animal deletes his thread

[Animalkits]

Admins feel free to comment on the fraud being perpetuated as you are now liars.

 

[Animalkits]

Also, if you don't have ANY insulin receptors, I'd say that's about the best insulin resistant you could be.

See how he twists stuff! I know used car salesman that aren't that bad.

 

[macro]

Also, if you don't have ANY insulin receptors, I'd say that's about the best insulin resistant you could be.

See how he twists stuff! I know used car salesman that aren't that bad.

insulin resistant and not having an insulin receptor in the tissue at all are quite different.

if you are insulin resistant it take more insulin to activate the signaling. Signalling that effects a lot more than fat storage at least in a human adult. if you have insulin resistant fat your body will produce more insulin to compensate.

now these mice have no receptor, none since birth (they were engineered that way). Their system is an adaptated one. If you were FIRKO from birth you would probably be fine as your system would adapt. However, to introduce fat specific insulin resistance into a adult human system will result in diabetes. If you were to make your self FIRKO, who knows what the impact would be...

they are two totally different things.

 

[Animalkits]

I think they plainly stated in english what the results are. I guess they are wrong.

Although FIRKO mice show insulin resistance in the adipose tissue, whole-body glucose metabolism is not affected.

BTW, fire or chemical resistant means what?

You don't catch on fire!

You seem to missing the point that I said it would be GREAT to be insulin resistant in the fat cells and there just so happens to be a study showing no adverse affects.

 

[macro]

I think they plainly stated in english what the results are. I guess they are wrong.

Although FIRKO mice show insulin resistance in the adipose tissue, whole-body glucose metabolism is not affected.

BTW, fire or chemical resistant means what?

You don't catch on fire!

You seem to missing the point that I said it would be GREAT to be insulin resistant in the fat cells and there just so happens to be a study showing no adverse affects.

if that quote were from the study.

unfortunately its from this article
http://www.signaling-gateway.org/update/updates/200209/nrd902.html

now the effect of insulin resistant fat cells on the other hand, this quote actually from the study

The role of white adipose tissue in overall glucose homeostasis is not clear. Although some studies suggest that adipose tissue in humans may metabolize up to 20% of an orally administered glucose load (Janssonet al., 1994; Kashiwagi et al., 1983), euglycemic hyperin-sulinemic clamp studies in rats indicate that adipose
tissue is responsible for only 3%–5% of glucose uptake
(James et al., 1985).Onthe other hand, adipose selective
inactivation of the GLUT4 gene causes glucose intolerance and hyperinsulinemia, and induces secondary alterations
in insulin action in muscle and liver (Abel et
al., 2001).

 

[Ifrit]

This has to be the longest a thread has gone with just two guys dukin it out,lol. You guys are nuts.

 

[TxLonghorn]

admin did not delete the thread. you did.

I haven't deleted any thread by animal...but I have edited several of his posts that called people jackasses and other similar things...this is not tolerated, nor is it called for.

I would like to thank ulter and macro for not going down the same path... instead they post up peer reviewed articles and other factual statements to support their arguments. I would like to urge animal to do the same in the future...I do not like having to continuously edit posts for ad hominem attacks

 

[Animalkits]

You might want to look at the all the 'stupid, idiot, fool, uneducated, etc in their posts and let's not forget who was posting pictures and personal information out.

Anyhow, I've gotten out all the info and exposed this for what it is and you can now do what you want with the info. You wanna believe studies on diabetics, obese, and post menopausal women, it's your $ lost. I'm done.

 

[Animalkits]

And hopefully you can also point out how I miraculously hacked into the board and reposted my thread to the frauds. They can't even lie good! And why would I delete a thread where I was right, anyhow.

At least they are good for a laugh. I'm training for world cup trials and olympic qualifiers while having moved to another state to do so for 3 months and I only have so much time for humor.

 

[EngiCream]

I haven't deleted any thread by animal...but I have edited several of his posts that called people jackasses and other similar things...this is not tolerated, nor is it called for.

I would like to thank ulter and macro for not going down the same path...

Might wanna edit the first post in this thread by Macro.

 

[SWALE]

Is it too late to inject a legitimate question into this thread?

Has anyone ever shown ALA to be effective in individuals who are NOT insulin resistent? That would seem to me to be a very important thing to consider.

At an Anti-Aging conference I recently spoke at, one of the other lecturers, a lady doc who possesses THREE Board Certifications (!) said that 600mg of ALA per day has been shown to depress thyroid function. I have not had time to research this, and am hoping someone else can?

 

[macro]

At an Anti-Aging conference I recently spoke at, one of the other lecturers, a lady doc who possesses THREE Board Certifications (!) said that 600mg of ALA per day has been shown to depress thyroid function. I have not had time to research this, and am hoping someone else can?

she probably misinterpreted this study on exogenous T4 use

Arzneimittelforschung. 1991 Dec;41(12):1294-8. Related Articles, Links


Effect of alpha-lipoic acid on the peripheral conversion of thyroxine to triiodothyronine and on serum lipid-, protein- and glucose levels.

Segermann J, Hotze A, Ulrich H, Rao GS.

Institute of Clinical Biochemistry, University of Bonn, Fed. Rep. of Germany.

