Quote (Balla @ Apr 19 2014 05:31pm)
This is great
Disagree on a few points, but Alan is of course only looking at studies that may have examined the issue
The major benefit of IF for me, is appetite control, for instance.
I also profoundly disagree with the notion put forth about breakfast.. especially the cognitive function. For me personally, breakfast makes me much sloppier/lazier in general and slows down my cerebration/cognitive function, without a doubt.
I think there's a lot of variables with the breakfast issue though.. such as they'd typically look at epidemiology and find correlations between populations. That can sometimes be fallacious, as is seen with the evidence for eating more frequently vs fewer meals, and the higher frequency eating tends to be leaner/healthier.. clearly asinine physiologically, but that's the "trend".
I also think not enough "health" benefit was touched on from chronic IF. He did talk about blood lipids, neuroprotection (of which is also largely mediated by GDNF, not ONLY BDNF), and insulin sensitivity, however there's probably more. Fasting will obviously lower insulin secretion and increase glucagon secretion.. one, lower insulin pathways/fasting will induce FOXO pathways (from Akt not being activated), which binds to IREs and upregulates PGC1alpha as well as upregulating transcription of several antioxidant genes. The glucagon response augments (through CREs) the PGC1alpha expression and these lead to increased mitochondrial efficacy/function and greater antioxidant capacity. You also have an increased AMPK response from short term fasting. Unfortunately, I didn't even realize the time and I have to go.. later tonight or tomorrow now I want to go into more detail into AMPK and Sirtuin expression and benefits of (and how it applies to short term fasting).
Now, let's get back into this a little bit.
To me, one of the biggest problems, health wise, is chronic mTOR expression that is customary of our society (and of course eating 6-8 meals a day=chronic expression). mTOR is the main anabolic pathway ofc, and as weight lifters we love this, however it can be deleterious (balance is key). It exhausts the stem cell pool and promotes senescence, increased ROS (and thus oxidative damage), accumulation of unfolded proteins (inhibited autophagy), and ER stress (part of the reason in the former), etc. Long story short - mTOR promotes aging, and this has been demonstrated through its inhibition/antagonism increasing lifespan. Anyway, herein comes AMPK - damaged/cancerous cells to undergo apoptosis, promotes autophagy, promotes DNA repair, promotes lipolysis and subsequent oxidation, inhibits adipogenesis as well as fatty acid and cholesterol synthesis, promotes insulin independent glucose uptake (GLUT4 expression), phosphorylates and activates PGC1 alpha, generally changes glucose metab toward ATP generating pathways ie glucose uptake, glycogenolysis and glycolysis. I could keep talking about the AMPK and mTOR for awhile and balance of, but you can just do more reading yourself if curious as there's a lot to say. Now, some words on the sirtuins - these are upregulated during fasting. As an aside - these are the main focus of the recent Harvard et al study on the age extending compound. AMPK also helps to activate these, by modifying NAD+/NADH ratio, augmenting the activation. Myriad benefits for the sirtuins - they also deacetylate and activate PGC1alpha as well as FOXO (AMPK also increases FOXO expression.. starting to see a nice pathway build?). They protect from diabetes from protecting pancreatic beta cells (induces expression of NeuroD & MafA), they prevent axonal caspase activation (apoptosis), sirt1 represses PPAR-gamma (and thus inhibits adipogenesis & fat storage), and promotes adiponectin secretion (largely through FOXO). Several other things I'll list off as well (not all ofc.. exorbitant list) - mediates neuroprotection esp against amyloid beta toxicity/buildup and NF-kappaB suppression, suppresses apoptosis and promotes cell survival (same as mTOR, but remember AMPK and others are also facilitating their DNA repair, autophagy and such), etc etc. Now, part of the reason exercise is such a powerful repartitioning agent is a huge increase in AMPK expression, and of course the well known mTOR. However, from exercise, it's the alpha 2 isoform of AMPK that's expressed, which doesn't antagonize mTOR expression.. so from exercise, you get enormous rises in both enzymes, and thus the anabolic response (hence muscle building), as well as lipolytic and insulin sensitizing responses, increases in mitochondrial biogenesis, plus a positive ROS response through mitohormesis increasing stress resistance, etc etc. Clearly exercise is king. As is balance. A lot of this is why I think a chronic IF protocol is so strongly beneficial for health. And as far as I can see, fasting for 16-20 hours a day isn't going to impede muscle gains compared to increased frequency. A recent study saw higher protein synthesis levels in a group consuming more evenly allotted boluses of protein vs a group consuming a skewed bolus (one large in the evening, very little before that).. and this response seems clear, as only so much per meal will be actually utilized to form new proteins. There are 2 problems though - none of the participants lifted, and the intake was quite low in comparison to what would be seen from physically active individuals.. not to mention the diets were (ostensibly) at maintenance.. so if one was in a surplus, protein synthesis rates will also be higher. Point being, an IF protocol should help maximize health & possible longevity through various pathways, and shouldn't impede skeletal muscle hypertrophy. A lot more could be written about these topics, but the main idea is conveyed.