In my opinion, vitamin K supplementation is potentially very dangerous, and I'm actually doubting, at this point, if vitamin K is even essential. It doesn't behave at all like an essential nutrient, in my view, but that's just my opinion. There's research showing that geranylgeraniol, an intermediate in cholesterol biosynthesis, possesses vitamin K activity (see Ronden et al., 1997: (http://hardcorephysiologyfun.blogspot.com/2009/06/squalene-as-potential-cholesterol.html)], and I wonder if there isn't some endogenous ligand for the vitamin K-cycle enzymes. The whole business with squalene 2,3-epoxide being an intermediate in cholesterol biosynthesis and vitamin K epoxide being a vitamin K cycle intermediate seems like it might also suggest that endogenous compounds can be utilized for the gamma-carboxylation of glutamic acid residues on vitamin K dependent proteins. There's also research discussing the extremely low amounts of vitamin K that are required for humans to manufacture clotting factors, and, in fact, the amounts are so tiny as to make the notion of the essentiality of vitamin K more or less "not valid," in my opinion. I don't buy it anymore. The vitamin K nonsense in the literature has bothered me for a long time and defies all attempts to integrate it into anything resembling "nutritional" science. The facts that vitamin K decreases des-carboxyprothrombin levels and under-gamma-carboxylated osteocalcin aren't evidence of essentiality. In any case, vitamin K supplementation has the potential to not only exacerbate thrombotic conditions or lead to de novo thromboses by elevating levels of serum prothrombin and other clotting factors, in any number of disease states, but to also cause thrombogenic effects by exotic mechanisms, such as by inducing osteoclast precursor cell apoptosis, etc. Obviously, one would want to discuss these things with one's doctor, but there's all this research on vitamin K that looks good on paper but just becomes very bizarre on closer examination. Why would an essential nutrient cause osteoclast apoptosis or potentially cause such serious effects? In any case, I don't think it's essential, and this leads into another point. I should note that the vitamin K topics are not pleasant to write about.
In my opinion, coenzyme Q10 can exhibit vitamin K activity, and there's a lot of indirect evidence that it can. Riboflavin, or vitamin B2, can also enhance the activities of vitamin K dependent enzymes by providing the FAD cofactor for vitamin K reductase(s). There's evidence that quinone reductases or other cytosolic enzymes can utilize coenzyme Q10 and increase clotting factor biosynthesis. In my view, these facts seriously compromise the usefulness of CoQ10 or high-dose vitamin B2. I personally do not take coenzyme Q10 and only take a minimal dosage of vitamin B2, and the potential I see for problems with high doses of vitamin B3, vitamin B6, and vitamin B2 has caused me to not even be able to use a B-complex or multivitamin. In the case of multivitamins, all of the copper and zinc and manganese and vitamin A or beta-carotene are also reasons I don't use them. CoQ10 is also a benzoquinone, and benzoquinones are known to be highly reactive. One would want to discuss these things with one's doctor, but, in my view, there are plenty of energy substrates or other "agents" that could potentially substitute for CoQ10 as approaches to dealing with mitochondrial dysfunction in people who do not have mitochondrial disorders that require supplementation with CoQ10.
In my opinion, the large numbers of cases of intracranial hemorrhage in people taking some Ginkgo biloba extracts (GBEs) seriously compromises their usefulness, and there are, potentially, similar risks with high doses of supplemental omega-3 fatty acids. The numbers of case reports showing hemorrhages in people taking GBEs sort of speak for themselves, and there's no way of really evaluating the hemorrhagic risks of any degree of antagonism of platelet activating factor (PAF) receptors by GBE constituents, such as ginkgolide B and ginkgolides A and C and bilobalide. All of those are PAF receptor antagonists, and ginkgolide B is potent enough to be utilized as a pharmacological PAF receptor antagonist in in vitro research, etc. As far as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), the major omega-3 fatty acids that are supplied in supplements, I don't know what the answer is. EPA and DHA are really reactive and have been shown to cause problems in animal models of fatty liver disease, but they're obviously essential and can have a lot of beneficial effects. One strategy might be to obtain small amounts of them in omega-3 egg yolk phospholipids, but I don't quite understand why hard-boiling eggs doesn't destroy all of the docosahexaenoyl- and eicosapentaenoyl-containing phospholipids. I also don't understand why egg yolk phospholipids, which supply choline in the form of sphingomyelin, more than phosphatidylcholine, do not cause depression, in my view, but supplemental phosphatidylcholine and other choline-containing compounds have been shown to cause severe depression in some humans. I think it might be that the sphingomyelin is utilized differently or that the elevations in plasma choline that result from egg-yolk phospholipid administration are not rapid enough to flood the brain with free choline and cause ATP depletion or inorganic phosphate sequestration, etc., thereby potentially causing depression. The omega-3 issues are really complex, and I don't really get into them much in my blog.
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