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Amino acid

Depression, 5HTP and L-Tryptophan: Laboratory Markers Matter

by Dr Charles Parker on April 4, 2010 · 15 comments

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L-Tryptophan or 5HTP: How Laboratory Markers Can Guide Evolved Treatment

Guest Post: Dr Richard Lord

Depression Treatment History
Consider the typical progression of a patient with major depression: They usually go through periods of poor appetite and limited food intake, and they systematically show decreases in average stomach acid output. So, their protein intake and digestive capacity become deteriorated. At the same time, they are placed on SSRI therapy that increases their demand for serotonin production. The major catabolic end product from serotonin metabolism is 5-hydroxyindoleacetic acid (5-HIA), which is mainly excreted in urine. {The important point here: 5-HIA [some call it 5-HIAA], the breakdown product from serotonin metabolism, can be measured accurately in the laboratory.}

The Details of Deterioration
The typical patient who has been placed on SSRIs will show levels of 5-HIA that are ~2 times the upper 95% reference limit, or 4-5 times the mean [the breakdown values are significantly elevated in the urine]. That means that the percentage of dietary tryptophan that is flowing into the serotonin pathway is now more like 4-5 times the usual ~10%. Tryptophan as a limiting amino acid, meaning that the amounts found in foods are relatively small in proportion to the other amino acids. When the cells of human tissues need to be replaced, synthesis of thousands of proteins comes to a halt the moment tryptophan is not available.

Neurotransmitter Organ Reserve Matters
Thus, patients with long term major depression can have serious difficulty with maintenance of organ reserve. So, which organs will most quickly show the effects of inadequate ability to maintain reserve? Is it not those that have the greatest turnover and routine demands? And, does that not take us straight to the gut and digestive organs? The parietal cells that make hydrochloric acid, the enterocytes that line the inner surface of the small intestines, and the pancreatic cells that must produce many grams of digestive enzymes daily, lose their ability to keep up with demand.

Treatment Failure: Deeper Cellular Consequences
Thus, it is no wonder that the progression of patients with major depression is so often a downward spiral as more and more drugs are used with less and less efficacy because the ability of their bodies to reverse the major organ reserve loss becomes more and more restricted. The energetic demands of the parietal cells cannot be met because they can’t crank up the rate of mitochondrial enzyme production. The massive daily loss of enterocytes is not matched by new formation of cells at the base of the villi because they can’t supply amino trytophanyl-t-RNA at sufficient rates for ribosomal protein synthesis of everything from calbindin to glutathione-S-transferase. The absence of L-tryptophan alone can produce all of these effects. And, no additional amounts of any other amino acids will help, because the protein synthesis process ceases the moment the ribosome fails to receive a single tryptophan for insertion.

What To Do Next
So, are you going to recommend therapy with large doses of tryptophan for patients on typical SSRI therapy for major depression? No, because you may induce the dangerous serotonin syndrome. This is one of the most challenging nutritional intervention decisions that you will face. A solution that has merit for your investigation is the use of customized free-form amino acid supplement powders based on plasma amino acid profile results. Because of the presence of the full spectrum of amino acids, the large neutral amino acids limit the rate at which blood tryptophan is transferred across the blood-brain barrier. Many clinicians are learning that their patients with major depression (and the frequently accompanying condition of chronic fatigue) respond very positively to this intervention.

Outcome Over Time
Once their organ reserves are restored, they can stop the free-form supplements and go back to dietary protein, or, for an interval, use isolated whey or other superior protein supplements.

Comments on 5-HTP Supplementation
What about the use of 5-HTP as an alternative therapy to support brain serotonin? It can help with mood stabilization. But, does it help with protein synthesis? No, because the conversion of tryptophan to 5-hydroxytryptophan (serotonin) is not a reversible process. So it serves only to slightly spare the loss of tryptophan. What is needed is a consistent increase in available L-tryptophan to drive protein synthesis everywhere, and allow the organ reserve capacity to be rebuilt, -  turning the course of the degenerative spiral towards rebuilding of health.

Ed Note
I’m very pleased to share with you this first guest post at CorePsych Blog, written by Dr Richard Lord, Chief Science Officer at Metametrix Laboratories - and teaches at the Metametrix Institute. For those interested in further understanding Laboratory Evaluations see Dr Lord and Dr Bralley’s book linked below. These three YouTube videos on Autism will provide an excellent window into Dr Lord’s engaging personality and deep insights into specific measurements for treating Autism. I strongly recommend you follow this link over to his presentations on file at Metametrix.

