Vitamins A-Zinc — Vitamin B1

On January 9, 2010, in Vitamins, by Andrea

Whole Grains

What is it?

Thiamin (sometimes spelled thiamine) was once called aneurine.  It was isolated and characterized in the 1930′s and was one of the first organic chemicals to be recognized as a vitamin.  Since it was the first B vitamin to be recognized, it was given the moniker of vitamin B1.

Thiamin occurs in the human body as free thiamin, and in several phosphorylated forms: thiamin monophosphate (TMP), thiamin triphosphate (TTP), and thiamin pyrophosphate (TTP), which is also known as thiamin diphosphate.

What is it good for?

Thiamin pyrophosphate (TPP) is a required enzyme for a small number of very important enzymes.  Additionally, all forms of thiamin play critical roles in the production of energy from food.

Cataracts – there is some limited evidence that thiamin will help prevent cataracts

Alzheimer’s – there is slight and inconsistent evidence that thiamin supplements are of benefit to those with Alzheimer’s

Congestive Heart Failure – diuretics used in the treatment of CHG, notably Lasix, have been found to increase thiamin excretion, potentially leading to marginal thiamin deficiency; however, studies have shown that CHF patients have a low incidence of thiamin deficiency, although older patients are at greater risk than their younger counterparts — thus thiamin supplementation in CHF patients is currently still very controversial

Cancer – thiamin deficiency has been observed in some cancer patients with rapidly growing tumors; studies have shown that some of these rapid cell-dividing tumors have a high requirement for thiamin;  thiamin supplementation is common in cancer patients to prevent deficiency due to frequent vomiting, but given these findings, perhaps supplementation should be given only to those who have a definitive need versus as a prophylaxis

Where do I get it?

Thiamin is mainly absorbed in the jejunum and is transported in the blood via the red blood cells (erythrocytes) and plasma.  Only a small percentage of a high dose of supplemental thiamin is actually absorbed and elevated serum values will result in active urinary excretion.  After an oral dose, peak excretion occurs in about 2 hours, and is nearly complete after 4 hours.

For all of that information, we still know very little about the bioavailability of this critical water-soluble vitamin.

Food Sources

Median intake of thiamin from food in the US by young men was approximately 2mg and young women 1.2mg.

Food Serving Thiamin (mg)
Lentils (cooked) 1/2 cup 0.17
Peas (cooked) 1/2 cup 0.21
Long grain brown rice (cooked) 1 cup 0.19
Long grain white rice, enriched (cooked) 1 cup 0.26
Long grain white rice, unenriched (cooked) 1 cup 0.04
Whole wheat bread 1 slice 0.10
White bread, enriched 1 slice 0.11
Fortified breakfast cereal 1 cup 0.5-2.0
Wheat germ breakfast cereal 1 cup 4.47
Pork, lean (cooked) 3 ounces* 0.72
Brazil nuts 1 ounce 0.18
Pecans 1 ounce 0.19
Spinach (cooked) 1/2 cup 0.09
Orange 1 fruit 0.10
Cantaloupe 1/2 fruit 0.11
Milk 1 cup 0.10
Egg (cooked) 1 large 0.03

Vitamin Sources

Thiamin can be purchased by itself, or in a package with other B-vitamins as a B-complex.

Recommended Dietary Allowance (RDA) for Thiamin
Life Stage Age Males (mg/day) Females (mg/day)
Infants 0-6 months 0.2 (AI) 0.2 (AI)
Infants 7-12 months 0.3 (AI) 0.3 (AI)
Children 1-3 years 0.5 0.5
Children 4-8 years 0.6 0.6
Children 9-13 years 0.9 0.9
Adolescents 14-18 years 1.2 1.0
Adults 19 years and older 1.2 1.1
Pregnancy all ages - 1.4
Breastfeeding all ages - 1.4

There is not sufficient data concerning adverse effects to set a Tolerable Upper Intake Level (UL).  There are no reports available of adverse effects from consumption of excess thiamin from food or supplements, and there have been no studies done for high-dose thiamin supplementation.  However, it should be noted that although there have been no adverse reactions associated with excess thiamin intake from food or supplements, this does not mean that there is no potential for adverse effects resulting from high intakes — just that there have been none associated with high-dose thiamin supplementation.

There have been occasional reports of severe adverse reactions and even death in relation to injected supplementation therapy of thiamin.  Sympotms of anaphylaxis include anxiety, respitory distress, nausea, abdominal pain, shock, and sometimes death.


Thiamin deficiency has severe implications.  A B1 deficiency alters mitochondrial function, impairs oxidative metabolism, and causes selective neuronal death by diminishing vitamin B1-dependant enzymes.  It affects the cardiovascular, nervous, muscular, and gastrointestinal systems, resulting in peripheral neuropathy, ataxia, encephalopathy, and may even lead to permanent impairment of recent memory.  It is important to note that the encephalopathy and neuropathy of a B1 deficiency may occur despite supplementation of thiamin because vomitting may preclude effective absorption.

