anxiety

Using amino acids for anxiety and depression: does the right dose ever change or need a tweak?

October 19, 2018 By Trudy Scott Leave a Comment

If you are using targeted individual amino acids for anxiety and/or depression and doing well on them, you’ll likely get to the point when you’re asking questions like how to discontinue them and does the right dose ever change or need a tweak, especially after some stressful life events. Amy posted this question in the comments section of the blog on using tyrosine to create a sense of calm energy (paraphrased and formatting for ease of reading)

Trudy you are a God send! I stumbled upon your work after following Julia Ross. I have depression and anxiety. I’m currently taking:

1000 mg tyrosine 2x daily

500 mg glutamine morning, 1000mg mid-morning and afternoon

500mg DPA (Endorphigen) 3 x daily (previously I was using DLPA but your recommended DPA was so much better and less stimulating)

50 mg 5-HTP afternoon and

1500mg tryptophan at night

I used the amino acids to treat what used to be referred to as “atypical” depression: loss of motivation, tiredness, lethargic, intense carb craving, feelings of guilt and hopelessness. I would become paralyzed with depression, barely able to get through the days. When I was younger I treated these episodes with antidepressants but as I got older could no longer tolerate the side effects. I’m also still on birth control pills at the age of 46 and believe I may be in perimenopause but can’t stop the pills for medical reasons.

Tyrosine gave me my energy back, glutamine cut the carb cravings. DPA and True Calm work wonders for my anxiety.

I watch my sugar intake and always consume lots of animal protein. I’m so grateful for this solution.

After trialing this seems to be the right combo. I always get confused when is it time to discontinue supplements? Do you stop or slowly reduce or taper?

Does the “right” dose ever change? I’ve been on this combo about 2 months. I’ve felt great but some anxiety/panic creeping back up …. wondering if supplements need a tweak or is this just the result of some stressful life events. Advice appreciated!

I was really pleased to hear the wonderful results she was having and glad that she had trialed the amino acids to find the correct amount for her unique needs and situation. I don’t see this happening often enough and it really is the most effective way to get results. It’s what I do with all my clients – methodical, step-by-step trialing of each amino acid, one at a time and carefully documenting results (both good and bad) in order to find the optimal dose of each one.

I also appreciate her sharing her results and posting these questions which are a great learning opportunity for you.

When and how to discontinue the amino acids?

To answer her question about when and how to discontinue this is my feedback:

You may choose to stop everything at once, but I prefer to slowly lower the amount of one amino acid at a time and add back if your symptoms come back. They don’t need to be “tapered” but doing it this way it helps with preventing your original anxiety and depression symptoms going back to really bad in one big swoop and having to start all over again.

I will add that I have had feedback from someone saying when she stopped tryptophan abruptly she felt the same withdrawal effects as when she weaned off meds but based on my experience this is very rare.

After posting her question Amy made some adjustments – taking less of all of them. As I mentioned above I find it better to lower the amount of one amino acid at a time – kind of reverse of the trialing method you use when starting the amino acids. Also, since she mentioned she felt anxiety/panic creeping back up, I would have expected her to increase some of the calming amino acids.

Does the right dose ever change or need a tweak?

And to answer Amy’s other question: does the right dose ever change or need a tweak?

Yes, the “right dose” can change based on stressful life events especially if you have pyroluria – stressful life events can cause you to dump more zinc and vitamin B6 affecting serotonin and GABA production and increasing the social anxiety.

Amy does mention that she’s on the birth control pill and this depletes zinc and vitamin B6 and hence serotonin) and has an impact on the microbiome – so this may well be playing a role in the need to tweak doses.

There are many other factors that could lead to the need to adjust the amino acids (or other supplement protocols):

hormonal changes like PMS, perimenopause or menopause
something contributing to leaky gut like adding back gluten or accidental exposure to gluten
antibiotics (affecting the microbiome and serotonin/GABA levels)
artificial sweeteners (because of their effect on the microbiome and hormones)
starting on other medications (since many cause nutritional depletions)
adding in a new food like collagen/gelatin (for some people collagen and gelatin may lower serotonin levels)
running a marathon (it likely depletes zinc and may ramp up cortisol)
a formulation changing completely without you knowing (one example is Seriphos – used to lower high cortisol – where the core ingredient changed completely and the labeling stayed the same)
a product changing from using gelatin to cellulose capsules (this may be problematic if you have SIBO)
you move into a new home and get mold exposure
you get a new dog or cat and start using Frontline Plus for fleas (fipronil, the active ingredient, targets GABA receptors and recent research points to increased anxiety, aggressive behavior, memory problems)
you have started using a sauna (depletion of zinc and other minerals, as well as stirring up toxins)
your need for serotonin support increases as you head into winter-time (some low serotonin folks are more susceptible to the winter blues)
a recent course of fluoroquinolone antibiotics (impacts on magnesium and GABA levels and the mitochondria)
you may no longer need them

