protein’s high glycine and alanine content (~75% of the total amino acid composition), paired with a unique molecular structure, offers the unique advantage of binding to and preventing the buildup of amyloid plaque in the human brain. [3][4]

In addition to fighting against beta-amyloid plaque buildup, Cera-Q can also increase glucose uptake to the brain which provides energy and support during both simple and complex cognitive tasks. [5] Multiple studies on humans, animals, and cells verify Cera-Q potency and efficacy as an anti-aging compound for the brain.

The process for isolating Cera-Q is somewhat complex. Researchers place the silkworm cocoon in a mixture containing water and proprietary enzymes to isolate the fibroin protein found into a combination of short chains of amino acids called peptides. [2] After isolating the protein in hydrolysate form, the mixture is dried to eliminate the water so that only the protein remains.

The result is Cera-Q powder. Cera-Q is a water-soluble tan to yellowish-tan powder with greater than 65% protein and less than 10% moisture by weight, a semi-sweet taste like the amino acid L-glycine, and a shelf life of up to two years. [4]

Cera-Q Uses

CeragenClick here to order Ceragen with Cera-Q today.

To fight aging and cognitive decline the manufacturers of Cera-Q recommend a dosage of 200mg to 400mg per day divided across two to three servings. [6] One study found minor benefit with a dosage as low as 10mg per day but most research uses a daily 200mg to 400mg dosage. The dosage varies slightly based on the desired application of Cera-Q, characteristics of the end user, and other ingredients that may be included in a supplement containing Cera-Q.

Higher doses offer a greater benefit when consumed for a short period but also carry a higher cost. A lower dose is more cost-efficient and beneficial when consumed chronically for a longer period but may not offer the immediate benefits seen with higher doses.

You can purchase Cera-Q Silk Protein Hydrolysate as a single ingredient supplement or as a part of a multi-ingredient blend in gummy chews, beverage, shot, powder, tablet, and capsule forms. [6] There is a form of Cera-Q for your regardless of how you prefer to take your supplements.

Cera-Q also works synergistically with caffeine when consumed together in a one to one ratio. 200 to 400mg of each compound can improve brain circulation, deliver more glucose to the brain, release more fatty acids, and create a blood pressure neutral environment. [4]Cera-Q decreases blood pressure whereas caffeine increases blood pressure.

Cera-Q Benefits

Studies on animals and human cells confirm silk protein hydrolysate’s ability to fight against harmful beta-amyloid plaques that build up in the brain as we age. Cera-Q also reduces the amount of dead tissue resulting after ischemia, an event in which a vital organ (usually the heart) or body part receives an inadequate blood supply.

Researchers injected beta-amyloid protein in the hippocampal region of rat brains and then provided 5 to 10mg per kilogram of bodyweight oral doses of Cera-Q to rats for two continuous weeks. The beta-amyloid protein reduced acetylcholine levels in the brain by 45%. Just 5 to 10mg of Cera-Q per kilogram of bodyweight restored acetylcholine levels to between 78 and 80% of the levels found in the control population. [7]

Low levels of acetylcholine significantly impair learning, memory, and cognitive function. A study on human cells found that administering Cera-Q two hours prior to administering beta-amyloid protein normalized cell appearance and prevented 85% of cell death compared to the control group. [8] Beta-amyloid protein buildup in the brain paired with high rates of cell death expedites the aging process and neurodegeneration.

Cera-Q exhibits antioxidant properties through its ability to protect against reactive oxygen species. High levels of reactive oxygen species in the body hamper our immune system and increase inflammation. Reactive oxygen species levels were 65% lower in cells receiving Cera-Q after receiving beta-amyloid proteins and just 15% higher than the control cells receiving no beta-amyloid proteins. [8]

As we age we also experience an increased likelihood of insufficient blood supply to vital organs. Researchers blocked the middle carotid artery of rats and then provided them with a 10mg per kilogram dose of Cera-Q daily or placebo for seven days.

Rats receiving Cera-Q had a smaller area of dead tissue around the area damaged insufficient blood supply, experienced a smaller loss of neurons, and improved memory compared to the control group. [9] Silk protein hydrolysates in the form of Cera-Q may become a staple compound in fighting against heart attacks and Alzheimer’s.

A sharp mind and lucid memory is critical for fighting the aging process. The studies on Cera-Q consumption in humans found that it benefits the memory and learning capabilities of children, adults, and seniors.