Beriberi, the disease resulting from severe thiamin deficiency was described in Chinese literature as early as 2600 B.C. and has four distinct types:

Dry (paralytic or nervous) beriberi is peripheral neuropathy.  Early in the course of the neuropathy, “burning feet syndrome” may occur.  Other symptoms are:

  • abnormal or exaggerated reflexes
  • diminished sensation
  • weakness in the legs and arms
  • muscle wasting
  • muscle pain and tenderness
  • difficulty rising from a squatting position
  • may have seizures

Wet (cardiac) beriberi is characterized by cardiovascular manifestations of thiamin deficiency

  • rapid heart rate
  • enlargement of heart
  • severe swelling (edema)
  • difficulty breathing
  • ultimately congestive heart failure

Cerebral beriberi may lead to Wernicke’s encephalopathy and Korsakoff’s psychosis, especially in people who abuse alcohol

  • Diagnosis of Wernicke’s based on a triad of signs in addition to the thiamin deficiency:
    - abnormal eye movements
    - stance & gait abnormalities
    - abnormalities in mental function that may include a confused, apathetic state or a profound memory disorder termed Korsakoff’s psychosis
  • without amnesiac state, only Wernicke’s disease
  • most WKS sufferers are alcoholics, but cases have been seen in other disorders of gross malnutrition including stomach cancer, AIDS, and bariatric surgery
  • administration of IV thiamin to WKS patients generally results in prompt improvement of the eye symptoms but motor coordination and memory may take longer or may have less recovery depending on how long symptoms were present before treatment began
  • classic presentation of Wernicke’s only happens in 20% of patients

Infantile beriberi is possible in breast-fed infants whose mothers are thiamin-deficient.
Beriberi may progress for years if left untreated, but has been known to progress as quickly as 3 days.  Substantial recovery typically occurs within 3-6 months of the initiation of therapy; however, neurological recovery may never be complete if left untreated for a long period of time.

Biochemical changes in thiamin status occur well before the appearance of overt signs of deficiency.  Because erythrocyte transketolase activity decreases early in thiamin deficiency, measurement of its activity in red blood cells has been used to assess thiamin nutritional status; however it has some limitations so additional indicators should be considered as well in testing for a possible deficiency.

Deficiency may result from inadequate intake, an increased requirement for thiamin, excessive thiamin loss from the body, consumption of foods high in anti-thiamin factors, or a combo of the above.

Inadequate Intake

Deficiency is common in low-income populations whose diets are high in carbohydrates and low in thiamin (ie milled or polished rice).  Alcoholism, which is associated with low intake of thiamin, among other nutrients, is the primary cause of thiamin deficiency in industrialized countries.

Increased Requirement

Those with an increased requirement include those who have strenuous physical exertion, high fever, pregnancy, breast-feeding, and adolescent growth.  Such conditions place individuals with marginal thiamin intake at risk for developing symptomatic thiamin deficiency.  Recently, malaria and HIV patients were found to be in increased need of thiamin as well.  Those being treated with hemodialysis or peritoneal dialysis and individuals with a malabsorption syndrome are also in need for additional thiamin.

Reduced blood levels of thiamin have been reported in individuals with seizure disorders (epilepsy) taking the anticonvulsent medication Phenytoin for long periods of time.  Lasix may increase risk of thiamin deficiency in individuals with marginal thiamin intake due to increased urinary excretion of thianmin, and chronic alcohol abuse is associated with thiamin deficiency so these individuals have an increased requirement.

Excessive Loss

By increasing urinary flow, diuretics may prevent reabsorption of thiamin by the kidneys and increase it’s excretion in the urine, although this point still remains quite controversial.  Women experiencing excessive vomiting during pregnancy are at additional risk for thiamin deficiency and should be monitored closely.

Anti-Thiamin Factors (ATF)

The presence of anti-thiamin factors in foods also contribute to the risk of thiamin deficiency.  Certain plants contain ATF which react with thiamin to form an oxidized, inactive product — rendering the thiamin useless.  Consuming large amounts of tea and coffee (including decaffeinated versions) has been associated with thiamin depletion.  Thiaminases are enzymes that break down thiamin in food and are found in raw freshwater fish, raw shellfish, and certain ferns.  When cooked, these enzymes are destroyed and the thiamin-eating enzymes are destroyed.


No well-established toxic effects from the consumption of excess thiamin in food or through long-term oral supplementation (up to 200mg / day) have been notated.  However, there have not been any studies into this, so that is not to say that there are no toxic effects to high-dose thiamin supplementation, or to long-term over-supplementation of thiamin.

WLS Concerns

We know that thiamin absorbs in the jejunum, which is partially bypassed in RNY folk.  It’s also completely bypassed in DS folk.  This is something that needs to be watched in both surgeries to make sure a deficiency does not arise.  Deficiencies in B1 are common enough after bariatric surgery that a new term has been coined — either “bariatric beriberi” or even the cuter and shorter “bariberi.”

Beyond the fact that we know it is a water-soluble vitamin that absorbs in the jejunum, we know that the body only absorbs a small portion of high-dose supplementation.  When we give the body a huge dose at once, it causes the body to excrete extra through the urine.

And that’s what we know about the bioavailability.  Which isn’t much in the grand scheme of things.  We don’t know if there is a maximum we can absorb at a time, or how often we should take it for max absorption.  There simply have not been enough studies to tell us this.  That’s why our labwork is so critical to tell us where we stand — and if you think there could possibly be a problem, it’s time to get it checked immediately, not in a week, or next month when you get your labs anyway.

Another concern comes from intractable vomiting.  Oral supplementation may not be enough if you are losing thiamin through vomiting.

Looking through medical database sites, I found multiple papers about the neurological complications after bariatric surgery.  There were two about thiamin alone — and another that also discussed B12, E and copper.  The point is that B1 needs to be on your labslip, and if it is not, there is a problem.

Information compiled from:

Linus Pauling Institute
The National Acadamies Press: Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline
The Neurological Complications of Bariatric Surgery
Thiamine Deficiency May Complicate Gastric Bypass