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Ketamine is emerging as a popular treatment for depression. New research suggests the drug acts like an opioid


Ketamine is emerging as a popular treatment for depression. New research suggests the drug acts like an opioid

  • Ketamine is emerging as a way to treat depression, but it appears to act like an opioid, Stanford researchers found.
  • Clinics are cropping up around the country where people receive ketamine infusions.
  • A handful of pharmaceutical companies, including Johnson & Johnson and Allergan, are using ketamine as inspiration for new prescription drugs to treat depression.
This is a vial of the animal tranquilizing drug ketamine hydrochloride, better known in the drug culture as "Special K."
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This is a vial of the animal tranquilizing drug ketamine hydrochloride, better known in the drug culture as “Special K.”

Ketamine is emerging as a way to treat depression, but it appears to act like an opioid — and it may carry similar risks, Stanford researchers found.

Clinics are cropping up around the country where people receive ketamine infusions. A handful of pharmaceutical companies are using ketamine as inspiration for new prescription drugs to treat depression. Yet the new research questions whether scientists know enough about chronic ketamine use to introduce it broadly.

The drug blocks NMDA receptors, which scientists think may treat depressive symptoms. Researchers wanted to test whether it was possible to elicit this reaction without activating the brain’s opioid receptors.

To block an opioid response, they gave participants naltrexone then infused them with ketamine. To compare that response with the normal response, they also gave participants a placebo before giving them the treatment.

Naltrexone so successfully blocked the anti-depressant effects of ketamine that researchers cancelled the study after the first interval because they felt it wasn’t ethical to continue it, said Dr. Nolan Williams, one of the study’s authors and a clinical assistant professor of psychiatry and behavioral sciences at Stanford University.

When patients took naltrexone, the opioid blocker, their symptoms did not improve, suggesting ketamine must first activate opioid receptors in order to treat depression, according to the study, published Wednesday in the American Journal of Psychiatry.

That’s not to say ketamine cannot be used occasionally, but it does raise questions about using it repeatedly over time, said Dr. Alan F. Schatzberg, co-author of the study and Stanford’s Kenneth T. Norris, Jr., professor of psychiatry and behavioral sciences. He likens it to opioid painkillers being an appropriate pain treatment when used once in the emergency room but posing problems, such as the risk of dependence, when used chronically.

“More studies need to be done to fully understand ketamine before it’s widely rolled out for long-term chronic use,” Schatzberg said.

Researchers planned on studying 30 adults but stopped enrolling patients once they decided combining ketamine and naltrexone was not only ineffective but also “noxious” for many participants. They tested a total of 12 people with both naltrexone and the placebo.

Of those 12, seven who received naltrexone experienced nausea after the ketamine infusion, compared to three in the placebo group. Two participants in each group also experienced vomiting.

Participants who received the placebo and ketamine treatment reported reduced depression symptoms. But those same participants did not see a decrease in depression symptoms after receiving ketamine and opioid-blocker naltrexone.

“We essentially blocked the mechanism for producing the anti-depressant effect, which were opioids,” said Williams.

The findings may have implications for clinics offering ketamine infusions and drug manufacturers trying to commercialize ketamine-like drugs.

Ketamine is meant to be used as an anesthetic. Since ketamine is currently not indicated to treat depression, insurance typically doesn’t cover the cost of infusions, so people tend to pay out of their own pocket. One session can run more than $500.

Meanwhile, drug giant Johnson & Johnson plans to seek approval from the Food and Drug Administration for its nasal spray esketamine this year after reporting positive results from a Phase 3 trial. Allergan plans to file its drug Rapastinel, which targets the NMDA receptors like ketamine, within the next two years. VistaGen Therapeutics is working on a similar drug.

In a statement, J&J said while the study reviewed ketamine and not esketamine, the findings “are difficult to interpret because of the study’s design.”

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What Is Traction Alopecia & Can It Be Reversed

What Is Traction Alopecia & Can It Be Reversed

When most of us think of the typical person suffering from severe balding, our mind usually imagines a greying, old man losing their hair thanks to genetics and age. Medically known as androgenetic alopecia, this may be the most common form of balding, affecting 80 million people in the U.S., but it’s far from the only way we lose our hair.

Traction alopecia occurs when hair has been pulled too tightly against the scalp. It’s also one of the few forms of hair loss attributed to mechanical causes, and not genetics, hormones, or other disease processes. Traction alopecia is commonly reported in women of African descent, though it has nothing to do with ethnicity or hair type. Instead, it’s the specific hair styles and techniques popular in these communities that ultimately cause traction alopecia. However, just because it’s more common in women, doesn’t mean that it doesn’t occur in men. With the recent surge in popularity of the “Man bun”, you may be putting your locks at risk.

Traction alopecia the root of the problem.

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As frustrating as any form of hair loss may be, the bright side of traction alopecia is that sufferers don’t have to fight against genetics. If caught early, traction alopecia is an easy form of hair loss to treat and prevent by simply changing your hairstyle.

What is Traction Alopecia?

Traction alopecia is essentially hair loss caused by hair regularly and aggressively pulling at the hair. As the hair follicles/bulbs/scalp is increasingly irritated, sufferers will feel stinging, pain, and tenderness. Small red bumps (folliculitis) may also appear. If these initial symptoms are ignored, permanent hair loss can occur. Early on, traction alopecia can be reversed. However, if trauma continues and irritation persists, scarring of the damaged hair follicle can occur. Once scarred, the hair stops growing entirely and cannot be reversed without invasive medical intervention.

What Causes Traction Alopecia?

Traction alopecia is almost always caused by hair styles that pull hair too tight against the fragile skin of the scalp. Though often associated with braids, weaves, and dreadlocks, traction alopecia also occurs with ponytails, buns, pigtails, extremely long hair, extensions, etc. Helmets and turbans are also known culprits.

What Are Symptoms of Traction Alopecia?

Telltale signs that you may have traction alopecia include:

  • Scalp tenderness
  • Red bumps on or near the scalp
  • Broken hairs near the hairline
  • Thinning or patchy areas of missing hair near the hairline
  • Relief in scalp when tight bun released.
  • Itching

If you notice these symptoms as soon as they appear, the damage can be reversed. However, waiting longer increases the chance of developing more severe, or even permanent hair loss.

Once scarring, or scarring alopecia occurs, treatment becomes significantly more difficult. Medical intervention by a dermatologist or hair restoration expert (703-844-0184) is strongly recommended as soon as symptoms occur.

How Can I Treat Traction Alopecia?

When caught early enough, traction alopecia can be completely treated and reversed without a doctor. If no scarring has occurred and there is no significant pain or swelling, simply letting your hair down and avoiding any hairstyles that causes scalp tension should resolve the issue.

However, be patient. The hair and scalp will need time to regrow. It can take several months, or even a full year to see progress. During this time, don’t be tempted to wear your hair tight at any time and be as gentle as possible to your hair and scalp.

If your traction alopecia has advanced to the point of significant balding, pain, swelling, or scarring—or you don’t see any new growth after a year of wearing your hair loose—it’s definitely time to see a dermatologist or hair restoration specialist (703-844-0184 | Neograft Hair transplantation | Dr. Sendi)

First, your specialist will likely test your hair to ensure the cause of your hair loss is in fact traction alopecia. This may include a biopsy of your scalp; a minor outpatient procedure where a small sample of your scalp is submitted to the lab for microscopic examination.

Then once officially diagnosed, typical treatments include:

  • Topical hair growth creams like minoxidil (Rogaine)
  • Biotin or other natural hair growth supplements
  • Oral or topical medications to reduce inflammation to the scalp

If scarring has occurred, no pills or creams will bring your hair back. The only way to reverse permanent hair loss is through a hair transplant procedure. Though this is an invasive surgery, it does have a high success rate for bringing your hair back to its former glory.

How Can I Prevent Traction Alopecia?

Traction alopecia is extremely preventable. Prevention doesn’t have to mean forever giving up the hairstyles that you love—though you might have to take regular breaks. Use proper hair styling techniques and strategies to minimize damage. Above all, avoid constantly pulling your hair too tightly into any style.

Maintaining your hair should never hurt. If you notice regular pain, stinging, or tension along your hairline, it’s time to try a different style. Braids or dreads, are better when they’re thick. Thin braids and dreads tend to pull more at the scalp. If you love the man bun but it’s giving you tension headaches, let it down and set your locks free.

Also, choose high-quality hair care products and minimize the use of chemicals. If you’re good to your hair and scalp, your hair and scalp will be good to you in return.

Minoxidil: Your Questions, Answered

Minoxidil is an FDA-approved drug for the treatment of androgenetic alopecia (hair loss). Prior to it being approved by the FDA for hair loss treatment, it was used as an oral pill to treat patients with high blood pressure. A common side effect of oral minoxidil is “hirsuitism” or increase hair growth on the body, face and scalp. In addition to increased (unwanted) body hair, in pill form, minoxidil has other side effects that made it impractical as an oral hair loss treatment.

In the 1980’s, the scientists at the UpJohn Corporation invented a topical formulation of minoxidil in a 2% and 5% strength, called Rogaine. When applied to the scalp it harnessed the benefit of hair growth in areas of balding while avoided the unwanted side effects that came with the pill form.

Who Should Use Minoxidil?

Minoxidil topical solution can be used by adults over 18 years old who are experiencing gradually thinning hair. People who have vertex/crown hair loss tend to respond best to the treatment, but it is effective throughout the scalp.

There are 2% and 5% formulations of the drug available for both men and women which both come in liquid solution or foam. There are also over-the-counter versions of both formulas except for the 5% strength for women, which is still under patent as it was not released until much later than the original 2%. There is really no difference between the men’s, women’s or the over-the-counter versions except the price or color of the boxes. We recommend all patients use the 5% strength and decide if they prefer the foam or solution.

How Does Minoxidil Work?

Minoxidil topical solution is intended for external use only. It is to be applied to a dry scalp per the instructions from your doctor. Once applied, it should be left on your head until it dries by itself – do not use a hairdryer in an attempt to speed up the process.

Science does not currently understand exactly how minoxidil works. It is known that unlike Propecia, minoxidil does not affect the levels of DHT. Some scientists believe that minoxidil works in part by having a vasodilatory effect upon the blood vessels. The dilation could allow for improved oxygen, blood, and nutrient flows to the hair follicles. What we do know is that it is activated in the scalp by an enzyme called sulfotransferase which is found in hair follicles. When activated it shortens the telogen (shedding) phase and prolongs the anagen (growth) phase therefore causing the miniaturized hair follicles to grow longer and stronger.

How Soon Before Results Start Showing?

Many people start seeing benefits after 4 months of using minoxidil. However, the full benefit usually isn’t realized until 12-14 months after starting treatment.

Minoxidil must be used on a continual basis in order to maintain hair growth. If you stop using minoxidil, you might experience “catch-up hair loss” in which you will start to lose hair at an accelerated rate until they catch-up with the level of hair loss that you would have had, had you never used minoxidil in the first place.

Who Shouldn’t use Minoxidil?

It was originally created to help people with high blood pressure. Therefore, if you suffer from low blood pressure, you should avoid using minoxidil unless directed by your doctor. Pregnant women and people with heart problems should also avoid using the drug.

People who have experienced hypersensitivity with the other components of minoxidil should avoid using it as well. Speak with your doctor if you have any questions regarding the drug or the ingredients.

Minoxidil will not regrow hair in areas of scarring hair loss. If you have experienced trauma or deep burns in your scalp, you should let your doctor know. People who have hair loss from hair grooming methods as cornrows or tight ponytails should also consult with their doctor because minoxidil may not be helpful.

Are there Any Side Effects of Minoxidil?

Topical minoxidil is considered safe for long-term usage to treat androgenetic alopecia. However, if you start to notice any side effects such as burning, redness, itching, or irritation, you should inform your doctor and discontinue its use.

