# Biotin

Category: Vitamins & Minerals

Also known as: vitamin B7

Biotin (vitamin B7) is a B vitamin that functions as a critical cofactor for mitochondrial oxidative metabolism, specifically by enabling an alternative entry point into the Krebs cycle when the primary pathway is blocked. Peat expressed caution about high-dose supplementation…

11 passages · 3 authors · 2015–2025 · Most-cited: [Georgi Dinkov](https://bioenergeticoracle.com/md/voices/georgi-dinkov/index.md)

Canonical page: https://bioenergeticoracle.com/concepts/biotin

## Synthesis

**Biotin** (vitamin B7) is a B vitamin that functions as a critical cofactor for mitochondrial oxidative metabolism, specifically by enabling an alternative entry point into the Krebs cycle when the primary pathway is blocked. [Source 5, 10] Peat expressed caution about high-dose supplementation, noting that animal studies from 50 years ago showed moderate overdoses could cause liver cancer, and he recommended sticking to around **1 milligram** per day. [Source 1] Dinkov has extensively investigated pharmacological doses of biotin, finding that it acts as a cofactor for the enzyme **pyruvate carboxylase**, which converts pyruvate into oxaloacetate, thereby bypassing a blocked pyruvate dehydrogenase complex and sustaining the Krebs cycle. [Source 5, 7, 10]

The therapeutic potential of high-dose biotin became apparent in a landmark human trial for *primary progressive multiple sclerosis*, a disease with no known remissions. [Source 2, 3, 5] In that study, 300 milligrams of biotin daily led to a striking amelioration of symptoms, with researchers concluding that biotin dramatically improved the energetic status of the organism by increasing carbon dioxide production, lowering lactate, and reducing free fatty acids and triglycerides in the blood. [Source 3, 5, 7] Dinkov has cited this trial and other in vitro work showing that pharmacological biotin concentrations tripled cellular carbon dioxide production, confirming its role as a **mitochondrial nutrient** that shifts metabolism away from *fatty acid oxidation* and toward *glucose oxidation*. [Source 3, 5, 11]

In Dinkov's own cancer experiments, biotin was the decisive addition that converted tumor growth arrest into regression. [Source 8, 9] While vitamin B1 (thiamine) alone flattened the tumor growth curve and the combination of B1 and B3 (niacinamide) stopped growth temporarily, adding biotin at a human-equivalent dose of 150–200 milligrams daily caused the tumor to start declining. [Source 3, 9, 11] The mechanism involves biotin's role in providing a bypass for pyruvate when the main gateway enzyme, pyruvate dehydrogenase, is completely blocked by excessive fatty acid oxidation, a state characterized by a low **NAD+/NADH ratio**. [Source 5, 10, 11] This combination of B1, B3, and B7 ultimately stopped tumor growth completely, achieving what Dinkov termed a dormant remission. [Source 3, 9]

Beyond cancer and multiple sclerosis, intracellular biotin deficiency has been implicated in other degenerative conditions. [Source 4] Dinkov has noted that normal blood levels of biotin do not reflect intracellular status, and autopsy studies of Huntington's disease patients confirmed a brain-specific deficiency of both thiamine and biotin, with pharmacological supplementation ameliorating symptoms by improving oxidative metabolism and increasing ATP and CO2 synthesis. [Source 4] He has also pointed out that a biotin deficiency leads to a buildup of unused electrons from food, which can be shunted into *lactate production*, *fat synthesis*, or uncontrolled tissue growth. [Source 6] Dietary sources like egg yolks and liver provide adequate biotin for healthy individuals, but the raw egg white protein avidin binds biotin and can induce a deficiency, adding to the reasons Dinkov advises against consuming egg whites without the yolks. [Source 7]

## People also ask

### How does biotin provide an alternative entry point into the Krebs cycle?

Biotin acts as a cofactor for pyruvate carboxylase, which converts pyruvate into oxaloacetate, thereby bypassing a blocked pyruvate dehydrogenase complex and sustaining the Krebs cycle.

