Vitamin B1, anti-estrogenic, pro-DHT, anti-serotonin, pro-dopamine

Thiamine, the first discovered B vitamin, is an essential water-soluble vitamin.

Even though thiamine is water soluble, it can be stored for up to 2-3 weeks in the liver before being excreted through the urine.

Vitamin B1 plays an important role in cellular energy production, is neuroprotective and is important for normal neuronal activity. It is required for numerous critical biochemical reactions in the body, including the synthesis of certain brain chemicals (i.e., neurotransmitters); production of the molecules making up the cells’ genetic material (i.e., nucleic acids); and production of fatty acids, steroids, and certain complex sugar molecules.

Magnesium is an important cofactor in converting thiamine to its active form, thiamine pyrophosphate. Hence, a magnesium deficiency can mimic a thiamine deficiency.

31%+ of people are deficient and 17%+ are depleted in this vitamin.


Vitamin B1 is particularly important for carbohydrate and BCAA metabolism and is a required cofactor in four enzyme pathways, namely, 1) oxoglutarate dehydrogenase, 2) branched-chain ketoacid decarboxylase, 3) pyruvate dehydrogenase and 4) transketolase. As your consumption of carbohydrates increase, so does the need for thiamine. And a deficiency interferes with glycogen storage, which may cause hyperglycemia, and other characteristic errors in carbohydrate metabolism.

Oxoglutarate dehydrogenase (a.k.a alpha-ketoglutarate dehydrogenase (α–KGDH)) is an enzyme responsible for the formation of succinyl CoA from α-ketoglutarate in the kreb/citric acid cycle and produces NADH which directly provides electrons for the respiratory chain. α–KGDH plays a role in maintaining the levels of the neurotransmitters glutamate, gamma–aminobutyric acid (GABA), and aspartate, and its also directly involved in muscle protein synthesis. Calcium can also increase the activity of this vitamin B1 dependent enzyme, thus increasing metabolism even further.

Branched-chain decarboxylase is an enzyme responsible for the catabolism of the branched-chain amino acids. The catabolism of the three BCAAs also contributes to the production of cholesterol and donates nitrogen for the synthesis of the neurotransmitters, glutamate and γ-aminobutyric acid (GABA) (1)

Pyruvate dehydrogenase (PDH) is the enzyme that is responsible for catalyzing pyruvate to acetyl CoA before entering the citric acid cycle. When pyruvate isn’t converted to acetyl CoA, it then accumulates and is then converted into lactic acid. 300mg+ thiamine a day is used to treat severe lactic acidosis. (2) PDH is essential for the production of the neurotransmitter acetylcholine as well as for the synthesis of a compound called myelin, which forms a sheath around the extensions (i.e., axons) of many neurons, thereby ensuring the ability of these neurons to conduct signals.

Transketolase (TK), which requires thiamine as a coenzyme, is part of the pentose phosphate pathway which helps maintain cellular NADPH levels. NADPH plays an intracellular role in regenerating glutathione (thus strengthening the immunity).

Certain toxins called, glyoxals, which are alpha-oxoaldehydes, are primarily formed during the breakdown of carbohydrates and polyunsaturated fatty acids. They are created directly from glucose via retroaldol condensation, and it is formed indirectly from glucose via a glycoaldehyde intermediate that undergoes autoxidation. A build-up of glyoxals increases oxidative stress and is toxic to the liver and mitochondria and also depletes glutathione.

Glyoxals are detoxified primarily by the glyoxalase system utilizing glutathione (GSH) and by the aldo-keto reductase enzymes which utilize NADPH as the co-factor. (3)


Thus, thiamine administration activates intermediate metabolism routes, enhancing cellular respiration, decreasing the generation of ROS and prevents toxin buildup. (4)

A deficiency in thiamine leads to mitochondrial dysfunction, brain and neural damage, neurotransmitter deficiency and Beriberi.  (56)


Thiamine is being used to improve brain function and it is also shown to help reverse neurodegenerative disease such as Alzheimers and Parkinsons (7)

A thiamine deficiency stresses the mitochondria and decreases ATP production. Less ATP in the brain decreases an enzyme that regulates dopamine levels and can lead to low levels of dopamine and bring feelings of tiredness, no motivation or focus, etc…

It is shown that a thiamine deficiency induces degeneration of dopamine neurons (8).

A deficiency in thiamine also increases serotonin synthesis and decreases its uptake, resulting in a stronger action of serotonin, which antagonizes dopamine further (9).

Increased intake of thiamine increases serotonin disposal and inhibits dopamine reuptake, thus resulting in a stronger action of dopamine. It is said that Steve Jobs took massive doses of thiamine when he was experimenting with LSD and said both were about equally effective as idea stimulators, but B1 did not have the “trip” effect.

50mg of thiamine improves mood, attention and faster decision times (10).

100mg+ of thiamine has a significant effect on memory recall and is very useful when studying or before a test…

Thyroid and fatigue

Administration of thiamine (600mg/day) in patients with Hashimoto’s thyroiditis, led to a partial or complete regression of the fatigue and related disorders within a few hours (11). Thiamine also prevents bad symptoms of hypermetabolism, such as the rapid action of the heart, nervousness and digestive disturbances, during thyroid treatment (12).


A thiamine deficiency also leads to low immunity and the development of autoimmune encephalomyelitis (autoimmune demyelination of the CNS) through activating CCL2 and inducing pathologic inflammation (degenerates the nervous system). (13)

Thiamine helps increase NADPH as a cofactor in the pentose phosphate pathway. NADPH is essential for the recovery and production of glutathione (GSH), which is the master antioxidant and detoxifier of the body. Thus leading to stronger immunity, less inflammation and infections.

