CLA & Insulin Resistence in Men

I just thought I’d post this for the board.

A study by the Journal of Lipid Research (arguable less “vendetta” than the American Heart Association), show that “Conjugated linoleic acid-mediated inflammation and insulin resistance in human adipocytes are attenuated (diminished) by resveratrol.”

Per the study [quote]Inflammation plays a role in trans-10, cis-12 (10,12)-conjugated linoleic acid (CLA)-mediated delipidation and insulin resistance in adipocytes. Given the anti-inflammatory role of resveratrol (RSV), we hypothesized that RSV would attenuate inflammation and insulin resistance caused by 10,12 CLA in human adipocytes. RSV blocked 10,12 CLA induction of the inflammatory response by preventing activation of extracellular signal-related kinase and induction of inflammatory gene expression (i.e., IL-6, IL-8, IL-1�²) within 12 h. Similarly, RSV suppressed 10,12 CLA-mediated activation of the inflammatory prostaglandin pathway involving phospholipase A2, cyclooxygenase-2, and PGF2. In addition, RSV attenuated 10,12 CLA increase of intracellular calcium and reactive oxygen species associated with cellular stress, and activation of stress-related proteins (i.e., activating transcription factor 3, JNK) within 12 h. 10,12 CLA-mediated insulin resistance and suppression of fatty acid uptake and triglyceride content were attenuated by RSV. Finally, 10,12 CLA-mediated decrease of peroxisome proliferator-activated receptor (PPAR) protein levels and activation of a peroxisome proliferator response element (PPRE) reporter were prevented by RSV. RSV increased the basal activity of PPRE, suggesting that RSV increases PPAR activity. Collectively, these data demonstrate for the first time that RSV prevents 10,12 CLA-mediated insulin resistance and delipidation in human adipocytes by attenuating inflammation and cellular stress and increasing PPAR activity./quote

I don’t know if you caught that last sentence, but it read: “these data demonstrate for the first time that RSV prevents 10,12 CLA-mediated insulin resistance and delipidation in human adipocytes”

So the question becomes A) how much RSV do you have to take and in what form? B) Are there any unknown sides of resveratrol? C) is it cost effective to most users to take CLA if they have to take resveratrol?


  1. Conjugated linoleic acid-mediated inflammation and insulin resistance in human adipocytes are attenuated by resveratrol http://www.jlr.org/cgi/content/abstract/50/2/225

BT

[quote]BulletproofTiger wrote:
limitatinfinity wrote:
The conclusion in this study is garbage.

It’s the same backwards thinking that claims that Omega-6 fatty acids cause inflammation.
It’s the fatty acid PROFILE AND BALANCE that is important to consider.

I think you might be confusing the conclusion of the study with some of the conclusions being made by people on this thread, i.e. their decision to discontinue use of CLA supplementation. If I’m wrong, then please let the readers know more specifically which part of the conclusion you disagree with so we can understand your point better.

Conclusionsâ??

  1. t10c12 CLA supplementation increases oxidative stress and inflammatory biomarkers in obese men.
  2. The oxidative stress seems closely related to induced insulin resistance, suggesting a link between the fatty acid-induced lipid peroxidation seen in the present study and insulin resistance.
  3. These unfavorable effects of t10c12 CLA might be of clinical importance with regard to cardiovascular disease, in consideration of the widespread use of dietary supplements containing this fatty acid.

Thanks,
BT
[/quote]

I’ll clarify:
No conclusion can be drawn on the effects of supplementation(specifically the addition of this isomer) of t10, c12 CLA without the consideration of the existing ratio’s and balance of concomitant consumption of other isomers.

An example with omega 6(AA) v omega 3(EPA, DHA):

Supplementation of omega 3 may yield no real benefits to someone who doesn’t already consume high RATIOS of 6 to 3. Further, beyond(roughly) a 1:1.2 ratio of omega 6 to omega 3 in serum may have deleterious effects.

A specific ingredient on the label of a product without the consideration of ALL of the ingredients tells you nothing of the quality and effectiveness of the product.

I would also like to point out that, in terms of body composition, it’s favorable for adipocytes to be insulin resistant as long as skeletal muscle insulin binding sites are not also down-regulated.

Why would you want an obese person’s adiposity to readily increase glycogen stores. You would want a large mobilization of triglycerides while carb consumption and liver glycogen stores were at a low levels in order to fuel the foreward process of gluconeogenesis.

SO…
Training: deplete SM glycogen, GH mobilizes fatty acids
PWO MEAL: reduce cortisol levels, spike insulin, replenish SM glycogen with minimal liver/adipose deposition
Rest of Your meals: low carb, keep blood sugar levels normalized, avoid insulin spikes, fuel gluconeogenesis with ample fats in diet
Being hypocaloric: “fat adapted” condition and the need to maintain blood glucose levels increases fatty acid mobilization from adiposity, but because there are no direct transporters of glucose out of SM, glycogen levels there aren’t depleted until the next training period.

