Thiamine deficiency: the silent epidemic of the modern world

B1: an energy conductor

Imagine that every cell in your body is a factory running on electricity. Thiamine (B1) is not the fuel — it is the electrical transformer that makes the fuel usable. Without it, the mitochondrial power plant slows, overruns, or partially breaks down, depending on the organs affected.¹

More concretely: thiamine is the limiting cofactor of three fundamental enzymes of energy metabolism: pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, and transketolase.²³

History: a century of ignored warnings

Thiamine deficiency has been known since the era of beriberi linked to polished rice, documented from the late 19th century in Asia.⁴⁵⁶

From the 1970s–2000s, Dr Derrick Lonsdale published dozens of papers showing that subclinical thiamine deficiency is widespread in the United States and linked to behavioural disorders, developmental problems, and chronic disease, while remaining largely ignored.⁷

In 2021, a review in Nutrients (Hiding in Plain Sight: Modern Thiamine Deficiency) emphasized that no current data on thiamine deficiency rates in the United States is available — not because the problem has been resolved, but simply because thiamine is not being measured.²

“TD is believed to be rare in developed, food-secure countries […] As a result of this perception, thiamine is not consistently assessed in healthcare practice or in the nutritional surveys that guide policy.”²

Demystifying: B1 is not “easy to obtain”

Officially, the recommended intake (≈1.1–1.2 mg/day) would be easily achieved through diet, but numerous modern factors destroy or deplete B1: cereal refining, high-temperature cooking, coffee/tea containing thiaminases, alcohol, diuretics, metformin, PPIs, stress, and chronic hyperglycaemia.^5891011

Body stores cover only 2–3 weeks, with a half-life of 9 to 18 days, so any increase in demand (infection, pregnancy, surgery, high carbohydrate intake) can unmask functional deficiency.²

The carbohydrate paradox: eating sugar consumes B1

Thiamine is indispensable to carbohydrate metabolism: several key steps of glycolysis and the Krebs cycle are B1-dependent.²³

The higher the diet in refined carbohydrates, the greater the thiamine requirement — creating a double trap: ultra-processed foods are both poor in B1 and major consumers of B1.²³

“Among the most common contributors to thiamine deficiency is the regular consumption of a high carbohydrate/highly processed food diet.”³

This phenomenon particularly affects type 2 diabetics, obese individuals in “high-calorie malnutrition,” and children raised on ultra-processed products.¹²¹³

Who is really at risk?

Contrary to the myth that confines B1 to alcoholics and low-income countries, measurable deficits have been observed in: psychiatric patients, pregnant women, emergency department patients, obese individuals (especially pre-bariatric surgery), dialysis patients, heart failure patients on diuretics, the elderly, people with chronic illness, and patients on artificial nutrition.¹⁰¹³¹⁴

“The number and variety of symptomatic thiamine-deficient adults identified in this review demonstrates that thiamine deficiency is not exclusive to LMICs and, in high-income settings, is not exclusive to alcoholic patients.”¹⁰

Genetics: when B1 meets its transporters

Polymorphisms in the SLC19A2 and SLC19A3 genes (THTR1 and THTR2 transporters) can reduce absorption or utilization of thiamine and predispose to early-onset diabetes, chronic inflammation, or neurological disorders.¹⁵¹⁶¹⁷

In these individuals, a “normal” intake may be insufficient, lowering the clinical deficiency threshold and modifying the response to supplementation.

B1, the “great imitator”: dysautonomia, SIBO, fatigue

The brainstem and autonomic nervous system, highly dependent on mitochondrial ATP, are particularly vulnerable to thiamine deficiency, which can cause dysautonomia (POTS, tachycardia, exercise intolerance, vasomotor disturbances), anxiety, and brain fog.¹⁸¹⁹

At the digestive level, B1 is necessary for acetylcholine synthesis for the vagus nerve; its deficiency can lead to gastroparesis, constipation, reflux, and presentations confused with SIBO or IBS.¹⁸²⁰

“The gastrointestinal tract is one of the main systems that can be affected by a deficiency of thiamine […] often non-responsive to antimicrobial treatments. Yet, sometimes the issues improve greatly with vitamin B1 repletion.”¹⁸

The testing problem: a false sense of security

Serum thiamine poorly reflects tissue stores and can remain “normal” despite functional deficiency.²¹

Measurement of TDP (thiamine diphosphate) in whole blood is more relevant but remains limited by the absence of standardised thresholds and inter-laboratory variations; some data also suggest increased vulnerability of certain populations (e.g. Black subjects) at lower concentrations.²²²³²⁴

Functional tests such as ETKAC also have important technical limitations; a study in thiamine-sensitive children showed that no biomarker could reliably identify them individually.²³²⁵

In practice, several authors conclude that it is often rational to supplement empirically when the clinical picture is compatible, since thiamine is very safe and inexpensive.¹¹⁰

Health authorities vs scientific reality

Official fact sheets (NIH, WHO, national agencies) state that thiamine deficiency is rare in developed countries and easily prevented through diet and fortification, but acknowledge not having recent data on actual deficiency rates.²⁸

Independent reviews show on the contrary that modern deficiency is widely underestimated, poorly measured, and affects a much broader spectrum of populations than just alcoholics or low-income countries.²¹⁰²⁶

The researchers who have sounded the alarm

• Derrick Lonsdale (1924–2024): more than 50 years of work on thiamine, author of Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition; three of his papers are cited by the WHO on sudden infant death syndrome.⁷²⁷
• Chandler Marrs (PhD): co-author of the reference book and founder of HormonesMatter.com, a platform documenting hundreds of clinical cases and thiamine effects.²⁸
• Elliot Overton (EONutrition): functional medicine practitioner who developed high-dose thiamine protocols (ThiamineProtocols), used by thousands of patients and carers.²⁹³⁰³

The hope: a simple, safe, often transformative intervention

Thiamine combines three rare properties: high safety (even at elevated doses), very low cost, and the potential for rapid reversibility of sometimes debilitating symptoms (extreme fatigue, mild to moderate dysautonomia, functional digestive disorders, paradoxical anxiety).¹⁰¹

Specific forms (benfotiamine, TTFD) can optimise tissue or neurological penetration depending on the case, with progressively titrated protocols to limit paradoxical reactions.¹⁰²⁹³⁰

“Treatment with intravenous thiamine resulted in partial or complete recovery from the symptoms (cardiac, neurologic, and metabolic disorders) for most patients.”¹⁰

Within the framework of the Right to Physiological Integrity, this grounds a right to an optimal thiamine status: the right to recognition of subclinical deficiency, access to relevant tests where available, and safe, low-cost supplementation strategies to correct a deficit that today is, quite literally, hiding in plain sight.

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