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ALA dosing info!!!

CRNT93

New member
I know many here advocate taking 1000-2000mg a day
of ALA but check out what AST says:

Q. What should my dosage be with ALA?

We recommend taking 200 milligrams (1 capsule) 3 times daily with meals. Research has shown that 200 milligrams increases blood levels of ALA the same as 600 milligrams, so there is no need to take more than 200 milligrams at any one time. Also 600 milligrams daily has been shown to be just as effective at muscle glucose uptake as 1200 milligrams per day so therefore there appears to be no need to take more than 600 milligrams per day.




http://www.ast-ss.com/Products/ala/qa/ala_qa-6.asp
 
why is it better?I mean blood levels are the same
whether you take 200 or 600 per dose.If it doesn't get
into circulation it can't do no good anyway.
 
No never did that...please explain what you mean.
Are you saying you can feel how your liver is doing?
I don't think so....bro,you better explain.
 
ultragainz said:
we are talking about the liver....you ever try ALA at 1000mgs when hitting high amounts of orals like d-bol?

How about var at 40-50mg? 500mg ALA enough? Gets damn expensive. More than my actual cycle.
 
I think i'm beginning to sound like a broken record.

ALA dosage DEPENDS on CARB INTAKE.

Low carbs= Less ALA
High Carbs= MORE ALA

For liver, dosage should range from 600mg to 1000mg
DEPENDING on the amount of 17-aa's being used.

600mg is the MINIMUM daily dosage for a THERAPEUTIC
effect to be seen in regards to blood glucose
levels and liver function.

Any less, and the ALA is a complete waste for BB'ing
purposes. At <600mg, ALA is only good for
an anti-oxidant effect.

So,

1g/lb carbs or less: 600mg
2-3g/lb of carbs: 1000mg
5g+ of carbs: 1400-2000mg(ALA at high dosage is VERY
BENEFICIAL during the carb-up phase of a CKD as
it increases the amount of nutrients that enter
the muscle-cell)

Fonz
 
CRNT93 said:
No never did that...please explain what you mean.
Are you saying you can feel how your liver is doing?
I don't think so....bro,you better explain.

you can't feel it but you can see it.... when you start turning yellow from jaundice... 600-1000mg for liver support when taking 17-aa orals
 
Once again,if it is true what AST says,that
600mg's raise levels just as well as 1200mg
then why would the higher dosage be better?

Fonz,is what you claim based on some research
or is it just something you came up with yourself?

IF IT DOESN'T ABSORB IT CAN'T DO NO GOOD!!!

It would make sense to me to stack 600mg with some
NAC instead to boost glutathione levels.
 
CRNT93 said:
Once again,if it is true what AST says,that
600mg's raise levels just as well as 1200mg
then why would the higher dosage be better?

Fonz,is what you claim based on some research
or is it just something you came up with yourself?

IF IT DOESN'T ABSORB IT CAN'T DO NO GOOD!!!

It would make sense to me to stack 600mg with some
NAC instead to boost glutathione levels.

is AST the only source you have or believe in? Also is AST's recommendation based on someone that is or is not taking steroids?
 
CRNT93 said:
Once again,if it is true what AST says,that
600mg's raise levels just as well as 1200mg
then why would the higher dosage be better?

Fonz,is what you claim based on some research
or is it just something you came up with yourself?


IF IT DOESN'T ABSORB IT CAN'T DO NO GOOD!!!

It would make sense to me to stack 600mg with some
NAC instead to boost glutathione levels.



I can't wait to see what Fonz says to that lol
 
CRNT93 said:
If Fonz can back up what he is saying I'll be
happy to hear it.

Oct.2001, I see........

Oh well. You sound very naive. Nearly all
supplement companies twist the data
to make their supplements look better.
Anyways, since I'm in Spain at the moment
I have access to my 5GB removable HD
which is absolutely full of studies about pretty
much everything.

So here goes, you might actually learn something cionstructive
today.

1: Am J Physiol 1997 Jul;273(1 Pt 1):E185-91 Related Articles, LinkOut, Books


Differential effects of lipoic acid stereoisomers on glucose metabolism in insulin-resistant skeletal muscle.

Streeper RS, Henriksen EJ, Jacob S, Hokama JY, Fogt DL, Tritschler HJ.