The influence of alpha-lipoic acid (LA, thioctic acid, CAS 62-46-4) on thyroid hormone metabolism and serum lipid-, protein- and glucose levels was investigated. In the first setup of experiments administration of LA together with thyroxine (T4) for 9 days suppressed the T4 induced increase of T3 generation by 56%. This suppression was similar to that affected by 6-propylthiouracil (54%). LA or T4 alone did not affect the cholesterol level, but together they led to a reduction. LA decreased the triglyceride level by 45%; the decrease induced by T4 or LA plus T4 was not significant. Total protein and albumin levels decreased by LA plus T4 treatment when compared to the LA control. The slight increase in glucose level by LA or T4 alone was not observed when they were administered together. In the second setup of experiments the administration of T4 for 22 days increased the serum T3 level 3-fold. When LA was combined with T4 and the treatment continued, the T3 production decreased by 22%. T4 reduced cholesterol level by 30%, and LA plus T4 further reduced it by 47%. The triglycerides were not affected. A moderate decrease in total protein was observed after treatment with T4 plus LA; T4 and LA plus T4 decreased the albumin level. The decrease in serum glucose by T4 recovers by LA treatment. These results demonstrate that LA interferes with the production of T3 from T4 when it is co-administered with T4. The elevated level of T3, after T4 administration, is reduced by treatment with LA.

 

[Drveejay11]

Is it too late to inject a legitimate question into this thread?

Has anyone ever shown ALA to be effective in individuals who are NOT insulin resistent? That would seem to me to be a very important thing to consider.

At an Anti-Aging conference I recently spoke at, one of the other lecturers, a lady doc who possesses THREE Board Certifications (!) said that 600mg of ALA per day has been shown to depress thyroid function. I have not had time to research this, and am hoping someone else can?

Well, if in fact r-ALA DOES clear glucose efficiently, THIS obviously results in lowered insulin release...which should translate to LESS T4-T3 coversion as a direct result of the decreased glucose circulation. I believe MACRO stated that this decrease in converted T3 is compensated by a rise in Somatomedin which has lipolytic activity independant of insulin/glucagon pathways. So, it SOMEWHAT becomes a NON-issue (with respect to fat loss anyway).

 

[macro]

J Oral Pathol Med. 2002 May;31(5):267-9. Related Articles, Links


Burning mouth syndrome (BMS): double blind controlled study of alpha-lipoic acid (thioctic acid) therapy.

Femiano F, Scully C.

Stomatology Clinic II, University of Medicine and Surgery, Napoli, Italy. femiano@libero.it

BACKGROUND: Burning mouth syndrome (BMS) has features of a neuropathy and could be related to the production of the toxic free radicals that are released in stress situations. Alpha-lipoic acid is an antioxidant able to increase the levels of intracellular glutathione and eliminate free radicals. This study aimed to examine the effectiveness of alpha-lipoic acid in the therapy of BMS. METHOD: This was a double blind, controlled study conducted for two months on 60 patients with constant BMS. Comparing alpha-lipoic acid (test) with cellulose starch (placebo), there was no laboratory evidence of deficiencies in iron, vitamins or thyroid function and no hyperglycaemia. RESULTS AND CONCLUSION: Following treatment with alpha-lipoic acid, there was a significant symptomatic improvement, compared with placebo, with the majority showing at least some improvement after 2 months, thus supporting the hypothesis that burning mouth syndrome is a neuropathy. This improvement was maintained in over 70% of patients at the 1 year follow-up

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


though will look more closely at the t4-t3 issue when time allows.

 

[Drveejay11]

Sweet.....r-ALA for BMS too...........why have you been holding out on this one? LOL..........

 

[dude]

Why the hell is everyone always fighting about R-ALA?! It is always the same people. If your product is good then it will get the good reviews that it should from the majority of people who use it and I would think you wouldn't need to be so defensive about it. I've never used R-ALA and don't plan to but I will say that these types of posts where there are such strong views upholding the value of their product makes me not want to buy it even more.

 

[Ifrit]

Sadly I agree with dude.

 

[heregothere]

ditto.

a good product will sell itself and definitely doesn't need studies dated from the early 90s to back up its efficacy.

 

[Animalkits]

I don't really sell it and why would I rip into a product that I could make big $ on?

It's about using it at the right time for the right reason.

If you are a glucose pig and think you are insulin resistant and don't believe exercise sensitizes you to insulin and you love to eat sugar all day every day, then it's a good way to spend your money.

I'd also call you a lazy ass for not controlling your food intake/style. The main point of all this is that goofs are fucking themselves up with piss poor diets and then thinking a pill is gonna solve it. Good luck.

BTW, if you keep eating like shit and take it, it's will still back fire on you over time. Much research is well documented in showing that when people get a metabolic increase they just eat more. When something is low fat or low carb, they just eat MORe!

So people will take their magic little fix and then eat more....................

 

[SWALE]

So ALA reduces T3 levels in the hyperthyrpoid state. What are its effcets regarding same in the euthyroidic individual.

It is an unwarranted leap in logic to say that an increase in IGF-1 "compensates" for a decrease in T3, though, just to be sure we are limiting claims to fat-loss. The overlap between the effects of these homones are not all inclusive.

Once again, is there any proof of ALA's claimed effcets in non-insulin resistant individuals?