This is not a complete list of reasons that could impact you but this will give you an idea of what to start to think about.

Hopefully this shows how important it is to monitor how you’re doing and adjust as needed (either up or down) and think about what is changing in your life.

If you’d like to read about the amino acids products Amy uses – the same ones I recommend and use with clients – you can find them listed on my supplements blog.

Have you found the ideal dose of amino acids and then needed to adjust them up or down based on any of the above? How methodical were you in doing your adjustments?

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

October 12, 2018 By Trudy Scott 4 Comments

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.

Integrative Cannabis: Therapeutic Value of CBD/Cannabinoids

October 11, 2018 By Trudy Scott 1 Comment

The Integrative Cannabis 6-week course, Therapeutic Value of CBD/Cannabinoids is just starting this week and it’s not too late to register and participate.

Razi Berry, founder of NDNR/Naturopathic Doctor News and Review, shares this about cannabis and this new training on the topic of CBD:

Since the legalization of medical cannabis, and more recently its recreational use, it has become more and more important that practitioners are aware, educated and fluent in this popular botanical medicine. Cannabis has an incredible and varied use profile and can also be a drug of addiction; it has the ability to serve as a highly beneficial opioid alternative, while at the same time causing social and psychological problems. It is a drug/botanical that is not going away anytime soon, and practitioners need more education in its therapeutic use. This multi-week course is sure to give you a solid foundation in understanding cannabis and cannabinoids and their interaction with physiological systems as well as their implications for clinical practice.”

Cannabis is a controversial subject! But, no matter where you stand on the political, moral, or ethical spectrum, in support or against this botanical medicine, cannabis is here to stay. The increase in legislative efforts allowing for its medical use, along with its growing recreational legalization is mandating that medical practitioners are aware and knowledgeable of the effects, interactions, benefits, and complications of its use. This multi-week course is intended to give a solid foundation of understanding for the clinical use and therapeutic understanding of cannabis, as well as the legal implications of its use in clinical practice. We hope you find it beneficial to your practice.

Love it or hate it, you’re going to have to learn about the use of cannabis in both a medical and non-medical context sooner or later. Currently, cannabis is not included in botanical medicine courses at most of the naturopathic or allopathic medical schools, however its use is rapidly increasing and a need for knowledge of its effects and therapeutic use are also increasing. This multi-week course includes the foundational elements necessary to understand the major and minor constituents of cannabis sativa/indica, as well as its therapeutic indications, physiological indications, dosing and complications. It will serve any practitioner needing or desiring a more in depth understanding of the plant.

Who is this Cannabis/CBD Training for?

Practitioners who are interested in the therapeutic use of cannabis.
Practitioners who want more information about the systemic effects of cannabis.
Practitioners who want more pharmacological knowledge of cannabis as a botanical medicine.
NDs in states where marijuana is legal – both medically and recreationally – regardless of whether it is in ND scope.
NDs who would like to gain Pharmacology CEU for a relevant botanical medicine that is used pharmacologically.
Individuals needing foundational knowledge about the physiological effects of cannabis.
Individuals who are looking for alternatives to opioids and pain medication.
Individuals who are interested in non-psychoactive uses of cannabis.

Someone asked this when I posted about it on Facebook:

Is it just for practitioners? What about parent who has a child who uses it therapeutically?

Razi responded as follows:

It is designed for practitioners, but as a parent it would answer all your questions and help you to navigate the journey. You might end up knowing more than your doctor/practitioner!

Here are the details of the first module – Stress, Adrenal Health, and Cannabidiol: The ECS-HPA Connection with Aimee Shunney, ND

Knowledge of the difference between hemp and marijuana.
Understand how the ECS/endocannabinoid system can support healthy HPA axis function.
Understand CBD as a regulatory or balancing agent of the ECS.
Evaluation of how baseline endocannabinoid levels can affect the stress response and anxiety.
Application of CBD as it relates to HPA axis function in clinical practice.
Understand quality, sourcing, safety, and legal issues surrounding medical cannabis.