Department of Physiology, University of Arizona, Tucson 85721-0093, USA.

The racemic mixture of the antioxidant alpha-lipoic acid (ALA) enhances insulin-stimulated glucose metabolism in insulin-resistant humans and animals. We determined the individual effects of the pure R-(+) and S-(-) enantiomers of ALA on glucose metabolism in skeletal muscle of an animal model of insulin resistance, hyperinsulinemia, and dyslipidemia:

R-(+) ALA is the common stereo-isomer used in all
Lipoic acid products btw.

the obese Zucker (fa/fa) rat. Obese rats were treated intraperitoneally acutely (100 mg/kg body wt for 1 h) or chronically [10 days with 30 mg/kg of R-(+)-ALA or 50 mg/kg of S-

Geee........30mg/Kg Thats 3000mg for a 100kg BB'er.

(-)-ALA]. Glucose transport [2-deoxyglucose (2-DG) uptake], glycogen synthesis, and glucose oxidation were determined in the epitrochlearis muscles in the absence or presence of insulin (13.3 nM). Acutely, R-(+)-ALA increased insulin-mediated 2-DG-uptake by 64% (P < 0.05), whereas S-(-)-ALA had no significant effect. Although chronic R-(+)-ALA treatment significantly reduced plasma insulin (17%) and free fatty acids (FFA; 35%) relative to vehicle-treated obese animals, S-(-)-ALA treatment further increased insulin (15%) and had no effect on FFA. Insulin-stimulated 2-DG uptake was increased by 65% by chronic R-(+)-ALA treatment, whereas S-(-)-ALA administration resulted in only a 29% improvement. Chronic R-(+)-ALA treatment elicited a 26% increase in insulin-stimulated glycogen synthesis and a 33% enhancement of insulin-stimulated glucose oxidation. No significant increase in these parameters was observed after S-(-)-ALA treatment. Glucose transporter (GLUT-4) protein was unchanged after chronic R-(+)-ALA treatment but was reduced to 81 +/- 6% of obese control with S-(-)-ALA treatment. Therefore, chronic parenteral treatment with the antioxidant ALA enhances insulin-stimulated glucose transport and non-oxidative and oxidative glucose metabolism in insulin-resistant rat skeletal muscle, with the R-(+) enantiomer being much more effective than the S-(-) enantiomer.

PMID: 9252495 [PubMed - indexed for MEDLINE]

Now, here's the correlation between ALA and carb-intake
(Which raises insulin levels)

1: Life Sci 1997;61(8):805-12 Related Articles, Books, LinkOut


Stimulation by alpha-lipoic acid of glucose transport activity in skeletal muscle of lean and obese Zucker rats.

Henriksen EJ, Jacob S, Streeper RS, Fogt DL, Hokama JY, Tritschler HJ.

Department of Physiology, University of Arizona, Tucson 85721-0093, USA. [email protected]

Alpha-lipoic acid (ALA), a potent biological antioxidant, improves insulin action of skeletal muscle glucose transport and metabolism in both human and animal models of insulin resistance. In order to obtain further insight into the potential intracellular mechanisms for the action of ALA on insulin-stimulated glucose transport in skeletal muscle, we investigated the effects of direct incubation with ALA (2 mM) on 2-deoxyglucose (2-DG) uptake by epitrochlearis muscle from either insulin-sensitive lean (Fa/-) or insulin-resistant obese (fa/fa) Zucker rats. ALA stimulated 2-DG uptake in muscle of lean animals by 76%, whereas ALA stimulated 2-DG uptake by only 48% in muscle from obese animals. The stimulation of 2-DG uptake due to ALA was enhanced 30-55% in the presence of insulin. In contrast, ALA action on 2-DG uptake was not additive with the effects of electrically-stimulated muscle contractions in either insulin-sensitive or insulin-resistant muscle. Wortmannin (1 microM), an inhibitor of phosphotidylinositol-3-kinase, completely inhibited insulin action on 2-DG uptake, but inhibited ALA action by only 25%.

And the point is:

Collectively, these results indicate that although a portion of ALA action on glucose transport in mammalian skeletal muscle is mediated via the insulin signal transduction pathway, the majority of the direct effect of ALA on skeletal muscle glucose transport is insulin-independent.

Stress on the INSULIN-DEPENDENT.....