### Why did high-dose biotin show benefit in a multiple sclerosis trial?

The trial found that 300 milligrams of biotin daily dramatically improved symptoms by increasing carbon dioxide production, lowering lactate, and reducing free fatty acids and triglycerides in the blood.

### What role did biotin play in Dinkov's cancer regression experiments?

Adding biotin at a human-equivalent dose of 150–200 milligrams daily converted tumor growth arrest into regression when combined with vitamins B1 and B3, achieving a dormant remission.

## Related concepts

- [Cancer](https://bioenergeticoracle.com/md/concepts/cancer/index.md)
- [Anemia](https://bioenergeticoracle.com/md/concepts/anemia/index.md)
- [Cancer metabolism](https://bioenergeticoracle.com/md/concepts/cancer-metabolism/index.md)
- [Chronic Fatigue Syndrome](https://bioenergeticoracle.com/md/concepts/chronic-fatigue-syndrome/index.md)
- [Cyproheptadine](https://bioenergeticoracle.com/md/concepts/cyproheptadine/index.md)
- [Estrogen-serotonin axis](https://bioenergeticoracle.com/md/concepts/estrogen-serotonin-axis/index.md)

## Cited passages

Passage numbers match the `[Source N]` markers in the synthesis above.

### Source 1 — Ask the Herb Doctor: Progesterone vs Estrogen, Listener Questions (Part 2)

Ray Peat · Interview · May 18, 2018

> ## B-Vitamins: Dosage and Safety
>
> **Caller:** What about B3?
>
> **Ray Peat:** It is important to get the **niacinamide** form. Niacin releases inflammatory mediators. Niacinamide is safe up to at least a couple hundred milligrams. I've seen people with terminal brain diseases cure themselves taking just 150 or 200 mg of niacinamide per day.
>
> **Caller:** What about Biotin (B7)? I hear it regulates glucose, but is there a negative?
>
> **Ray Peat:** I've seen good results from big doses, but 50 years ago animal studies showed moderate overdose could cause liver cancer. I've always been leery about it. I would stick to around 1 milligram of biotin per day.
>
> **Caller:** And folic acid? I read you think it's dangerous.
>
> **Ray Peat:** I think it's safe at a dose of around 1 mg, maybe as high as 5 mg. However, you have to be cautious with Vitamin B2 (Riboflavin) and folic acid. Something in the synthetic process makes a lot of people get migraine headaches, hemorrhoids, and bowel inflammation from them. They are yellow molecules, and I think their sensitivity to light and oxidation makes the pure chemical allergenic for many people.

### Source 2 — Sugar Doesn’t Cause Cancer with Georgi Dinkov

Georgi Dinkov · Interview · Oct 2, 2024 · https://www.youtube.com/watch?v=xXq4S2Dx_b8

> **Georgi Dinkov:** There is no known cases of cure in an animal model with this human tumor. So they said, okay, let's go with it. So thiamine by itself, a little benefit. Niacinamide by itself, more benefit. Together, the curve started to flatten. And I said, okay, so, but they still died. They lived long enough, but they still died. So I said, okay, what else can we do? And I remember that there was a recent clinical study with multiple sclerosis patients, specifically the most aggressive form of the disease known as primary progressive multiple sclerosis. So typically, you know, the multiple, I have a relative who has that condition, but the close relative, but the condition is basically the remittance relapsed form. In other words, you have periods of exacerbation, and then you have periods of recovery, followed by periods of exacerbation, periods of recovery. That's the, you know, it's not a good disease to get, but if you have to get that one, then that's the least dangerous form of it. There's also secondary progressive and the primary progressive, which is basically these people invariably progress. They're usually in a wheelchair within two to three years after diagnosis. Nothing stops that condition, right? But then this human trial administered as a single therapy. Nothing else was given, no steroids, no other drug. The B vitamin known as biotin or also known as vitamin B7. And then it was a striking, striking amelioration of the symptoms for a disease that has no, basically nothing can stop it, right? And the proposal of the researchers was that biotin was acting as a stimulator of basically the oxidation of glucose. In other words, removing again the block from the, you know, from the pyruvate step and then converting pyruvate, pushing pyruvate through the Krebs cycle in the electron transport chain. And then I found other studies, both in vitro and in vivo, demonstrating that administration of relatively high doses of biotin also drops lactate, right?

