[quote]Apoklyps wrote:
[quote]Facepalm_Death wrote:
Even if correlation implied causation, how would the study determine which way the causality operated?
Think about this: what if, by the very nature of what insulin resistance is (think about it), it was actually the case that insulin resistance was a prior condition that caused increases in bf%. Furthermore, what if diet and training improvements affected insulin sensitivity first, and the improved insulin sensitivity subsequently affected bf%? Are there any thoughts on this?
[/quote]
Best post regarding the insulin sensitivity debate here. Finally, someone’s thinking like a scientist here.
Additionally, as correlation does not equal causation, we cannot discount the possibility of confounding factors. It is quite possible that leanness or low BMI also positively correlate with differences in diet, physical activity, stress, mental health, socioeconomic status, general health, etc. in the general population. These third factors may or may not have associations (causal or not) with insulin sensitivity.
Even the study posted subsequent to Pangloss’s cannot demonstrate direct causation. It does not demonstrate that reduced body fat causes increased insulin sensitivity, it demonstrates that reduced body fat resulting from a “1-year lifestyle intervention” causes increased insulin sensitivity.
Additionally, if you do believe that there is direct causation, this places the burden of proof on you to come up with a physiological mechanism for this.
That said, for day to day (not scientific) training purposes, we should take a pragmatic approach. While it is debatable at best to imply a direct causal mechanism with the information at hand, we all know the effects of diet on insulin sensitivity. And we all slack on our diets at least a little more when we’re at stages where don’t care about BF. If you don’t, you get a cookie (or not… THINK ABOUT YOUR INSULIN SENSITIVITY!!!).
Cliffs:
The scientific approach: too many confounding factors to determine direct causation, no physiological mechanism provided
The pragmatic approach: I think it’s safe to assume that we live different lifestyles when we are maintaining low BF% or in a “not giving a shit about weight” phase, and this would likely affect insulin sensitivity.[/quote]
You were asking for a specific mechanism?
“Endocrine, inflammatory, and neuronal pathways link obesity to insulin resistance. (A) The obesity-associated increase in FAs can trigger insulin resistance through intracellular metabolites that activate PKC, leading to the activation of serine/threonine kinases that inhibit insulin signaling. (B) Obesity-associated changes in secretion of adipokines that modulate insulin signaling. (C) Obesity-associated inflammatory factors. Obesity is characterized by an increase in the accumulation of ATMs, which increase the adipose tissue production of inflammatory cytokines that inhibit insulin signaling. (D) Endocrine and inflammatory mediators converging on serine/threonine kinases that inhibit insulin signaling. (E) Obesity-associated activation of NF-κB heightens inflammatory responses that exacerbate insulin resistance. (F) SOCS family proteins, induced by adipokines, induce insulin resistance either by interfering with IRS-1 and IRS-2 tyrosine phosphorylation or by targeting IRS-1 and IRS-2 for proteosomal degradation. (G) FAs also trigger insulin resistance by direct activation of TLR4 and the innate immune response. (H) Obesity-related alteration in the central response to hormonal and nutrient signals alters peripheral insulin sensitivity.”