Best way to dose Biotin -

[Guest guest]

,

Thanks for all the good information.

I have been starting higher dose Biotin with (2000

mcg) to help with his yeast issue.

So far he has been tolerating it fine, and I have seen

reduction in yeasty symptoms.

Should Biotin be dosed all in the a.m. or spread throughout

the day?

Can it keep the kids up at night?

How do you know when the dose is right? Yeast testing?

Thanks for any information that you can give.

Lori

Re: Can biotin

cause yeast die-off?

Posted by:

" Owens " lwo@...

susancostenowens

Sat Jan 19, 2008 3:19 pm (PST)

,

You said:

>I believe biotin can cause yeast die-off from what I've seen on the

>other boards. we just started using it also.

That could happen, but I'd like to explain WHY it might happen and some

other things it would be good to know about biotin.

Biotin is a cofactor for a whole class of enzymes called carboxylases that

are used by us and our flora.

Biotin works as a swinging arm inside those molecules which allows the

enzymes to do their job. Carboxylases (and also some biotin-dependent

decarboxylases, especially in bacteria) have many functions, but the best

way to understand those functions is to look at the list of things that

might happen to you if you have biotin deficiency or a deficiency of the

enzyme that recycles biotin or another reason for these enzymes to be

impaired..

One influence we've just learned about in recent years is oxalate, a very

reactive molecule found to be high in some plant foods that if it gets

absorbed through a leaky gut, and finds a carboxylase enzyme, it will

replace another cofactor in the enzyme complex that usually hooks to biotin

and makes the enzyme work. Unfortunately, the oxalate keeps that swinging

arm from accomplishing the job of the enzyme.

Because there are so many ways that biotin's job can be hindered,it is

sometimes appropriate to take biotin in doses that are far higher than the

RDA and it is not unusual for an effective dose to get as high as 10

mgs. Having greater than normal amounts of biotin around will help most of

these problems, but it is also a very good idea to spend some time figuring

out what caused the biotin problem in the first place and see if you can

correct that. Ideas about that are below!

Here is a list of things that go wrong in biotin deficiency and you will

notice it includes problems with yeast infections which finally gets to

your question! The problems with yeast are believed to derive from a lack

of proper immune defense agains candida. What might change in regards to

yeast when you've taken biotin is that the immune system may be suddenly

enabled to start to recognize the problem in overgrowth and start to kill

the candida. That may explain the die-off that did not come from using any

anti-anything medicine, but instead from enabling immune defense. You have

to wonder why that immune defense is so often not up to the task of keeping

yeast within bounds in autism and some other conditions.

Anyway, this is a list of other biotin-deficiency related symptoms:

hypotonia

ataxia

hair loss (alopecia)

seizures

encephalopathy

neurodevelopmental delay

motor limb weakness

loss of visual acuity

hearing loss

chronic candidiasis

Immunological deficiencies especially cellular immunity abnormalities

Breathing abnormalities including apnea, hyperventilation, and laryngeal

stridor.

swallowing difficulties

jaundice

secretory diarrhea

eczematous and other skin rashes (dermatitis)

metabolic acidosis

ketolacticacidosis

hemianopia

optic atrophy

Leigh syndrome

spastic paraparesis

The lab test for biotin deficiency finds the following elevated in a

urinary organic acid test, but you won't see all these reported on typical

OATs we get in the autism community:

3-Methylcrotonylglycine

3-Hydroxyisovaleric acid

3-Hydroxypropionic acid

Methylcitric acid

The carboxylase enzymes also need CoA, which is a product of pantothenic

acid and cysteine and ADP. That means if there is not enough

intracellular cysteine around to make enough CoA, biotin-dependent enzymes

may not work well and you might also see some problems with energy.

Apparently, one of the mechanisms that might break down with low

intracellular biotin might be the handling of the ammonia that is produced

when glutamine is converted into glutamate: an important step for the

making of inhibitory GABA and for making glutathione.

I think that the people who are most likely to respond to biotin are those

who have used biotin depleters. This can include anticonvulsants such as

phenytoin, primidone, carbamezepine, and phenobarbital which may incease

urinary excretion of biotin. Valproic acid or depakote can cause

biotinidase deficiency, which is a problem in recycling biotin. I have yet

to meet a child with autism on depakote that progressed with biomedical

interventions as much as other children, and I wonder if this might be why.

I would like to also mentione alpha lipoic acid because it competes with

biotin for transport, as discussed in an article below. That means the

biotin you got from your diet or from your flora may not have competed well

for absorption in the gut or for reabsorption in the kidneys, and that may

mean that your would-have-been adequate biotin may have ended up in the

toilet. For children who were biotin depleted because of use of

antibiotics which killed their biotin-making flora or because of being on

depakote, this loss of reabsorption may have more serious consequences.

There are tests to measure lack of activity of certain biotin dependent

carboxylases, mainly using the organic acid profile. It seems

3-hydroxyisovaleric acid is the first one that moves during deficiency, but

the others come " online " if you get really deficient or under stress.

Here

below I've put a listing of the different carboxylases, and which markers

are associated with deficient activity of each one.

These enzymes may have a lot of organ specificity, because we know that

some people with biotin-responsive conditions in the brain have not had

these markers in the urine so don't assume if you lack these markers that

biotin won't do you some good.

For those who want to know more, there is a mini-section on biotin that I

wrote a number of years ago that was included in the very back of the DAN!

manual that was written and edited by Jon Pangborn and Sid Baker.

I hope this helps.

