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low biotin, fat synthesis and gluconeogenesis.

learner2life

David Pain
Messages
71
Location
Tijuana-San Jose, Ca
For the last year I haven't been able to regain any reasonable amount of fat to help hide my tendons and ligaments on my hands and wrists. I took acetyl l carnitine out of desperation to help gain energy but this may have contributed to my biotin deficiency. Once I added mb12 then the fat really went away.

Biotin is a component of the acetyl CoA carboxylase enzyme. This enzyme converts acetyl coA to Malonyl-CoA.
http://en.wikipedia.org/wiki/Acetyl-CoA_carboxylase

Malonyl-CoA is a highly-regulated molecule in fatty acid synthesis; as such, it inhibits the rate-limiting step in beta-oxidation of fatty acids. Malonyl CoA inhibits fatty acids from associating with carnitine by regulating the enzyme carnitine acyltransferase, thereby preventing them from entering the mitochondria where fatty acid oxidation and degradation occur.

So to limit the use of the carnitine induced oxidation, malonyl-CoA is trying to prevent the fatty acids from being oxidized. The biotin is used to help create the malonyl CoA. It sounds like that this reaction would be enough to create a biotin deficiency honestly. You are feeding fatty acids into b oxidation thru the use of carnitine all the while your body may be trying to hold onto the fatty acids thru the use of a biotin related enzyme.

Another point to make is the reactions with pyruvate. Pyruvate carboxylase is a biotin dependent enzyme that is used in the first chain of gluconeogenesis reactions. This probably isn't the best reaction for us to make, but I think because of the high ketones that I saw on my test results it is probably used extensively just trying to survive sometimes. But, the drawback too is this enzyme is used to help control blood glucose levels and other things. I doubt it would explain my hypoglycemic symptoms but it could play a role in it.
 

learner2life

David Pain
Messages
71
Location
Tijuana-San Jose, Ca
just continuing on with my thread.
So, I have been adding about 50mg of biotin in hopes of preparing myself for the addition of copper. I feel I have a copper deficiency aswell. The biotin has helped stabilize me in some way. I wouldn't say I have any more energy per se, but I don't feel on the fringe of collapse sometimes and overwhelmed.

Would this be enough to conclude that if the biotin stores were replenished then fatty acid synthesis would ensue. Would it be a stretch to think this would help with my thyroid issues and help relieve the stress on my adrenals and lead to an overall better sense of well being. I don't know what the biotin stores are, I read they are widespread in the endoplasmic reticulum. But, these are some interesting points I am trying to discover. Also, would it help my hormones as well. There are alot of questions here but the biotin relationship seems fairly reasonable. It would explain the very low reading in comparison to normal readings of everything else. There is still alot of what if's but it seems reasonable.
David
 

learner2life

David Pain
Messages
71
Location
Tijuana-San Jose, Ca
Hmm, rereading my first post is seems very abstract. Here are some good links to help give some insight into the acetyl CoA...


The citric acid cycle. How many times have we all been to this link?
http://en.wikipedia.org/wiki/Citric_acid_cycle

Pyruvate dehydrogenase complex. This is the transformation of pyruvate right to Acetyl CoA. Thiamin and fad are involved with it.
http://en.wikipedia.org/wiki/Pyruvate_dehydrogenase_complex

Pyruvate carboxylase, biotin, manganese and magnesium used.
http://en.wikipedia.org/wiki/Pyruvate_dehydrogenase_complex

http://en.wikipedia.org/wiki/Gluconeogenesis

http://en.wikipedia.org/wiki/Fatty_acid_synthesis

Some of this info might aid some people who are very fat deficient to finally gain fats. There is still alot of things I need to look up but it's pretty interesting.
David
 

xks201

Senior Member
Messages
740
This is more info than anyone here probably will comprehend. I've found CFS responds better to hormone replacement than anything...specifically T3.

You are talking about enzymes that detox the body in the liver that are biotin dependent. It's all great. I've tried mega doses of all vitamins and nothing works except t3 daily and replacing all the deficient hormones.
 

determined

Senior Member
Messages
307
Location
USA: Deep South
Thanks for this, learner2life! I have a new plan to try to learn a bit more about CFS every day, and your post is at the top of my list. Yes, it's complicated but there is so much power in knowledge, especially for us!
 

learner2life

David Pain
Messages
71
Location
Tijuana-San Jose, Ca
I came across a post that said that friendly bacteria can produce biotin which is also needed to suppress the growth of candida by not allowing it to change into the fungal form. So, according to what I've read candida overgrowth can cause a biotin deficiency. I didn't know that, just wanted to share.
Thanks.
David
 

Radio

Senior Member
Messages
453
Hmm, rereading my first post is seems very abstract. Here are some good links to help give some insight into the acetyl CoA...