Unwanted hair growth can occur in areas adjacent to where it is being applied. It’s also suggested that you wash your hands completely after touching the medication. If topical minoxidil comes into contact with other areas of skin on your body, unwanted hair growth can occur.

Many people use minoxidil or finasteride before they undergo a hair transplant to help improve the native hair. Recent studies have shown that using a combination of both works best in treating male androgenetic alopecia. Your doctor may suggest that you take minoxidil at the same time you take finasteride.

Combined Treatment with oral finasteride and topical minoxidil in males androgenetic alopecia


What is the Success Rate of Minoxidil?

Researchers conducted a 1-year study of 984 men who had male-pattern hair loss and were using minoxidil 5%. At the end of the study they found that the hair loss areas in the scalp had become smaller in 62% of the study participants. Hair loss remained unchanged in 35.1% of the participants and grew larger in 2.9% of them.

Each person reacts differently to minoxidil and results will vary from person to person. Normal hair usually only grows ¼ – ½” per month so it will take at least 4 months before you start to notice hair regrowth.

Do Shampoos Help With Hair Loss?

Do Shampoos Help With Hair Loss?

Androgenic alopecia, most commonly known as male pattern hair loss, is an extremely common issue for many men as they age. In fact, approximately half of all men over the age of 50 are afflicted. Though many happily embrace a hairless future, others choose to fight it in hopes of gaining back the confidence connected to their locks.

Thanks to scientific breakthroughs and innovations, there are a multitude of options when it comes to improving hair growth. Surgical procedures are incredibly successful but invasive and often reserved for when previous methods have failed. Several medications also boast great results, but many also don’t want to rely on daily pills, and their possible side effects.

Instead, most men prefer to start with simple, noninvasive solutions—most notably, shampoos. With so many products on the market, some companies will try to take advantage of those desperately seeking their old head of hair.

So, how can you be sure you’re not wasting money on snake oil? You can spend $3-$100 on a bottle of shampoo, but it is worth it? First, let’s look at how shampoos developed to minimize hair loss and increase hair growth actually work.

How Do Hair Growth Shampoos Work?

Though there are various ways that people lose hair, our own hormones and genetics are almost always to blame. Typically, this is due to the effects of testosterone and dihydrotestosterone (DHT). Hair loss shampoos will use various ingredients intended to suppress these hormones. Ingredients include:


Widely regarded as the most important ingredient to look for in shampoos made to treat hair loss, ketoconazole is actually an antifungal solution which also has anti-androgenic properties that may prevent hair growth. Similar to finasteride, ketoconazole can prevent the action of testosterone or DHT on the hair.

There currently are few large studies proving ketoconazole actually is absorbed into the scalp enough to fully achieve this goal. However, some smaller studies have shown that shampoos with 2% ketoconazole may be as effective as minoxidil regimens. Ketoconazole also has anti-inflammatory effects which can help keep the scalp healthy and free of the grease and scale that may impede hair growth.Promotive effect of topical ketoconazole, minoxidil, and minoxidil with tretinoin on hair growth in male mice.


An all-natural nutrient essential for creating healthy hair, biotin, also known as Vitamin B7, Vitamin H, or Coenzyme R helps strengthen hair. Essentially, it’s a co-enzyme that helps synthesize the fatty acids and amino acids needed to produce keratin, which is what hair is mostly made of.

Though results have not been scientifically proven, a quick Google search shows that anecdotally, many believe biotin has helped them thicken and strengthen their hair, especially when taken orally. Less is known about biotin’s benefit when used topically in a shampoo.

It is indisputable that biotin is required for hair synthesis and is incredibly safe to use. From a marketing standpoint, it also makes for a great ingredient to add to hair loss shampoos. It might help—and it certainly won’t hurt—your hair.


It’s good for so much more than getting you out of bed in morning. Caffeine has been scientifically proven to potentially promote hair growth in human tissue . Basically, the stimulant plays a role in counteracting the effects of testosterone, which in turn increases hair growth potential.  Role of Caffeine in the Management of Androgenetic Alopecia

Don’t think drinking coffee will help though. For results, data suggests you’ll have to apply caffeine topically so it can be absorbed into the scalp and directly to the hair follicles themselves, making shampoos a great way to get it on your head.

Saw Palmetto

Though official research has yet to confirm its effectiveness, saw palmetto has been used for centuries to treat hair loss and many believe they’ve had positive, all-natural hair growth results. Saw palmetto may work because it blocks the 5-alpha-reductase, one of the enzymes that converts your testosterone into DHT.

Like biotin, there has been little verified scientific proof of its effectiveness. Also like biotin, it won’t hurt or hinder hair growth. Especially if you’re seeking a drug-free solution, it may be worth a try.

How Do I Choose the Right Shampoo?

First off, always visit a doctor or hair growth specialist before starting any treatment. An expert will be able to pinpoint exactly why you are losing your hair. This can be an essential step in developing a comprehensive plan in battling your baldness. Don’t wait until it’s too late for noninvasive methods to be effective.

Also, don’t expect a simple bottle of shampoo to work miracles. Shampoos are most helpful for keeping your hair clean and your scalp healthy. In addition, shampoo removes debris that could increase irritation or inflammation that may impede hair growth. However, they do little to change the actual biology of your hair growth.

Once you’ve decided to try hair growth shampoos, always do these three things:

1. Check the Ingredients

You’ll always want to ensure you know what ingredients are included in the shampoo. When it comes to over-the-counter shampoos, the ingredients listed above have the most potential benefit based on current data. Others may be helpful as well, like niacin and argan oil, or tea tree oil, but have even less scientific backing or testimonials.

2. Look at Reviews

If a product doesn’t have at least a year of consistently high unbiased reviews by many users, skip it. The product pages should also always link to scientifically backed studies proving thorough research and effectiveness. Like the saying says—if it’s too good to be true, it probably is.

3. Give it Time

Remember—hair growth is slow. Even the best products take several months to show results. Don’t become frustrated and toss the bottle after a few weeks. Try to give it at least 4 months before deciding the product isn’t right for you.

Minoxidil and Prescription Hair Growth Shampoos

Minoxidil is widely regarded as the most effective topical FDA-approved drug to fight hair loss. Commonly used under the well-known brand Rogaine, this topical solution is used in several brands of hair loss shampoos, creams, serums and foams in both over-the-counter and prescription strengths.

Unlike the ingredients above, minoxidil has a higher likelihood of side effects including scalp irritation and increased body hair in places other than your scalp. If other treatments haven’t proven successful however, this is a great option with high success rates for both men and women suffering from hair loss. Users should expect approximately 4-6 months for results, with full results taking about a year.

Hair Loss Benefits of Finasteride

Approximately 85% of individuals who routinely use Finasteride see a stabilization of their hair loss or dramatic slowing of the loss.

Over 65% of patients who use this medication see an actual increase in hair numbers. While we typically see a greater response on the crown, it also helps the mid-portion of the scalp and to a lesser degree the frontal region.

The vast majority of patients will see an increase in hair weight. This means more volume of hair even if the actual numbers do not increase.

Side effects are rare and there are no reported medication interactions between Finasteride and other prescription medications. You should always consult with your primary physician before starting a new medication.

About Finasteride and Dutasteride

This category of drugs is known as 5-alpha reductase inhibitors. These medications prevent testosterone from being converted to DHT (dihyrdotestosterone) in the prostate, hair follicles and oil glands. DHT is the active form of testosterone that causes hairloss. The two medications available are Finasteride (Propecia and Proscar) and Dutasteride (Avodart). Neither drug blocks testosterone activity throughout your body as a whole, only in the specific areas that contain these enzymes. Proscar & Avodart are FDA approved to treat benign prostatic hypertrophy (BPH or enlarged prostate). Only Finasteride 1mg is FDA approved to treat hair loss. Dutasteride can be used to treat hair loss, but this is off label.

The vast majority of men (and some women) can benefit from these medications without adverse side effects.

    • Women who are pregnant or potentially could become pregnant CAN NOT take these medications, as they interfere with the developing baby’s hormones.
    • You CAN NOT donate blood while taking these medications, because a pregnant woman might be the one who receives your blood.
    • Tell your doctor you are taking one of these medications as they can lower your PSA score. Your PSA is used to monitor for possible prostate cancer development.
    • Although there is no proven risk the fetus, men may choose to stop this medication if you and your partner plan to conceive a child.

Finasteride and Dutasteride Side Effects

Decreased sex drive and difficulty in achieving an erection has been reported in ~2% of men using these medications compared to placebo groups. In all major studies the side effects went away upon discontinuing the use of the medication. There have been rare reports of men who claim to continue to have problems after they stopped the medication. In most of these reports, the men continued taking the medication for several years in spite of their symptoms. A class action law-suit is ongoing claiming “Post Finasteride Syndrome.” The true validity of this syndrome is still under debate and research.

Breasts or testicular tenderness can be seen but is rare (<1%) and goes away upon stopping the medication.

Allergic reactions are possible but in over 20 years of prescribing these medications I have not seen a person have an allergic reaction to any of these medications.

Depression – While not reported as a side effect in any of the major studies, there have been rare reports of depression in the literature and on the internet.  The validity of these reports remains unclear.

Decreased sperm counts – While not a reported problem during FDA trials, there have been rare cases reported in the literature and a positive link between use and decreased sperm count. In trials evaluating this side effect, upon discontinuation sperm counts returned to normal within 3 months.

Breast cancer is very rare in men in general and no association between using these medications and breast cancer has been shown.  However, if you experience any lumps, bumps, pain or nipple discharge you should report it to your physician.

Prostate cancer is the 2nd most common form of cancer in men in the United States and over 15% will be diagnosed with it during their lifetime.  Prostate cancers are graded on a Gleason Score scale from 1 to 10.  The vast majority of prostate cancers are low to mid grade types with Gleason Scores of 6 or less.  In two large clinical trials of these medications there was a 15-25% reduction in the incidence of prostate cancer.  However, if you developed prostate cancer there was a small increased risk that your cancer would be a higher grade Gleason Score 8-10.  For those taking 5mg of Finasteride the risk was 1.8% vs. 1.1% on placebo and for those taking Dutasteride the risk was 1.5% vs. 1.0% on placebo.  The data regarding the link between these medications and possible increased/decreased risk of prostate cancer remains controversial and under intense review.

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Brain fog is a term that’s commonly used to describe cloudy mental thinking, difficulty with focus or concentration or sometimes difficulty with memory, or the ability to memorize new information.

Some of the key drivers of brain fog include:








How often do you see a patient who is complaining of cloudy mental thinking, difficulty with focus or concentration or sometimes difficulty with memory, or the ability to memorize new information?

In just 28 days, both healthy adult women and adolescent males showed significant improvements in attentional focus and motor speed when taking citicoline or one (1) Cerenx per day.

Cerenx works on attentional focus by increasing dopamine, increasing dopamine receptors, and protecting dopamine related neurons. Further evidence has shown that citicoline improves attention in a variety of patient populations including individuals with neurocognitive degeneration after a stroke, and elderly participants.

Cerenx works on attentional focus by increasing dopamine, increasing dopamine receptors, and protecting dopamine related neurons. Further evidence has shown that citicoline improves attention in a variety of patient populations including individuals with neurocognitive degeneration after a stroke, and elderly participants.

Objective: This study assessed the effects of citicoline, a nutraceutical, on attention, psychomotor function, and impulsivity in healthy adolescent males. Method: Seventy-five healthy adolescent males were randomly assigned to either the citicoline group (n = 51 with 250 or 500 mg citicoline) or placebo (n = 24). Participants completed the Ruff 2&7 Selective Attention Test, Finger Tap Test, and the Computerized Performance Test, Second Edition (CPT-II) at baseline and after 28 days of supplementation. Results: Individuals receiving citicoline exhibited improved attention (p = 0.02) and increased psychomotor speed (p = 0.03) compared with those receiving placebo. Higher weight-adjusted dose significantly predicted increased accuracy on an attention task (p = 0.01), improved signal detectability on a computerized attention task (p = 0.03), and decreased impulsivity (p = 0.01). Discussion: Adolescent males receiving 28 days of Cognizin® citicoline showed improved attention and psychomotor speed and reduced impulsivity compared to adolescent males who received placebo.

