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tryptophan

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

By Trudy Scott 14 Comments

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.

When and how to discontinue the amino acids?

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

Once you are feeling back to your old self with no more anxiety, panic attacks or depression, 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.

We appreciate Amy for allowing me to share her results and posting these questions which are a great learning opportunity for you.  She shared this with me:

I hope my “story” is helpful. Keep doing this important work! I work in the behavior health field. My colleagues think this is radical thinking and continue to only support the medical model. I’ve done a lot of my own research and trial and error. I wish there were more-open minded clinicians.

Hopefully with success stories like this, all the nutritional psychiatry research and behavioral health practitioners like Amy who have experienced it first hand and/or with clients/patients and family, we’ll change how mental health care is approached.

Do success stories like this lead you to be more open-minded about anxiety nutrition solutions? Have they worked for you?

And 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?

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

By Trudy Scott 43 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.

Vitamin B6 improves dream recall (which can be used to monitor vitamin B6 status)

By Trudy Scott 40 Comments

It’s exciting to see new research confirming the connection between vitamin B6 and dream recall. In this new study, Effects of Vitamin B6 (Pyridoxine) and a B Complex Preparation on Dreaming and Sleep (which was randomized, double-blind and placebo-controlled), 100 participants from across Australia were given 240 mg vitamin B6 (pyridoxine hydrochloride) before bed for five consecutive days. Other study participants were given a B complex. This is the outcome of the study:

  • vitamin B6 significantly increased the amount of dream content participants recalled but did not significantly affect dream vividness, bizarreness, or color, nor did it significantly affect other sleep-related variables
  • participants in the B complex group showed significantly lower self-rated sleep quality and significantly higher tiredness on waking

Here are my thoughts on these results:

  • It’s wonderful to read that Vitamin B6 improves dream recall – this is what I see with my clients all the time.
  • With an optimal dose of vitamin B6, I would expect changes in “dream vividness, bizarreness, or color” and this also what I also see with my clients. If they are having horrible/vivid/bizarre dreams, the vitamin B6 changes them to pleasant dreams OR if dreams were not recalled prior to supplementation, they are now remembered and pleasant. The dose of 240 mg was used across the board but based on what we know about biochemical individuality, 240mg may be too much for some folks and not enough for others, so this could have impacted the results.
  • It’s not surprising that the B complex taken at bedtime impacted sleep. It’s known to be stimulating and it’s not something I’d advise any client to do. For this reason, I don’t feel it was the ideal control for this study.

The lead researcher is Dr. Denholm Aspy and his primary research focus is lucid dreaming. On his researcher profile on the University of Adelaide website, he describes lucid dreaming and the potential benefits:

In a lucid dream, the dreamer realizes that they are dreaming and can then explore and even control the dream. Lucid dreaming has a wide range of potential benefits and applications such as creative problem solving, treatment for recurrent nightmares and improvement of motor skills through rehearsal in the dream environment (e.g. for elite athletes or people recovering from physical trauma).

He shares that the purpose of his research is to address exploration of the potential applications of lucid dreaming and to “develop reliable ways to induce lucid dreams.” Looking for potential applications of lucid dreaming is very interesting and new to me.

Vitamin B6/dream recall research and pyroluria (a social anxiety condition)

However, this vitamin B6/dream recall research is of particular interest to me because of my work with pyroluria, a social anxiety condition which responds really well to supplementation with zinc, vitamin B6 or P5P (pyridoxal-5-phosphate) or a combination of both, and a few other key nutrients.  Here is the pyroluria questionnaire.

One of the classic signs of pyroluria is poor dream recall, stressful or bizarre dreams, or nightmares, signs which the late Carl Pfeiffer, MD attributed to low vitamin B6 status. He suggested that your dreams and dream recall serve as a good indicator of your need for vitamin B6. You should dream every night and you should remember your dreams. They should be pleasant—the kind of dreams where you wake up and want to close your eyes and continue dreaming.

Going back to the above discussion of lucid dreaming, in lucid dreams “the dreamer is aware of dreaming and often able to influence the ongoing dream content.” This is exactly how I would describe my dreams when I have good levels of vitamin B6 and my clients say the same.

Keep in mind that if you do have pyroluria, you may need to increase your dose of vitamin B6 in times of stress. Vitamin B6 can also be depleted by oral contraceptives because they cause both low vitamin B6 and zinc, reduce serotonin levels and increase anxiety. Vitamin B6 can also be depleted by antidepressants, diuretics, and cortisone, so if you start or stop taking any of these, you may need to adjust the amount you supplement.

