ken
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- Joined
- Oct 31, 2012
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- 288
Lexis posted a link to an article about an Italian doctor doing a stint to drain blood from the Brian. As I recall he thought that iron built up or something.
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Lexis posted a link to an article about an Italian doctor doing a stint to drain blood from the Brian. As I recall he thought that iron built up or something.
Well, we'll have to wait for the results of the clinical trial to find out how biotin helped. In the meantime, I still maintain that it is the big increase in CO2 and ATP that I posted about in the biotin thread for controlling blood glucose. But I may be wrong...
OK, as I suspected, my original guess that biotin helped MS through improvement in ATP levels and oxidative metabolism has turned out to be correct. This follow up study, confirmed the results of the first one and explained that the primary mechanism of action of biotin in MS is through improvement of cellular energy status.
http://www.sciencedirect.com/science/ar ... 0815300733
"...However, evidence suggests that, in MS patients, axonal ATP production is simultaneously compromised due to defects in their neuronal mitochondria (Dutta et al., 2006, Mahad et al., 2009 and Su et al., 2009). The resulting imbalance between energy supply and energy demand causes a state of ‘virtual hypoxia’ which may be the trigger for neuron degeneration (Luessi et al., 2012 and Trapp and Stys, 2009). If insufficient ATP is available for Na+/K+ ATPase to restore the membrane potential, the neuron will enter a state of depolarization characterized by a further influx of Na+. This state can activate the Na+/Ca2+ exchanger in reverse mode, leading to an increase in intra-axonal Ca2+ as Na+ ions are removed from the neuron (Trapp and Stys, 2009). Excessive levels of Ca2+ in the neuron can activate a number of Ca2+-mediated degenerative pathways (Trapp and Stys, 2009). In chronic MS lesions, axonal levels of Na+/K+ ATPase are decreased, which may exacerbate the state of membrane depolarization (Young et al., 2008)."
"...We hypothesize that treatment with high-dose biotin reverses this state of virtual hypoxia through its role as a cofactor for PC, MCC, and PCC. These three enzymes are central to aerobic energy production and generate intermediates for the tricarboxylic acid (TCA) cycle (Fig. 3) (Tong, 2013). All three of these enzymes are known to be expressed in astrocytes and neurons (Ballhausen et al., 2009 and Hassel, 2000)...By increasing the available intraneuronal pool of ATP, high-dose biotin may reduce demyelinated neural dysfunction and the adverse effects of hypoxia (Lazzarino et al., 2010 and Trapp and Stys, 2009)."
This is pretty exciting, since it suggests that biotin can be used to reverse tissue hypoxia. The brain is the most sensitive organ to hypoxia and if biotin can reverse hypoxia there it should be able to reverse it anywhere else. Hypoxia is one of the primary triggers of cancer and one of the main drivers of cancer growth. I posted a study earlier this year showing that reversing tumor hypoxia is a possible cancer treatment.
viewtopic.php?f=123&t=6067
The reversal of hypoxia in tumors was done by opposing adenosine, so it suggests using caffeine. The MS study suggests that biotin can do the same, so combining caffeine and biotin can be synergistic for hypoxic conditions. High doses of thiamine, niacinamide, riboflavin and aspirin also have been shown to reverse hypoxia.
Now the bad news. The companies that ran the MS studies have applied to the FDA for designating high-dose biotin as a drug called MD1003.
http://www.bioworld.com/content/meddays ... -iii-trial
"...MD1003, a concentrated, patented, formulation of biotin (vitamin H), administered orally at 300 mg per day, was well tolerated. One patient in the treatment arm committed suicide but that was not considered to be related to the drug. It also emerged that MD1003 confounded immunoassay tests that use biotinylated antibodies or substrates."
"...MD1003 is thought to have a twofold effect, activating acetyl-CoA carboxylases that are the rate-limiting enzymes in the production of fatty acids required for myelin synthesis, and also activating the Krebs cycle in axons that have been demyelinated, increasing their energy supply."
"...Assuming positive results, there will be sufficient data to file for approval in Europe. "For the FDA we would have to discuss whether there needs to be a U.S. study or [if it will be sufficient] to show the data we have are applicable to a U.S. population," said Sedel."
As far as I can see the application is likely to be successful, which will lead to the FDA forcing biotin vendors to further lower the dose per capsule available in supplements. The current legal maximum is 10mg per capsule, which is already low enough to be inconvenient for use in MS. When MD1003 officially becomes a new drug, the biotin capsules will likely be limited to no more than 1mg per capsule in order to make self-medication with biotin impractical and very costly. I don't know if this will affect the powder vendors, but given the recent FDA action against caffeine powder vendors I would not be surprised if biotin powder vendors suffer the same fate.
Probably because 5mg needs a ***t ton of silicon dioxide.
Hey @TubZy, you obviously have first-hand experience that I'm looking for. I bought biotin to possibly fix my metabolism. However, there are tons of reports that biotin increases sebum production, but, unfortunately, I have sebum in excess already. Conversly, panthothenic acid is used to decrease sebum production.
What would you think is a good ratio of biotin-to-B5 ? And did you really mean microgram amounts (or rather milligram)? Thank you in advance!
. Malonyl-CoA also coordinates the balance between fatty acid synthesis and fatty acid oxidation. As cytosolic levels of malonyl-CoA increase, the rate of fatty acid synthesis increases; as peri-mitochondrial levels of malonyl-CoA from the reaction catalyzed by ACC2 increase, carnitine palmitoyltransferase 1 (CPT1) is inhibited and the rate of fatty acid transport into mitochondria decreases leading to reduced fatty acid beta oxidation (Foster, 2012; McGarry et al., 1978). Therefore, high-dose biotin may be acting as a promyelinogenic agent through its role as a cofactor for ACC1 and ACC2.
and high dose biotin can effect vitamin b5 status in body,it blocks b5 actions.i read something about that a while ago.should be careful about that if use heavy doses of biotin i guess.
From 'Nutrition for all the women out there':
"Very large doses of biotin cause experimental animals to develop fatty livers (developing into liver cancer), but this effect can be offset by feeding the animal another B vitamin, inositol."
"Biotin is involved in the synthesis of fats in the nervous system, and so should probably be given special attention in the MS [Microsoft] diet. Liver is a good source of it. If it is taken as a supplement, inositol (and probably choline) should be taken with it, because large doses of biotin by itself were toxic in animal experiments."