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MDMA-Assisted Psychotherapy for Treating Chronic PTSD: Why I feel we can do better and the role of nutrition and amino acids like GABA

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You may be familiar with MDMA (3,4-methylenedioxymethamphetamine), also known as “ecstasy”, because of its reputation as a party drug. And you have likely seen some of the media reports on the new research and growing support for MDMA-Assisted psychotherapy for treating chronic PTSD (post-traumatic stress disorder). Due to adverse effects I’d like to share my concerns about this research and treatment and why I feel we can do better – by addressing nutrition and using amino acids like GABA and others.

In a recent press release, Colorado Study Shows Lasting Benefits of MDMA-Assisted Psychotherapy for Treating Chronic PTSD, the non-profit organization, Multidisciplinary Association for Psychedelic Studies (MAPS) reports these study results:

28 participants found that one month after their second day-long experimental session, 42.9% in the active-dose (100 mg and 125 mg) MDMA groups did not qualify for a diagnosis of PTSD, compared to 33.3% in the low-dose MDMA (40 mg active placebo) control group.

The results were even more notable 12 months after the third active-dose experimental session, which found that one year following treatment with MDMA-assisted psychotherapy, 76% of participants no longer had PTSD.

It is the largest U.S. FDA-regulated double-blind, placebo-controlled clinical trial of MDMA-assisted psychotherapy for the treatment of chronic PTSD and the results are impressive: 76% of the study participants no longer had PTSD after a year and 3 treatment sessions. I’m really happy for the participants BUT I believe we can do better because there are adverse reactions to this treatment and there are other safer approaches for recovery.

This comment about an acceptable risk profile and adverse reactions concerns me (and I suspect it concerns you too):

The study replicated previous research showing an acceptable risk profile for MDMA, with the most frequently reported adverse reactions during experimental sessions being anxiety, jaw clenching, headache, muscle tension, dizziness, fatigue, and low mood.

Adverse reactions one week following treatment included insomnia, low mood, irritability, and ruminations. Temporary elevations in pulse, blood pressure, and temperature were also recorded during MDMA sessions, and did not require medical intervention.

A common theme we see in the research on psychedelics is how effective it is for PTSD that doesn’t respond to therapy or medications. This paper states:

There is an immense need for innovative treatment options that improve outcomes, especially for PTSD refractory to psychotherapy and/or pharmacotherapies

I agree there is an immense need for successful treatment approaches, but jumping to MDMA from psychotherapy and/or psychiatric medications is skipping out the entire nutritional and biochemical step which is SO powerful and doesn’t have the above adverse effects. I’m concerned too many who have not seen benefits from therapy or medications are seeing MDMA as THE solution and are going to be harmed even further.

This paper, The Potential Dangers of Using MDMA for Psychotherapy, the author is concerned about the fact that “acute MDMA can stimulate the release of difficult feelings and memories, which may be distressing” and also the negative moods that occur after MDMA treatment:

This period of negative cognitions may be counter-productive, especially in psychiatrically vulnerable clients, for instance those with predispositions to anxiety, depression, or psychosis. For example, it could increase the likelihood of suicide in those individuals with strong post-recovery feelings of depression.

Because of this, I wholeheartedly agree with the author’s position:

it will always be far safer to undertake psychotherapy without using co-drugs. In selected cases MDMA might provide an initial boost, but it also has far too many potentially damaging effects for safe general usage.

In addition to psychotherapy, there are also so many nutritional and biochemical factors we can consider when it comes to PTSD. These don’t have any of the above damaging effects seen with MDMA. Here are a few to consider:

I feel it is these above approaches and others like this that we need to be using to address PTSD, rather than subjecting individuals who are already suffering to treatments that have adverse reactions AND are not addressing underlying nutritional deficiencies of low GABA, low serotonin, out of balance endocannabinoid system and overall health, to name a few of many possible underlying biochemical factors.

If this treatment approach is approved, I would hope that all the adverse effects and dangers are clearly explained and I’d also like there to be informed consent before it is used – so individuals know exactly what they are getting into. Hopefully, by the time it is approved, nutritional psychiatry will be more accepted.

I’d love to hear your thoughts on this research and treatment approach. Is it something you have considered or would possibly consider in the future – you personally or with patients?

Or do you have similar concerns that I have?