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Now that the days are getting shorter, the air is getting cooler, Virginians have had the first glimpse of cold for the season, some of us begin to feel the winter blues. These feelings of low energy and sleepiness may actually be Seasonal Affective Disorder, or SAD.

SAD is a form of depression related to the changing seasons. It usually starts in the late fall, especially in our northern climes. The decreasing hours of sunlight, along with the cold and snow, cause our bodies to retreat into the warmth and coziness of our homes. We tend to crave carbohydrates, eat comfort foods, and socially KWC_SADwithdraw as we sleep more, and move less; much like we are hibernating!

Those most at risk for SAD are people already suffering from major depression or bipolar disorder. Risk factors include being female, family history, young age, and the further you live from the equator, the higher your risk.   However, there are ways to decrease your risk, and increase your mood.

What can you do to improve your mood? Soak up the sun! When the weather allows, go for a walk on those bright, crisp sunny days. If the temperature or the ice and snow don’t allow you to venture outside, open the curtains and let the sun shine in. Exercise and eating healthy are both options to make you feel better. Vitamins, especially vitamin D, the sunshine vitamin can help with mood. Be social, visit with friends. A phone call, visit, or even a vacation to visit your “snowbird” friends will keep you socially involved.

So, if these options aren’t working or you just need something more to improve your mood, your healthcare provider may recommend seeking help from a psychotherapist. They may offer medications, light box therapy, or talk therapy.


Ketamine therapy is an option to help make it through dark times when nothing else seems to work. Contact 703-844-0184 for a consultation.



Seasonal Affective Disorder


Seasonal Affective Disorder (SAD) is a type of depression that comes and goes with the seasons, typically starting in the late fall and early winter and going away during the spring and summer. Depressive episodes linked to the summer can occur, but are much less common than winter episodes of SAD.

Signs and Symptoms

Seasonal Affective Disorder (SAD) is not considered as a separate disorder. It is a type of depression displaying a recurring seasonal pattern. To be diagnosed with SAD, people must meet full criteria for major depression coinciding with specific seasons (appearing in the winter or summer months) for at least 2 years. Seasonal depressions must be much more frequent than any non-seasonal depressions.

Symptoms of Major Depression

  • Feeling depressed most of the day, nearly every day
  • Feeling hopeless or worthless
  • Having low energy
  • Losing interest in activities you once enjoyed
  • Having problems with sleep
  • Experiencing changes in your appetite or weight
  • Feeling sluggish or agitated
  • Having difficulty concentrating
  • Having frequent thoughts of death or suicide.

Symptoms of the Winter Pattern of SAD include:

  • Having low energy
  • Hypersomnia
  • Overeating
  • Weight gain
  • Craving for carbohydrates
  • Social withdrawal (feel like “hibernating”)

Symptoms of the less frequently occurring summer seasonal affective disorder include:

  • Poor appetite with associated weight loss
  • Insomnia
  • Agitation
  • Restlessness
  • Anxiety
  • Episodes of violent behavior

Risk Factors

Attributes that may increase your risk of SAD include:

  • Being female. SAD is diagnosed four times more often in women than men.
  • Living far from the equator. SAD is more frequent in people who live far north or south of the equator. For example, 1 percent of those who live in Florida and 9 percent of those who live in New England or Alaska suffer from SAD.
  • Family history. People with a family history of other types of depression are more likely to develop SAD than people who do not have a family history of depression.
  • Having depression or bipolar disorder. The symptoms of depression may worsen with the seasons if you have one of these conditions (but SAD is diagnosed only if seasonal depressions are the most common).
  • Younger Age. Younger adults have a higher risk of SAD than older adults. SAD has been reported even in children and teens.

The causes of SAD are unknown, but research has found some biological clues:

  • People with SAD may have trouble regulating one of the key neurotransmitters involved in mood, serotonin. One study found that people with SAD have 5 percent more serotonin transporter protein in winter months than summer months. Higher serotonin transporter protein leaves less serotonin available at the synapse because the function of the transporter is to recycle neurotransmitter back into the pre-synaptic neuron.
  • People with SAD may overproduce the hormone melatonin.Darkness increases production of melatonin, which regulates sleep. As winter days become shorter, melatonin production increases, leaving people with SAD to feel sleepier and more lethargic, often with delayed circadian rhythms.
  • People with SAD also may produce less Vitamin D. Vitamin D is believed to play a role in serotonin activity. Vitamin D insufficiency may be associated with clinically significant depression symptoms.

Treatments and Therapies

There are four major types of treatment for SAD:

  • Medication
  • Light therapy
  • Psychotherapy
  • Vitamin D

These may be used alone or in combination.


Selective Serotonin Reuptake Inhibitors (SSRIs) are used to treat SAD. The FDA has also approved the use of bupropion, another type of antidepressant, for treating SAD.

As with other medications, there are side effects to SSRIs. Talk to your doctor about the possible risks of using this medication for your condition. You may need to try several different antidepressant medications before finding the one that improves your symptoms without causing problematic side effects. For basic information about SSRIs and other mental health medications, visit NIMH’s Medications webpage. Check the FDA’s website for the latest information on warnings, patient medication guides, or newly approved medications.

Light Therapy

Light therapy has been a mainstay of treatment for SAD since the 1980s. The idea behind light therapy is to replace the diminished sunshine of the fall and winter months using daily exposure to bright, artificial light. Symptoms of SAD may be relieved by sitting in front of a light box first thing in the morning, on a daily basis from the early fall until spring. Most typically, light boxes filter out the ultraviolet rays and require 20-60 minutes of exposure to 10,000 lux of cool-white fluorescent light, an amount that is about 20 times greater than ordinary indoor lighting.


Cognitive behavioral therapy (CBT) is type of psychotherapy that is effective for SAD. Traditional cognitive behavioral therapy has been adapted for use with SAD (CBT-SAD). CBT-SAD relies on basic techniques of CBT such as identifying negative thoughts and replacing them with more positive thoughts along with a technique called behavioral activation. Behavioral activation seeks to help the person identify activities that are engaging and pleasurable, whether indoors or outdoors, to improve coping with winter.

Vitamin D

At present, vitamin D supplementation by itself is not regarded as an effective SAD treatment. The reason behind its use is that low blood levels of vitamin D were found in people with SAD. The low levels are usually due to insufficient dietary intake or insufficient exposure to sunshine. However, the evidence for its use has been mixed. While some studies suggest vitamin D supplementation may be as effective as light therapy, others found vitamin D had no effect.


Ketamine for Depression

Everyone occasionally feels blue or sad. But these feelings are usually short-lived and pass within a couple of days. When you have depression, it interferes with daily life and causes pain for both you and those who care about you. Depression is a common but serious illness.

Many people with a depressive illness never seek treatment. But the majority, even those with the most severe depression, can get better with treatment. Medications, psychotherapies, and other methods can effectively treat people with depression.

There are several forms of depressive disorders.

Major depression,—severe symptoms that interfere with your ability to work, sleep, study, eat, and enjoy life. An episode can occur only once in a person’s lifetime, but more often, a person has several episodes.

Persistent depressive disorder—depressed mood that lasts for at least 2 years. A person diagnosed with persistent depressive disorder may have episodes of major depression along with periods of less severe symptoms, but symptoms must last for 2 years.

Some forms of depression are slightly different, or they may develop under unique circumstances. They include:

  • Psychotic depression, which occurs when a person has severe depression plus some form of psychosis, such as having disturbing false beliefs or a break with reality (delusions), or hearing or seeing upsetting things that others cannot hear or see (hallucinations).
  • Postpartum depression, which is much more serious than the “baby blues” that many women experience after giving birth, when hormonal and physical changes and the new responsibility of caring for a newborn can be overwhelming. It is estimated that 10 to 15 percent of women experience postpartum depression after giving birth.
  • Seasonal affective disorder (SAD), which is characterized by the onset of depression during the winter months, when there is less natural sunlight. The depression generally lifts during spring and summer. SAD may be effectively treated with light therapy, but nearly half of those with SAD do not get better with light therapy alone. Antidepressant medication and psychotherapy can reduce SAD symptoms, either alone or in combination with light therapy.

Bipolar depression, also called manic-depressive illness, is not as common as major depression or persistent depressive disorder. Bipolar disorder is characterized by cycling mood changes—from extreme highs (e.g., mania) to extreme lows (e.g., depression).


Most likely, depression is caused by a combination of genetic, biological, environmental, and psychological factors.

Depressive illnesses are disorders of the brain. Brain-imaging technologies, such as magnetic resonance imaging (MRI), have shown that the brains of people who have depression look different than those of people without depression. The parts of the brain involved in mood, thinking, sleep, appetite, and behavior appear different. But these images do not reveal why the depression has occurred. They also cannot be used to diagnose depression.

Some types of depression tend to run in families. However, depression can occur in people without family histories of depression too. Scientists are studying certain genes that may make some people more prone to depression. Some genetics research indicates that risk for depression results from the influence of several genes acting together with environmental or other factors. In addition, trauma, loss of a loved one, a difficult relationship, or any stressful situation may trigger a depressive episode. Other depressive episodes may occur with or without an obvious trigger.

Signs & Symptoms

“It was really hard to get out of bed in the morning. I just wanted to hide under the covers and not talk to anyone. I didn’t feel much like eating and I lost a lot of weight. Nothing seemed fun anymore. I was tired all the time, and I wasn’t sleeping well at night. But I knew I had to keep going because I’ve got kids and a job. It just felt so impossible, like nothing was going to change or get better.”

People with depressive illnesses do not all experience the same symptoms. The severity, frequency, and duration of symptoms vary depending on the individual and his or her particular illness.

Signs and symptoms include:

  • Persistent sad, anxious, or “empty” feelings
  • Feelings of hopelessness or pessimism
  • Feelings of guilt, worthlessness, or helplessness
  • Irritability, restlessness
  • Loss of interest in activities or hobbies once pleasurable, including sex
  • Fatigue and decreased energy
  • Difficulty concentrating, remembering details, and making decisions
  • Insomnia, early-morning wakefulness, or excessive sleeping
  • Overeating, or appetite loss
  • Thoughts of suicide, suicide attempts
  • Aches or pains, headaches, cramps, or digestive problems that do not ease even with treatment.

Who Is At Risk?

Major depressive disorder is one of the most common mental disorders in the United States. Each year about 6.7% of U.S adults experience major depressive disorder. Women are 70 % more likely than men to experience depression during their lifetime.  Non-Hispanic blacks are 40% less likely than non-Hispanic whites to experience depression during their lifetime.  The average age of onset is 32 years old. Additionally, 3.3% of 13 to 18 year olds have experienced a seriously debilitating depressive disorder.


“I started missing days from work, and a friend noticed that something wasn’t right. She talked to me about the time she had been really depressed and had gotten help from her doctor.”

Depression, even the most severe cases, can be effectively treated. The earlier that treatment can begin, the more effective it is.

The first step to getting appropriate treatment is to visit a doctor or mental health specialist. Certain medications, and some medical conditions such as viruses or a thyroid disorder, can cause the same symptoms as depression. A doctor can rule out these possibilities by doing a physical exam, interview, and lab tests. If the doctor can find no medical condition that may be causing the depression, the next step is a psychological evaluation.

The doctor may refer you to a mental health professional, who should discuss with you any family history of depression or other mental disorder, and get a complete history of your symptoms. You should discuss when your symptoms started, how long they have lasted, how severe they are, and whether they have occurred before and if so, how they were treated. The mental health professional may also ask if you are using alcohol or drugs, and if you are thinking about death or suicide.