DHT and estrogen

NADPH (created via the pentose phosphate pathway, which uses thiamine as a cofactor) provides hydrogen atoms in the chemical reaction in the production of steroids, specifically DHT. NADPH is a cofactor in 5-alpha reductase, and is also needed for the production of glutathione which is the master antioxidant and protects the body against oxidative stress.

Furthermore, androstenedione (a weak intermediate steroid hormone) also requires NADPH to be converted to testosterone.

Chronic thiamine administration results in higher testosterone and antioxidant enzymes and less oxidative stress. (14)

An interesting rat study indicated that a combination of pyruvate (end breakdown product of glucose) and thiamine pyrophosphate (active form of thiamine) exhibited a strong potentiation of steroidogenesis in intact isolated rat adrenocortical cells in presence of threshold concentrations of cyclic AMP or other cyclic nucleotides. (15) With enough glucose, vitamin B1 and a cAMP promoter (such as forskolin and caffeine) in the testes can powerfully stimulate steroidogenesis.


The complete inactivation of estradiol in the liver is dependent on vitamin B1 and B2.

Without adequate amounts of either one of these vitamins, full inactivation cannot occur, and readministration of vitamin B1 or B2 enables the liver to fully deactivate estradiol. (16)


For those who exercise, thiamine may be a great additive to your supplement regiment, as it reduces ammonia and lactic acid build-up. This will help you squeeze out extra reps and recover faster during sets as well as to improve recovery post-workout. Optimal lactate and ammonia clearance will improve mental clarity (less brain fog), less inflammation, better sleep, better energy, etc… Start with 100mg and try working up to 1000mg thiamine HCL. Allithiamine would be the best, as it’s fat-soluble and stays much longer in your system (can last months) and the absorption is also much better, so smaller doses can be used. A good combination would be thiamine and sodium bicarbonate to decrease lactic acid and ammonia and increase pH.

Extras & supplements

Protein and folate assist in thiamine absorption.

Its been shown that thiamine deficient rats develop aggressive reflex and it’s speculated that this deficiency also causes aggression in humans, likely to more estrogen.

If you feel on edge, agitated, irritated with a lack of physical/mental energy, or you just want to seriously boost your immunity, testosterone, DHT and decrease estrogen, pop a thiamine cap.

  • Energin – 50mg Thiamine HCL, combined with Vitamin B2, B3, B6 and biotin, while all works together in synergy (topical and oral application with over 90% bio-availability and 99.9% purity)
  • Thiamine – 100mg Thiamin HCL, 100 caps

Want more awesome content like this?

Success! You're on the list.

22 thoughts on “Vitamin B1, anti-estrogenic, pro-DHT, anti-serotonin, pro-dopamine”

  1. nadph 5ar cofactor, is not thiamine, thats vitamin b3, how could you not correct such a massive blunder, this puts question marks on everything youve said here.

  2. Hi Hans,
    I take a B Complex with 40mg Thiamine with no side effects. One day I tried an additional separate 100mg thiamine cap, but a few hours later got a bad headache.Is this normal?

    P.S. Love your newsletter.

      • Thanks for the reply Hans.

        The cap just had thiamine, so no fillers. Maybe not eaten enough carbs, will make sure eat more next time.

  3. Hi Hans, I’ve been experimenting with B1, I was just curious there is a lot of information out there saying you shouldn’t isolate any B vitamin. I’ve been reading from Dr Lonsdale and Dr Berg (he takes nutritional yeast) with his B1. I can’t take nutritional yeast due to celiac cross reactivity, and I don’t really want to take the other synthetic B’s especially B12 and folate. Is it absolutely necessary to take the complex or not? I would prefer to get them from food, but have a feeling I could be thiamine deficient, hence the experimentation. Is there any reliable testing to check if low in the other b’s, my methylation status is ok.

  4. Hey Hans, thanks for the reply. Just another question, I’m experiencing a bit of hypoglycemia, is this usual when first introducting b1? I’m taking benfotiamine and hcl. Or am I not eating enough carbs?

  5. I’m trying high dose Thiamin (1500mg/day) to help lower fasting blood glucose of over 300. For diabetics, is it still necessary to take with high carbs? Will the excess sugar in a diabetics blood be enough carbs for the Thiamin to work at lowering blood glucose? Also, how soon (days, weeks,?) can I expect to see lowered BG levels? Thanks for all your great work!

  6. Too much of that article seems relevant to me. Previously & now consistently I have been taking 100mg HCL in the morning, 100 mg Benfo & 50mg TTFD with meals for an improved tolerance to carbs with carnivore as my fall back. I have had hair loss & with B1 urine colour could not be achieved unless I took R5P but intermittent Biotin seems more relevant in ameliorating skin repair with a history of bouts of acute Berri Berri. Magnesium [& Potassium] depletion manifest as cramps with B1 use. My most recent breakthrough has been treating histrionic [diarrhea] Serotonin Syndrome with a NDRI [bupropion]. But acidosis & monitoring urine pH seems less relevant now with a marked improvement in chronic fatigue although I don’t seem to be able to break the 3hr glycogen storage barrier. Peripheral neuropathy, is almost unnoticeable now.


Leave a Reply

This site uses Akismet to reduce spam. Learn how your comment data is processed.

%d bloggers like this: