A friend of mine who suggested I adopt bone broth into my diet to heal my gut knows I’m a ketogenic eater, and sent me this. Apparently there is concern about lack of vitamin B/thiamin in a ketogenic diet that treats for seizures. I myself eat plenty of red meat and supplement with vitamin B so I don’t think that would ever be an issue.
My eye doctor saw that I had a diabetic neuropathy dot in my eye earlier this year, but within 5 weeks it was completely gone. Soooo… I’m not sure what all the fuss is about.
I have not supplemented with Vitamin B, but just started because I’m taking a regimen to help with fatty liver, and they recommended B vitamins. But never too them before now and have been low carb almost 5 years. Like you, I eat a lot of beef, beef liver, beef heart, etc.
I’ve heard that metformin can make you B12 depleted, so any t2d’s taking metformin may want to look into that. I’ve started adding nutritional yeast to my scrambled eggs, it’s delicious, nutritious and a great source of b vitamins.
I think another difference may also be in the fat solubility and water solubility of vitamins being administered and how long it is in the circulation and not a lack of the B complex vitamins but the ability to absorb them through the gut and a more fat soluble form of a particular vitamin to penetrate the myelin sheath and get into the nucleus of the nerve cell to regenerate it?
“…Specifically, the methylcobalamin (like in fat soluble grass fed livestock?) form of vitamin B-12 could increase the production of proteins that regenerate nerve cells, which is particularly useful for the myelin sheath. …” …More
Re: Receptor proteins: A key difference between water-soluble and fat-soluble hormones is that: •Water-soluble hormones bind to receptors on the surface of the target cell, while •Fat-soluble hormones bind to receptors inside the target cell. Hence water-soluble hormones can affect cells without actually entering the target cell while fat-soluble hormones first pass through the cell membrane, then go on to enter the nucleus of the cell in order to adjust its biochemical activity. Note: A cell may have several different receptors that recognize the same hormoneand activate different signal transduction pathways. Alternatively, a cell may have several different receptors that recognize different hormones and activate the same biochemical pathway (see also metabolic pathways and characteristics of metabolic pathways). …” …More
This might be more about a biotin deficiency, as biotin deficiency can affect thiamine status. Biotin deficiency is not uncommon in the ketogenic diet because gluconeogenesis increases the need for biotin.
The biotin deficiency might be more common in people with seizures, not sure, just a thought.
Things going on in the gut can affect biotin status, also if one has the genetics for biotinidase deficiency, biotin deficiency is almost guaranteed.
I saw a study of a case study of a child who had severe thiamine deficiency that was cured with biotin alone.
The place where I read about gluconeogenesis increasing need of biotin was in reference to a rash which sounds similar to keto rash. It said that increasing carbs is a way to cure the rash. So maybe increasing carbs to supply adequate glucose decreases the need for biotin because of gluconeogenesis, but maybe a diet very high in carbs also increases the need for biotin. I don’t know. I am pretty sure that a diet high in processed carbs increases the need for thiamine. I should look this up but I’m running out of energy at the moment.
Looking at these articles, the impression I’ve come away with is that saying that gluconeogenesis increases the need for biotin is backward, or upside-down, or something. The first article is a review discussing the use of biotin to inhibit gluconeogenesis in type I diabetics:
The second article reports an experiment (n = 90) on using biotin to inhibit gluconeogenesis in rats:
The third article purports to show that gluconeogenesis worsens biotin deficiency in rats (n = 32) that were already biotin-deficient:
I’m not sure how much value to place in the third article. For one thing, this sounds like a preliminary study, and the sample-size is small. Secondly, I’m not sure that I agree with the logic chain. And thirdly, it’s a mouse model, so it’s not clear exactly what this implies for biotin-deficient human beings. And I don’t believe it says anything about the effect on biotin in mice or people that are not biotin-deficient.
I’m going to bed now. Will take a look at the rest of my PubMed search tomorrow, and see if anything interesting turned up.
Very interesting articles. I have to run out to do some errands, I’ll reread them when I get home, after I feed and take out the dogs and get the laundry started.
I find this stuff so interesting it’s hard to take care of my house.
Just one quick thought that I will probably think about while driving is, why does administration of biotin or raising carbs both have the same effect on the rash caused by ketosis?
Oh wait, the original presumption that gluconeogenesis uses up biotin is wrong, the correct conclusion for it helping should have been that it shuts down gluconeogenesis?
Well, this study may have part of the answer. It looked at effects of biotin deficiency in a yeast species, in a nematode species, and in lab rats, and found that severe lack of biotin inhibits glycolysis and lipolysis, and promotes fatty acid β-oxidation and gluconeogenesis, even in the presence of abundant glucose. In other words, it appears that biotin starvation causes the body to ignore dietary glucose and act ketogenically. The authors speculate that because the same mechanism exists in such widely diverse species, it is quite possible that it also exists in human beings.
I am coming to the conclusion that, far from gluconeogenesis causing biotin deficiency, biotin deficiency enables gluconeogenesis and ketogenesis. High levels of biotin inhibit both processes, which I consider to be rather undesirable in nutritional ketosis.