Have you already tried MDMA recreationally (possibly for therapeutic reasons) and what were your experiences like?

Metal-on-metal hip replacement and cobalt toxicity: anxious, tearful, lowered self-esteem, social withdrawal and poor sleep

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I’m always on the look-out for out-of-the-box root causes for anxiety, insomnia and low mood and the role of targeted amino acids like GABA, tryptophan and tyrosine in easing symptoms clients and boy was I surprised to learn about the connection between metal-on-metal hip replacements and mental health symptoms.

I first learned about this in the new Netflix documentary called The Bleeding Edge which is an “eye-opening look at the fast-growing medical device industry” and “reveals how the rush to innovate can lead to devastating consequences for patients.”

With metal-on-metal hip replacements it’s the cobalt and chromium in the metal-on-metal hip replacements that are causing toxicity in many individuals. In the Guardian article The Bleeding Edge: behind the terrifying new Netflix documentary we hear about Stephen Tower, an orthopedic doctor who shared his story in the documentary:

He had developed a tremor and was having a hard time thinking when he decided to scrawl all over the walls and ceiling of a hotel room during a medical conference, eventually using soap as ink.

Tower, his friends and family knew he was in the throes of mental health crisis, but no one was sure why. So, Tower studied himself until he found the answer in a blood and urine sample: his levels of cobalt, a metal used in rechargeable batteries, were more than a hundred times higher than normal.

Tower thought it might be related to his metal-on-metal hip replacement and had it redone. On the operating table, his surgeon found metal sludge seeping from the device before it was removed.

Dr. Tower shares that within a month of having his hip replacement redone his recovery was remarkable – he could think again, and his psychiatric symptoms resolved.

The sad thing is that he actually admits that he would never have believed this could be possible without having had experienced it himself. We see this all too often in the medical profession.

But he is now enlightened and of course he’s passionate about sharing what he experienced and has started documenting similar adverse experiences in his patients. He says the EPA and FDA should be studying this and reporting it and so they should be.

I was curious to find out how serious an issue this was and how long it’s been an issue because surely we’d be hearing more about it.

A paper published in 2017: Neuropsychiatric symptoms following metal-on-metal implant failure with cobalt and chromium toxicity reports depression and short term memory problems, as well as “disorientation in place, problems with tests of concentration and word finding difficulties.”

The paper includes feedback from some of the study participants. This is what two of them shared about their mood, sleep and anxiety post-hip replacement:

Ms. X … persistent anxieties about the need for future surgery and a feeling she must always be cautious about protecting her hip, tearfulness, lability of mood, lowered self-esteem – “I used to be very active and now I feel a mess”, guilt about being a burden on her husband, a fear about the effects of ions on her body and poor concentration.

Mrs. Z … complained of poor sleep with early morning wakening, low mood and emotional lability, social withdrawal, poor appetite, forgetfulness and a tendency to repeat herself reported by relatives, her frustration at being unable to do day to day activities such as cleaning, she felt she was a burden to relatives, and complained of anhedonia [or an inability to feel pleasure in normally pleasurable activities]. She was disorientated in person, was unable to perform serial sevens and was able to register, but not able to retain any elements of a new name and address on cognitive testing.

The study authors state that “in order preserve neurocognitive function implant removal conceivably should be as soon as possible after toxicity is detected.”

They admit it’s a small sample and that some of the depression and anxiety may be typical after a surgery HOWEVER once I looked at how long metal-on-metal cobalt toxicity has been an issue I feel we really need to take this very very seriously. Here are just a few of the studies from 2017 going back to 2011:

Cobalt can be responsible for local toxicity (including metallosis, hypersensitivity reaction, and benign tumor) or systemic toxicity (including cardiomyopathy, polycythemia, hypothyroidism, and neurological disorders).

  • Systemic toxicity related to metal hip prostheses (published 2014) This systematic review states toxicity is rare but reported cases of cardiotoxicity, thyroid toxicity, peripheral neuropathy, hearing loss, cognitive decline and visual impairment.

Prosthetic hip-associated cobalt toxicity (PHACT) is gaining recognition due to the use of metal-on-metal total hip replacements

And then we have this study reporting toxicity issues as far back as 1999:

Our findings suggest that in total hip replacements using metal-metal pairings, metal ions of the alloys are released. This release may lead to significantly elevated metal concentrations in biological fluids. Long-term studies are needed to determine the risk of metal-metal implants as a potential cause of cobalt and chromium toxicity.