Here are 2 slides from Aimee’s Adrenal/HPA presentation:

…Science has linked the ECS [endocannabinoid system] with complex processes from anxiety to immunity…This research bonanza is revealing more and more about the ECS master control system and it’s shining star, cannabidiol [CBD].

Preliminary human studies show baseline endocannabinoid tone regulates HPA axis reactivity to stress; low baseline AEA [anandamide] leads to greater increase in cortisol after stress AND high baseline AEA seem to be protective against anxiety.

And here is a short video snippet from “The Role of CBD Targeted Clinical Strategies on the Microbiome and Gut-Brain Axis” presented by Dr. Chris Meletis.

Understand the role of CBD receptors in the GI tract.
Understand how CBD receptor activation can alter microbiome microenvironment.
Appreciation of the clinical utility of HEMP derived CBD on Brain and Gut Health.

I’m enjoying it already and I’ve only done one module so far. I hope to get some additional clarification on the following: how the endocannabinoid system interacts with and supports neurotransmitters like serotonin, GABA and endorphins; safety aspects and cautions about THC and worsening mental health; understanding how best to assess for an out of balance endocannabinoid system; how to assess quality; a better understanding of the different strains – how they work and what symptoms they help; and how we talk about cannabis in terms of CBD percentages.

Click here for information and registration details about the Integrative Cannabis 6-week course, Therapeutic Value of CBD/Cannabinoids or share this link with your practitioner.

It started on Monday Oct 8^th and runs for 5 weeks. As soon as you register you’ll get access to the first module on stress and adrenal health (see below) with delivery of the other modules each Monday thereafter. Registration closes on Friday and will reopen in 2019 sometime. Apologies for the late notice – I just found out about it late last week!

If you have feedback on how you’ve benefited from hemp-based CBD products please post below in the comments. If you have questions please post them too and I’ll try and get answers from the presenters if I don’t have an answer.

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

October 5, 2018 By Trudy Scott 2 Comments

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

September 28, 2018 By Trudy Scott 4 Comments

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?

How do I taper tryptophan without withdrawal symptoms: a tight band around my head, brain zaps and agitated free-floating anxiety?

September 21, 2018 By Trudy Scott 8 Comments

I have not had any clients experience the need to taper or slowly wean their tryptophan dose or report tapering side-effects similar to those they experienced when tapering off an antidepressant. However, I recently had someone ask this question on the blog (and then had someone else ask a similar question) so I’m sharing these questions and my responses in the hope of gleaning some additional information (and educating you if this applies to you). I never say never and am always learning. I’m also very interested to know how common this is and what some of the underlying factors could be.

Here is the question that was asked by Lara (we’ll call her Lara) and slightly paraphrased for clarity:

I’ve been taking 1500 mg of tryptophan for 3 months, and it has helped a lot with sleep and depression. I dropped to 1000 mg about a week ago then 500mg just to see how I’d do without it. I didn’t think it was numbing my feelings, but I am experiencing a return of feeling good.

I’ve been on antidepressants before and I am feeling the same withdrawal effects as when I weaned off meds. This is exactly why I chose to not go back to pharmaceuticals. It was difficult to wean off. How do I taper tryptophan without experiencing withdrawal symptoms? Thank you for your valuable knowledge.

These are the kinds of questions I’d ask a client in this situation:

Was the 1500mg helping and which low serotonin symptoms were eased?
How did this change when you reduced to 1000mg and then reduced to 500mg? i.e. did the low serotonin symptoms come back?
Which antidepressant are you comparing these affects to? And how long ago did you wean off the antidepressant?
Which brand of tryptophan you are using? (I find Lidtke is the best quality)

Keep in mind that we always want to be sure it’s not a one-off situation. In order to be sure someone is observing mild adverse effects from a supplement I’ll often have my client stop it and then add it back to make sure. And sometimes more than once.

In this instance repeating the process may be a good idea i.e. going back to 1000mg and then 1500mg and then reducing again, carefully documenting in a food mood supplement log.

