CLA dosage

tai4ji2x

New Member
if i'm already taking flax and fish oils, do i still need to take in 6-10g of CLA to get an effect from it? or could i stretch out my purchase with just 3 or 4g a day?
 
Dear tai4ji2x,

The effective therapeutic dosage for CLA is 3.4gm per day. Check the label on your CLA bottle - how much CLA is contained per capsule? Then take as many capsules necessary to get your 3.4gm per day.

This is regardless of how much fish/flax oil you are taking.

Godspeed, and happy HSTing :)
 
bryan? anyone? further comments? sorry for prodding.
tounge.gif
 
ok, bryan seems to have answered my original question re: CLA in the fish oil thread. but i have one more, for anyone who might have advice:

should CLA be counted in my daily caloric intake, given that i'm trying to have it after a meal and actually have it act as "excess" calories so as to make it get stored as fat?
 
heh, looks like my final question didn't get answered.
tounge.gif
well, i got another one as well now... :D

- is it better to take small amounts of CLA, spread out over several meals? or will just taking your desired daily dosage with just one or two meals be okay (given that the meals are large enough to satiate oneself)?
 
interesting thought. Apparently, CLA is 'burnt' primarily before the eccess makes it to the fat cells. So perhaps eating larger doses would ensure that more gets to the fat cells. perhaps taking lots of small doses spread throughout the day would simply get burt up. Anyone?
 
I didn't like CLA. I took it for a while (6 months).

It did seem to stabilize my body weight.

However, when I got back to the bulking phase and I had difficulty gaining muscle weight. Eventually, my weight started moving upwards, but I was not gaining that much muscle ...

My conclusion is that CLA makes body insulin "insensitive" for both fat AND muscle. [Like a hard gainer]. This is consistent with a number of pubmed abstracts on this -- increased insulin insensitivity in muscles due to CLA administration.

I won't cite the abstracts here, as I am too lazy.

Just do search on "insulin insensitivity CLA" at pubmed.com.
 
I am under the opinion that CLA is better consumed in one or two larger doses rather then smaller. Like glutamine needs to be dosed in larger doses (over 2 grams at a time i think) just to get by the stomache, the same probably goes for CLA so the bulk of it can avoid oxidation by the liver. And while CLA does cause insulin resistence in the muscles this is actually a good thing in terms of preventing muscle loss according to lyle. The best way around that would be a large dose of ALA around your post workout meal(s). That way you get the best of both worlds.
 
I have had opportunities to discuss with others at AvantLabs about muscle and insulin insensitivity. It is not a good thing. There is overwhelming evidence against it. Again, pubmed abstracts support my view.
 
But alot of studies indicate a simultaneous loss of fat mass and an increase in muscle mass at the higher end doses. If CLA is not having an anabolic effect on the subjects then it must be having some sort of an anti-catabolic effect to acheive such results, right? Am i missing something?
 
I must admit, my knowledge in this area is lacking -- so, I'd welcome any new insights in this area.

For muscles, insulin has two main effects (1) glycogen synthesis and (2) anti-catabolism. The first effect occurs through cell volumization, by increasing sodium and potassium concentration in the cells. The second effect is important because without it, pure anabolism in muscle generally would not be sufficient to induce net positive muscle accrual.

Anti-catabolic effect becomes inhibited when muscles become insensitive to insulin. [Again, the negative impact of insulin resistance in muscle is very well documented -- there are pubmed abstracts after abstracts on this topic.]

Ideally, you'd want muscles to respond well to insulin and the fat cells to become insulin insensitive. But it seems that in general, muscle and fat tend to become insulin sensitive and insensitive together.

As far as I know, there are a couple of things that one can do to cause muscle to become more insulin sensitive and fat cells to become insulin insensitive.