You may wonder how this toxicity problem has been ignored and swept under the rug for so long. If you watch the documentary, you’ll soon see that the medical devices industry is far more powerful than the pharmaceutical industry and has its own set of rules for medical device approval. It’s basically the wild west and the FDA is doing nothing about it (even though it is acknowledged to be a problem)!

I’m not suggesting we shouldn’t be doing hip replacements – they are amazing surgical innovations that give many people their mobility and lives back – but instead I suggest we consider the following:

  • Know what you’re getting into before you embark on a major medical procedure
  • Understand that the testing for medical devices is very inadequate
  • Ask questions and get detailed information about the medical device: what materials are being used, how long it’s been around, any known adverse effects etc.
  • Search for information using terms like “horror stories metal-on metal hip replacement” and “law suits metal-on metal replacement”
  • Have a plan in place should you start to notice adverse symptoms after a hip replacement (or other major procedure). You may even want a medical directive in case you become cognitively incapacitated

I have no expertise on what the safest type of hip replacement is and will find an expert for a part 2 of the blog. If you know of someone please do share in the comments.

How do we address the cobalt and chromium toxicity?

  • Tower, the orthopedic doctor in The Bleeding Edge documentary found his symptoms resolved once the metal-on-metal hip replacement was removed. The research seems to support this approach too
  • A 2-person case study supports the use of N-acetyl-cysteine (NAC) for reducing blood levels
  • An in vivo (test tube) study found astaxanthin “mitigated cobalt cytotoxicity … by modulating oxidative stress”

How do we address the anxiety, insomnia and associated mood issues?

I recommend using the above amino acids short-term to ease symptoms before the hip revision surgery is done and for as long afterwards as they are needed. And, as always, base the use of the amino acids on trials per the amino acid questionnaire.

Also, work with a thyroid expert for thyroid support which will also help the mood and cognitive issues. And work with a heart specialist to rule out any damage to the heart.

If you’ve had a metal-on-metal hip replacement in the past and have chronic anxiety or cognitive issues (that started or got worse after the surgery), then I encourage you to look into cobalt toxicity as a possible root cause or contributory root cause.

Please feel free to share your experiences with this surgery – both good and bad – so we can all learn. And if the amino acids have helped ease anxiety and mood symptoms and helped you sleep while going through this.

And do let us know what you think about the Netflix documentary The Bleeding Edge.

CBD oil resolves anxiety and insomnia in young girl with PTSD caused by sexual abuse

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There is growing evidence that cannabidiol (also called CBD) is effective for many individuals suffering from anxiety and sleep issues.

A case study published in 2016, Effectiveness of Cannabidiol Oil for Pediatric Anxiety and Insomnia as Part of Posttraumatic Stress Disorder, reports that cannabidiol oil was effective for reducing the anxiety and improving the sleep of a young girl who was experiencing these problems due to posttraumatic stress disorder (PTSD).

She had been sexually abused at the age of three and the medication (Clonidine) had not helped and had caused side major effects (hallucinations).

In the discussion the authors state the following:

Cannabidiol oil, an increasingly popular treatment of anxiety and sleep issues, has been documented as being an effective alternative to pharmaceutical medications.

This case study provides clinical data that support the use of cannabidiol oil as a safe treatment for reducing anxiety and improving sleep in a young girl with posttraumatic stress disorder.

Prior to the prescribing of the CBD a functional medicine workup included ruling out thyroid dysfunction and low levels of iron and vitamin D deficiency. The following helped initially but were not sufficient to reduce all her symptoms: 1 -5mg/night of melatonin, 3g inositol 3 times a day, 500 mg/day of fish oil/EPA, 300mg magnesium/day. She also had psychotherapy sessions for 3 years.

Once it was decided to trial CBD she was given 25 mg at bedtime, and 6-12 mg of CBD sublingual spray during the day as needed for her anxiety: A gradual increase in sleep quality and quantity and a decrease in her anxiety were noted. After 5 months, the patient was sleeping in her own room most nights and handling the new school year with no difficulties. No side effects were observed from taking the CBD oil.

In this case study, the CBD was from industrial hemp, providing the medicinal benefits of CBD without the “high” of the THC.

