Weight Loss with Trimethylaminuria (Fish Odour Syndrome) in South Africa

Trimethylaminuria (TMAU), commonly called Fish Odour Syndrome, is a metabolic disorder in which the body cannot adequately convert trimethylamine (TMA) — a pungent, fishy-smelling compound — into its odourless form. As a result, TMA accumulates and is excreted through sweat, urine, breath, and reproductive secretions, producing a persistent fishy body odour. For many people with TMAU, the social and emotional consequences of the condition are profound — isolation, shame, anxiety, and depression are common, and these often drive emotional eating and weight gain. If you have TMAU and want to lose weight, this guide explains the biochemistry, the dietary restrictions that reduce TMA production, and how to address the emotional eating patterns that are almost universal in this condition.

What Is Trimethylaminuria?

Trimethylamine (TMA) is produced in the gut by intestinal bacteria that break down certain dietary compounds — primarily choline, lecithin (phosphatidylcholine), carnitine, and TMAO (trimethylamine N-oxide, found in marine fish). The TMA produced in the gut is absorbed into the bloodstream and transported to the liver, where the enzyme flavin-containing monooxygenase 3 (FMO3), encoded by the FMO3 gene on chromosome 1q24.3, converts TMA to TMAO (trimethylamine N-oxide) — the odourless, water-soluble form. TMAO is then excreted harmlessly in urine.

In Trimethylaminuria, mutations in both copies of the FMO3 gene reduce or abolish FMO3 enzyme activity. TMA can no longer be efficiently oxidised to TMAO. It builds up in the bloodstream and is excreted unchanged through:

TMAU is more common than once thought — primary (genetic) TMAU from homozygous or compound heterozygous FMO3 mutations is relatively rare, but secondary TMAU — caused by increased TMA load from diet, certain gut bacteria, liver disease, or hormonal factors — is estimated to affect 1% or more of the population in some form. Women are more commonly and severely affected than men, partly because oestrogens reduce FMO3 activity and androgens enhance it.

Dietary Sources of TMA Precursors

The key insight in managing TMAU is: TMA is not a nutrient you eat directly — it is produced by gut bacteria from precursor compounds in food. Reducing TMA production requires reducing the dietary substrates that gut bacteria convert to TMA:

Choline

Choline is the most significant TMA precursor in most people's diets. Gut bacteria (including Clostridium and Erysipelotrichaceae species) convert choline to TMA via TMA lyase enzymes. Foods very high in choline include:

Lecithin (Phosphatidylcholine)

Lecithin is a phospholipid found in many foods and used as an emulsifier in processed foods (label: E322). Lecithin is hydrolysed in the gut to release choline, which is then converted to TMA. High-lecithin foods include egg yolks, liver, and many processed foods and supplements (lecithin supplements are commonly marketed as a "health food" for brain function — avoid completely in TMAU).

Carnitine

L-carnitine is converted to TMA by gut bacteria. Carnitine is found in high concentrations in:

TMAO in Marine Fish

Marine (saltwater) fish contain TMAO in their muscle tissue as an osmoprotectant. When fish dies, bacteria convert TMAO to TMA — the familiar fishy smell of aging fish. When TMAU patients eat marine fish, the TMAO is absorbed and provides a direct additional TMA load to the liver (which cannot convert it efficiently). Avoid:

Freshwater fish (trout, tilapia, catfish) contain negligible TMAO and are generally tolerated, though this varies by individual.

The Emotional Eating Cycle in TMAU

This aspect of TMAU is underappreciated in medical literature but is extremely common in practice:

Addressing the emotional dimension of TMAU is as important as addressing the dietary dimension. If you recognise emotional eating patterns in yourself — eating in secret, eating in response to emotional pain rather than hunger, feeling out of control around food — speak to a clinical psychologist or counsellor. Cognitive-behavioural therapy (CBT) has good evidence for emotional eating and is available in South Africa through several channels (SADAG, the South African Depression and Anxiety Group, can provide referrals: 0800 456 789).

Safe Weight Loss with TMAU

The good news is that the core dietary restrictions for TMAU (low choline, low carnitine, avoid marine fish) are compatible with a calorie-controlled, nutrient-rich weight loss diet. The restricted foods — organ meats, egg yolks, red meat, fatty processed foods, marine seafood — are not nutritionally essential when replaced correctly. Here is what a well-planned TMAU weight loss diet looks like:

Protein Sources (Low TMA Precursor)

Foods to Build the Plate Around

Caloric Deficit Strategy

A target deficit of 400–500 kcal/day is safe and appropriate for most adults with TMAU. Unlike many of the other rare metabolic disorders discussed on this site, TMAU does not carry a risk of metabolic crisis from caloric restriction — the primary concern is odour worsening, not acute metabolic decompensation. Practical approach:

Other Management Strategies for TMAU

Beyond diet, several management approaches can reduce TMA load and improve quality of life:

Exercise and TMAU

Exercise is not metabolically dangerous in TMAU — it does not trigger metabolic crises. The challenge is social: sweating during exercise increases TMA exhalation and skin release, potentially making odour more noticeable. Practical approaches:

South African Context

TMAU is underdiagnosed in South Africa. Many patients are told they have a hygiene problem or are dismissed without metabolic investigation. Diagnosis requires a urine TMA/TMAO ratio test — this is available through National Health Laboratory Service (NHLS) at some centres or via referral to a metabolic physician. The test should ideally be done after a choline challenge (eating 300 mg supplemental choline before the test) to maximise diagnostic sensitivity.

If you suspect TMAU and have not been diagnosed, ask your GP to refer you to a metabolic physician or clinical geneticist. TMAU is likely more common in South Africa than current diagnostic rates suggest, particularly given the genetic diversity of the South African population and the prevalence of certain FMO3 polymorphisms in sub-Saharan African populations.

Key Takeaways

This article is for educational purposes only and does not replace advice from your metabolic physician, dietitian, or mental health professional. If you are struggling with the emotional impact of TMAU, please seek support from SADAG (0800 456 789) or a qualified clinical psychologist.