Other illnesses may come on before depression, cause it, or be a consequence of it. But depression and other illnesses interact differently in different people. In any case, co-occurring illnesses need to be diagnosed and treated.

Anxiety disorders, such as post-traumatic stress disorder (PTSD), obsessive-compulsive disorder, panic disorder, social phobia, and generalized anxiety disorder, often accompany depression. PTSD can occur after a person experiences a terrifying event or ordeal, such as a violent assault, a natural disaster, an accident, terrorism or military combat. People experiencing PTSD are especially prone to having co-existing depression.

Alcohol and other substance abuse or dependence may also co-exist with depression. Research shows that mood disorders and substance abuse commonly occur together.

Depression also may occur with other serious medical illnesses such as heart disease, stroke, cancer, HIV/AIDS, diabetes, and Parkinson’s disease. People who have depression along with another medical illness tend to have more severe symptoms of both depression and the medical illness, more difficulty adapting to their medical condition, and more medical costs than those who do not have co-existing depression. Treating the depression can also help improve the outcome of treating the co-occurring illness.


Once diagnosed, a person with depression can be treated in several ways. The most common treatments are medication and psychotherapy.


Antidepressants primarily work on brain chemicals called neurotransmitters, especially serotonin and norepinephrine. Other antidepressants work on the neurotransmitter dopamine. Scientists have found that these particular chemicals are involved in regulating mood, but they are unsure of the exact ways that they work. The latest information on medications for treating depression is available on the U.S. Food and Drug Administration (FDA) website .

Popular newer antidepressants

Some of the newest and most popular antidepressants are called selective serotonin reuptake inhibitors (SSRIs). Fluoxetine (Prozac), sertraline (Zoloft), escitalopram (Lexapro), paroxetine (Paxil), and citalopram (Celexa) are some of the most commonly prescribed SSRIs for depression. Most are available in generic versions. Serotonin and norepinephrine reuptake inhibitors (SNRIs) are similar to SSRIs and include venlafaxine (Effexor) and duloxetine (Cymbalta).

SSRIs and SNRIs tend to have fewer side effects than older antidepressants, but they sometimes produce headaches, nausea, jitters, or insomnia when people first start to take them. These symptoms tend to fade with time. Some people also experience sexual problems with SSRIs or SNRIs, which may be helped by adjusting the dosage or switching to another medication.

One popular antidepressant that works on dopamine is bupropion (Wellbutrin). Bupropion tends to have similar side effects as SSRIs and SNRIs, but it is less likely to cause sexual side effects. However, it can increase a person’s risk for seizures.


Tricyclics are older antidepressants. Tricyclics are powerful, but they are not used as much today because their potential side effects are more serious. They may affect the heart in people with heart conditions. They sometimes cause dizziness, especially in older adults. They also may cause drowsiness, dry mouth, and weight gain. These side effects can usually be corrected by changing the dosage or switching to another medication. However, tricyclics may be especially dangerous if taken in overdose. Tricyclics include imipramine and nortriptyline.


Monoamine oxidase inhibitors (MAOIs) are the oldest class of antidepressant medications. They can be especially effective in cases of “atypical” depression, such as when a person experiences increased appetite and the need for more sleep rather than decreased appetite and sleep. They also may help with anxious feelings or panic and other specific symptoms.

However, people who take MAOIs must avoid certain foods and beverages (including cheese and red wine) that contain a substance called tyramine. Certain medications, including some types of birth control pills, prescription pain relievers, cold and allergy medications, and herbal supplements, also should be avoided while taking an MAOI. These substances can interact with MAOIs to cause dangerous increases in blood pressure. The development of a new MAOI skin patch may help reduce these risks. If you are taking an MAOI, your doctor should give you a complete list of foods, medicines, and substances to avoid.

MAOIs can also react with SSRIs to produce a serious condition called “serotonin syndrome,” which can cause confusion, hallucinations, increased sweating, muscle stiffness, seizures, changes in blood pressure or heart rhythm, and other potentially life-threatening conditions. MAOIs should not be taken with SSRIs.

How should I take medication?

All antidepressants must be taken for at least 4 to 6 weeks before they have a full effect. You should continue to take the medication, even if you are feeling better, to prevent the depression from returning.

Medication should be stopped only under a doctor’s supervision. Some medications need to be gradually stopped to give the body time to adjust. Although antidepressants are not habit-forming or addictive, suddenly ending an antidepressant can cause withdrawal symptoms or lead to a relapse of the depression. Some individuals, such as those with chronic or recurrent depression, may need to stay on the medication indefinitely.

In addition, if one medication does not work, you should consider trying another. NIMH-funded research has shown that people who did not get well after taking a first medication increased their chances of beating the depression after they switched to a different medication or added another medication to their existing one.

Sometimes stimulants, anti-anxiety medications, or other medications are used together with an antidepressant, especially if a person has a co-existing illness. However, neither anti-anxiety medications nor stimulants are effective against depression when taken alone, and both should be taken only under a doctor’s close supervision.

Report any unusual side effects to a doctor immediately.





IV Ketamine Therapy

One of the most exciting new treatment options for depression is with a long known drug, ketamine. Ketamine has been used historically as an anesthetic. Recently, it has emerged as an effective treatment option for severe depression (citations below). The mechanism of action for ketamine’s antidepressant effects is not fully understood and hotly debated. However, studies of the neurobiology of depressed patients have revealed possible abnormalities that may have a causal link to depression such as increased inflammatory cytokines, decreased BDNF, and reduced hippocampal volume. Interestingly, there is much overlap in the neurobiology of depression and known consequences of ketamine treatment. Ketamine has been found to reduce neuroinflammation, increase BDNF production and hippocampal volume. Thus, it is highly likely that ketamine possesses a robust pharmacological profile that works collectively to correct abnormalities common to severe depression. Although only FDA-approved as an anesthetic, ketamine is used off-label by many physicians in cases of severe, treatment-resistant depression.

Resources for Ketamine and Depression:

Schwartzman, R. J., G. M. Alexander, J. R. Grothusen, T. Paylor, E. Reichenberger and M. Perreault (2009). “Outpatient intravenous ketamine for the treatment of complex regional pain syndrome: a double-blind placebo controlled study.” Pain 147(1-3): 107-115.

Best, S. R. and B. Griffin (2015). “Combination therapy utilizing ketamine and transcranial magnetic stimulation for treatment-resistant depression: a case report.” Int J Neurosci125(3): 232-234.

Clark, P. (2014). “Treatment-refractory depression: a case of successful treatment with intranasal ketamine 10%.” Ann Clin Psychiatry 26(2): 145.

Galvez, V., E. O’Keefe, L. Cotiga, J. Leyden, S. Harper, P. Glue, P. B. Mitchell, A. A. Somogyi, A. DeLory and C. K. Loo (2014). “Long-lasting effects of a single subcutaneous dose of ketamine for treating melancholic depression: a case report.” Biol Psychiatry 76(3): e1-2.

Hu, Y. D., Y. T. Xiang, J. X. Fang, S. Zu, S. Sha, H. Shi, G. S. Ungvari, C. U. Correll, H. F. Chiu, Y. Xue, T. F. Tian, A. S. Wu, X. Ma and G. Wang (2016). “Single i.v. ketamine augmentation of newly initiated escitalopram for major depression: results from a randomized, placebo-controlled 4-week study.” Psychol Med 46(3): 623-635.

Li, C. T., M. H. Chen, W. C. Lin, C. J. Hong, B. H. Yang, R. S. Liu, P. C. Tu and T. P. Su (2016). “The effects of low-dose ketamine on the prefrontal cortex and amygdala in treatment-resistant depression: A randomized controlled study.” Hum Brain Mapp 37(3): 1080-1090.

Murrough, J. W., K. E. Burdick, C. F. Levitch, A. M. Perez, J. W. Brallier, L. C. Chang, A. Foulkes, D. S. Charney, S. J. Mathew and D. V. Iosifescu (2015). “Neurocognitive effects of ketamine and association with antidepressant response in individuals with treatment-resistant depression: a randomized controlled trial.” Neuropsychopharmacology 40(5): 1084-1090.

Murrough, J. W., D. V. Iosifescu, L. C. Chang, R. K. Al Jurdi, C. E. Green, A. M. Perez, S. Iqbal, S. Pillemer, A. Foulkes, A. Shah, D. S. Charney and S. J. Mathew (2013). “Antidepressant efficacy of ketamine in treatment-resistant major depression: a two-site randomized controlled trial.” Am J Psychiatry 170(10): 1134-1142.

Murrough, J. W., A. M. Perez, S. J. Mathew and D. S. Charney (2011). “A case of sustained remission following an acute course of ketamine in treatment-resistant depression.” J Clin Psychiatry 72(3): 414-415.

Price, R. B., D. V. Iosifescu, J. W. Murrough, L. C. Chang, R. K. Al Jurdi, S. Z. Iqbal, L. Soleimani, D. S. Charney, A. L. Foulkes and S. J. Mathew (2014). “Effects of ketamine on explicit and implicit suicidal cognition: a randomized controlled trial in treatment-resistant depression.” Depress Anxiety 31(4): 335-343.

Singh, J. B., M. Fedgchin, E. J. Daly, P. De Boer, K. Cooper, P. Lim, C. Pinter, J. W. Murrough, G. Sanacora, R. C. Shelton, B. Kurian, A. Winokur, M. Fava, H. Manji, W. C. Drevets and L. Van Nueten (2016). “A Double-Blind, Randomized, Placebo-Controlled, Dose-Frequency Study of Intravenous Ketamine in Patients With Treatment-Resistant Depression.” Am J Psychiatry: appiajp201616010037.

Living With Depression

How do women experience depression?

Depression is more common among women than among men. Biological, life cycle, hormonal, and psychosocial factors that women experience may be linked to women’s higher depression rate. Researchers have shown that hormones directly affect the brain chemistry that controls emotions and mood. For example, women are especially vulnerable to developing postpartum depression after giving birth, when hormonal and physical changes and the new responsibility of caring for a newborn can be overwhelming.

Some women may also have a severe form of premenstrual syndrome (PMS) called premenstrual dysphoric disorder (PMDD). PMDD is associated with the hormonal changes that typically occur around ovulation and before menstruation begins.

During the transition into menopause, some women experience an increased risk for depression. In addition, osteoporosis—bone thinning or loss—may be associated with depression. Scientists are exploring all of these potential connections and how the cyclical rise and fall of estrogen and other hormones may affect a woman’s brain chemistry.

Finally, many women face the additional stresses of work and home responsibilities, caring for children and aging parents, abuse, poverty, and relationship strains. It is still unclear, though, why some women faced with enormous challenges develop depression, while others with similar challenges do not.

How do men experience depression?

Men often experience depression differently than women. While women with depression are more likely to have feelings of sadness, worthlessness, and excessive guilt, men are more likely to be very tired, irritable, lose interest in once-pleasurable activities, and have difficulty sleeping.

Men may be more likely than women to turn to alcohol or drugs when they are depressed. They also may become frustrated, discouraged, irritable, angry, and sometimes abusive. Some men throw themselves into their work to avoid talking about their depression with family or friends, or behave recklessly. And although more women attempt suicide, many more men die by suicide in the United States.

How do older adults experience depression?

Depression is not a normal part of aging. Studies show that most seniors feel satisfied with their lives, despite having more illnesses or physical problems. However, when older adults do have depression, it may be overlooked because seniors may show different, less obvious symptoms. They may be less likely to experience or admit to feelings of sadness or grief.

Sometimes it can be difficult to distinguish grief from major depression. Grief after loss of a loved one is a normal reaction to the loss and generally does not require professional mental health treatment. However, grief that is complicated and lasts for a very long time following a loss may require treatment. Researchers continue to study the relationship between complicated grief and major depression.