I am very much in favor of CBD rather than THC because of the high risk of psychosis, schizophrenia and increased anxiety with THC. Dr. Hyla Cass and I share our concerns in this Anxiety Summit interview: Marijuana and anxiety: Panacea or Pandora’s Box?

The authors of this case report provide a very thorough overview of the mechanism of action of CBD via the two cannabinoid receptors in the body, CB1 and CB2:

  • CBD has an indirect effect on the CB1 receptors by stopping the enzymatic breakdown of anandamide, allowing it to stay in the system longer and provide medical benefits. The CB1 receptors are located mainly in the brain and modulate neurotransmitter release in a manner that prevents excessive neuronal activity (thus calming and decreasing anxiety), as well as reduces pain, reduces inflammation, regulates movement and posture control, and regulates sensory perception, memory, and cognitive function.
  • CBD has a mild effect on the CB2 receptors, which are located in the periphery in lymphoid tissue. CBD helps to mediate the release of cytokines from the immune cells in a manner that helps to reduce inflammation and pain

They explain other mechanisms that include “stimulation of vanilloid pain receptors (TRPV-1 receptor)”, “activating adenosine receptors” to reduce anxiety, “a potentially new third cannabinoid receptor GPR55”, and “directly activating the 5-HT1A serotonin receptor.”

I find the latter mechanism very interesting – activation of the serotonin receptor – given the work I do with supporting my clients who have low serotonin and do well with targeted supplementation with tryptophan and 5-HTP. As well as anxiety and insomnia, this young girl was also impulsive and disobedient, had aggressive outbursts at school and was self-destructive, and had low self-esteem and suicidal ideation. These symptoms are all classic signs of low serotonin.

I’d have loved to see how she would have done on a trial of tryptophan instead of 25mg of diphenhydramine (Benadryl), which acts in a similar way to SSRI antidepressants. Interestingly, diphenhydramine was the medication that led to the development of fluoxetine (Prozac) and high doses can mimic serotonin syndrome. Diphenhydramine also has side-effects that include “drowsiness, dizziness, constipation, stomach upset, blurred vision, or dry mouth/nose/throat.”

Based on my experience with tryptophan and 5-HTP – and all her low serotonin symptoms, I’d definitely consider this a better choice for a young girl like this, especially because we see results so quickly, often within a week and sometimes up to 2 or 3 weeks rather than the 5 months it took to completely resolve her sleep issues and anxiety.

Since low GABA can also lead to physical anxiety and insomnia, and with new research suggesting CBD also acts on GABAA receptors a trial of GABA may also have led to quicker results.

Aimée Gould Shunney, ND, summarizes this perfectly in the module on “Stress, Adrenal Health, and Cannabidiol: The ECS-HPA Connection” in the Integrative Cannabis course

CBD impacts the serotonin receptors, in particular the 5-HT1A receptors which has a lot to do with depression [and anxiety]. It impacts the GABA receptors, the dopamine receptors, the glutamine receptors. It also impacts different receptors that effect the inflammatory environment in the body like TRPV-1 and PPAR. There are so many different ways both within the ECS [endocannabinoid system] at the cannabinoid receptors and outside at these other receptors that CBD can help create balance and calm within the HPA axis. In short, CBD balances the system that keeps you balanced.

In summary, doing trials of tryptophan (or 5-HTP) and GABA, together with CBD oil, seems like an ideal approach to consider. I recommend doing this together with dietary changes that support serotonin production, like real whole quality food, quality protein, healthy fats, fermented foods, foods high in zinc, exercise, time in nature etc. so long-term use isn’t needed – for the CBD oil and the amino acids.

I’m excited about this emerging use of CBD oil, all the recent research, and using it in conjunction with dietary and lifestyle changes, and the amino acids and other nutritional approaches.

You can read more about the GABA and tryptophan products I use with clients here.

The two CBD products I’ve had the best results with are Elixinol (read here on using Elixinol for benzodiazepine tapers) and CV Sciences +CBD Oil.

Please share if you’ve used CBD oil or CBD supplements with good results.

We’d also love to hear if using CBD in conjunction with tryptophan (or 5-HTP) and GABA has improved your symptoms even more than just using the amino acids alone, or if the amino acids alone provided relief.