PMID: 9275010 [PubMed - indexed for MEDLINE]

And another regarding MAXIMUM THERAPEUTIC LEVEL...

1: Diabetes 1996 Aug;45(8):1024-9 Related Articles, LinkOut, Books


The antioxidant alpha-lipoic acid enhances insulin-stimulated glucose metabolism in insulin-resistant rat skeletal muscle.

Jacob S, Streeper RS, Fogt DL, Hokama JY, Tritschler HJ, Dietze GJ, Henriksen EJ.

Department of Physiology, University of Arizona College of Medicine, Tucson, USA.

Insulin resistance of muscle glucose metabolism is a hallmark of NIDDM. The obese Zucker (fa/fa) rat--an animal model of muscle insulin resistance--was used to test whether acute (100 mg/kg body wt for 1 h) and chronic (5-100 mg/kg for 10 days) parenteral treatments with a racemic mixture of the antioxidant alpha-lipoic acid (ALA) could improve glucose metabolism in insulin-resistant skeletal muscle. Glucose transport activity (assessed by net 2-deoxyglucose [2-DG] uptake), net glycogen synthesis, and glucose oxidation were determined in the isolated epitrochlearis muscles in the absence or presence of insulin (13.3 nmol/l). Severe insulin resistance of 2-DG uptake, glycogen synthesis, and glucose oxidation was observed in muscle from the vehicle-treated obese rats compared with muscle from vehicle-treated lean (Fa/-) rats.

Here it comes.....

Acute and chronic treatments (30 mg.kg-1.day-1, a maximally effective dose) with ALA significantly (P < 0.05) improved insulin-mediated 2-DG uptake in epitrochlearis muscles from the obese

Thats 30mg/Kg again.....

rats by 62 and 64%, respectively. Chronic ALA treatment increased both insulin-stimulated glucose oxidation (33%) and glycogen synthesis (38%) and was associated with a significantly greater (21%) in vivo muscle glycogen concentration. These adaptive responses after chronic ALA administration were also associated with significantly lower (15-17%) plasma levels of insulin and free fatty acids. No significant effects on glucose transporter (GLUT4) protein level or on the activities of hexokinase and citrate synthase were observed. Collectively, these findings indicate that parenteral administration of the antioxidant ALA significantly enhances the capacity of the insulin-stimulatable glucose transport system and of both oxidative and nonoxidative pathways of glucose metabolism in insulin-resistant rat skeletal muscle.

PMID: 8690147 [PubMed - indexed for MEDLINE]


And for future reading..........which just might be
the next generation of glucose disposal type
products.




1: Antioxid Redox Signal 1999 Winter;1(4):523-35 Related Articles, Books


Metabolic effects of gamma-linolenic acid-alpha-lipoic acid conjugate in streptozotocin diabetic rats.

Khamaisi M, Rudich A, Beeri I, Pessler D, Friger M, Gavrilov V, Tritschler H, Bashan N.

Department of Clinical Biochemistry, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.

Data suggesting the involvement of increased oxidative stress in the pathophysiology of diabetes has raised interest in the potential therapeutic benefit of antioxidants. Although beneficial metabolic effects of antioxidant supplementation have been suggested, an antioxidant mode of action, particularly in skeletal muscle, has not been documented. In the present study, we evaluate the metabolic effects of a gamma-linolenic acid-alpha-lipoic acid conjugate (GLA-LA) in streptozotocin-induced diabetic rats, and assess its potential mode of action by comparing its effects with equimolar administration of LA and GLA alone. Ten days of oral supplementation of 20 mg/kg body weight GLA-LA, but not LA or GLA alone, caused a mild reduction in fasting blood glucose concentration as compared with vehicle-treated diabetic rats (375 +/- 11 vs. 416 +/- 16 mg/dl, p = 0.03), with no change in fasting plasma insulin levels. A peripheral insulin-sensitizing effect could be observed with GLA-LA, LA, and GLA treatments, as demonstrated by a significant (p < 0.04) 23%, 13%, and 10% reduction, respectively, in the area under the glucose curve following an intravenous insulin tolerance test. This effect was associated with a 67% and 50% increase in GLUT4 protein content in the membranes of gastrocnemius muscle of GLA-LA and LA-treated animals, respectively; however, no change was observed with GLA treatment alone. Interestingly, both GLA-LA and LA treatments corrected a diabetes-related decrease in the gastrocnemius muscle low-molecular-weight reduced thiols content. These data demonstrate insulin-sensitizing properties of the GLA-LA conjugate by distinct mechanisms attributable to each of its components, which are associated with antioxidant effects.