If this intrigues you and you’re new to pyroluria, I write about dreams and vitamin B6 in the pyroluria chapter of my book, The Antianxiety Food Solution. My blog is also a wealth of information on pyroluria:

Dream recall and vitamin B6 status is important even if you don’t have pyroluria

Observing your dream recall and hence vitamin B6 status is important even if you don’t have pyroluria. This is because vitamin B6 it has been implicated as a co-factor in more than 140 biochemical reactions in the cell, playing a role making amino acids and neurotransmitters, making fatty acids, and even quenching reactive oxygen species (ROS).

This is partial list showing the importance of vitamin B6 (with both research and clinical evidence) for:

You may also wonder what the mechanism of action is? How does vitamin B6 impact your dream recall? One hypothesis is that vitamin B6 is a co-factor nutrient used in the conversion of tryptophan to serotonin which is then used to make melatonin. Vitamin B6 is also an antioxidant, is anti-inflammatory, and modulates immunity and gene expression.

If you’re looking for a quality vitamin B6 product, my supplements blog lists a range of vitamin B6 supplements that I use with clients and those in my group program.

Monitoring your dream recall is one very simple way to assess changes in your vitamin B6 status. And we now have new research supporting this. I look forward to follow-on studies by these authors, learning more from them about lucid dreaming and I hope to be able to offer some of my insights from clinical practice.

*** I address some concerns about vitamin B6 toxicity in this blog: Why is vitamin B6 toxic for some and why don’t symptoms resolve when vitamin B6 is stopped? I have yet to see any signs of toxicity in my clients, but I have also not ever recommended more than 500mg/day. However, I was recently made aware (thanks to some folks in my community) that there are some individuals who have issues with very small amounts of vitamin B6.  If you have experienced any issues with using vitamin B6 supplementation please share.

What are your dreams like and do you use your dreams to monitor your vitamin B6 status? What improvements have you noticed by addressing low vitamin B6 levels?

If you’re a practitioner do you use dream recall as an indication of vitamin B6 status?  Have you seen adverse issues with vitamin B6 supplementation and at what doses?

Delayed IgG food sensitivities: depression and anxiety due to inflammation, leaky gut, leaky blood brain barrier and low serotonin

By Trudy Scott 7 Comments

It’s really encouraging and exciting to see a major study confirming what we’ve known about IgG food sensitivities or IgG food reactivity for years, and also reporting a link to irritable bowel syndrome (IBS) and depression. The paper, published in May this year, The Food-Specific Serum IgG Reactivity in Major Depressive Disorder Patients, Irritable Bowel Syndrome Patients and Healthy Controls states

There is an increasing amount of evidence which links the pathogenesis of irritable bowel syndrome (IBS) with food IgG hyperreactivity. Some authors have suggested that food IgG hyperreactivity could be also involved in the pathophysiology of major depressive disorder (MDD).

The following diagram and excerpt illustrates the gut-immune-inflammatory-brain model for depression that is associated with food IgG hyperreactivity or sensitivity.

The gut-immune-inflammatory-brain model for Major Depressive Disorder associated with food IgG hyperreactivity. According to the hypothesis proposed in our previous work, we present a possible mechanism underlying the MDD [major depressive disorder] development, suggesting that the interplay between genetic and environmental factors may lead to disruption of tight junctions, the loss of their integrity and both gut and BBB [blood brain barrier] permeability. Undigested food compounds, which would normally break down in the gut, translocate into the blood circulation, and trough epitopes combine with food IgG antibodies to form immune complexes. This, in turn, provokes an abnormal response and triggers immune-inflammatory cascade. Uncontrolled release of the proinflammatory mediators may contribute to low-grade systemic inflammation and low-grade neuroinflammation, which, via pathological processes in CNS [central nervous system], i.e., changes in neurotransmitter metabolism, neurogenesis, glutamate excitotoxicity, may in consequence induce and then maintain and prolong depression.

[diagram and excerpt from The Food-Specific Serum IgG Reactivity in Major Depressive Disorder Patients, Irritable Bowel Syndrome Patients and Healthy Controls]

I wrote my book, The Antianxiety Food Solution, in 2011 and there wasn’t research on the gut-immune-inflammatory-brain model, but I do write extensively about delayed IgG food sensitivities (as well as other types of food issues). If you don’t have my book I’m including some of the highlights related to this (and I encourage you to pick up a copy too!). If you do have my book I hope this next section encourages you to go back and read chapter 4 again (and even check out the other books I mention below).