Older adults also may have more medical conditions such as heart disease, stroke, or cancer, which may cause depressive symptoms. Or they may be taking medications with side effects that contribute to depression. Some older adults may experience what doctors call vascular depression, also called arteriosclerotic depression or subcortical ischemic depression. Vascular depression may result when blood vessels become less flexible and harden over time, becoming constricted. Such hardening of vessels prevents normal blood flow to the body’s organs, including the brain. Those with vascular depression may have, or be at risk for, co-existing heart disease or stroke.

Although many people assume that the highest rates of suicide are among young people, older white males age 85 and older actually have the highest suicide rate in the United States. Many have a depressive illness that their doctors are not aware of, even though many of these suicide victims visit their doctors within 1 month of their deaths.

Most older adults with depression improve when they receive treatment with an antidepressant, psychotherapy, or a combination of both. Research has shown that medication alone and combination treatment are both effective in reducing depression in older adults. Psychotherapy alone also can be effective in helping older adults stay free of depression, especially among those with minor depression. Psychotherapy is particularly useful for those who are unable or unwilling to take antidepressant medication.

How do children and teens experience depression?

Children who develop depression often continue to have episodes as they enter adulthood. Children who have depression also are more likely to have other more severe illnesses in adulthood.

A child with depression may pretend to be sick, refuse to go to school, cling to a parent, or worry that a parent may die. Older children may sulk, get into trouble at school, be negative and irritable, and feel misunderstood. Because these signs may be viewed as normal mood swings typical of children as they move through developmental stages, it may be difficult to accurately diagnose a young person with depression.

Before puberty, boys and girls are equally likely to develop depression. By age 15, however, girls are twice as likely as boys to have had a major depressive episode.

Depression during the teen years comes at a time of great personal change—when boys and girls are forming an identity apart from their parents, grappling with gender issues and emerging sexuality, and making independent decisions for the first time in their lives. Depression in adolescence frequently co-occurs with other disorders such as anxiety, eating disorders, or substance abuse. It can also lead to increased risk for suicide.

An NIMH-funded clinical trial of 439 adolescents with major depression found that a combination of medication and psychotherapy was the most effective treatment option. Other NIMH-funded researchers are developing and testing ways to prevent suicide in children and adolescents.

Childhood depression often persists, recurs, and continues into adulthood, especially if left untreated.

How can I help a loved one who is depressed?

If you know someone who is depressed, it affects you too. The most important thing you can do is help your friend or relative get a diagnosis and treatment. You may need to make an appointment and go with him or her to see the doctor. Encourage your loved one to stay in treatment, or to seek different treatment if no improvement occurs after 6 to 8 weeks.

To help your friend or relative

  • Offer emotional support, understanding, patience, and encouragement.
  • Talk to him or her, and listen carefully.
  • Never dismiss feelings, but point out realities and offer hope.
  • Never ignore comments about suicide, and report them to your loved one’s therapist or doctor.
  • Invite your loved one out for walks, outings and other activities. Keep trying if he or she declines, but don’t push him or her to take on too much too soon.
  • Provide assistance in getting to the doctor’s appointments.
  • Remind your loved one that with time and treatment, the depression will lift.

How can I help myself if I am depressed?

If you have depression, you may feel exhausted, helpless, and hopeless. It may be extremely difficult to take any action to help yourself. But as you begin to recognize your depression and begin treatment, you will start to feel better.

To Help Yourself

  • Do not wait too long to get evaluated or treated. There is research showing the longer one waits, the greater the impairment can be down the road. Try to see a professional as soon as possible.
  • Try to be active and exercise. Go to a movie, a ballgame, or another event or activity that you once enjoyed.
  • Set realistic goals for yourself.
  • Break up large tasks into small ones, set some priorities and do what you can as you can.
  • Try to spend time with other people and confide in a trusted friend or relative. Try not to isolate yourself, and let others help you.
  • Expect your mood to improve gradually, not immediately. Do not expect to suddenly “snap out of” your depression. Often during treatment for depression, sleep and appetite will begin to improve before your depressed mood lifts.
  • Postpone important decisions, such as getting married or divorced or changing jobs, until you feel better. Discuss decisions with others who know you well and have a more objective view of your situation.
  • Remember that positive thinking will replace negative thoughts as your depression responds to treatment.
  • Continue to educate yourself about depression.

Information adapted from the National Institute of Mental Health (NIMH).

Article Links:

The National Institute of Mental Health Highlights Ketamine for Depression

IV Ketamine Shows Promise in Clinical Trial with Depressed Teens

Researchers from the University of Minnesota and The Mayo Clinic found that ketamine caused an average decrease of 42% on the Children’s Depression Rating Scale(CDRS)—the most widely used rating scale in research trials for assessing the severity of depression and change in depressive symptoms among adolescents. The study recruited adolescents, 12-18 years of age, with treatment-resistant depression (TRD; failure to respond to two previous antidepressant trials). The teens were administered intravenous ketamine (0.5 mg/kg) by infusion six times over two weeks.

The study reported that the average decrease in CDRS-R was 42.5% (p = 0.0004). Five (38%) adolescents met criteria for clinical response (defined as >50% reduction in CDRS-R). Three responders showed sustained remission at 6-week follow-up; relapse occurred within 2 weeks for the other two responders. The ketamine infusions were generally well tolerated; dissociative symptoms and hemodynamic symptoms were transient. Interestingly, higher dose was a significant predictor of treatment response.

“Adolescence is a key time period for emergence of depression and represents an opportune and critical developmental window for intervention to prevent negative outcomes,” the authors wrote in the study.

“Unfortunately, about 40% of adolescents do not respond to their first intervention and only half of non-responders respond to the second treatment,” they said. “Because standard interventions require prolonged periods (e.g., weeks to months) to assess efficacy, serial treatment failures allow illness progression, which in turn worsens the outcome. Hence, novel treatment strategies to address treatment-resistant depression in adolescents are urgently needed.”

The authors concluded that their results demonstrate the potential role for ketamine in treating adolescents with TRD. Additionally, evidence suggested a dose–response relationship; future studies are needed to optimize dose


Yale study found no safety issues with long-term ketamine treatment

 August 08, 2018

Researchers at Yale published a new study titled “Acute and Longer-Term Outcomes Using Ketamine as a Clinical Treatment at the Yale Psychiatric Hospital” in Clinical Psychiatry.  In late 2014, Yale began providing ketamine as an off-label therapy on a case-by-case basis for patients who could not participate in research protocols.  The authors observed 54 patients that received IV ketamine infusion for the treatment of severe and treatment-resistant mood disorders such as depression.

“Ketamine is being used as an off-label treatment for depression by an increasing number of providers, yet there is very little long-term data on patients who have received ketamine for more than just a few weeks,” Samuel T. Wilkinson, MD,from the department of psychiatry, Yale School of Medicine and Yale Psychiatric Hospital, told Healio Psychiatry.

The Yale researchers studied the acute and longer-term outcomes in this patient population. Importantly, a subset of patients (n=14) received ketamine on a long-term basis, ranging from 12 to 45 total treatments, over a course of 14 to 126 weeks.  The researchers found no evidence of cognitive decline, increased proclivity to delusions, or emergence of symptoms consistent with cystitis in this subset of long-term ketamine patients.  They also reported that the infusions were generally well-tolerated.

Although this study population was relatively small, limiting the conclusions that can be drawn, this is still an important first step in establishing the long-term safety of ketamine for the treatment of a myriad of diseases that it’s being used to treat

CNN Reports ‘Ketamine offers lifeline for suicidal thoughts’

CNN featured a segment on the use of ketamine for treating suicidal ideation–a novel, off-label use for ketamine that is currently being explored in human clinical trials.  The segment featured Dr. Sanjay Gupta sharing the story of Alan Ferguson.  Mr. Ferguson discussed his experience with suicidal ideation, stating that he had planned his own suicide prior to a psychiatrist suggesting the off-label use of ketamine.  Fortunately, ketamine worked for him as it has for many others, completely eliminating all thoughts of suicide and depression.

While ketamine is a long-known, FDA-approved anesthetic, new uses for this old drug have recently been discovered.  The new indication that is probably the farthest along is for the treatment of depression.  It’s even undergoing phase III clinical trials for the treatment of depression, which are expected to be completed next year.  In depression, ketamine’s mechanism of action is still being explored. Scientists know that ketamine antagonizes the NMDA receptor, which causes a number of downstream cascades that may be relevant to it’s antidepressant effects. Ketamine also increases important neuronal growth factors that can create new synaptic connections.

While there are numerous anti-depressants that are already FDA-approved, they don’t always work and–even when they do–it takes weeks to see the effect.  This is what’s special about ketamine.  The anti-depressant effects of ketamine are instantaneous.  In the case of Alan Ferguson, his depression went from severe to mild after the first infusion, and was gone after the second. In cases of depression that involve suicidality, this rapid improvement can be the difference between life and death.  Even though ketamine is not yet approved for the treatment of depression or suicidal ideation, there is an abundance of data showing that it works and it’s already being used off-label in the clinic.

First study shows ketamine is safe and effective for depression in elderly patients


Australian researchers completed the world’s first randomized control trial (RCT), assessing the efficacy and safety of ketamine as a treatment for depression in elderly patients.

In this double-blind, controlled, multiple-crossover study with a 6-month follow-up, 16 participants (≥60 years) with treatment-resistant depression who relapsed after remission or did not remit in the RCT were administered an open-label phase. Up to five subcutaneous doses of ketamine (0.1, 0.2, 0.3, 0.4, and 0.5 mg/kg) were administered in separate sessions (≥1 week apart), with one active control (midazolam) randomly inserted. Twelve ketamine treatments were given in the open-label phase. Mood, hemodynamic, and psychotomimetic outcomes were assessed by blinded raters. Remitters in each phase were followed for 6 months.

The results, published in the latest American Journal of Geriatric Psychiatry, provide preliminary evidence that ketamine is effective as an antidepressant – when delivered in repeated intravenous doses.

Pilot Randomized Controlled Trial of Titrated Subcutaneous Ketamine in Older Patients with Treatment-Resistant Depression

“What we noticed was that ketamine worked incredibly quickly and incredibly effectively,” Professor Colleen Loo, who led the pilot program told ABC News. “By incredibly effective, we mean going rapidly from severely depressed to being completely well in one day.”

“Some people think, ‘oh maybe it was just a drug induced temporary high’ — and it wasn’t,” she said. “You had the woozy effects in the first hour or so, but the antidepressant effects kicked in later.”

None of the participants experienced problematic side effects, according to the research team who administered the drug through a small injection under the skin.

“Our results indicate a dose-titration method may be particularly useful for older patients, as the best dose was selected for each individual person to maximize ketamine’s benefits while minimizing its adverse side effects,” she said.

The authors noted that further study is needed, however, to understand the risks of ketamine use and possible side effects, such as its impact on liver function in the elderly.

IV Ketamine “most important breakthrough in antidepressant treatment in decades”

PTSD Treatment – Ketamine is a novel treatment for several psychiatric disorders including: Major Depressive Disorder, Bipolar Depression, Postpartum Depression, Obsessive-Compulsive Disorder (OCD), and Posttraumatic Stress Disorder or PTSD.  It was originally FDA approved for anesthesia but is now frequently used off-label due to its positive effects on the various disorders listed above.  PTSD is an devastating disorder that has become more and more common but medical treatments overall are still lacking.

What is PTSD?

PTSD Treatment

PTSD is a disorder that develops after a traumatic experience.  Such trauma sometimes involves combat, car accidents, natural disasters or sexual assaults.  Up to 80% of individuals in their life will experience at least one traumatic event but, fortunately, most people do not go on to develop PTSD.  The lifetime prevalence of developing PTSD is about 10% and women are twice as likely as men to develop PTSD.  Those who do go on to develop PTSD typically will have one or more of the following symptoms:

• traumatic nightmares
• flashbacks taking them back to the event
• distress after exposure to traumatic reminders or stimuli
• hypervigilance/hyperarousal
• avoidance of certain thoughts and situations
• negative thoughts and mood including shame, despair and depression.