The citric acid cycle. How many times have we all been to this link?
http://en.wikipedia.org/wiki/Citric_acid_cycle

Pyruvate dehydrogenase complex. This is the transformation of pyruvate right to Acetyl CoA. Thiamin and fad are involved with it.
http://en.wikipedia.org/wiki/Pyruvate_dehydrogenase_complex

Pyruvate carboxylase, biotin, manganese and magnesium used.
http://en.wikipedia.org/wiki/Pyruvate_dehydrogenase_complex

http://en.wikipedia.org/wiki/Gluconeogenesis

http://en.wikipedia.org/wiki/Fatty_acid_synthesis

Some of this info might aid some people who are very fat deficient to finally gain fats. There is still alot of things I need to look up but it's pretty interesting.
David
Check This out.... (one of a very few Vitamin B12-dependent enzymes)???

Propionyl-CoA carboxylase
catalyses the carboxylation reaction of propionyl CoA in the mitochondrial matrix. The enzyme is biotin-dependent. The product of the reaction is (S)-methylmalonyl CoA. Propionyl CoA is the end product of metabolism of odd-chain fatty acids, and is also a metabolite of most methyl-branched fatty acids. It is also the main metabolite of valine, and together with acetyl-CoA, is a metabolite of isoleucine, as well as a methionine metabolite. Propionyl-CoA is thus of great importance as a glucose precursor. (S)-Methylmalonyl-CoA is not directly utilizable by animals; it is acted on by a racemase to give (R)-methylmalonyl-CoA. The latter is converted by methylmalonyl-CoA mutase (one of a very few Vitamin B12-dependent enzymes) to give succinyl-CoA. The latter is converted to oxaloacetate and then malate in the Krebs cycle. Export of malate into the cytosol leads to formation of oxaloacetate, phosphoenol pyruvate, and other gluconeogenic intermediates.

B12 could be the main cause of the biotin problem...MTR, MTRR gene defect?

Biotin is a big player in healing...Check out the protocol i used to completely recover from CFS...

NT factor / Simplified protocol
1,000-5,000 B12 Methylcobalamin, B12 Adenosylcobalamin 1-2xday. (Lower the dose if you have COMT +/+ , Every-other-day)
Solgar 400mcg Metafolin 1-3xday.
Potassium Gluconate 500mg 2-4xday
Jarrow carntine 600 2xday
Jarrow Formulas, Borage GLA oil 1-2xday (Great Anti-inflammatory, bypass the Delta(6)-desaturase gene-defect)
NT Factor (Nutri cology Nt factor) powder 2-4xday, you could try (Smart youthful energy) (Repairs Mitochondria)
Now foods, COQ 10 Ubiquinol 100mg
Now foods super enzymes take with NT Factor 2-4xday
Now foods Magnesium citrate 200mg 2-3xday
Now Foods Biotin 5000mcg 1xday (repairs nerves and helps make key aminos acids)
Now Foods Vitamin D-3 5,000iu 1-2xday
Pure encapsulations Trace mineral 1-2xday (Minerals make B-Vitamins active)
Source naturals Coenzymated B-2, B-3 25mg 1-2x day. (Bypass MAO Gene, B-3 makes NADH)
Seeking Health Probiota Maximum Support Dairy-free probiotic 50 Billion CFU's (Best Mast-cell probiotic, Help make B vitamins)

(NO Vitamin B-6) <-- (Over-drives CBS Pathway and prevents neuropathy and nerve demyelination from healing)

The first critical step is healing the mitochondria and eating a super clean diet. The key is to give the methylation cycle a break and eat the right foods with the least amount of metabolic waste. ( low animal protein foods ) Also, i wanted to add that digestive support is recommended when supplementing with NT factor. I take (Now foods super enzymes). I've had great success implementing the low histamine chef diet, combined with a low protein paleo diet.

The Mitochondria becomes damaged and leaky from an overload of metabolic waste.
NT Factor is a blend of phospholipids and glycolipids whose mechanism of action is to repair cellular membranes by increasing cell membrane fluidity. By repairing the membranes of the mitochondria , we allow our cells to increase their nutrient uptake so that the mitochondria may product more ATP.