I write about how with delayed food reactions, it may take a few hours to several days before symptoms appear, which can make it difficult to identify the offending food or foods. In these reactions, the body responds by creating a type of antibody known as IgG (immunoglobulin G).

I also write about how food sensitivities can have effects beyond physiological symptoms, including creating imbalances in key chemicals in the brain, which can cause anxiety, phobias, depression, irritability, and mood swings. When food sensitivities have these effects, they are sometimes termed “brain allergies” or “cerebral allergies.” Dr. Carl Pfeiffer wrote extensively about this and used these terms in his wonderful book, Nutrition and Mental Illness, way back in 1987. (This book is a quick read and is one of my favorite older books on the subject of mental health and biochemical imbalances.)

I also reference the work of my colleague and friend, clinical nutritionist Liz Lipski. In her 2004 book, the 3rd edition of Digestive Wellness she shares that

24 percent of American adults claim they have delayed food and environmental reactions.

She feels that these sensitivities are often the result of leaky gut syndrome, a condition characterized by damage to the microvilli lining the intestinal walls. This allows undigested food particles to travel across the intestinal wall and into the blood, where the immune system responds to them as foreign, harmful substances and creates antibodies to neutralize them.

All this sounds very similar to what the new study is reporting doesn’t it? I’d prefer it not to take so long for the knowledge from as far back as 1987 to get into mainstream journals but it’s the world we live in and we can just appreciate that we are moving forward and in the right direction!

The 2018 paper mentioned above concludes the following:

Our findings suggest more common food-specific serum IgG hyperreactivity among patients with IBS and MDD [major depressive disorder], which may be one of the mechanisms leading to the development of immune activation and low-grade inflammation observed in these disorders.

They do support an elimination diet for IBS but not for depression:

There is no causal relationship which could confirm clinical utility of an elimination diet in patients with depression

I do love research, but this really bothers me as it’s just common-sense and we do have some case studies supporting the use of elimination diets. In this case study the patient’s “treatment-resistant” depression improved considerably with an elimination diet, with similar results in another case study where a gluten-free elimination diet improved both anxiety and depression and everyday functioning.

In the meantime, we’ll continue to rely on the wisdom of practitioners like Dr. Pfeiffer and Liz Lipski, and all the clinical evidence showing how an elimination diet does help with both depression and anxiety. Just read some of the success stories on this blog – Paleo and grain free diets: anxiety and depression success stories.

Other mechanisms: nutrient malabsorption and serotonin production

There are other mechanisms that I also cover in my book – nutrient malabsorption and a more direct impact on serotonin production.

One possible mechanism is indirect effects of gastrointestinal damage due to eating problem foods, resulting in nutrient malabsorption. In a 2009 double blind placebo-controlled study:

65 celiac patients aged 45-64 years on a strict gluten-free diet for several years [and showing signs of low folate, low vitamin B12 and low vitamin B6] were randomized to a daily dose of 0.8 mg folic acid,0.5 mg cyanocobalamin and 3 mg pyridoxine or placebo for 6 months

I doubt folic acid or this form of B12 would be used today but even with these forms at these low doses, the study participants showed homocysteine in a good range and reported improvement in general well-being – after just 6 months of supplementation.

Another possible mechanism is the fact that gluten sensitivity and the resulting damage to the gut can limit the availability of tryptophan and therefore lead to decreases in levels of serotonin. Research published in 2005, Gluten-free diet may alleviate depressive and behavioural symptoms in adolescents with coeliac disease: a prospective follow-up case-series study, reports that:

serotonergic dysfunction due to impaired availability of tryptophan may play a role in vulnerability to depressive and behavioral disorders among adolescents with untreated coeliac disease

In addition to removing the foods that are causing the sensitivities, you need to heal the gut and boost serotonin levels with a targeted individual amino acid like tryptophan.

Give the link between anxiety and depression, all of the above could apply if you have anxiety too.

Have you had IgG food sensitivity testing and found that an elimination diet helped reduce your depression or anxiety symptoms?

