That LC can be used as a powerful therapeutic tool is without a doubt, but it has tricked more than just me into
mistaking the effect of a therapeutic intervention for a cause. For more than 100 years medical practitioners recommended a LC approach for weight loss, but for the reasons related to specific individual insulin resistance AND satiety. Some folks do well on higher carb, some better on lower. We can do theory and internet flame wars all day and never get to a point that helps people. Or, we can take general guidelines, encourage folks to tinker, and actually see some results for our efforts.
One of the best explanations I have seen to date on both the important role of dietary carbohydrate in human health, and a credible mechanistic explanation of the pathogenesis of insulin resistance, is encapsulated in Chris Masterjohn’s talk at AHS 2012. I have seen similar proposed mechanisms of insulin resistance and fat gain being an adaptation to reduce oxidative stress since perhaps 2008, but Chris nails this.
Please watch the entire video and ponder upon it’s implications a bit, especially if you are leaning towards the Insulin hypothesis crowd.
Chris Masterjohn — Oxidative Stress & Carbohydrate Intolerance: An Ancestral Perspective from
Ancestral Health Society on
Vimeo.
We have a mechanism whereby excess calories can be either pushed through the mitochondria, causing severe oxidative stress, or we have fat gain and insulin resistance occurring in an effort to “lock up” excess calories and glucose, which can both pose significant metabolic problems. Let me say this again, as it’s important that folks get this: Insulin resistance is likely an effort to prevent cellular death due to free-radical production. This is facilitated by pushing substrates (primarily fat and carbs) into adipose tissue, which is RELATIVELY inert (aside from the hormonal messengers that adipose tissue produces). We also see elevated lipoproteins, triglycerides, and blood glucose as the body is trying to put nutrients ANYWHERE other than through the mitochondria.