Fipronil insecticide: GABA/glutamate and anxiety, aggressive behavior, memory and Alzheimer’s disease in humans?

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The insecticide called fipronil has me concerned because there is increasing evidence that it can be toxic to humans and, much to my surprise, I’ve just discovered that the main mechanism of action is by targeting the gamma-aminobutyric acid (GABA) receptor and recent research points to increased anxiety, aggressive behavior, memory problems and even Alzheimer’s disease in animal studies.

Based on a rather surprising conversation I had with someone a few weeks ago (let’s call her Sue), I felt compelled to get more information on fipronil. Before that I was not aware about the specific effects I mention above.

We were in Sue’s front yard and the dog kept sniffing these small white plastic squares in the flower beds. Sue kept pulling the dog away and I asked “why? what are those?” It turns out they were ant-bait devices. Yes, I’m this clueless simply because I’ve never purchased anything like this. I expressed my concerns about toxicity and possible endocrine/hormone effects but didn’t have enough concrete facts, so I went digging through the research. Needless to say I am very concerned with what I found.

What was equally concerning is that Sue had not even considered that it could be harmful. Looking into possible harms was not even on her radar. When pressed, Sue said “it’s only a small amount in each container so I’m sure it’ll be fine” and “the poison is inside the container so none of it will come out – so it’ll be fine.”

This is what went through my mind (which is pretty typical for me – I’m always in questioning mode): What is it and how toxic is it? Does it have impacts on humans and by what mechanism? Could it cause anxiety or increase existing anxiety symptoms? Are there additional concerns about it being in a flower-bed near the front door where you could possibly walk some into the house or breathe it in as you come and go?

Organophosphates and psychological effects

Organophosphates are a commonly used pesticide used on fruits and vegetables and research going as far back as 1994 reports that acute exposure can cause psychological effects because they

act directly on the nervous system by inhibiting the neurotransmitter acetylcholine … [contributing to] … acute psychological and behavioral effects, such as anxiety, depression, and cognitive impairments.

The researchers also suggest that long-term psychological effects of low-level exposure have not been determined satisfactorily.

We hear less about insecticides such as fipronil

We hear less about insecticides such as fipronil and how they work.

According to the National Pesticide Information Center Fipronil is a broad use insecticide that

belongs to the phenylpyrazole chemical family. Fipronil is used to control ants, beetles, cockroaches, fleas, ticks, termites, mole crickets, thrips, rootworms, weevils, and other insects.

Fipronil is used in a wide variety of pesticide products, including granular products for grass, gel baits, spot-on pet care products, liquid termite control products, and products for agriculture.

It can be found in ant-bait and anti-cockroach products as well as Frontline Plus for cats and dogs. You can find a partial list of products here and a fact sheet here.

GABA & glutamate: anxiety, aggressive behavior and neurotoxic effects

Fipronil works to kill insects via the inhibition of glutamate- and GABA-activated chloride channels resulting in uncontrolled neural excitation. It also blocks GABAA receptor function and is typically considered toxic to insects but not humans.

As soon as I read the GABA-glutamate mechanism I started searching for anxiety and neurotoxic connections.

There are no human studies on increased anxiety due to fipronil exposure but research on zebrafish larvae exposed to fipronil at typical environmental levels, finds anxiety-like behavior.   In the paper, A metabolomic study of fipronil for the anxiety-like behavior in zebrafish larvae at environmentally relevant levels, the authors report decreased levels of glycine and serine with higher levels of glutamate saying fipronil may be a potential neurotransmitter disruptor. Here are some of the possible mechanisms they discuss related to this:

  • The decreased metabolite glycine caused by fipronil may contribute to the excitatory swimming performance. Whether the glycinergic reciprocal receptor (GlyR)…inhibitory mechanism is also involved in low level of fipronil [exposure] requires further investigation.
  • Additionally, as one of the most abundant amino acids in microenvironment stress, proline is biosynthetically derived from the amino acid L-glutamine. Low levels of L-proline detected in fipronil-treated group may indicate the accumulation of glutamine. As an excitatory neurotransmitter, high level of glutamine would associate with the excitatory behavior of the fish.

In another study, Prenatal exposure to fipronil disturbs maternal aggressive behavior in rats, the authors suggest fipronil impacts the central nervous system areas that control aggression and increases in maternal aggressive behavior are via impacts on GABA(A) receptors.