Candida: anxiety and low serotonin, testing and parasites, sugar cravings, EMFs and your genes

By Trudy Scott 9 Comments

My interview on anxiety on The Candida Summit with host Evan Brand, addresses anxiety, the tie in to low serotonin and the sugar cravings aspect. I was so excited to find a connection between serotonin and candida and share this in our interview. 

with low serotonin you’ve got the mental anxiety – the worry, the ruminating thoughts, the obsessive thinking, the reprocessing, insomnia, lying awake in bed, trying to shut down the busy mind. And the two amino acids I use for this is tryptophan; that’s my first choice. And my second choice is 5-HTP. That being said, some people do better on one versus the other.

The reason I like tryptophan is 5-HTP can raise cortisol and make people who are wired/tired feel a little bit more wired/tired. So until I’ve seen cortisol results in saliva, I like to use tryptophan first.

But let me share some of this interesting research that I’ve found. And why I’m so excited about it is because as I said earlier, I will use the amino acids first before I’m specifically addressing the candida. But it seems like using tryptophan first, as well as helping with the low serotonin, it’s starting to have an impact on the candida, which I didn’t know about, until I did the research for this. So thank you for inviting me to speak. It just reinforces what I know about the amino acids – that they are pretty powerful.

There was a study done in 2003, and the title is Antifungal Properties of Serotonin Against Candida species. And they looked at various different candida strains: albicans, glabrata, tropicalis, and a few others. And they exposed these candida strains to serotonin. The study concludes: “Serotonin showed antifungal activity towards all isolates of candida.”

What they didn’t know is what the mechanism of action was. They stated: “Identifying the mode of action would be of great help in developing and research new antifungal drugs.” I don’t agree with that. I’m just excited to see that there is this connection with serotonin, which reinforces how beneficial tryptophan is.

Of course, my solution is to provide serotonin support via diet, exercise and the use of the targeted individual amino acid tryptophan or 5-HTP.

You can read more about this serotonin-candida connection in my blog post: Symptoms, nutrient malabsorption, worsening psychiatric symptoms and the serotonin connection

In our interview I also discuss how I use the amino acids and how tryptophan/5-HTP as well as GABA, DPA, tyrosine and glutamine, can actually help with so much of the sugar craving we see in candida, PLUS how I use this approach to gauge when candida is really serious.

EMFs and the dangers of 5G – and candida

Dr. Schaffner talks about EMFs and the dangers of 5G and shares how they are protecting the Sophia Institute Clinic (which she shares with Dr. Dietrich Klinghardt):

What we have done at the clinic—and again, this is an evolving art—the two things that I think are going to make the most difference in what we can do right now is, first, of course we always say avoid exposure, try to distance yourself. Distance is your friend with any technology, when we’re looking at EMF.

But we actually shielded the clinic. We have a cell phone tower within a mile of the clinic. And so, we wanted to be mindful of that exposure. We ask everybody to turn off their cell phones when they come in to the clinic. And we don’t have Wi-Fi. So everything is ethernet corded. And then, we don’t have cell phone exposure while we’re practicing.

But we do two things that I think people should be aware of. And one is we use a type of graphite paint. It’s called YSHIELD. And that actually comes from Germany. And it has properties to, essentially, try to create a Faraday cage environment and block the incoming microwave radiation. And so, that has to be grounded, of course. And you want to always work with somebody who knows what they’re doing with this technology. Because if you don’t do it right, you can actually increase your exposures or create an unhealthy environment.

And then, Dr. Klinghardt works with the woman who creates these silver-lined curtains that actually help to block the microwave radiation coming in through the windows.

There’s a really great website—LessEMF has a lot of this technology. And then, YSHIELD, you can Google, I think it’s yshield.com. And then, the silver-lined curtains, I believe, is a fabric called, Swiss Shield. And so, you can either make them yourself or hire somebody to do that.

Learn more about candida, low serotonin, low melatonin, and your glymphatic system in the second half of Dr. Schaffner’s interview.

Candida, sugar cravings and COMT and MAOA genes

Evan Brand brings up the topic of sugar and carbs in the diet with Dr. Ben Lynch in the Candida, sugar cravings and COMT and MAOA genes interview: No one is discussing the influence of the whole epigenetic piece, and how people and their decision making with foods could be influenced by their genes?

Dr. Ben Lynch shares how he has a unique angle on this fascinating topic of our genes and sugar/carb cravings:

It’s one that always ties back to what came first—the chicken or the egg, right? So what came first, the genetic propensity towards carbohydrate binging or addictive personalities for high-caloric dense foods like ice cream and cakes, doughnuts, pastries, which then leads us to candida?