### Source 3 — #367 Cancer pt2. Inflammation, Metabolism, & Ozempic. With Georgi Dinkov & Alannah Connealy.

Georgi Dinkov · Interview · Mar 29, 2025

> **Georgi Dinkov:** Well, I've been looking at biotin starting back in 2014, and it was a very interesting study that the addition of pharmacological doses of biotin concentrations to cells tripled their production of carbon dioxide, which can only happen if biotin stimulates the function of the Krebs cycle, which theory says it should because it's a cofactor for one of the enzymes that enter into it. And then there was a really remarkable study with patients with primary progressive multiple sclerosis, about 30 of them. And they gave them really high doses of biotin, 300 milligrams daily. For comparison, the daily requirement, I think it's like only about a milligram or maybe even less. So those were pharmacological doses of biotin. So these patients went into remission. And primary progressive multiple sclerosis is not known to go into remission. That's why it's called progressive. It just keeps getting worse. And when they looked at the metabolic profile of those patients, they saw that their carbon dioxide production had increased, the production of lactate had decreased, right? And the level of free fatty acids and triglycerides in the blood was lower. So this means these patients started oxidizing more glucose, less fat, and their lipolysis levels were lower. I said, excellent, let's try biotin. So I added that to... to the B1 and B3. So I added biotin, which is B7. And I added a slightly lower dose than what was used in humans. In humans, they use 300 milligrams daily. The dosage that I basically used, the equivalent for mice converted to humans would be about 150 to 200 milligrams daily. And then I added the biotin with the three vitamins. the tumor growth was completely stopped. So no matter how long we kept the mice alive, they did not die. The tumor did not disappear, but also did not grow. So that combination alone achieved, I would call for remission, right? Tumor's still there, but it's dormant, right? So I said, okay, so far so good.

### Source 4 — Vitamin B1 and/or biotin may treat Huntington Disease (HD)

Georgi Dinkov · Article · Oct 20, 2021 · https://haidut.me/?p=1649

> As some of my own studies with cancer recently demonstrated, vitamins are no laughing matter when it comes to their ability to treat very serious conditions. This seems to be especially true in regards to the B vitamins, which are required co-factors for most of the metabolic reactions inside our organisms. The study below adds more to that line of evidence by demonstrating that conditions such as HD may be little more than organ-specific symptoms of intracellular deficiency of one or more of the B vitamins. I emphasized the word “intracellular”, because doctors have tested blood levels of those vitamins in patients with various conditions (including HD) and the levels have invariable came back normal. However, as is often the case (and mainstream medicine refuses to admit), normal blood levels of a substance does not imply normal intracellular levels as well. Aware of this discrepancy, the study authors checked thiamine (vitamin B1) and biotin (vitamin B7) levels in brains of animals with the equivalent of HD, as well as in autopsy samples of people who died with HD, and confirmed intracellular deficiency in both of these vitamins. So, the authors surmised that giving pharmacological doses of those vitamins may be able to reverse that intracellular deficiency, and indeed that’s exactly what happened, with the end result being great amelioration of HD symptoms. I can’t get access to the full study so I can get the actual doses, but human studies with Crohn’s disease(CD) and Multiple Sclerosis (MS) have also confirmed intracellular deficiency of those vitamins and has successfully treated the deficiencies (as well as the actual pathology, at least in regards to MS) with about 600mg thiamine (for CD) and 300mg biotin (for MS) daily. The mechanism of action for the therapeutic benefit of those vitamins in both conditions has already been confirmed to be improvement of oxidative metabolism, with consequent increase in ATP and CO2 synthesis.
>
> [references]