(1) exercise
(2) take drugs that affect the brain. This include AAS.
 
blade:

whoa, where did that come from?
tounge.gif
i was being semi-sarcastic about you (and bryan) having a different interpretation of CLA research than virtualcyber (if indeed your opinions are different). i actually have faith in you guys' thoughts, and i did read the FAQ about supplements before. i was just amused that there was an apparent disagreement amongst two forum vets and quipped about it in jest.

in fact, i still feel my specific questions weren't actually addressed fully by the FAQ entry, nor by anyone in this or other threads that i've come across. namely: 1) should one take larger doses of CLA only once or twice daily, or spread evenly amongst three or more meals? 2) should CLA be counted in your daily calorie totals?

yes, perhaps the answers might be inferred from the FAQ, but i guess i just want to confirm what others might have inferred.
laugh.gif
 
Blade certainly knows much about supplements.

I think though, his conclusions on CLA is somewhat outdated. There have been recent pubmed research abstracts that have revealed more about CLA's effects on muscle.

Perhaps further research will reveal that Bryan was right after all. (I think it is too early to say). But as of now, the tide of research has turned against it. If you don't believe it, do a pubmed search.

I repeat, muscle insensitivity to insulin is not a good thing. Currently, CLA has been shown to promote that.
 
[b said:
Quote[/b] (tai4ji2x @ Mar. 12 2003,4:15)]blade:
whoa, where did that come from?
tounge.gif
I wasn't directing my post at anyone in particular, I just remember someone saying after the FAQ section was up that "now no one will ask questions anymore". But then you see a multitude of posts asking the same questions over and over again - even to the point where you have three-four threads in succession in the same forum related to the same topic, so I was just suggesting that people do their homework first... :)

Virtualcyber, I'll look into that thread on Avant, but a quick search revealed a study related to the one in the FAQ section demonstrating the effects of CLA on insulin sensitivity in muscle:

Am J Physiol Endocrinol Metab 2003 Mar 4; [epub ahead of print]

Isomer-specific Actions of Conjugated Linoleic Acid on Muscle Glucose Transport in the Obese Zucker Rat.

Henriksen EJ, Teachey MK, Taylor ZC, Jacob S, Ptock A, Kramer K, Hasselwander O.

Department of Physiology, University of Arizona, Tucson, AZ, USA.

The fatty acid conjugated linoleic acid (CLA) enhances glucose tolerance and insulin action on skeletal muscle glucose transport in rodent models of insulin resistance. However, no study has directly compared the metabolic effects of the two primary CLA isomers, cis-9,trans-11-CLA (c9,t11-CLA) and trans-10,cis 12-CLA (t10,c12-CLA). Therefore, we assessed the effects of a 50:50 mixture of these two CLA isomers (M-CLA) and of preparations enriched in either c9,t11-CLA (76% enriched) or t10,c12-CLA (90% enriched), on glucose tolerance and insulin-stimulated glucose transport in skeletal muscle of the insulin-resistant obese Zucker (fa/fa) rat. Animals were treated daily by gavage with either vehicle (corn oil), M-CLA, c9,t11-CLA, or t10,c12-CLA (all CLA treatments at 1.5 g total CLA/kg body wt) for 21 consecutive days. During an oral glucose tolerance test, glucose responses were reduced (P<0.05) by 10% and 16%, respectively, in the M-CLA and t10,c12-CLA animals, while insulin responses were diminished by 21% and 19% in these same groups. There were no significant alterations in these responses in the c9,t11-CLA group. Insulin-mediated glucose transport activity was enhanced by M-CLA treatment in both type I soleus (32%) and type IIb epitrochlearis (58%) muscles, and by 36% and 48%, respectively, with t10,c12-CLA. In the soleus these increases were associated with decreases in protein carbonyls (index of oxidative stress, r=-0.616, P=0.0038) and intramuscular triglycerides (r=-0.631, P=0.0028). Treatment with c9,t11-CLA was without effect on these variables. These results suggest that the ability of CLA treatment to improve glucose tolerance and insulin-stimulated glucose transport activity in insulin-resistant skeletal muscle of the obese Zucker rat are associated with a reduction in oxidative stress and muscle lipid levels, and can be specifically ascribed to the actions of the t10,c12 isomer. In the obese Zucker rat, the c9,t11 isomer of CLA is metabolically neutral.
 
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