In 2004, 53 healthy Korean females and 13 healthy Korean males with an average age of 42 consumed either 0mg, 200mg, or 400mg of Cera-Q daily for three weeks. These individuals then completed Digit Symbol Test portion the Korean-Wechsler Adult Intelligence Scale. [10]The Digit Symbol Test is a variation of number memorization used to measure brain damage, dementia, age, and depression. [11]

Individuals consuming placebo did not show improvement over baseline but those consuming 200mg and 400mg of Cera-Q increased their scores by 11.3% and 22.2%, respectively. [12] These results are staggering after just three weeks of supplementation.

A larger study of 99 healthy Korean adults asked individuals to consume 0mg placebo, 200mg, or 400mg of Cera-Q daily for three weeks and perform the Rey-Kim Memory Test. [13] This test measures both auditory and visual memory. [14] The placebo group experienced no improvements but both Cera-Q groups experienced significant improvements in memory maintenance as measured by word recall in a dose dependent manner. [13]

This means that the 400mg group had superior improvements in word recall compared to the 200mg group. The 200mg and 400mg groups also improved memory recall efficiency by 90% and 60%, respectively, compared to their intra-group baseline. [13] The baseline memory recall efficiency was higher for those in the 400mg group compared to the 200mg group.

This 99-person study also examined everyone’s memory quotient (MQ) and found the pre-study average to be 105. [13] Memory quotient assesses memory for content, location, and sequence as measured by questions related to short-term recall and recognition of both meaningful and abstract material. [15] A low memory quotient indicates diminished or impaired memory and logic.

At the end of the study researchers found that those in the placebo group increased their memory quotient by 3% but those in the 200mg and 400mg Cera-Q groups increased their memory quotient by a staggering 12% and 21%, respectively. [13] Keeping a sharp memory is critical for fighting the aging process and silk protein hydrolysate may be one of the most potent substance to help you do so.

References

1) “Alzheimer’s Brain Plaques.” Alzheimer’s Association, 2016, Accessed Dec. 2016.
2) “Cera-Q: FAQS.” Cera-Q, 2016, Accessed Dec. 2016.
3) “Cera-Q – Function. Focus. Freedom.” Novel Ingredients, July 2016, Accessed Dec. 2016.
4) Cera-Q Silk Protein Hydrolysate Brain Effects & Human Clinical Studies White Paper. Novel Ingredients, 2016. Accessed Dec. 2016.
5) “Cera-Q: How It Works.” Cera-Q, 2016, Accessed Dec. 2016.
6) “Cera-Q: Products and Applications.” Cera-Q, Accessed Dec. 2016.
7) Kim DK, Kang YK, Lee MY, Lee KG, Yeo JH, Lee WB, Kim YS, Kim SS. Neuroprotection and enhancement of learning and memory by BF-7. J Health Sci 2005; 51(3):317-324.
8) Chae HS, Kang YK, Shin YK, Lee HJ, Yu JI, Lee KG, Yeo JH, Kim YS, Sohn DS, Kim KY, Lee WB, Lee SH, Kim SS. The role of BF-7 on neuroprotection and enhancement of cognitive function. Kor J Physiol Pharmacol 2004 Aug; 8:173-179.
9) Lee JY, Lee SH, Sung JJ, Kim ET, Cho HJ, Kim KH, Kang YK, Kim SS, Kwon OS, Lee WB. [The effect of BF-7 on the ischemia-induced learning and memory deficits]. Kor J Anat 2005; 38(2):181-188. Korean
10) Lee et al.,[BF-7 improved memory function and protected neurons from oxidative stress]. Kor J Phys Anthropol 2004c; 17(4):313-320. Korean
11) “Digit/Symbol Coding Test.” Cognitive Atlas, National Institute of Mental Health, 2016, Accessed Dec. 2016.
12) Lee et al.,[BF-7 improved memory function and protected neurons from oxidative stress]. Kor J Phys Anthropol 2004c; 17(4):313-320. Korean
13) Kim et al., Neuroprotection and enhancement of learning and memory by BF-7. J Health Sci 2005; 51(3):317-324.
14) Na, Kyoung-Sae et al. “Mediating Effects of Cognitive Effort and Depression on Intelligence, Memory, and Executive Functions in Individuals with Mild Traumatic Brain Injury.” Psychiatry Investigation 11.2 (2014): 112-118. PMC. Web. Dec. 2016.
15) “Universal Nonverbal Intelligence Test (UNIT).” Eastern Washington University, 2016, Accessed Dec. 2016.

TigerFitness

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