Enzyme

Acetyl-CoA Carboxylase (cytosolic active ACC1 and mitochondrially active ACC2)

*most enhanced by supplement of biotin

sensitive to insulin

Reaction

ATP+ acetyl-CoA+ HCO(3)(-) <=>ADP+ phosphate + malonyl-CoA

Organic acid deficiency marker:

elevated hexanoic acid

including 2-ethyl-3-keto-hexanoic

2-ethyl-3-hydroxy-hexanoic acid

2-ethyl-hexanedioic acid

---------------------------------------------------

Enzyme

Pyruvate Carboxylase

Reaction

ATP+ pyruvate+ HCO(3)(-) <=>ADP+ phosphate + oxaloacetate

Deficiency markers:

lactic acidemia

hyperammonemia, and citrullinemia

hyperlysinemia

decreased beta hydroxybutyrate/acetoacetate ratio

------------------------------------------------------

Enzyme

propionyl-CoA carboxylase

Reaction catalyzed

(S)-2-methyl-3-oxopropanoyl-CoA <=> propanoyl-CoA + CO(2)

Deficiency marker in organic acid profile:

elevated 3-hydroxypropionic acid

elevated methylcitrate

--------------------------------------------------------

Enzyme

beta-methylcrotonyl-CoA carboxylase

Reaction

ATP+ 3-methylcrotonyl-CoA + HCO(3)(-)

<=>ADP+ phosphate + 3-methylglutaconyl-CoA

Organic acid deficiency marker:

elevated 3-Methylcrotonylglycine

elevated 3-Hydroxyisovaleric acid

also: secondary carnitine deficiency

--------------------------------------------------------

J Gastroenterol 1995 Jun;30(3):351-5 Related Articles, Books, LinkOut

Effect of biotin on ammonia intoxication in rats and mice.

Nagamine T, Saito S, Kaneko M, Sekiguchi T, Sugimoto H, Takehara K,

Takagi H.

First Department of Internal Medicine, Gunma

University School

of

Medicine, Maebashi, Japan.

The effects of biotin on ammonia concentration in blood and brain were

evaluated in hyperammonemic rats and mice. Rats were injected with 5

mmol/kg BW of ammonium acetate, and mice were injected with 10 mmol/kg BW.

Increases in blood ammonia levels in rats 15-30 min after ammonia loading

were prevented by treatment with 0.2 ml/100 g BW of biotin or 0.04 ml/100 g

BW of arginine-glutamate with statistical significance. Blood ammonia

levels after ammonia loading were lower, although not significantly, in the

arginine glutamate-treated rats than in the biotin-treated animals. In mice

also, increases in blood and brain ammonia levels after ammonia loading

were prevented by the administration of biotin. The decrease in brain

glutamate and aspartate after ammonia loading was lower and the brain

glutamine level was higher in biotin-treated mice than in the controls.

These findings indicate the protective effect of biotin against ammonia

intoxication.

PMID: 7647902 [PubMed - indexed for MEDLINE]

J Nutr 1997 Sep;127(9):1776-81 Related Articles, Books, LinkOut

[Click here to read]

Lipoic acid reduces the activities of biotin-dependent carboxylases in

rat liver.

Zempleni J, Trusty TA, Mock DM.

Department of Pediatrics, University of Arkansas for Medical Sciences

and the Arkansas Children's Hospital Research Institute, Little Rock, AR

72202, USA.

In the past, lipoic acid has been administered to patients and test

animals as therapy for diabetic neuropathy and various intoxications.

Lipoic acid and the vitamin biotin have structural similarities. We sought

to determine whether the chronic administration of lipoic acid affects the

activities of biotin-dependent carboxylases. For 28 d, rats received daily

intraperitoneal injections of one of the following: 1) a small dose of

lipoic acid [4.3 micromol/( kg.d)]; 2) a large dose of lipoic acid [15.6

micromol/(kg.d)]; or 3) a large dose of lipoic acid plus biotin [15.6 and

2.0 micromol/(kg.d), respectively]. Another group received n-hexanoic

acid

[14.5 micromol/(kg.d)], which has structural similarities to lipoic acid

and biotin and thus served as a control for the specificity of lipoic acid.

A fifth group received phosphatidylcholine in saline injections and served

as the vehicle control. The rat livers were assayed for the activities of

acetyl-CoA carboxylase, pyruvate carboxylase, propionyl-CoA carboxylase,

and beta-methylcrotonyl-CoA carboxylase. Urine was analyzed for lipoic

acid; serum was analyzed for indicators of liver damage and metabolic

aberrations. The mean activities of pyruvate carboxylase and

beta-methylcrotonyl-CoA carboxylase were 28-36% lower in the lipoic

acid-treated rats compared with vehicle controls (P < 0.05). Rats treated

with lipoic acid plus biotin had normal carboxylase activities. Carboxylase

activities in livers of n-hexanoic acid-treated rats were normal despite

some evidence of liver injury. Propionyl-CoA carboxylase and acetyl-CoA

carboxylase were not significantly affected by administration of lipoic

acid. This study provides evidence consistent with the hypothesis that

chronic administration of lipoic acid lowers the activities of pyruvate

carboxylase and beta-methylcrotonyl-CoA carboxylase in vivo by competing

with biotin.

PMID: 9278559 [PubMed - indexed for MEDLINE]

At 01:04 PM 1/19/2008, you wrote:

>Hi ,

>

>I believe biotin can cause yeast die-off from what I've seen on the

>other boards. we just started using it also.

>

>