Phospholipids Sources
Egg yolks, liver, wheat germ and peanuts contain the phospholipid lecithin. Your body can only synthesize lecithin if you have sufficient choline in your diet, however. You can also find phospholipids in soy, milk and lightly cooked meats. Most fats, oils and fat-containing foods contain phospholipids as well.
 
Last edited:

douglasmich

Senior Member
Messages
311
Check This out.... (one of a very few Vitamin B12-dependent enzymes)???

Propionyl-CoA carboxylase
catalyses the carboxylation reaction of propionyl CoA in the mitochondrial matrix. The enzyme is biotin-dependent. The product of the reaction is (S)-methylmalonyl CoA. Propionyl CoA is the end product of metabolism of odd-chain fatty acids, and is also a metabolite of most methyl-branched fatty acids. It is also the main metabolite of valine, and together with acetyl-CoA, is a metabolite of isoleucine, as well as a methionine metabolite. Propionyl-CoA is thus of great importance as a glucose precursor. (S)-Methylmalonyl-CoA is not directly utilizable by animals; it is acted on by a racemase to give (R)-methylmalonyl-CoA. The latter is converted by methylmalonyl-CoA mutase (one of a very few Vitamin B12-dependent enzymes) to give succinyl-CoA. The latter is converted to oxaloacetate and then malate in the Krebs cycle. Export of malate into the cytosol leads to formation of oxaloacetate, phosphoenol pyruvate, and other gluconeogenic intermediates.

B12 could be the main cause of the biotin problem...MTR, MTRR gene defect?

Biotin is a big player in healing...Check out the protocol i used to completely recover from CFS...

NT factor / Simplified protocol
1,000-5,000 B12 Methylcobalamin, B12 Adenosylcobalamin 1-2xday. (Lower the dose if you have COMT +/+ , Every-other-day)
Solgar 400mcg Metafolin 1-3xday.
Potassium Gluconate 500mg 2-4xday
Jarrow carntine 600 2xday
Jarrow Formulas, Borage GLA oil 1-2xday (Great Anti-inflammatory, bypass the Delta(6)-desaturase gene-defect)
NT Factor (Nutri cology Nt factor) powder 2-4xday, you could try (Smart youthful energy) (Repairs Mitochondria)
Now foods, COQ 10 Ubiquinol 100mg
Now foods super enzymes take with NT Factor 2-4xday
Now foods Magnesium citrate 200mg 2-3xday
Now Foods Biotin 5000mcg 1xday (repairs nerves and helps make key aminos acids)
Now Foods Vitamin D-3 5,000iu 1-2xday
Pure encapsulations Trace mineral 1-2xday (Minerals make B-Vitamins active)
Source naturals Coenzymated B-2, B-3 25mg 1-2x day. (Bypass MAO Gene, B-3 makes NADH)
Seeking Health Probiota Maximum Support Dairy-free probiotic 50 Billion CFU's (Best Mast-cell probiotic, Help make B vitamins)

(NO Vitamin B-6) <-- (Over-drives CBS Pathway and prevents neuropathy and nerve demyelination from healing)

The first critical step is healing the mitochondria and eating a super clean diet. The key is to give the methylation cycle a break and eat the right foods with the least amount of metabolic waste. ( low animal protein foods ) Also, i wanted to add that digestive support is recommended when supplementing with NT factor. I take (Now foods super enzymes). I've had great success implementing the low histamine chef diet, combined with a low protein paleo diet.

The Mitochondria becomes damaged and leaky from an overload of metabolic waste.
NT Factor is a blend of phospholipids and glycolipids whose mechanism of action is to repair cellular membranes by increasing cell membrane fluidity. By repairing the membranes of the mitochondria , we allow our cells to increase their nutrient uptake so that the mitochondria may product more ATP.


Phospholipids Sources
Egg yolks, liver, wheat germ and peanuts contain the phospholipid lecithin. Your body can only synthesize lecithin if you have sufficient choline in your diet, however. You can also find phospholipids in soy, milk and lightly cooked meats. Most fats, oils and fat-containing foods contain phospholipids as well.


please PM me. I had MTR + MTRR
 

Violeta

Senior Member
Messages
2,895
I know, I just found his posts recently and was finding them very informative.

I am having the same problem as the original poster and nothing seems to help, it just keeps getting worse.
 