It’s a full circle approach to nutrient timing, and as far as I’m concerned, t10, c12 reinforces this structure.

lim@infinity

[quote]limitatinfinity wrote:
BulletproofTiger wrote:
limitatinfinity wrote:
The conclusion in this study is garbage.

It’s the same backwards thinking that claims that Omega-6 fatty acids cause inflammation.
It’s the fatty acid PROFILE AND BALANCE that is important to consider.

I think you might be confusing the conclusion of the study with some of the conclusions being made by people on this thread, i.e. their decision to discontinue use of CLA supplementation. If I’m wrong, then please let the readers know more specifically which part of the conclusion you disagree with so we can understand your point better.

Conclusions�¢??

  1. t10c12 CLA supplementation increases oxidative stress and inflammatory biomarkers in obese men.
  2. The oxidative stress seems closely related to induced insulin resistance, suggesting a link between the fatty acid-induced lipid peroxidation seen in the present study and insulin resistance.
  3. These unfavorable effects of t10c12 CLA might be of clinical importance with regard to cardiovascular disease, in consideration of the widespread use of dietary supplements containing this fatty acid.

Thanks,
BT

I’ll clarify:
No conclusion can be drawn on the effects of supplementation(specifically the addition of this isomer) of t10, c12 CLA without the consideration of the existing ratio’s and balance of concomitant consumption of other isomers.

An example with omega 6(AA) v omega 3(EPA, DHA):

Supplementation of omega 3 may yield no real benefits to someone who doesn’t already consume high RATIOS of 6 to 3. Further, beyond(roughly) a 1:1.2 ratio of omega 6 to omega 3 in serum may have deleterious effects.

A specific ingredient on the label of a product without the consideration of ALL of the ingredients tells you nothing of the quality and effectiveness of the product.

I would also like to point out that, in terms of body composition, it’s favorable for adipocytes to be insulin resistant as long as skeletal muscle insulin binding sites are not also down-regulated.

Why would you want an obese person’s adiposity to readily increase glycogen stores. You would want a large mobilization of triglycerides while carb consumption and liver glycogen stores were at a low levels in order to fuel the foreward process of gluconeogenesis.

SO…
Training: deplete SM glycogen, GH mobilizes fatty acids
PWO MEAL: reduce cortisol levels, spike insulin, replenish SM glycogen with minimal liver/adipose deposition
Rest of Your meals: low carb, keep blood sugar levels normalized, avoid insulin spikes, fuel gluconeogenesis with ample fats in diet
Being hypocaloric: “fat adapted” condition and the need to maintain blood glucose levels increases fatty acid mobilization from adiposity, but because there are no direct transporters of glucose out of SM, glycogen levels there aren’t depleted until the next training period.

It’s a full circle approach to nutrient timing, and as far as I’m concerned, t10, c12 reinforces this structure.

lim@infinity

[/quote]
OK so you think people should be supplementing with CLA?

[quote]fightnews10 wrote:
limitatinfinity wrote:
BulletproofTiger wrote:
limitatinfinity wrote:
The conclusion in this study is garbage.

It’s the same backwards thinking that claims that Omega-6 fatty acids cause inflammation.
It’s the fatty acid PROFILE AND BALANCE that is important to consider.

I think you might be confusing the conclusion of the study with some of the conclusions being made by people on this thread, i.e. their decision to discontinue use of CLA supplementation. If I’m wrong, then please let the readers know more specifically which part of the conclusion you disagree with so we can understand your point better.

Conclusions�?�¢??

  1. t10c12 CLA supplementation increases oxidative stress and inflammatory biomarkers in obese men.
  2. The oxidative stress seems closely related to induced insulin resistance, suggesting a link between the fatty acid-induced lipid peroxidation seen in the present study and insulin resistance.
  3. These unfavorable effects of t10c12 CLA might be of clinical importance with regard to cardiovascular disease, in consideration of the widespread use of dietary supplements containing this fatty acid.

Thanks,
BT

I’ll clarify:
No conclusion can be drawn on the effects of supplementation(specifically the addition of this isomer) of t10, c12 CLA without the consideration of the existing ratio’s and balance of concomitant consumption of other isomers.

An example with omega 6(AA) v omega 3(EPA, DHA):

Supplementation of omega 3 may yield no real benefits to someone who doesn’t already consume high RATIOS of 6 to 3. Further, beyond(roughly) a 1:1.2 ratio of omega 6 to omega 3 in serum may have deleterious effects.