A constellation of these symptoms must persist for at least a month for a diagnosis of PTSD to be made.
Most PTSD Treatment are ineffective for some patients and their all generally slow acting—meaning that the patient must wait weeks to have a meaningful impact on the patient’s wellness. Ketamine has now been shown to be effective at managing PTSD in several clinical studies. Moreover, physicians are beginning to present case reports where ketamine has helped their patients. One of the largest benefits of using Ketamine off label for the treatment of depression is that it is generally very fast-acting. Patients typically report feeling better after the first infusion or two. Sometimes, they report feeling 100% better after 5 days of IV ketamine therapy.



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Trippy depression treatment? Hopes and hype for ketamine

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Lauren Pestikas sits as she receives an infusion of the drug ketamine during a 45-minute session at an outpatient clinic in Chicago on July 25, 2018. Pestikas struggled with depression and anxiety and made several suicide attempts before starting ketamine treatments earlier in the year. (AP Photo/Teresa Crawford)

CHICAGO (AP) — It was launched decades ago as an anesthetic for animals and people, became a potent battlefield pain reliever in Vietnam and morphed into the trippy club drug Special K.

Now the chameleon drug ketamine is finding new life as an unapproved treatment for depression and suicidal behavior. Clinics have opened around the United States promising instant relief with their “unique” doses of ketamine in IVs, sprays or pills. And desperate patients are shelling out thousands of dollars for treatment often not covered by health insurance, with scant evidence on long-term benefits and risks.

Chicago preschool teacher Lauren Pestikas long struggled with depression and anxiety and made several suicide attempts before trying ketamine earlier this year.

The price tag so far is about $3,000, but “it’s worth every dime and penny,” said the 36-year-old.

Pestikas said she feels much better for a few weeks after each treatment, but the effects wear off and she scrambles to find a way to pay for another one.

For now, ketamine has not received approval from the U.S. Food and Drug Administration for treating depression, though doctors can use it for that purpose.

Some studies show ketamine can provide relief within hours for tough-to-treat depression and suicidal behavior and clinics promising unproven benefits have popped up nationwide. But more research is needed to know long-term benefits and risks. (Oct. 31)

Ketamine has been around since the 1960s and is widely used as an anesthesia drug during surgery because it doesn’t suppress breathing. Compared to opioids such as morphine, ketamine isn’t as addictive and doesn’t cause breathing problems. And some studies have shown that ketamine can ease symptoms within hours for the toughest cases.

Its potential effects on depression were discovered in animal experiments in the late 1980s and early 1990s showing that glutamate, a brain chemical messenger, might play a role in depression, and that drugs including ketamine that target the glutamate pathway might work as antidepressants.

Conventional antidepressants like Prozac target serotonin, a different chemical messenger, and typically take weeks to months to kick in — a lag that can cause severely depressed patients to sink deeper into despair.

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A vial of ketamine, which is normally stored in a locked cabinet, on display in Chicago on July 25, 2018. AP Photo/Teresa Crawford)

Ketamine’s potential for almost immediate if temporary relief is what makes it so exciting, said Dr. Jennifer Vande Voort, a Mayo Clinic psychiatrist who has used ketamine to treat depression patients since February.

“We don’t have a lot of things that provide that kind of effect. What I worry about is that it gets so hyped up,” she said.

The strongest studies suggest it’s most useful and generally safe in providing short-term help for patients who have not benefited from antidepressants. That amounts to about one-third of the roughly 300 million people with depression worldwide.

“It truly has revolutionized the field,” changing scientists’ views on how depression affects the brain and showing that rapid relief is possible, said Yale University psychiatrist Dr. Gerard Sanacora, who has done research for or consulted with companies seeking to develop ketamine-based drugs.

But to become standard depression treatment, he said, much more needs to be known.

Last year, Sanacora co-authored an American Psychiatric Association task force review of ketamine treatment for mood disorders that noted the benefits but said “major gaps” remain in knowledge about long-term effectiveness and safety. Most studies have been small, done in research settings and not in the real world.

When delivered through an IV, ketamine can cause a rapid increase in heart rate and blood pressure that could be dangerous for some patients. Ketamine also can cause hallucinations that some patients find scary.

“There are some very real concerns,” Sanacora said. “We do know this drug can be abused, so we have to be very careful about how this is developed.”

Dr. Rahul Khare, an emergency medicine specialist in Chicago, first learned about ketamine’s other potential benefits a decade ago from a depressed and anxious patient he was preparing to sedate to fix a repeat dislocated shoulder.

“He said, ‘Doc, give me what I got last time. For about three weeks after I got it I felt so much better,’” Khare recalled.

Khare became intrigued and earlier this year began offering ketamine for severe depression at an outpatient clinic he opened a few years ago. He also joined the American Society for Ketamine Physicians, formed a year ago representing about 140 U.S. doctors, nurses, psychologists and others using ketamine for depression or other nonapproved uses.

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Dr. Rahul Khare poses for a portrait at his outpatient Chicago clinic on July 25, 2018. (AP Photo/Teresa Crawford)

There are about 150 U.S. ketamine clinics, compared with about 20 three years ago, said society co-founder Dr. Megan Oxley.

Khare said the burgeoning field “is like a new frontier” where doctors gather at meetings and compare notes. He has treated about 50 patients with depression including Pestikas. They’re typically desperate for relief after failing to respond to other antidepressants. Some have lost jobs and relationships because of severe depression, and most find that ketamine allows them to function, Khare said.

Typical treatment at his clinic involves six 45-minute sessions over about two weeks, costing $550 each. Some insurers will pay about half of that, covering Khare’s office visit cost. Patients can receive “booster” treatments. They must sign a four-page consent form that says benefits may not be long-lasting, lists potential side effects, and in bold letters states that the treatment is not government-approved.

At a recent session, Pestikas’s seventh, she leaned back on a reclining white examining-room chair as a nurse hooked her up to a heart and blood pressure monitor. She grimaced as a needle was slipped into the top of her left palm. Khare reached up with a syringe to inject a small dose of ketamine into an IV bag hanging above the chair, then dimmed the lights, pulled the window curtains and asked if she had questions and was feeling OK.

“No questions, just grateful,” Pestikas replied, smiling.

Pestikas listened to music on her iPhone and watched psychedelic videos. She said it was like “a controlled acid trip” with pleasant hallucinations. The trip ends soon after the IV is removed, but Pestikas said she feels calm and relaxed the rest of the day, and that the mood boost can last weeks.

Studies suggest that a single IV dose of ketamine far smaller than used for sedation or partying can help many patients gain relief within about four hours and lasting nearly a week or so.

Exactly how ketamine works is unclear, but one idea is that by elevating glutamate levels, ketamine helps nerve cells re-establish connections that were disabled by depression, said ketamine expert Dr. Carlos Zarate, chief of experimental therapies at the National Institute of Mental Health.

A small Stanford University study published in August suggested that ketamine may help relieve depression by activating the brain’s opioid receptors.

Janssen Pharmaceuticals and Allergan are among drug companies developing ketamine-like drugs for depression. Janssen leads the effort with its nasal spray esketamine. The company filed a new drug application in September.

Meanwhile, dozens of studies are underway seeking to answer some of the unknowns about ketamine including whether repeat IV treatments work better for depression and if there’s a way to zero in on which patients are most likely to benefit.

Until there are answers, Zarate of the mental health institute said ketamine should be a last-resort treatment for depression after other methods have failed.

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Ketamine in the News October 2018

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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:  NMDA receptor function, memory, and brain aging Case-control study of genotypes in multiple chemical sensitivity CYP2D6, NAT1, NAT2, PON 1, MTHFR

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.


  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



  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: Overview of air pollution and endocrine disorders  |  Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment


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.




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




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. 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



More Helpful Resources:



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.


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.



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The pros and cons of ketamine

Geuris “Jerry” Rivas, a native of New York, was diagnosed with severe obsessive-compulsive disorder when he was 15. Obsessions with organizing and reorganizing the belongings in his bedroom — posters, comic books, videos — took over most of his life.

Forced by germ obsessions to compulsively wash and rewash his hands, he started wearing gloves all day to both protect him from the germs and stop him from washing his hands raw. Now, at 36, OCD symptoms continue to cost him jobs and relationships. He’s managed to turn his organizational skills into a profession — he’s a home organizer and house cleaner — but still he struggles daily with his obsessions.

“It’s caused me a great deal of suffering,” Rivas says. “I’ve tried many, many medications. I’ve wasted so much of my life.”

In 2012, running out of answers, Rivas took part in the first clinical trial to test ketamine as a treatment for OCD. While ketamine is approved by the U.S. Food and Drug Administration as an anesthetic, it is also an illicit party drug known as “Special K,” with hallucinogenic effects and the potential for abuse. Over the past 10 years, dozens of small studies of ketamine’s ability to treat a variety of mood and anxiety disorders have reported remarkable results — including the sudden alleviation of treatment-resistant depression, bipolar disorder and post-traumatic stress disorder. And these effects lasted days, sometimes weeks, after the hallucinogenic effects of the drug wore off.

With a single infusion of the drug, Rivas experienced for two weeks what it was like to live without the compulsions and obsessions that had for years controlled his life.

“I felt like, for the first time, I was able to function like a regular person,” he says.

Illustration of a giant K being painted by a man in a white coat

Pros and cons

Ketamine has brought hope to a psychiatric field desperate to find new treatments for severe OCD, a chronic condition marked by debilitating obsessions and repetitive behaviors. Current treatments, which include antidepressants such as Prozac, can take months to have any effect on the disease, if they work at all.

“Severe OCD takes such a toll on patients,” says Carolyn Rodriguez, MD, PhD, who as a researcher at Columbia University ran the OCD trial. Now an assistant professor of psychiatry and behavioral sciences at Stanford, she has continued to explore the pros and cons of using ketamine to treat OCD. “The constant, intrusive thoughts that something is contaminated, the checking and rechecking, the repetitive behaviors. It interferes with your life, your jobs, your relationships.”

Ketamine was developed in the 1960s and has been used for decades as an anesthetic during surgery. It remains a mystery just how the drug works in the brain, and there are safety concerns. There is evidence from people who take the drug routinely — in much higher doses — that chronic, high-frequency ketamine use may be associated with increased risk of bladder inflammation and cognitive impairment, Rodriguez says. And if taken regularly, it can lead to dependence.

But researchers like Rodriguez are intrigued about the drug’s potential to help them identify a whole new line of medicines for fast-acting treatment of mental health disorders.

“What most excites me about ketamine is that it works in a different way than traditional antidepressants,” Rodriguez says. “Using ketamine, we hope to understand the neurobiology that could lead to safe, fast-acting treatments. I feel that is part of my mission as a physician and researcher.”

‘Right out of a movie’

Rodriguez’s interest in ketamine as a treatment for OCD was sparked about a decade ago when she was starting out as a research scientist at Columbia. A small, placebo-controlled study published in 2006 by a mentor of hers, Carlos Zarate, MD, now chief of the section on neurobiology and treatment of mood disorders at the National Institute of Mental Health, had shown that ketamine induced dramatic improvement in treatment-resistant depression within two hours of infusion. It was a landmark study, drawing attention among the psychiatric community and launching a new field of research into the use of ketamine to treat various mood and anxiety disorders.

“What most excites me about ketamine is that it works in a different way than traditional antidepressants.”

Rodriguez, intent on searching for better, faster treatments for her patients like Rivas with OCD, took note. There was an emerging theory that ketamine affects the levels of the neurotransmitter glutamate in the brain and increasing evidence that glutamate plays a role in OCD symptoms, she says. Perhaps ketamine could help regulate OCD symptoms as well as depression.