It turns out that Lara was using the Lidtke tryptophan and she was seeing wonderful benefits for her low serotonin symptoms with none of the typical SSRI side-effects:

the 1500mg before bed with a small carb helped me get to sleep and stay asleep. It also helped with anxiety and depression during day. I tend to be a worrier, have social anxiety, and get stuck with negative thoughts about myself and others. And have very little interest in life.

I was on Zoloft from 2005 – 2009. Got off of that and did Lexapro for only 6 months in 2012. The Zoloft was life changing for me but I did not like the side effects and being on an antidepressant for the rest of my life.

The tryptophan is superior to these SSRIs [selective serotonin reuptake inhibitors] – no sexual side effects, no weight gain, or anhedonia [inability to feel pleasure in normally pleasurable activities].

She describes how she reduced the tryptophan and how her withdrawal symptoms were similar to those she experienced when tapering off her SSRIs in the past:

The withdrawal effects were felt when dropping from 1500mg to 1000mg, to 500mg, then zero over 2 days and they lasted about 3 days. By the 4th day I was no longer feeling bad.

The symptoms are hard to explain – it felt like a tight band around my head, also brain zaps (this is a common SSRI withdrawal symptom many describe feeling in their head).

The worst of it was a deep agitated free-floating anxiety like you’re walking along the edge of a cliff and there’s a physical pain in your gut. Fortunately, it was only present from waking up till around 2pm.

These are questions I’d ask or wonder about

As I mentioned in the introduction, I have not had any clients experience the need to taper or slowly wean their tryptophan dose or report tapering side-effects similar to those they experienced when tapering off an antidepressant. But if this is an issue some individuals experience I’d like to know about it

I’d also like to know how long the tapering side-effects of tryptophan last and how severe the symptoms are. In Lara’s case the symptoms were pretty severe but fortunately they only lasted 3 days which is very much shorter than SSRI tapers.

There could be confounding factors and here are additional questions I’d ask or wonder about if a client experienced similar adverse tapering effects. These are questions you could ask yourself if you have experienced this when stopping tryptophan abruptly:

Could the prior use of SSRI prescriptions be a factor? (but I have worked with many clients with prior use of SSRIs and not have tryptophan tapering issues)
What else has changed in terms of stress, diet, hidden gluten exposure, or even the something like a recent introduction of collagen (which may deplete serotonin levels in susceptible folks)?
Are there hormonal changes that could affect serotonin levels – like in a woman with PMS or perimenopausal or menopausal symptoms? (again, I’ve worked with many women of all ages and haven’t observed this to be an issue)
If you are prone to the winter blues and reduced winter serotonin, could stopping the tryptophan in the winter play a role? (I have had clients have SSRI tapering issues in winter because of being prone to the winter blues and choose to work with their doctors on their SSRI taper in the spring and summer for this reason)
Could this also be an issue with summer blues in hot states like Arizona?
Could any of these play a role: a recent medical procedure, a course of antibiotics (especially fluoroquinolones) or antifungals, poor gut health, a new infection, decreased immunity or increased inflammation?
Could low levels of these nutrients play a role: vitamin B6, ferritin, magnesium and zinc?
Would using high doses of vitamin C during the “taper” help reduce some of the symptoms? (this works well as an antidote when you take tryptophan and don’t need it and want to negate some of the negative effects, so may help in this situation)

Stopped tryptophan and felt very angry and down

The other question I had about tryptophan weaning is this one from someone who shared that she had suggested tryptophan for a friend. This friend was

experiencing a lot of ruminating and anxiety. She responded beautifully and felt great. About a year later, she tried to stop taking it, and said she felt very angry and down. Is there a weaning process for the tryptophan?

This could possibly be related to the above and you could pose similar questions but based on on what I see with clients I feel this is more of a matter of stopping the tryptophan too soon while she still had low serotonin – especially if the ruminating and anxiety came back. Feeling angry and down are classic signs of low serotonin.

The questions asked were specifically about tryptophan but they could also possibly apply to some individuals who stop 5-HTP abruptly.

I’d love to hear if you’ve experienced anything like this with either tryptophan or 5-HTP and if yes please share your answers to some of the above questions.

Right now, I’m afraid I don’t have an answer for you on how to taper tryptophan without these withdrawal symptoms: a tight band around the head, brain zaps and agitated free-floating anxiety. Right now, I’m not sure how big an issue this is. If it is common, I’m hoping some of the feedback I receive may provide some answers.