This 2016 paper lists a variety of toxic effects to both animals and humans: Fipronil insecticide toxicology: oxidative stress and metabolism:

because of accidental exposure, incorrect use of fipronil or widespread fipronil use leading to the contamination of water and soil, there is increasing evidence that fipronil could cause a variety of toxic effects on animals and humans, such as neurotoxic, hepatotoxic, nephrotoxic, reproductive, and cytotoxic effects

They explore oxidative stress as a possible mechanism as to how fipronil causes these toxic effects.

Does concrete make fipronil more toxic?

One of the questions I asked myself was this: Are there additional concerns about it being in a flower-bed near the front door where you could possibly walk some into the house?

It turns out that this may be a valid concern. In this 2016 paper, Conversion of pesticides to biologically active products on urban hard surfaces, the researchers report that urban landscapes that include concrete can actually convert pesticides to other biologically active and more toxic intermediates, likely caused by the alkalinity and metal oxides in concrete. They report that fipronil:

was quickly transformed to desulfinyl and sulfone derivatives, with the desulfinyl level exceeding that of parent in the runoff water only 1week after treatment. Fipronil derivatives have aquatic toxicity similar or even greater than the parent fipronil.

Impacts on memory and a possible factor in Alzheimer’s disease

This 2016 animal study, Memory impairment due to fipronil pesticide exposure occurs at the GABAA receptor level, in rats concludes that fipronil can

have toxic interactions with the CNS [central nervous system] of mammals and lead to memory impairment by modulating the GABAergic system.

We also have to ask how big a role this insecticide could be playing in Alzheimer’s disease? In a paper published earlier in 2018, Induction of Amyloid-β42 Production by Fipronil and Other Pyrazole Insecticides, they use the term “Alzheimerogens” when writing about insecticides such as fipronil and the metabolite fipronil sulfone:

Focusing on fipronil, we showed that some of its metabolites, in particular the persistent fipronil sulfone, also favor the production of Aβ42/Aβ43 in both cell-based and cell-free systems.

Fipronil administered orally to mice and rats is known to be metabolized rapidly, mostly to fipronil sulfone, which stably accumulates in adipose tissue and brain.

In conclusion several widely used pyrazole insecticides [such as fipronil] enhance the production of toxic, aggregation prone Aβ42/Aβ43 peptides, suggesting the possible existence of environmental “Alzheimerogens” which may contribute to the initiation and propagation of the amyloidogenic process in sporadic AD.

The paper shares that amyloid-β peptides (Aβs), especially increased production of Aβ42/Aβ43 over Aβ40, represent a characteristic feature of Alzheimer’s disease.

Why wait for long-term human studies?

Hopefully you’re like me and don’t buy ant-bait or roach-bait products.

My bigger concern is the wide-spread use of spot-on pet-care products which contain fipronil, exposing our beloved pets to this toxin and all the humans they come into contact with. Pet-groomers are especially cautioned. And I’d also add a caution for children playing with pets where these flea and tick products are used since “the developing brain is particularly vulnerable to the action of insecticides.”

We don’t know for sure how harmful this insecticide is for humans and it’s not clear what the mechanisms are – GABA-glutamate and/or glycine and/or oxidative stress – but why wait for long-term human studies, especially given that chronic and long-term effects are difficult to investigate and based on what we already know about their effects on Parkinson’s disease, amyotrophic lateral sclerosis, and depression.

I have found enough information to be very concerned and to feel justified in continuing to avoid fipronil. I encourage you to avoid fipronil as well.

This is especially the case if you already suffer from long-term anxiety, insomnia or another chronic health condition as it may be one more possible contributory factor.

Given that fipronil blocks GABAA receptor function, I have to wonder if chronic long-term exposure could play a role in difficulties with benzodiazepine tapering.

If this is old news to you feel free to share with family and friends who may not be as informed as you.

If this is news to you, I hoping this gets you thinking and questioning. I’d love to hear your thoughts, concerns and questions.

Pharma-GABA: study participants with an irrational fear of heights are relaxed and less anxious when crossing a swaying suspension bridge

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Based on clinical evidence, we know that gamma-aminobutyric acid (GABA), a calming amino supplement, reduces anxiety. There isn’t as much research on GABA or Pharma-GABA as we’d like to see, so we’ll take small studies that are done on humans.