In 2013, Rodriguez and colleagues published their results from that first clinical trial of ketamine in OCD patients. The trial randomized 15 patients with OCD to ketamine or placebo.

In those patients who were given ketamine, the effect was immediate. Patients reported dramatic decreases in their obsessive-compulsive symptoms midway through the 40-minute infusion, according to the study. The diminished symptoms lasted throughout the following week in half of the patients. Most striking were comments by the patients quoted in the study: “I tried to have OCD thoughts, but I couldn’t,” said one. Another said, “I feel as if the weight of OCD has been lifted.” A third said, “I don’t have any intrusive thoughts. … This is amazing, unbelievable. This is right out of a movie.” And while nearly all initially had dissociative effects like feelings of unreality, distortions of time or hallucinations, they were gone within two hours after the start of the infusion.

“Carolyn’s study was quite exciting,” Zarate says, adding that there were a number of similar, small but rigorous studies following his 2006 study that found fast-acting results using ketamine to treat bipolar disorder and post-traumatic stress disorder.

“We had no reason to believe that ketamine could wipe out any symptoms of these disorders within hours or days,” he says.

So how does it work?

Virtually all of the antidepressants used in the past 60 years work the same way: by raising levels of serotonin or one or two other neurotransmitters. Ketamine, however, doesn’t affect serotonin levels. Exactly what it does remains unclear.

“There’s a recognition that people like me and others are using the drug to treat patients now. There’s an incredible need for something.”

Since coming to Stanford in 2015, Rodriguez has been funded by the National Institute of Mental Health for a large clinical trial of ketamine’s effects on OCD. This five-year trial aims to follow 90 OCD patients for as long as six months after they’ve been given a dose of ketamine or an alternative drug. Rodriguez and her research team want to observe how ketamine changes participants’ brains, as well as test for side effects.

Ultimately, Rodriguez says, she hopes the study will lead to the discovery of other fast-acting drugs that work in the brain like ketamine but without its addictive potential.

Recent research in the field indicates that the glutamate hypothesis that triggered her pilot study might be further refined.

“Ketamine is a complicated drug that works on many different receptor sites,” she says. “Researchers have fixated on the NMDA receptor, one of the glutamate-type receptors, but it might not be the only receptor bringing benefit.”

In May 2016, researchers from NIMH and the University of Maryland — Zarate among them — published a study conducted in mice showing that a chemical byproduct, or metabolite, created as the body breaks down ketamine might hold the secret to its rapid antidepressant actions. This metabolite, hydroxynorketamine, reversed depressionlike symptoms in mice without triggering any of the anesthetic, dissociative or addictive side effects associated with ketamine, Zarate says.

“Ideally, we’d like to test hydroxynorketamine and possibly other drugs that act on glutamate pathways without ketamine-like side effects as possible alternatives to ketamine in OCD,” Rodriguez says.

Beyond the clubs

Meanwhile, dozens of commercial ketamine clinics have popped up across the country, making treatments available to patients who are searching for help to stop their suffering now. Medical insurance companies usually cover ketamine’s FDA-approved use as an anesthetic but won’t cover its use for other purposes, such as mental health disorders. So patients who have run out of treatment options are paying hundreds of dollars a dose for repeated ketamine infusions.

“The fact that these clinics exist is due to the desperation of patients,” says Rodriguez.

She and other researchers are calling for guidelines to protect patients and more research to learn how to use the drug safely.

“I think it’s a game changer, and it’s here to stay,” says David Feifel, MD, PhD, professor emeritus of psychiatry at UC-San Diego, who studies the effect of ketamine on clinical depression. Feifel began prescribing the drug for patients with treatment-resistant depression in 2010.

“I’ve found it to be very safe,” Feifel says, adding that the American Psychiatric Association this year issued safety guidelines on how to use ketamine clinically for treatment of depression.

“There’s a recognition that people like me and others are using the drug to treat patients now,” he says. “There’s an incredible need for something.”

The drug hasn’t worked for everyone he’s treated, Feifel says, but for many it’s been “life-changing.”

Rodriguez says she understands what motivates the clinicians to prescribe the drug now to patients in dire straits — those who are suicidal or who have tried every possible medication and therapeutic option and continue to suffer each day.

“I see it as a way to treat people whose OCD is very, very severe,” she says. “People who can’t come out of the house, who are suicidal, who have no other options.

“I just don’t like the idea of people being in pain,” Rodriguez adds. “I want to see science translated into treatments now.”

Meanwhile, researchers are learning more about the drug. Janssen Pharmaceutical is testing the efficacy of a version of ketamine, known as esketamine, as a therapy for treatment-resistant depression and for major depressive disorder with imminent risk for suicide. The FDA has fast-tracked both investigations. At Stanford, Alan Schatzberg, MD, a professor of psychiatry and behavioral sciences, along with other faculty including Rodriguez, is studying the mechanism of action for ketamine in treating depression.

Rodriguez is also interested in using ketamine to kick-start a type of cognitive behavioral therapy called exposure and response prevention, an evidence-based psychological treatment designed to help patients overcome OCD. The therapy involves teaching patients with OCD to face anxieties by refraining from ritualizing behaviors, then progressing to more challenging anxieties as they experience success.

Relaxation and other techniques also help patients tolerate their anxiety — for example, postponing the compulsion to wash their hands for at least 30 minutes, then extending that time period.

“My goal isn’t to have people taking ketamine for long periods of time,” Rodriguez says. But perhaps a short-term course of ketamine could provide its own kind of exposure and response prevention by allowing patients to experience that it is possible not to be controlled by their OCD, she says.

Rivas well remembers that infusion of ketamine he received during Rodriguez’s first clinical trial to test the drug. The rush made him feel “like Superman.”

“I felt like my body was bigger, that I was more muscular, that I could tackle anything,” he says. But that feeling only lasted the duration of the 40-minute infusion. His OCD symptoms disappeared immediately and were still gone for two weeks after.

“I was amazed that something like that would work and work so fast,” he says. His OCD symptoms today are still intrusive, but he manages to keep them under control by taking antidepressants and seeing a therapist. Still, each day when he comes home from work, he has to put gloves on before he enters his apartment building, and as soon as he enters his apartment, he must wash his hands.

“It’s a ritual now,” he says. “There has never been a time that I haven’t done that, except those two weeks after the ketamine.”

When he heard that certain private ketamine clinics are now offering the drug as treatment for OCD, he said he understands why patients take the risks and pay the high prices. As more research has become available, he’s begun considering it himself.

“I’ve been suffering through my OCD for so long, I’ve gotten to the point where I’d try anything,” he says.

USING KETAMINE TO TREAT SEVERE MENTAL ILLNESSA conversation with Stanford psychiatrist Carolyn Rodriguez, MD, PhD, about how she got interested in the use of ketamine to treat obsessive-compulsive disorder and how she is determined to find out why, in studies, the drug has provided relief from symptoms.

AUDIO Interview

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The Psychopharmacology of Depression: Strategies, Formulations, and Future Implications


With well over two dozen traditional antidepressants available in the US, and an ever-growing list of other psychotropic compounds with apparent antidepressant properties, pharmacological options for treating clinical depression today are broad and vast. However, recent findings suggest that the magnitude of efficacy for most antidepressants compared with placebo may be more modest than previously thought.1Most depressed patients do not respond fully to a first antidepressant trial, and with each consequent trial, there is less chance of symptom remission.2 About one-third of patients receiving long-term treatment report persistent moderate-to-severe depression.3 Hence, there remains more than a little room for improvement.

Since the late 1950s, the traditional view of treating depression has focused on the role of monoamines (serotonin, norepinephrine, and dopamine) as the main targets for medications. Newer treatments are looking beyond effects on monoamines as potential strategies to leverage depressive symptoms.

A major challenge for progress in novel pharmacotherapies has been our lack of a full understanding about the causes of depression. Advances in functional neuroimaging and genetic markers have begun to shed new light on brain regions and pathways associated with aberrant neural functioning in depression, but not in ways that have led to treatments aimed at remedying its pathogenesis. This makes it hard to think of antidepressant medications as “treating” the pathophysiology of depression (as when antibiotics eliminate the cause of an infection); rather, antidepressant relieve symptoms by counteracting or compensating for depression’s consequences (as when diuretics alleviate peripheral edema regardless of its etiology).

Gone are the days of oversimplified theories that depression is caused by a “chemical imbalance.” More likely, depression involves changes in brain architecture and the interplay of complex circuits in which chemicals, or neurotransmitters, are the messengers of information, rather than the causes of faulty functioning. Table 1 summarizes some of the major conceptual shifts that have occurred in thinking about the probable causes of depression (or at least its neurobiological context), which sets the stage for new ways to consider innovative treatment strategies. Looking beyond the role of monoamines as treatment targets in depression, a number of novel therapeutic strategies have begun to receive growing interest in preclinical and clinical trials. Key points about emerging novel depression pharmacotherapies are summarized in Table 2, and described more fully below.

Subanesthetically dosed intravenous (IV) ketamine currently represents perhaps the most dramatic and innovative antidepressant pharmacotherapy to emerge in decades.4,5 It is pharmacodynamically unique in its rapid onset (hours rather than days to weeks) and its potential ability to reduce suicidal ideation after a single dose, independent of its antidepressant properties.6 (While both lithium and clozapine have been shown to reduce suicidal behaviors, neither has been shown to reduce ideation, much less in the same day after a single dose.) Meta-analyses suggest that 0.5 mg/kg IV ketamine produces nearly a 10-fold greater likelihood of response than placebo at day 1 and a 4- to 5-fold likelihood of sustained response after one week.7

The exact psychotropic mechanism of action of ketamine remains elusive. Initial work focused on blockade of ionotropic N-methyl-D-aspartate (NMDA) receptors as accounting broadly for its antidepressant effects. However, subsequent negative randomized trials with other NMDA receptor antagonists (such as riluzole8) redirected interest toward ketamine’s other, non-NMDA receptor-related mechanisms, such as sigma receptor agonism, mu opioid receptor antagonism, or midbrain monoaminergic inhibition. Other authors have suggested that at low doses, ketamine’s antidepressant effects may derive from an increase in glutamate transmission with increased α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor expression, leading to increased release of brain-derived neurotrophic factor (BDNF).9Murrough and colleagues10 recently observed the necessity of AMPA receptor activation for the antidepressant effects of ketamine. They reported that “directly targeting the NMDA [receptor] may not be required.” As noted by the American Psychiatric Association Council on Research Task Force on Novel Biomarkers and Treatments,11 future advances will depend on a better understanding of the many mechanisms of action relative to the antidepressant properties of ketamine.

Ketamine is currently not approved by the FDA as a treatment for depression. Uncertainty remains as to whether repeated dosing is safe, effective, and necessary to avoid relapse and, if so, when, at what frequency, and for how long. The aforementioned APA Council on Research Consensus Statement on ketamine treatment for depression11 stated that while some clinics already offer 2- to 3-week courses of ketamine delivered 2 to 3 times per week, “there remain no published data that clearly supports this practice, and . . . the relative benefit of each ketamine infusion [should] be considered in light of the potential risks associated with longer term exposure to ketamine and the lack of published evidence for prolonged efficacy with ongoing administration.” 11 Thus far, studies of other pharmacotherapies to sustain an initial ketamine response (such as riluzole or lithium) have proven no better than placebo.