A specific ingredient on the label of a product without the consideration of ALL of the ingredients tells you nothing of the quality and effectiveness of the product.

I would also like to point out that, in terms of body composition, it’s favorable for adipocytes to be insulin resistant as long as skeletal muscle insulin binding sites are not also down-regulated.

Why would you want an obese person’s adiposity to readily increase glycogen stores. You would want a large mobilization of triglycerides while carb consumption and liver glycogen stores were at a low levels in order to fuel the foreward process of gluconeogenesis.

SO…
Training: deplete SM glycogen, GH mobilizes fatty acids
PWO MEAL: reduce cortisol levels, spike insulin, replenish SM glycogen with minimal liver/adipose deposition
Rest of Your meals: low carb, keep blood sugar levels normalized, avoid insulin spikes, fuel gluconeogenesis with ample fats in diet
Being hypocaloric: “fat adapted” condition and the need to maintain blood glucose levels increases fatty acid mobilization from adiposity, but because there are no direct transporters of glucose out of SM, glycogen levels there aren’t depleted until the next training period.

It’s a full circle approach to nutrient timing, and as far as I’m concerned, t10, c12 reinforces this structure.

lim@infinity

OK so you think people should be supplementing with CLA?
[/quote]

As long as they understand that supplement means in addition to a sound and effective diet, then yes, most definitely.

The fact is though there are more studies then the one I posted, Maybe even like 10 or more. There is to much conflicting data and you can’t draw a legit conclusion from it. So why take the risk? At least that’s how I feel about it.

Something to consider here, is that many single elements in nature work in conjunction with others present as well. Taking one supplement because its been tested to work in isolation doesn’t mean it works as well when it’s other necessary partners in crime are present.

[quote]fightnews10 wrote:
The fact is though there are more studies then the one I posted, Maybe even like 10 or more. There is to much conflicting data and you can’t draw a legit conclusion from it. So why take the risk? At least that’s how I feel about it.[/quote]

Or just take Rez-V with your tonalin and you’ll be set.

BT

Something else to consider…

Y’all not think ye overthinking the HELL out of this ??

Just eat proper food and you will be grand.

Your REALLY getting into the minor worries here something non professional people really shouldnt be worrying over.

Its just bodybuilding not nuclear physics !

[quote]300andabove wrote:
Something else to consider…

Y’all not think ye overthinking the HELL out of this ??

Just eat proper food and you will be grand.

Your REALLY getting into the minor worries here something non professional people really shouldnt be worrying over.

Its just bodybuilding not nuclear physics ![/quote]

FWIW, I am a professional.

Trainer, Strength coach, bodybuilder(amateur), and Biochem. Graduate student.

[quote]300andabove wrote:
Something else to consider…

Y’all not think ye overthinking the HELL out of this ??

Just eat proper food and you will be grand.

Your REALLY getting into the minor worries here something non professional people really shouldnt be worrying over.

Its just bodybuilding not nuclear physics ![/quote]

How do you figure? It’s a matter of using a supplement or not? Are you saying the merit of a supplement shouldn’t be debated especially when it has possible negative effects? How is it different then discussing any other supplement or program for that matter? This is a supplement website in the supplement section of a forum you know. What is your point exactly because I’m sure you won’t just admit you’re wrong?

[quote]limitatinfinity wrote:
300andabove wrote:
Something else to consider…

Y’all not think ye overthinking the HELL out of this ??

Just eat proper food and you will be grand.

Your REALLY getting into the minor worries here something non professional people really shouldnt be worrying over.

Its just bodybuilding not nuclear physics !

FWIW, I am a professional.

Trainer, Strength coach, bodybuilder(amateur), and Biochem. Graduate student.

[/quote]

So 1 person that should be worried in the WHOLE thread and even then why get caught up in the minors lol.

if your still worried about the little things like will cla do xyz to me then ugh your head must be wrecked lol

[quote]300andabove wrote:
limitatinfinity wrote:
300andabove wrote:
Something else to consider…

Y’all not think ye overthinking the HELL out of this ??

Just eat proper food and you will be grand.

Your REALLY getting into the minor worries here something non professional people really shouldnt be worrying over.

Its just bodybuilding not nuclear physics !

FWIW, I am a professional.

Trainer, Strength coach, bodybuilder(amateur), and Biochem. Graduate student.

So 1 person that should be worried in the WHOLE thread and even then why get caught up in the minors lol.

if your still worried about the little things like will cla do xyz to me then ugh your head must be wrecked lol[/quote]

Stupid way to look at it in my opinion. Why do you have to be worried just because you want to know? It’s retarded, Why would you continue taking something you know is unhealthy?