And then, they go on all these candida treatments. And they beat it. And they’re all happy again. But then their genetic propensity drives them yet again for the yeast overgrowth and the food binging.

He gives an example of how some people, when they’re down and out, may be drawn to sugar and carbs to self-medicate (this is something I see with my anxious clients all the time):

They’ll hit the chocolate. They’ll hit the doughnuts, the ice cream to make them feel good. And what these do is they spike your dopamine.

You’re not really aware of it, but you just do it. And you know you shouldn’t do it. But what happens here is, is some individuals, they have genes, which eliminate their dopamine out of their body pretty quickly. This gene is called COMT. And one of its jobs is to move dopamine out. You don’t want to always have neurotransmitters in your brain. That’s not good.

So some of these folks are born with a COMT gene that actually works faster, which is really good because they can calm down really quick in stressful environments. They can perform at a high level in stressful situations like surgeons, or EMT, or firefighters, or policemen, policewomen. They strive in these high-risk, highly-attentive situations.

But when they come home, everything’s a low normal. And they need that hit of dopamine. So they might come home and binge on sugars and carbs to drive their dopamine back up. And that’s a significant one.

Dr Lynch also shares about another gene, MAOA, which deals with our serotonin:

If you have a faster MAOA gene, which moves through your serotonin, then you are craving carbohydrates, and you’re craving pastas, and breads, and all the things that candida love, and beer. These things which increase your tryptophan levels, support your MAOA, and thus your serotonin. These are two major foods that our candida love. And these are two very, very common genes in the population which predispose us to having these issues

Candida testing, parasites and intractable yeast overgrowth 

Evan Brand asks this question about candida testing in the Candida, Mitochondrial Dysfunction, and Meditation interview with Dr. Dan Kalish: I’m guessing your statistics are similar to mine, 9 out of every 10 organic acids I find Candida overgrowth. Stool test, the GI map is missing a lot of Candida. Maybe you could help me understand why that’s happening.

Dr. Dan Kalish shares why candida testing can be challenging:

Because Candida can be commensal where it’s growing within the digestive tract itself, or it can be invasive where it penetrates into the tissue of the gut. And then it’s not going to be found in any of the stool tests. So stool tests can miss it easily. And in fact, the more severe it gets, the harder it is to find on a test.

That’s what happens with the yeast when it gets bad. It gets invasive. It goes up into the actual lining of the gut. So if it penetrates there, it causes leaky gut. But then it’s invasive, so it’s penetrating into the tissues. And you’re not going to see it in the stool. And that’s when it gets worse. In fact, it’s going to cause more symptoms. But then it’s almost impossible to find on the stool test.

He also shares this gem about intractable yeast overgrowth that just won’t go away:

You can have a Candida overgrowth, treat it and feel better, but have there be another underlying cause for the Candida. So there’s a lot of patients that will come to me and be like, “I had this Candida overgrowth. As long as I eat this radical and extreme and ridiculous diet, and take all these herbs, I’m fine. But every time I stop, it just comes back.”

Then, that leads the person to assume that it’s this horrific Candida overgrowth that’s never going to go away. And in those patients, there’s almost always Giardia, or Crypto [Cryptosporidium], or E. histo [Entamoeba histolytica], or some other bug that’s screwing up the ecology of the gut that’s allowing the Candida to keep coming back. So that’s just something to be on the lookout for.

If you feel like you have this intractable yeast overgrowth that just won’t go away, you should find a functional medicine doctor and do all the stool testing. Because you’re almost guaranteed there will be some other infection.

Click here to register for The Candida Summit which runs online from July 9-15, 2018!

Do share if you’ve successfully addressed candida overgrowth and how your symptoms improved and how bad your sugar cravings were.

Let us know if you’re EMF-aware and how addressing low serotonin has helped you.

If you have questions post them below in the blog comments.

Melatonin improves sleep quality and reduces anxiety after a TBI (traumatic brain injury)

By Trudy Scott 11 Comments

New research shows that melatonin improves sleep quality and reduces anxiety after a TBI (traumatic brain injury). The study, Efficacy of melatonin for sleep disturbance following traumatic brain injury: a randomised controlled trial was completed in Australia and used a prolonged-release (also called timed-release) melatonin product.

The study participants, 67% of whom were male, had mild to severe TBI and sleep disturbances as a result of their injuries (most of which were from car accidents). There were 2 study groups, with one group given 2mg of prolonged-release melatonin for 4 weeks and then switched to a placebo for 4 weeks (with a 48-hour window in between). The other group did the opposite.

