D-Biotin, not necessary for Lipoic Acid??

I recommend reading the whole article:

Question: “Several companies selling R-lipoic acid or alpha lipoic acid claim it is essential to take supplemental biotin with lipoic acid products. Why doesn’t GeroNova add biotin to their products? Since biotin is cheap and might be beneficial, why don’t you recommend people take it with lipoic acid?”

Answer: I call this issue the “lipoic acid–biotin mandate”. Scientists, doctors and companies making claims for the necessity of supplemental biotin with lipoic acid use made this determination after reading the conclusions of a single study by Zempleni et al1 issuing strong warnings to lipoic acid users with inherited carboxylase (the biotin-dependent enzymes) deficiencies that was I believe inappropriately extrapolated to the general lipoic acid using public. This article is frequently cited and is the first reference to appear on the lipoic acid page on encyclopedia.com.

Surprisingly, Zempleni et al did NOT recommend supplemental biotin either for people with or without carboxylase deficiencies. I speculate on the possible reasons for this omission below.

Source: http://www.geronova.com/content/lipoic-acid-biotin

This study is not from Zempleni et al. Also, the role in biotin and blood sugar and hair growth is important.

J Invest Dermatol. 2003 Mar;120(3):428-33.
Transport of biotin in human keratinocytes.

Grafe F, Wohlrab W, Neubert RH, Brandsch M.

Biozentrum of the Martin-Luther-University, Membrane Transport Group, Institute of Pharmaceutics and Biopharmaceutics, Martin-Luther-University Halle-Wittenberg, Halle, Germany.

Comment in:

* J Invest Dermatol. 2003 Mar;120(3):xi-xii.

Biotin is an essential micronutrient for normal cellular function, growth, and development. Biotin deficiency leads to pathologic, dermatologic, and neurocutaneous manifestations in skin and its appendages. Previous studies described the presence of specific biotin transport systems in the epithelia of the intestine, liver, kidney, and placenta, and in blood mononuclear cells. The aim of this study was to examine biotin transport into human keratinocytes. Uptake of [3H]biotin was measured both in the HaCaT cell line and in native keratinocytes in primary culture. Uptake of [3H]biotin (6 nM) in HaCaT cells was linear for up to 5 min of incubation. In the presence of an Na+ gradient total biotin uptake was 4- to 5-fold higher than in the absence of sodium ions. Biotin uptake was not altered by H+ and Cl- gradients. This transport system exhibited a Michaelis-Menten constant for biotin of 22.7+/-1.0 microM and a maximal velocity of 163.6+/-3.5 pmol per 5 min per mg protein. [3H]Biotin uptake (6 nM) was strongly inhibited by lipoic acid (oxidized form, Ki=4.6 microM; reduced form, Ki=11.4 microM), pantothenic acid (Ki=1.2 microM), and desthiobiotin (Ki=15.2 microM), but not by biocytin or biotin methyl ester. Measured at [3H]biotin concentrations of 0.1-10 nM we obtained kinetic evidence for the presence of a second transport component that is saturable at very low biotin concentrations (Kt=2.6+/-0.1 nM). Unlabeled lipoic acid and pantothenic acid (20 nM) did not inhibit the [3H]biotin uptake (1 nM). We conclude that human keratinocytes express the Na+-dependent multivitamin transporter with preference for pantothenate and a very high affinity transport component with specificity for biotin.

Interesting, thanks CS!

However, one thing pointed out in her article...she said that they shouldn't be taken together, because they share some of the same transporation mechanisms or something in the body. So, in other words, it may be better to take d-Biotin at a different time than at the same time as R-Lipoic Acid so they don't compete for the same pathways.

My stomach hurts a bit when I take them at the same time.

nidhogge - For the most part agree with their position on biotin, however a number of problems can contribute to its deficiency. Use of accutane, antibiotics, anticonvulsants, etc. Extra biotin is a good safe guard and improves glucose metabolism.

A little offtopic but here is a good post at the low oxalate forum regarding biotin and oxalates

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"This last week I came across a study that shows that oxalates impair the
function of biotin-dependent enzymes called carboxylases.

This study looks at the "ping-pong" exchange reactions between
propionyl-CoA and Methylmalonyl-CoA and between pyruvate and
oxaloacetate. Oxalate is considered an analogue of oxaloacetate, but it
was found that oxalate inhibits both of these reactions and was proposed to
inhibit all carboxylases similarly.

The study, after analyzing kinetic data, proposed that there are two places
for the biotin binding site in carboxylases which are adjacent to the two
substrate sites, and that the presence of oxalate impairs the migration of
biotin between the two sites, which would affect the completion of the dual
reaction. Basically, by making biotin unavailable for both sides of the
reaction, oxalate impairs these carboxylase reactions, producing effects
that may look like biotin deficiency.

The paper says: "Trapping of biotin by oxalate may be a cooperative event;
ie. uncarboxylated biotin bound near the keto acid site appears to be
necessary for the binding of oxalate."

It is not clear (because they didn't look at it) that adding extra biotin
in this situation would help but getting rid of the excess oxalate would
probably help.

What are the implications? The presence of excess oxalate may need to be
assessed before assuming a biotin deficiency in someone with impaired
carboxylase function....especially if all the carboxylases seem relatively
weak. We might find that the impairment of these enzymes with oxalate
would not be as severe as you would see in the genetic disorder
holocarboxylase synthetase deficiency, or in biotinidase deficiency, but if
oxalates are the problem, we might find that this situation would be less
responsive to correction with biotin."

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"Q. Why does low oxalate diet help with yeast overgrowth?

> I have two theories on this. The first is that oxalate inhibits
> biotin-dependent carboxylase activity. People who have genetic problems
> with the same enzymes have awful problems with yeast overgrowth. It is
> thought that the ability of the immune system to control yeast is
> compromised when you have poor carboxylase activity.
>
> Also, if you step back and think about the purpose of fungi in the earth,
> it is generally to break down biological material that has died. How does
> it recognize that something has died and it is time for the fungi to get
> busy degrading? Probably there are chemical signals, and perhaps those
> signals are present in those who are susceptible to yeast infection."