### Source 5 — #367 Cancer pt2. Inflammation, Metabolism, & Ozempic. With Georgi Dinkov & Alannah Connealy.

Georgi Dinkov · Interview · Mar 29, 2025

> **Georgi Dinkov:** And we know that lipolysis is high in cancer patients. They have an oversupply of fatty acids. As I mentioned earlier, they oxidize primarily fatty acids, the tumor at least, and they easily resist them. So, okay, so niacinamide has two roles here. First, it increases NAD plus. Second, it inhibits excessive lipolysis. So I did a second experiment, vitamin B1 and B3. Really good results, encouraging. Again, control group exponential growth. Timing in B1 flat. Flat, flat, flat, flat for about 30 days, and then it started growing again. But at least I stopped the tumor growth initially, completely stopped. And I said, okay, what else can we do? Well, let's say if pyruvate dehydrogenase is really, really blocked because there's a tremendous oxidation of fatty acids. So it's, you know, the B1 and B3 by itself are not sufficient to activate it. Well, there's a kind of like a bypass you can do. Whenever you have pyruvate, it has to get into the Krebs cycle in order to get properly oxidized. So if PDH, which is the main gateway to it, is completely blocked, what else can we do with pyruvate? Well, there's another enzyme called pyruvate decarboxylase, the main cofactor for which is biotin, which is vitamin B7. So if you have a buildup of pyruvate, you cannot go through pyruvate dehydrogenase. Maybe you can go through this other enzyme and still enter a Krebs cycle. Now, by the way, no matter which one of the steps of the Krebs cycle you enter, that's as good if you enter through pyruvate dehydrogenase. Basically, that's why it's called a cycle. Any of the intermediate metabolites in it are basically going to stimulate the rest of the cycle and then continue on to the end of the oxygen-phosphorylation. So why did I choose biotin?

### Source 6 — The Myths of Supplementation with Giorgi Dinkov

Georgi Dinkov · Interview · Oct 9, 2024 · https://www.youtube.com/watch?v=bHQnx-5PjFM

> **Georgi Dinkov:** So if you have a deficiency of biotin, again, you're going to have a buildup of electrons that are unused. And then it's going to create all kinds of problems. Initially, it will raise the levels of lactate. But then over time, like I said, excessive electrons can only go to... one of very few alternative pathways. One is synthesizing fat. Another one is basically using it to synthesize new tissue, but without control, the tissue can become problematic, grow out of control, right? And then the third thing is basically emergency oxidation by using some of the energy mediators such as pyruvate. And when pyruvate oxidizes NADH, when there's an excessive electrons, you get lactate. So you're going to get excess lactate, excess fat, or excessive growth somewhere if you have low metabolic rate or other causes that ultimately result in inability to process those extra electrons from food.

### Source 7 — A Bioenergetic View of Autoimmunity [Generative Energy #12]

Danny Roddy · Interview · Nov 10, 2015 · https://www.youtube.com/watch?v=veBLg1OwDJw