Last edited:

Violeta

Senior Member
Messages
2,895
I recently started taking biotin and had been wondering if it's good to take lysine along with it since biotin in food usually contains lysine. It enters the body as biocytin and biotinidase breaks it down to it's constituents. If you have partial biotinidase deficiency, as I saw Radio describe it, you could end up being deficient in both. I also tried to find out if/how lysine might play into the same cycle as biotin, and I just got started on that last night. Lysine is part of acetyl CoA.

Biotinidase deficiency supposedly can be affected by oxalates, and I don't know if/how that would work, but if so, candida in the gut producing oxalates inhibits biotin deficiency by first of all using biotin and secondly by reducing biotinidase.

That would cause a worsening of biotin deficiency, and somewhat of a lysine deficiency. Lysine being important for building muscle and bone.

Biotin deficiency can cause build up of iron on the cellular level and at the same time heme-a deficiency. Heme-a deficiency impairs Complex IV, (I hope I have the # correct), which of course impairs ATP production, which of course would leave one short of energy.

I might have more in my brain but I have to get ready for work.

So this is all starting to tie together for me, but I would have appreciated Radio's input.
 
Messages
27
Location
Russia
When I was taking biotin as most people do (just swallow) - I did not notice improvements of my brain energy level. But when I opened the capsule (10000 mcg by Solgar) and took the powder under the tongue - I noticed much improvements almost immediately (just after 1 to 5 minutes)! So that is how I live now, holding the powder under the tongue almost all the time. If you are interested in details, you may look at my first thread.
 

keenly

Senior Member
Messages
814
Location
UK
For the last year I haven't been able to regain any reasonable amount of fat to help hide my tendons and ligaments on my hands and wrists. I took acetyl l carnitine out of desperation to help gain energy but this may have contributed to my biotin deficiency. Once I added mb12 then the fat really went away.

Biotin is a component of the acetyl CoA carboxylase enzyme. This enzyme converts acetyl coA to Malonyl-CoA.
http://en.wikipedia.org/wiki/Acetyl-CoA_carboxylase

Malonyl-CoA is a highly-regulated molecule in fatty acid synthesis; as such, it inhibits the rate-limiting step in beta-oxidation of fatty acids. Malonyl CoA inhibits fatty acids from associating with carnitine by regulating the enzyme carnitine acyltransferase, thereby preventing them from entering the mitochondria where fatty acid oxidation and degradation occur.

So to limit the use of the carnitine induced oxidation, malonyl-CoA is trying to prevent the fatty acids from being oxidized. The biotin is used to help create the malonyl CoA. It sounds like that this reaction would be enough to create a biotin deficiency honestly. You are feeding fatty acids into b oxidation thru the use of carnitine all the while your body may be trying to hold onto the fatty acids thru the use of a biotin related enzyme.

Another point to make is the reactions with pyruvate. Pyruvate carboxylase is a biotin dependent enzyme that is used in the first chain of gluconeogenesis reactions. This probably isn't the best reaction for us to make, but I think because of the high ketones that I saw on my test results it is probably used extensively just trying to survive sometimes. But, the drawback too is this enzyme is used to help control blood glucose levels and other things. I doubt it would explain my hypoglycemic symptoms but it could play a role in it.

Makes sense as to why Dr Yasko tells people to add Biotin when using cartinine and the likes of butyric acid. At what dose is the question?
 
Messages
1
For background, I'm trying to find the cause of my idiopathic, whole body, sensory neuropathy.

Whole exome testing turned up that I'm a carrier of the primary biotinidase deficiency variant.

BTD: c.1330G>C* rs13078881

Biotinidase is the enzyme that allows your body to make use of biotin in food sources. On a reference scale of 4.8 to 12.0, my biotinidase levels are 4.9. The foremost researcher on Biotinidase Deficiency (BD) actually called me twice and explained that I'm not clinically deficient by definition, but said he also wouldn't say my low levels had nothing to do with my problems.

I've decided to supplement with Meribin biotin supplements which are the OTC supplements recommended for biotinidase deficient children and adults. I feel like my symptoms have improved somewhat, but that could just be the usual wax and wane I experience. What has definitely happened, though, is that a bad patch of skin has cleared up, and I have significant new hair growth. (My hairdresser noticed, and I never mentioned the biotin to her.) I also am losing weight, which is a good thing.

I'm trying to figure out if if low biotinidase levels, perhaps in conjunction with other problems are the root cause of my neuropathy. I also have glucose issues, both too high and too low, and can't metabolize alcohol any longer.