PMID: 11233149 [PubMed - indexed for MEDLINE]

Seems like a GLA-ALA conjugate is superior to ALA
by quite a margin.
Supplement companies seem to have largely
ignored this fact.

Fonz
 
Just a side note guys.. AST isn't the most honest company.. They don't even "distribute" (aka "make") there own products. They buy it off of other companys. For example: there ANDRO is comes straight from ERGO PHARM ..

bye
mb
 
Okay,these studies were on rats and
as we all know it doesn't always mean
it works the same,or that the same dosage
is required or even tolerated in humans.
Why don't you recommend 3000mg then?
I mean that's what was effective here,right?
You still haven't explained why 1000mg is better
than 600.
Also,these studies were on glucose metabolism,
not on antioxidant or liver protecting action.
I think,but am not certain,that there are studies
performed on HUMANS out of germany available
and those would be much more relevant in this case.
The GLA connection seems interesting though.

Fonz,you see it's not me who is ignorant.If you want to
extrapolate data like that I have some animal clenbuterol studies
you can try on yourself:)
 
CRNT93 said:
Okay,these studies were on rats and
as we all know it doesn't always mean
it works the same,or that the same dosage
is required or even tolerated in humans.
Why don't you recommend 3000mg then?
I mean that's what was effective here,right?
You still haven't explained why 1000mg is better
than 600.
Also,these studies were on glucose metabolism,
not on antioxidant or liver protecting action.
I think,but am not certain,that there are studies
performed on HUMANS out of germany available
and those would be much more relevant in this case.
The GLA connection seems interesting though.

Fonz,you see it's not me who is ignorant.If you want to
extrapolate data like that I have some animal clenbuterol studies
you can try on yourself:)

You seem to have missed the correlation.

Its what we call an asymptotal curve.

As ALA dosage increases, glucose disposals
rate of change(or derrivative) at a certain
dosage approaches zero.

While 3000mg will stimulate glucose disposal by say
X.
2000mg will stimulate it by 90% X
1000mg by 40% X

And so on.....

So, the actual question is, are you willing to increase
your dosage of ALA to 3000mg/day instead of 2000mg/day
for a 10% increase in effectiveness? It really is a cost
vs productiveness analisis.

Some people just want to strive for perfection.
This board is all about MAXIMIZING every single
mg of every supplemment so that it is better
used by your body.

One thing(Very important) that you failed to mention
is that ALA, since its both FAT and water soluble is
present BOTH inside the cells and outside the cells.
So, while there will be an amount in the blood-stream,
THERE WILL ALSO BE A FAIR AMOUNT INSIDE THE
CELLS THEMSELVES, which is not measurable by
a simple blood assay. And ALA works when its
INSIDE THE CELL. So, a blood assay really
doesn't give you a good perspective about the
reall effectiveness of ALA.

Hence, what AST is saying is scientifically unsound.
However, how many people out there actually
understand the science?

Very Few. Hence they will get away with it.

And I do have those german studies, BUT how many
people here actually speak german?

I suggest you look under the name THIOCTIC ACID, which was used in the 60's and 70's instead of the modern name Alpha-lipoic Acid, because it was thought to be a simple B-Vitamin.

In reference to its Hepatocyte-regenarating properties,
it is a simple of case of more muscle cells need more
ALA than liver cells, which in comparison to muscle
cells are relatively few.

Fonz
 
Last edited:
can anyone comment if the ALA from kilosports is any good? I heard some products are more potent than others.
thanks.
 
Fonz,I know results don't always increase linearly.
ALA being fat soluble is a good point.
However,the liver protecting properties are
related to the glutathione boosting effect,I think.
Saturating the cells doesn't therefore seem to be
the goal.
Some anti-oxidants actually become PRO-oxidants when
taken in too high dosages(CoQ10).It would make sense
to me then to stack it with NAC,vitamin C,Milk Thistle etc.
for maximum effect instead of boatloading just one of them.

I will see if I can find the German studies...
 
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