> **Danny Roddy:** And some people, you're talking about specific experiments and advanced stages of disease, but say you were relatively healthy, like egg yolks would be a good source of biotin, liver is a good source of biotin. You don't necessarily have to supplement all the things you're talking about.
>
> **Georgi Dinkov:** Yeah, I don't think you have to take them in the high doses that were used for clinical trial. These people have primary progressive multiple sclerosis. Basically, these people officially have about five years between diagnosis and needing a wheelchair, right? Or basically needing help with artificial breeding even sometimes because they get a paralysis of basically the trachea and the muscles that are responsible for breeding. So these were people that are in desperate condition. And in those people, 300 milligrams of biotin within six months reversed all of it. all of it right and then this is to me is a positive sign that there's a turnaround that i think people are starting to realize how wrong current medicine is the official at the conclusion of the study the official explanation was biotin dramatically improves the energetic status of the organism so there you have it biotin is one of the vitamins that Ray writes about too. Now, here's another important thing why you don't want to eat the egg whites. Not only are egg whites, because now they're very popular. Everybody eats egg whites because there's cholesterol, right? So we already talked about cholesterol, but I'll mention it for another reason. Cholesterol is vital for the functioning of your immune system. If you have low cholesterol, you can get symptoms of autoimmunity just by having low cholesterol. With low cholesterol, you can die from the flu. That's one of the primary purposes of cholesterol is to deactivate viruses that are invading your body. So And many people with autoimmune conditions are actually on cholesterol drugs because, you know, oh, it's bad cholesterol. It's going to give you cardiovascular disease. Anyways, so the reason you don't want to eat egg whites, two main reasons. First, you're getting an abnormally high amount of tryptophan. And that's the amino acid that will convert into serotonin in your body. And especially so in sick people.

### Source 8 — Sugar Doesn’t Cause Cancer with Georgi Dinkov

Georgi Dinkov · Interview · Oct 2, 2024 · https://www.youtube.com/watch?v=xXq4S2Dx_b8

> **Georgi Dinkov:** And by the way, keep in mind, the trials between starting with thiamine and reaching the biotin probably did seven or eight studies. We're basically like trying different dosages because, you know, I had to see what dosage works best. So maybe seven or eight studies that are encouraging, but failure. And now we have the biotin, which now the tumor is starting to regress. So it's flattening, it's reaching a certain plateau, which at that level, by the way, for a human case, will be considered a success because medicine is not trying to cure cancer. It's trying to convert into a chronic manageable disease so that your client for life. Many people say, well, that's just a conspiracy theory, Georgi. No, it's not. So there was a company, I'm blanking on the name, but they came up with a cure for hepatitis C. And they priced it like relatively steeply. I think it was like $80,000 to $100,000 per treatment. But of course, the insurance is going to cover most of that. And as soon as they did that, there was the chief analyst of Goldman Sachs, who was responsible for medical analysis, because they invest in, you know, obviously medical companies as well, came out with a blistering statement, said, short that company stock right now. That's the dumbest thing a medical company can do. And that analysis is on Forbes. I can send it to whoever wants it to. He said, the dumbest thing a medical company can do is kill its clients by curing them. So he's like, from a financial point of view, this makes absolutely no sense. So as soon as I started sending the article around to the people accusing me of conspiracy, some of whom are doctors, silence. So I said, OK, so we have three vitamins. We have a regression of a tumor, but not complete. What else can we do?

### Source 9 — #367 Cancer pt2. Inflammation, Metabolism, & Ozempic. With Georgi Dinkov & Alannah Connealy.

Georgi Dinkov · Interview · Mar 29, 2025

> **Georgi Dinkov:** Why would you use it? It's so dangerous. Then I started providing studies with patients with Crohn's disease, multiple sclerosis, cardiovascular disease, and they were actually given... four aspirin tablets daily, each tablet is 325 milligrams. That's right about 1.2, 1.3 grams, which is what they gave to the mice. And there was no side effects. So just, and I consider that like a super physiological, but not really pharmacological dose of aspirin like the one for rheumatoid arthritis. So as soon as I added the aspirin, I did another, so mind you, each one of these separate experiments, first, all the one would only be one. vitamin B1. Then one with only vitamin B3. Then one with only biotin, vitamin B7. Then started combining two of them. Then started combining three of them. And when the three of them stopped the tumor growth, I said, let's add aspirin to it. And as soon as I added the aspirin, and I posted this study on Twitter about a year ago. uh there were three mice um and then all three had the tumor completely disappeared there was initial growth but you know over time we had basically the tumor shrank uh to baseline and then even the scar tissue disappeared and the reason the scar tissue is that when they take the mice that have been immunocompromised they do a little incision in the skin and that's where they inject the tumor cells and then they stitch it up So it forms a little bit of a scar, right? There's scar tissue there. But with continued treatment, not only the tumor completely disappears, even the scar tissue disappears. And then I asked the lab to keep the mice alive and stop the treatment because, as you well know, in human trials, like when you go to a doctor, you have a tumor, they cut it out with surgery. Then you ask, am I cured? They said, no, you're in remission. And we can only declare you cured if you stay in remission for five years or more.