In a 2006 study, Relaxation and immunity enhancement effects of gamma-aminobutyric acid (GABA) administration in humans, Pharma-GABA was used to determine if it would increase relaxation and reduce anxiety during the stressful event of crossing a suspension bridge:

Eight healthy volunteers, with no clinical evidence of any illness, (5 males and 3 females) aged 25 to 30 years who had a history of acrophobia [extreme or irrational fear of heights], were recruited.

Subjects crossed … a pedestrian suspended bridge at Nara Prefecture, Japan (Totsu River Bridge) with 54 m height, 300 m length, and 2 m width.

I believe it’s also called the Tanize Suspension bridge and is one of the longest suspension bridges in Japan. You can see pictures of the bridge here and here. They say this: “though quite safe, the swaying motion can be disconcerting, or fun, depending on your perspective.”

If we convert that to feet, it’s 177 feet high, almost 1000 feet long (about 3 times the length of a football field) and 6 feet wide.

There were 2 groups: placebo and Pharma-GABA. Salivary immunoglobulin A (IgA) levels (also known as secretary IgA or sIgA) was measured in both groups and used as a marker of relaxation and stress, as well as immunity. Saliva was collected before crossing the bridge, half way across and at the end. The study found that the

placebo group showed marked decrease of their IgA levels, while GABA group showed significantly higher levels.

And concludes as follows:

GABA could work effectively as a natural relaxant and its effects could be seen within 1 hour of its administration to induce relaxation and diminish anxiety. Moreover, GABA administration could enhance immunity under stress conditions.

The paper is reporting about 2 studies and it’s not clear how much Pharma-GABA was used in this bridge study – it was either 100mg or 200mg. Results were observed within 60-90 minutes. Also, this study was conducted by the company who makes the Pharma-GABA product, and they do say that this bridge study includes unpublished data.  Notice that they use the term GABA in the paper – I prefer to differentiate since Pharma-GABA and GABA are actually different.

Other than this and the very small number of participants, I’m always encouraged by any research we have. Clinically, we see very similar results with GABA or Pharma-GABA when someone has a fear of something – heights, flying, spiders etc. – and it typically addresses the physical fear and anxiety symptoms.

Here are some of my thoughts as to why results were only observed after 60 minutes:

  • Pharma-GABA was used in the study and for some folks this is not as effective as using GABA. I typically start my clients on GABA.
  • Using GABA sublingually often has calming results in under 10 minutes, so a chewable Pharma-GABA may have been a better option and would be something I’d recommend
  • Low serotonin is commonly a factor with fears and phobias and I’d recommend a trial of tryptophan

The resources in this blog and my other articles are intended to be used in conjunction with my book: The Antianxiety Food Solution – How the Foods You Eat Can Help You Calm Your Anxious Mind, Improve Your Mood, and End Cravings (Amazon link). If you do not have my book I highly recommend getting it and reading it before jumping in and trialing/taking amino acid supplements: There is a complete chapter on the amino acids and one for pyroluria, plus information on real whole food, sugar and blood sugar, gluten, digestion and much more.

You can find the GABA and tryptophan products I recommend on this blog: The Antianxiety Food Solution Amino Acid and Pyroluria Supplements

How would you feel walking across a swaying suspension bridge like this?

Have you used Pharma-GABA, GABA and/or tryptophan to help you with the stress and anxiety caused by a phobia like this or another phobia?

Tyrosine for alleviating anxiety and panic attacks and creating a feeling of calm focus

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If you had anxiety, felt hugely stressed and were having panic attacks would you consider using tyrosine to help calm you? It’s not the first approach I use with a client as I typically want to calm things down first by addressing the low serotonin symptoms of anxiety (such as worry, overwhelm, insomnia and panic attacks) and the low GABA physical symptoms of anxiety (physical tension, stiff and tense muscles, overwhelm and panic attacks).

However, for some individuals addressing low catecholamines with tyrosine is the best approach to take, even if it feels counter-intuitive. Since everyone is different using the trial method is the best way to figure out what you need.

Here is another success story from someone using tyrosine, as shared in the comments on a recent blog post on tyrosine:

Tyrosine for anxiety has done wonders for me! I have tried GABA and Tryptophan. The GABA seemed to take the edge off a little when panic attacks occurred but wasn’t keeping anxiety from occurring.