Enantiomeric esketamine remains investigational as a possible easier-to-administer intranasal (IN) antidepressant, although IN bioavailability is only about half that of IV ketamine’s 100%. Two randomized multi-site trials of IN esketamine added to antidepressants showed dose-related better efficacy than placebo: Daly and colleagues12 found that 28 mg to 84 mg of IN ketamine twice weekly over two weeks produced significant improvement in depressive symptoms as compared to placebo beginning after 1 week and continuing through week 9 for the majority of responders. A study by Canuso and colleagues13 demonstrated a significant reduction in depressive symptoms within 4 hours of administration (56 mg to 84 mg insufflated over 15 minutes) and a medium to large effect size, sustained after 25 days; suicidal ideation reduced significantly at 4 hours but not beyond that time. Another recent randomized pilot trial of IN racemic ketamine (the mixture of S- and R-ketamine) was prematurely discontinued due to poor tolerability (including cardiovascular and neurological adverse effects) and highly variable absorption across subjects.14

Modulation of the endogenous opioid system has long been a target of interest in the treatment of mood disorders, but it is limited by safety risks, tolerance, and addiction potential. Recent work has focused on a proprietary combination of the μ-opioid partial agonist/kappa antagonist buprenorphine plus the μ-opioid receptor antagonist samidorphan (ALKS 5461). The potent blockade of μ-opioid receptors in samidorphan, which prevents buprenorphine access to these receptors, effectively renders buprenorphine a selective kappa opiate receptor (KOR) antagonist, which is its putative antidepressant mechanism. After initial favorable Phase II trials, in 2013 the FDA granted ALKS 5461 fast track status for accelerated regulatory review as an antidepressant adjunct. Subsequent randomized trials in treatment-resistant major depression revealed statistically significant differences from placebo on some, but not all, depressive symptom outcome measures and at some, but not all, doses studied.15,16 The FDA initially refused to review the new drug application for ALKS 5461 as an adjunctive therapy for depression because of concerns about bioavailability and lack of evidence, but then reversed its position. ALKS 5461 is currently under regulatory review and a decision regarding its possible approval is expected by early 2019.

Antiinflammatories and immunomodulators

There has been growing recognition of complex interrelationships between depression and inflammation. Some but not all patients with clinically significant depression appear to have elevated serum markers of systemic inflammation, such as high sensitivity C-reactive protein (hs-CRP) and inflammatory cytokines. While causal relationships between depression and inflammation are poorly understood and questions remain whether depression causes inflammation or vice versa, randomized trial data suggest potential antidepressant value of nonsteroidal anti-inflammatory drugs (NSAIDs), particularly the COX-2 inhibitor celecoxib. A pooled meta-analysis of 5447 participants from 10 NSAID trials and 4 cytokine inhibitors (as mono- or add-on therapy for depression) revealed statistically significant advantages over placebo, with small to medium effect sizes, for response (odds ratio = 6.6; 95% confidence interval=2.2-19.4) or remission (odds ratio = 7.9; 95% confidence interval=2.9-21.1)17It has not been established whether adding celecoxib or other NSAIDs to an antidepressant may be more useful only in the setting of elevated serum markers of inflammation. Elsewhere, preliminary studies reveal that inflammatory depressive subtypes (ie, high baseline hs-CRP) may respond better to a tricyclic than SSRI,18 adjunctive L-methylfolate,19 or the tumor necrosis factor (TNF) antagonist infliximab (admnistered IV at 5 mg/kg over 3 doses).20

The antimicrobial minocycline exerts anti-inflammatory and anti-oxidative properties and has been preliminarily studied mostly in small or open/nonrandomized trials. A meta-analysis of 3 randomized controlled trials found an overall significantly greater effect than placebo with a medium to large effect size and good tolerability, although the small number of well-designed studies and samples sizes (total N = 158) limits their generalizability.21

Anticholinergic muscarinic agents

Harkening back to the 1970s hypothesis that depression could reflect cholinergic-adrenergic dysregulation, interest has turned to the possible antidepressant effects of the muscarinic cholinergic antagonist scopolamine. Preliminary studies of intravenous scopolamine dosed at 4 µg/kg in both unipolar and bipolar depression have produced remission rates from 45% to 56% (Cohen’s d ranged from 1.2-3.4) typically within several days of administration, with persistence for 10 to 14 days.22Antimuscarinic adverse effects such as sedation, dry mouth, and blurry vision are common but transient. Neurocognitive measures reaction time during selective attention tasks reveal no significant delays following IV scopolamine infusion.23 Analogous to IV ketamine, questions remain about the optimal number of infusions to minimize relapse as well as the use of nonparenteral formulations.

Brexanolone (SAGE-547), also known as allopregnanolone, is a positive allosteric modulator of GABA-A receptors. It is a progesterone metabolite that exerts neuroprotective, pro-cognitive, and possible antidepressant/anxiolytic properties. Precipitous drops in progesterone and allopregnanolone after childbirth prompted interest in the use of allopregnanolone specifically in postpartum depression. A small (N = 21) initial trial of brexanolone (administered intravenously because of its short half-life and poor oral bioavailability) or placebo for severe postpartum depression yielded a substantial reduction in depressive symptom severity within 60 hours (effect size = 1.2).24 Further data remain pending. SAGE-217 is reformulated brexanolone that has good oral bioavailability, allowing for oral administration, as well as a longer half-life allowing once-a-day dosing. It is currently being studied as an adjunctive agent for treatment resistant depression.

PPAR-γ agonists and incretins

Thiazolidinediones are insulin sensitizers that also demonstrate antidepressant properties in animal studies and appear to possess anti-inflammatory, neuroprotective, antioxidant and anti-excitatory properties. Pioglitazone, a PPAR-γ agonist thiazolidinedione, has been studied versus placebo or metformin in major depression, both as monotherapy and in combination with antidepressants or lithium. A meta-analysis of 4 trials revealed significantly higher remission rates than controls (27% versus 10%, respectively; odds ratio of remission in major depression = 5.9 (95% confidence interval=1.6-22.4), p = .009), with an NNT = 6.25 Even though PPAR-γ agonists can decrease insulin resistance, weight gain can be an undesired adverse effect that is possibly a result of a combination of fat cell proliferation, fluid retention, and increased appetite. Pioglitazone also carries serious adverse risks for congestive heart failure and bladder cancer.

Glucagon-like peptide 1

Another class of antidiabetic drugs known as glucagon-like peptide 1 (GLP-1) agonists mimic the action of insulin (so-called incretins) and are of interest as a potential target for depression. GLP-1 agonists such as liraglutide possess neuroprotective and antiapoptotic properties, and animal studies suggest it has antidepressant and pro-cognitive effects, particularly involving reward and motivation. Human studies have thus far focused more on weight-reducing and possible cognitive benefits of liraglutide more than its potential antidepressant efficacy, but its mechanism represents a promising direction for further study.

Future directions

This brief overview has focused on emerging novel pharmacotherapies for depression. While the provisional nature of proof-of-concept studies may be encouraging, they are far from definitive. The aforementioned findings are largely preliminary and meant more to prompt larger randomized trials to establish efficacy, safety, and generalizability rather than inspire premature immediate uptake into clinical practice.

Given the focus on neuroprotection and enhanced neuroplasticity as proposed targets of treatment, it would seem remiss not to at least mention the neurobiological impact of depression-specific psychotherapies, mindfulness meditation, and related psychosocial interventions. Psychotherapy is, among other things, a behavioral learning paradigm, presumably rendering alterations in cognitive functions (memory, attention, and decision-making), fear extinction, and emotional processing. Evidence-based psychotherapies for depression have been shown to produce changes in brain network connectivity26 (recapitulating the idea of Hebbian synapses, where “neurons that fire together wire together”) and upregulation of intracellular transcription factors involved in neuronal plasticity.27Enhanced neuroplasticity may represent a common denominator target for effective biological or psychosocial treatments for depression.

Increasingly, drugs we call antidepressants are diversifying to include broader classes of molecules. A more neuroscience-based nomenclature for psychotropic drugs has already been proposed28 and will no doubt invoke more novel drug mechanisms, supplanting older concepts about depression as a chemical imbalance as perspectives continue to evolve about how antidepressants impact neuronal viability and brain microarchitecture.


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2. Trivedi MH, Rush AJ, Wisniewski SR, et al. Evaluation of outcomes with citalopram for depression using measurement-based care in STAR*D: implications for clinical practice. Am J Psychiatry. 2006;163:28-40.

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5. Murrough JW, Iosifescu DV, Chang LC, et al. Antidepressant efficacy of ketamine in treatment-resistant major depression: a two-site randomized controlled trial. Am J Psychiatry. 2013;170:1134-1142.

6. Wilkinson ST, Ballard ED, Bloch MH, et al. The effect of a single dose of intravenous ketamine on suicidal ideation: a systematic review and individual participant data meta-analysis. Am J Psychiatry. 2018;175:150-158.

7. Newport DJ, Carpenter LL, McDonald WM, et al. Ketamine and other NMDA antagonists: early clinical trials and possible mechanisms in depression. Am J Psychiatry. 2015;172:950-966.

8. Mathew SJ, Gueorguieva R, Brandt C, et al. A randomized, double-blind, placebo-controlled, sequential parallel comparison design trial of adjunctive riluzole for treatment-resistant major depressive disorder. Neuropsychopharmacol 2017;42: 2567-2574.

9. Duman RS, Li N, Liu RJ, et al. Signaling pathways underlying the rapid antidepressant actions of ketamine. Neuropharmacol. 2012;62:35-41.

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11. 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;74:399-405.

12. Daly EJ, Singh JB, Fedgchin M, et al. Efficacy and safety of intranasal esketamine adjunctive to oral antidepressant therapy in treatment-resistant depression: a randomized clinical trial. JAMA Psychiatry. 2018;75:139-148.

13. Canuso CM, Singh JB, Fedgchin M, et al. Efficacy and safety of intranasal esketamine for the rapid reduction of symptoms of depression and suicidality in patients at imminent risk for suicide: results of a double-blind, randomized, placebo-controlled study. Am J Psychiatry. April 2018; Epub ahead of print.

14. Gálvez V, Li A, Huggins C, et al. Repeated intranasal ketamine for treatment-resistant depression – the way to go? Results from a pilot randomised controlled trial. J Clin Psychopharmacol. 2018;32:397-407.

15. Ehrich E, Turncliff R, Du Y, et al. Evaluation of opioid modulation in major depressive disorder. Neuropsychopharmacol. 2015;40:1448-1455.

16. Fava M, Memisoglu A, Thase ME, et al. Opioid modulation with buprenorphine/samidorphan as adjunctive treatment for inadequate response to antidepressants: a randomized double-blind placebo-controlled trial. Am J Psychiatry. 2016;173:499-508.

17. Köhler O, Benros ME, Nordentoft M, et al. Effect of anti-inflammatory treatment on depression, depressive symptoms, and adverse effects: a systematic review and meta-analysis of randomized clinical trials. JAMA Psychiatry. 2014;71:1381-1391.

18. Uher R, Tansey KE, Dew T, et al. An inflammatory biomarker as a differential predictor of outcome of depression treatment with escitalopram and nortriptyline. Am J Psychiatry. 2014;171:1278-1286.

19. Papakostas GI, Shelton RC, Zajecka JM, et al. Effect of adjunctive L-methylfolate 15 mg among inadequate responders to SSRIs in depressed patients who were stratified by biomarker levels and genotype: results from a randomized clinical trial. J Clin Psychiatry. 2014;75:855-863.

20. Raison CL, Rutheford RE, Woolwine BJ, et al. A randomized controlled trial of the tumor necrosis factor antagonist infliximab for treatment-resistant depression: the role of baseline inflammatory biomarkers. JAMA Psychiatry. 2013;70:31-41.

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25. Colle R, de Larminat D, Rotenberg S, et al. Pioglitazone could induce remission in major depression: a meta-analysis. Neuropsychiatr Dis Treat 2016;13: 9-16.

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27. Koch JM, Hinze-Selch D, Stingele K, et al. Changes in CREB phosphorylation and BDNF plasma levels during psychotherapy of depression. Psychother Psychosom. 2009;78:187-192.

28. ECNP Neuroscience Applied. Neuroscience-based Nomenclature. Accessed June 6, 2018.

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