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WHAT IS TMAU? It’s Not a Hygiene Thing… It’s Not a Imaginary Thing…


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2 .0 1 .1 0 .0 To Balance… BARS THE SKIN YOU LOVE … LOVE THE SKIN YOU’RE IN Body Washes & Facial Cleanser Products One of the suggestions on The trimethylaminuria paper written for the NIH Gene reviews site (written by Phillips/Shephard, London) for a TMAU (trimethylaminuria) management protocol is the use of an acid soap/cleanser to attempt to neutralize some of the highly alkaline trim ethylamine. Use of acid soaps and body lotions. Trimethylamine is a strong base (pKa 9.8). Thus, at pH 6.0, less than 0.02% of trimethylamine exists as the volatile free base. The use of soaps and body lotions with a pH close to that of normal skin (pH 5.5-6.5) helps retain secreted trimethylamine in a less volatile salt form that can be removed by washing. BORC does not promote nor endorse any product, brand name or commercial supplier. Check with your physician or health-care provider before using or taking any product featured on this site. All products are posted for informational and educational purposes. Note: The use of soaps and body lotions with a pH close to that of normal skin (pH 5.5-6.5) helps retain secretion in a less volatile salt form can be removed by washing, choose a bar with low pH levels, check here to find your body wash or facial cleansers' pH level, then decide what’s best for you. Trimethylaminuria is a rare disorder in which the body's metabolic processes fail to alter the chemical trimethylamine. Trimethylamine is notable for its unpleasant smell. It is the chemical that gives rotten fish a bad smell. When the normal metabolic process fails, trimethylamine accumulates in the body, and its odor is detected in the Trimethylaminuria is a rare disorder in which the body's metabolic processes fail to alter the chemical trimethylamine. Trimethylamine is notable for its unpleasant smell. It is the chemical that gives rotten fish a bad smell. When the normal metabolic process fails, trimethylamine accumulates in the body, and its odor is detected in the person's sweat, urine and breath. The consequences of emitting a odor can be socially and the psychologically damaging among adolescents and adults. person's sweat, urine and breath. The consequences of emitting a odor can be socially and the psychologically damaging among adolescents and adults.

There is no known cure or treatment for the disorder. People affected by the disorder live relatively normal lives by managing their symptoms and with counseling. When the condition is suspected or known to occur in a family, genetic testing can be helpful in identifying the specific individuals who have or carry the disorder. Ways of reducing the fishy odor may include: Avoiding foods such as egg yolks, legumes, red meats, fish, beans and other foods that contain choline, carnitine, nitrogen, sulfur and lecithin


Exclusion of the major source of TMAO from the diet, namely marine fish, is the primary dietary modality, and should not present a major difficulty. Choline is essential to the human and to some extent can be synthesized endogenously by methylation of phosphatidylethanolamine. But despite this endogenous production, a dietary deficiency may possibly lead to liver damage, neurological disease, and carcinogenesis. Dietary reference intakes, based on observed and experimental estimates and the content of various foods have been published. A low substrate diet that requires minimizing the intake of choline, lecithin and glycine betaine containing foods as well as marine fish is rigorous and potentially dangerous enough that professional dietary guidance and advice are necessary to prevent various dietary inadequacies. Requirements are higher in pregnant women, so restricting choline might be ill-advised. Given that only excess choline, lecithin and glycine betaine passing to the colon are metabolized to TMA by gut bacteria, it is far from clear whether ordinary dietary intake

NO dairy, RED MEATS OR seafoods seafoods! the Diet! A classification scheme for trimethylaminuria has been proposed [Mitchell & Smith 2001, Mitchell 2005]. Primary genetic trimethylaminuria. Caused by FMO3 mutations that result in loss of


function of FMO3 enzyme activity, this subtype accounts for the majority of reported cases [Phillips et al 2007]. Combinations of certain FMO3 polymorphisms may cause a less severe form of the condition [Zschocke et al 1999]. Acquired trimethylaminuria emerges during adult life as a consequence of hepatitis in individuals with no previous personal history or familial history of the disorder. The metabolic changes persist after the liver problems have resolved, suggesting a permanent change in the expression or activity of the FMO3 enzyme.


Transient childhood trimethylaminuria has been reported in preterm infants fed a choline-containing infant formula. Symptoms disappear as the children mature or when the choline source is discontinued [Pardini & Sapien 2003]. Young children who are heterozygous for a loss-of-function mutation of FMO3 or have certain combinations of FMO3 polymorphisms may exhibit mild symptoms of the disorder [Mayatepek & Kohlmuller 1998, Zschocke et al 1999, Zschocke & Mayatepek 2000]. Transient childhood forms are a consequence of the immaturity


of FMO3 expression, which is switched on after birth and continues to increase throughout childhood [Koukouritaki et al 2002]. Transient trimethylaminuria associated with menstruation. A short episode of trimethylaminuria can occur in women during menstruation [Mitchell & Smith 2001, Shimizu et al 2007]. The effect is more pronounced in women homozygous for polymorphic variants that result in a limited decrease in FMO3 enzyme activity [Shimizu et al 2007].


Precursor overload can cause a transient form of trimethylaminuria that results from saturation of the enzyme FMO3. It can occur in individuals with Huntington disease or Alzheimer disease who have been given large oral therapeutic doses of choline (=20 g/day) [Mitchell & Smith 2001, Mitchell 2005].

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