### Source 10 — The Metabolic Cancer Revolution with Dr. Thomas Seyfried, Georgi Dinkov

Georgi Dinkov · Interview · Apr 3, 2025

> **Georgi Dinkov:** And just using the vitamin B1 flattened the growth curve of the tumor compared to the animals that didn't get anything. So there was an effect there, but it wasn't sufficient. um and i said okay what else can be done well uh one of one of the reasons the peru the headquarters doesn't work aside from you know lacking timing is that it also depends on the mitochondrial redox ratio uh personified by the ratio of nad plus to nadh that ratio is low in cancer So in other words, cancer cells are in a state of a reduction, at least in their mitochondria. So in theory, raising that ratio, in other words, shifting it in favor of NAD+, should have beneficial effects, and that has also been known to be another factor controlling the activity of pyruvate hydrogenase. Lower ratio means lower activity of the enzyme. Higher ratio means higher activity of the enzyme. So it should be synergistic with thiamine, which is one of the cofactors for the enzyme as well. So they did a second study with just vitamin B1 and B3. And then that basically stopped the tumor from growing. The curve was completely flat. The control animals died after 14, 15 days. But it didn't cure it. And if you continue the administration long enough, eventually the tumor started growing again. So they said, okay, good, but not enough. What else can be done? And I found some studies showing that when pyruvate dehydrogenase is completely blocked, there is an alternative pathway into the Krebs cycle out of glycolysis. And that's another enzyme called pyruvate decarboxylase. And a cofactor for that one is the vitamin B7, also known as biotin. And there have been some very promising research with high-dose biotin recently showing that a really high pharmacological dose of about 300 milligrams daily, which is massive considering that the normal RDA requirements are about one milligram per day.

### Source 11 — The Metabolic Cancer Revolution with Dr. Thomas Seyfried, Georgi Dinkov

Georgi Dinkov · Interview · Apr 3, 2025

> **Georgi Dinkov:** So 300 milligrams daily stopped the progression of primary progressive multiple sclerosis, which is a really kind of like very aggressive form of multiple sclerosis that doesn't really, is not amiable to any treatment. These people usually they will share with a couple of years after diagnosis. So I think they did about 30 patients. And the results were remarkable. And the opinion of the researchers who published the paper said, we discovered a normalization of a number of different biomarkers related to oxidative pulsation. The pyruvate to lactate ratio increased. The NAD plus to the NADH ratio increased. The ratio of acetoacetate to hydroxybutyrate also increased. And the production of carbon dioxide also increased. So I said, okay, well, sounds like biotin is a mitochondrial nutrient. Let's try it out and see what happens with the three vitamins together. So with the three vitamins together, with biotin being administered in those roughly equivalent to what the people with multiple sclerosis got, the tumor actually started declining. The tumor growth started declining. We were experiencing regression. um and then i continued to study for as long as it was ethically reasonable because there they had these rules for how long the animals can be kept alive so the tumor growth was about a regress to about half of what it was originally but it didn't disappear And then I decided to add something else. Dr. Sievert, I'm sure you've seen, there's a tremendous amount of research on aspirin and cancer, mostly in regards to preventing cancer. But for some reason, these studies never address why aspirin actually has an effect on cancer or preventing cancer. Well, one thing is aspirin actually acidifies the cell, and we know the cancer cells are highly alkaline. When you acidify a defective cell, it usually commits apoptosis if it cannot recover. So that's one potential anti-cancer mechanism of aspirin.

_Generated 2026-07-20 from the Bioenergetic Oracle corpus._