Dr Richard Lord
- Received his BS in Chemistry from Georgia State University, and his PhD in Biochemistry from the University of Texas in 1970. Postdoctoral and staff fellowships were completed at the Clayton Foundation Biochemical Institute (oligopeptide properties), the University of Arizona (insulin self-association), and the National Institutes of Health – Institute of Arthritis and Metabolic Diseases (human thyroid-binding globulin). He served as clinical laboratory director at Horizon Laboratories from 1974-1981, then, for the next eight years, Dr. Lord was Professor and Chairman in the Department of Chemistry for Life University where he was instrumental in the initiation and design of a BS degree in Nutritional Science. Dr. Lord joined Metametrix in 1989 where he currently fills the role of Chief Science Officer.

In addition to co-authoring and editing the books, Laboratory Evaluations in Molecular Medicine and Laboratory Evaluations for Integrative and Functional Medicine, Dr. Lord also publishes technical articles, lectures live at the Applying Laboratory Evaluations to Improve Clinical Outcome Seminars, and consults with health professionals regarding clinical applications of testing for metabolites and toxicants. Dr. Lord has participated in Think Tanks on Orthomolecular Medicine, Environmental Medicine and Autism.

Thanks Richard for this excellent review [emphasis with italics and subheadings my own],
cp

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Tagged as: 5-Hydroxytryptophan, 5HTP, Amino acid, Blood-brain barrier, Major depressive disorder, Neuroscience, neurotransmitter precursors, neurotransmitters, protein, Protein biosynthesis, Psychiatric Medications, Serotonin, SSRI, Tryptophan

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Vyvanse diminishes Memory? Watch The Top of The Therapeutic Window

by Dr Charles Parker on November 14, 2009 · 21 comments

Taking Vyvanse – and Losing Your Memory?

There are several likely explanations, so let’s review. Most importantly, remember these small Vyvanse challenges do teach us – they point the way to the next logical intervention for the most effective medication dosage strategies.

Vyvanse and Time

Vyvanse and Time

Vyvanse Question from Lara

I am in my late 30’s and have been on Vyvanse 50mg for over 6 months. Like some previous posters I experience some unsettling memory problems even though I have great focus. I can’t remember simple things like my children’s teachers names, or the name of a store. My word retrieval skills are terrible, or I will reverse words thought, example: “I am going to the bananas to get the store.”

This is quite common and it is only after I utter this nonsense that I notice the error. My children even pick up on it sometimes. Also, for several months I experienced a shortness of breath that seemed similar to my asthma symptoms as a child. This seems to come and go now, but is bizarre. Do you think these could be related to the Vyvanse?

Vyvanse, the Window and other Neurotransmitters: My Reply

Do look very carefully at your duration, your DOE as discussed in this post on Vyvanse dosing, and assess if it has crept up to the 14 hr range. While not always the accurate barometer [having only misrepresented Vyvanse dosage efficacy with careful questioning only 2x in my experience], it will often tell the tale.

The phenomenon of decreased memory can be related to several different issues, the most frequent, and the reason for measuring the DOE, is simply adhd-medication-management-series-measuring-the-top-of-the-window/”>too much Vyvanse, leading to an excessively long DOE [somewhere over 12 hr with some folks]. Said another way, sounds like you are coming out of the Top of the Therapeutic Window. These findings in the office are less common, as many adults have done well in specific work simulated studies with 14 hr DOE.

Shortness of breath can also be associated if the dose is slightly too high.

Another possibility, also quite likely, is that your ADHD is simply caused by a dysregulation with one of several different neurotransmitters, for example PEA. Phenylethylamine, PEA, is not commonly appreciated by the current ADHD psychopharmacology practitioners simply because we haven’t had a medication to address levels. Low PEA can create ADHD issues, and an abundance of PEA can drive the stimulant consequences [side effects] out the top of that window.

Measuring PEA, as I do now in every challenging presentation, saves big time – months of speculation and trial and error, and real dollars as the evidence will tell the practitioner exactly what to do. As you may know from these pages I am a strong advocate of science and measurement, and disparage the Missouri Turkey Shoot method of dosing – such as taking a blurb like this one from the Internet and running out to find the amino acid precursor for PEA, phenylalanine.

However, if you are interested in PEA do take a look at this article [PEA noted on pg 269] from Psychiatry and Clinical Neurosciences, for verification of this possible targeted amino acid neurotransmitter precursor for intervention, should that be the correction needed.

Neurotransmitter measurement possibilities discussed in detail on the Neuroscience page here.

Interesting Vyvanse/neurotransmitter question, thanks,
cp

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Tagged as: ADD and ADHD, Amino acid, Attention-deficit hyperactivity disorder, Child, DOE, dopamine, Mental health, neurotransmitter precursors, neurotransmitters, PEA, Pharmaceutical drug, Therapeutic Window

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Neurotransmitters & Psychiatric Medications: The Turkey Shoot Revisited

November 7, 2009 Brain/Body Evidence

Let’s target the symptoms precisely. The approach of Turkey Season serves as a great reminder for what-not-to-do with psychiatric medications and supplements, and how to consider withdrawal from gluten with neurotransmitters.

15 comments Read the full article here →