Three main protocols of TMAU diet

There is some confusion about food issues regarding TMAU and other possible metabolic BO conditions because usually what works for one person may not necessarily work for another. However, it is always best to ‘arm’ ourselves with knowledge about the content of foods, then to try to ‘read’ our respective body to determine what our saturation point is for the various foods with respect to our body’s ability or inability to metabolize them. Unfortunately, without more scientific tests to help us with the process of understanding the physiology of our bodies, we just have to experiment on ourselves using the trial and error method.

...the choline content alone of the foods is not the only factor to consider in a TMAU odor-management effort; instead, the trimethylamine-N-oxide/trimethylamine (TMAO/TMA) content of the foods as well as their inhibiting effects of FMO3 enzyme activity need to be taken into account as well. An attempt is made in this post to shed some light on this question by presenting 3 different points of interest, but in the end, each sufferer will have to ‘test’ their respective saturation levels to determine how much choline and TMAO rich foods can be ingest without the body odors going off the roof. We as sufferers also have a choice as to when and how much we are willing to smell in order to enjoy foods every once in a while and in order to provide the nourishment our bodies need.

Feeling physically ill while smelling: One important thing we do need to keep in mind is that when our bodies do fail to metabolize TMA and the TMA builds up in our blood, we may be in an unhealthy state with a high level of compounds that should not be in our blood, as our bodies will try very hard to clean it out. These compounds makes some of us feel sluggish, sort of ‘hangoverish’ and some may even develop ‘Chronic Fatigue Syndrome,’ anxiety and depression, and possibly other more serious physical and emotional/mental conditions as a result of toxins flowing around our bodies in our blood. Some sufferers have found that as their odor increases, so do their allergies and chemical sensitivities also increase. See post, TMA and Epilepsy, learning disabilities, anxiety, and more, which presents studies of high TMA serum levels triggering seizure activity, increased symptoms of learning disabilities; and it also discuses a case of a small boy with severe seizures linked to a metabolic condition controlled with diet.

Point #1:
http://www.nal.usda.gov/fnic/foodcom...ne/Choln02.pdf
“In 1998, the Food and Nutrition Board of the Institute of Medicine established dietary recommendations for choline intake, estimating an Adequate Intake (AI) at 550 mg per day for men and 425 mg per day for women.”

*(Discussion) For a sufferer with a weak or deficient FMO3 enzyme, or a gut dysbiosis consisting of an overgrowth of TMA-producing bacteria, perhaps taking this recommended level of choline will produce high under-metabolized TMA level in the blood, which would not only produce strong odor, but also may make the person feel sick as described above. Therefore, each person needs to find ways to weigh the options and make the necessary decisions to consume the amount of choline recommended without over-saturating the metabolic enzymes too much, so as not to trigger negative side effects.

Point #2:
The NIH recommended Trimethylaminuria Management Protocol.

Treatment of manifestations recommended by NIH: dietary restriction of: (1) trimethylamine (present in milk obtained from wheat-fed cows) and its precursors including choline (present in eggs, liver, kidney, peas, beans, peanuts, soya products, and brassicas [Brussels sprouts, broccoli, cabbage, cauliflower]), lecithin and lecithin-containing fish oil supplements, (2) trimethylamine N-oxide (present in seafood [fish, cephalopods, and crustaceans]), (3) inhibitors of FMO3 enzyme activity such as indoles (found in brassicas)…

*(Discussion) Note that this recommendation is broken up into three parts.

Part #1: refers to choline being a Trimethylamine precursor in this food group. A precursor is a substance, cell, or cellular component from which another substance, cell, or cellular component is formed. In this case, the choline is the precursor that is broken down by bacteria which then produces trimethylamine. A person with this bacteria producing excessive amounts of TMA may overwhelm a healthy FMO3 metabolic enzyme level. This form of TMAU is referred to Secondary TMAU. In this case, a low choline diet and possibly antibiotic treatment is recommended. See Treatment of Manifestations of the Gene Reviews article on Trimethylaminuria

PART #2: refers to the trimethylamine N-oxide (TMAO)ALREADY PRESENT IN SEAFOOD. This is a different precursor. So in this case, we are more concerned with the actual TMAO content of the food as well as the choline content.

In a Google book, Advances in Fish Processing Technology, by D.P. Sen 2005 (pg 240, #6.4.2 Trimethylamine) it states,

Trimethylamine (TMA) is a most known compound to indicate freshness quality and degree of spoilage of marine fish. TMA is associated with “fishy” odour and with the odour of fish spoilage and is clearly a part of the spoilage pattern of many fish species; odour goes, more or less, hand in hand with TMA concentration…

TMA is formed from trimethylamine oxide (TMAO) [in fish] which is an osmoregulatory and buffering compound found in many marine teleosts, elasmobranchs and shellfish…

Small amount of TMA may be produced by the endogenous enzymes* of fish. But main degradation of TMAO to TMA is due to enzymes of psychrotrophic bacteria particularly Achromobacter that invade the fish after death…

*Definition of endogenous enzymes: Developing or originating within the organisms or arising from causes within the organisms.

PART #3: refers to foods that act as inhibitors of FMO3 enzyme activity. This concern is independent of the choline content or TMAO content of the food, because this food group actually inhibits FMO3 enzyme activity, which can be very detrimental to someone who has a weakness or deficiency of this enzyme. It is most detrimental to Primary TMAU, which is a genetic metabolic disorder inherited in an autosomal recessive manner. This type of TMAU, is determined by DNA mutation analysis of the FMO3 gene indicating a deficiency in the FMO3 metabolic enzyme produced in the liver. This deficiency of FMO3 enzyme results in an inefficient FMO3 function with a failure to metabolize (add an oxygen molecule)to the chemical Trimethylamine(TMA), which smells of rotting fish, as well as other compounds that contain nitrogen, sulfur or phosphorous. Symptoms are usually present from birth and may worsen during puberty. In females, symptoms are more severe just before and during menstruation, after taking oral contraceptives, and around the time of menopause. This condition benefits from reduction in all three diets, low choline, low TMAO/TMA-rich foods, and low consumption of inhibitors of FMO3 enzyme activity, such as indoles (found in brassicas)…

IN SUM, It is important that we understand how these three food groups differ and how the choline content of the foods alone is not the only factor to consider in a TMAU odor-management effort; instead, the TMAO/TMA content of the foods and their inhibiting effects of FMO3 enzyme activity need to be taken into account as well.

Translated into Spanish
by Natalia


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