I have been under tremendous pressure at work. The internal stress has been overwhelming! I haven’t been able to remember anything, even things I’ve done for years! I am in the process of learning new software at work. In the very first class my mind just went blank. The more I tried to focus the more stressed I became. All I could do was sit and stare at my screen while the rest of the class moved forward.

In short order I developed a migraine and panic. The internal pressure felt as if someone was wringing out my brain like one would do to a wash rag! I had to leave the class earlier. From this point on I was struggling to even do my job as I have done the last few years. Every time I tried to think I’d immediately become overwhelmed and shut down. I felt like crying most of the time from the sheer force of the internal pressure (this is embarrassing to admit as I’m someone with a competitive career). This stress just completely shut down my ability to learn and problem solve.

So, I decided to start some tyrosine. I was hesitant because I have heard it can cause panic attacks and I definitely don’t need more of those! I bought some powder and took 400mg on an empty stomach about 30 minutes before breakfast. WOW!!! Within an hour the stress just melted away!

I wasn’t stressed on my way to work either which normally I am. I was able to sit down and think thru my problems without feeling overwhelmed at all. Also, I was communicating with people much more easily. I noticed better eye-contact. I seemed less concerned of anyone’s opinions too.

I take another 400mg 30 minutes before lunch. I simply cannot believe how much better I am doing!

Just a few weeks prior I was telling my wife that I may need to start thinking about starting the process for disability because I simply could not function well enough to do my job.

I’d also add that the stress from the anxiety was so bad I felt like I had the flu for a few weeks. This also has dissipated since starting the tyrosine.

It’s still early in this experiment but I am hopeful for once. Nothing, and I mean NOTHING has worked so well so fast for me than tyrosine. It’s the closest thing to a miracle I’ve ever experienced. A night and day experience!

What wonderful results! I’m thrilled to hear about his “miracle” and that he’s doing so much better, that he has hope and that the stress from the anxiety has dissipated!

What approach to follow if you can relate to this situation

Of course, I thanked him for sharing his success story with tyrosine and added my response for other blog readers who may relate to this situation and may consider a trial of tyrosine as a first step when anxiety is an issue.

I still stand by my advice to start with GABA and tryptophan when you have anxiety whether it’s the low serotonin-type anxiety (worry in the head) or the low GABA-type anxiety (physical anxiety). I always have clients start by addressing these deficiencies first before adding tyrosine for the low catecholamine symptoms because tyrosine is too stimulating for many and can increase anxiety and insomnia (and may also cause a panic attack).

With the majority of the anxious clients that I’ve worked with, the order of doing trials is as follows: tryptophan or GABA first and then tyrosine.

Addressing his low catecholamine symptoms was what he needed

For this gentleman, clearly GABA and tryptophan support was not what he needed or was not enough to ease his anxiety. Addressing his low catecholamine symptoms was what he needed to do.

In case you’re wondering how he’s doing now – I reached out to him and he reports he’s still taking tyrosine and is still doing great!

He is the third person that I know of who has experienced these types of results with tyrosine so I expect there are others who could benefit too – which is why I decided to share his story.

Increased anxiety because of lack of focus and low motivation

Here is another similar story from a prior client of mine. She had terrible anxiety, and we trialed both GABA and tryptophan. While she did get some benefits with both it just wasn’t enough.

She was sleeping better but still felt so stressed and anxious when preparing for an important meeting at work which she was in charge of running. The anxiety also seemed to get worse during the meetings. She did also score high on the low catecholamines section on the amino acid questionnaire (poor focus, low motivation, fatigue, ADHD, depression) but were working on the low serotonin and low GABA types of anxiety before addressing poor focus and low motivation.

It turned out that her anxiety escalated around her work meetings because of her lack of focus and low motivation – she was pushing herself to get through them. Once she added tyrosine her anxiety was under control. In this instance tyrosine actually helped ease the anxiety because her ADHD symptoms diminished and her motivation and drive improved!

This is what biochemically individuality is all about and how we all have our own unique needs. And is why I love the trial-method for determining which amino acid is best for your own unique needs.

Here are some related blog posts that you may find helpful:

Do let us know if you have experienced less anxiety and a sense of calm focus when taking tyrosine?