The prolonged-release melatonin was made by Sigma Pharmaceuticals Australia and called Circadin. Each night 2 hours before bedtime, 2mg of Circadin was taken by study participants. They received a reminder text message each night.

These are the study results for sleep:

Melatonin was associated with a significant and moderate reduction in PSQI [Pittsburgh Sleep Quality Index] global scores, indicating improved sleep quality.

There was no significant reduction in sleep onset latency with melatonin compared to placebo.

What this means is that overall quality of sleep improved but there was no change in the time it takes to fall asleep (sleep onset latency). The latter is to be expected with prolonged-release or timed-release melatonin.

The study concluded that:

The present results, therefore, suggest that melatonin may be useful in treating sleep disturbances in patients with TBI.

With better sleep quality you would expect reduced fatigue and improved vitality – both were reported by study participants.

Melatonin associated with a small decrease in self-reported anxiety

What is interesting is that melatonin was also associated with a small decrease in self-reported anxiety (no differences in depression were reported.) The authors suggest that one possible mechanism of this may be that melatonin acts a muscle relaxant. In this commentary: Potential action of melatonin in insomnia, the authors equate the beneficial effects of melatonin to benzodiazepines:

many of the actions of melatonin on sleep propensity, anxiety, thermoregulation, and convulsions resemble those reported following administration of benzodiazepines. It is possible that some of these actions of melatonin may be mediated via peripheral benzodiazepine receptors

They are suggesting that with melatonin we get the sleep improvement (sleep propensity is the readiness to transit from wakefulness to sleep, or the ability to stay asleep if already sleeping), relaxation effects and antianxiety benefits of benzodiazepines.

But you get none of the side-effects, tolerance issues and withdrawal nightmares with a benzodiazepine which do more harm than good. On a side notes: this month World Benzodiazepine Day is celebrated to create awareness and offer support for benzo sufferers.

I would have picked something more inert for the placebo ingredients

I would have picked something more inert for the placebo ingredients: mannitol (106mg), acacia (11 mg) and pure icing sugar (106 mg). Mannitol, a sugar alcohol, can cause bloating and diarrhea in some individuals and although the amount is tiny (5g of sugar equals 1 teaspoon), sugar consumption is not ideal before bed. As I would expect adverse symptoms:

were more frequently reported during placebo treatment. The most commonly reported symptoms were neurological, followed by bodily pain, gastrointestinal and dermatologic.

In Australia, melatonin cannot be purchased over the counter (OTC) at health stores or via online retailers, unlike in the USA, and is only available by prescription. I’m all for melatonin being available OTC but the silver lining to this is that companies that make melatonin, such as Circadin, have a vested interest in the research. Research is expensive and time-consuming and we get to benefit too.

Keep in mind that this research is applicable to anyone with low melatonin, whether or not a prior TBI has occurred.

There are many root causes of insomnia – how I work with clients

In those with TBI, sleep disturbances are common, and the authors do report reduced evening and overnight melatonin production in this population. However, there are many root causes of insomnia, with low melatonin being one possible root cause – in TBI and in those who have not had a TBI.

One study limitation is that they didn’t measure melatonin levels or circadian rhythm (salivary cortisol) in all of the study participants so we can’t be sure everyone did have low melatonin.

And melatonin isn’t going to work in all instances of insomnia. It’s one root cause I look at.

This is how I work with clients who have insomnia:

  • I start with low serotonin and address this with tryptophan observing improvements in sleep and easing of worry and anxiety (on a side note, low serotonin is common after a TBI so this makes total sense)
  • Then I have my client use sublingual melatonin if they have issues falling asleep AND timed-release melatonin if they have issues staying asleep (you can see some of the melatonin products I recommend here)
  • When saliva results come back, we address the adrenals as needed, often adding Seriphos when cortisol is high
  • Other factors are addressed based on each person’s need: gluten issues, SIBO, parasites, candida, EMFs, sex hormone imbalances, medication side-effects, sleep habits

We’d love to hear if timed-release melatonin has helped you improve your sleep quality? And if it also helped with easing anxiety?

What about tryptophan or sublingual melatonin for helping you fall asleep? And the other root causes?

If you’re a practitioner, do you use tryptophan or sublingual or timed-release melatonin with your clients? And address the other root causes of insomnia?

Feel free to post your questions too.