You are a genius. This explains so many things about me. Thanks.

I agree on pretty much all, except this piece about glycogen:
"Furthermore, glycogen cannot be shuttled out of or between muscles: it’s only available to the muscle containing it."

There's at least one study (Intramuscular Glycogen and Intramyocellular Lipid
Utilization during Prolonged Exercise and Recovery in
Man: A 13C and 1H Nuclear Magnetic Resonance
Spectroscopy Study*
MARTIN KRSSAK†, KITT FALK PETERSEN‡, RAYNALD BERGERON,
THOMAS PRICE, DIDIER LAURENT, DOUGLAS L. ROTHMAN, MICHAEL RODEN,
AND GERALD I. SHULMAN§)
concluding the following in the abstract (pay attention to 3)!):
"In summary, we found during
prolonged running 1) significantly greater muscle glycogen utilization
in the calf muscle group than in the thigh muscle group, 2) significant
utilization of IMCL in the soleus muscle, and 3) a decrease in glycogen
content in nonexercising muscle and an increase in glycogen content
in recovering muscles during the postexercise phase. These latter
data are consistent with the hypothesis that there is transfer of
glycogen by the glucose3lactate and the glucose3alanine cycle from
the resting muscle (forearm) to recovering muscles (thigh and calf)
after running exercise."

Btw, this entry made me think about my cheese cravings (I think I told you here once).
It just might be that cheese has the right ratios of fat, protein and salt I need after the IF-period! The craving goes away completely after dinner, regardless if it did contain indeed cheese or just other sources of animal protein and fat (salt is a given with my cooking anyways).

Hello John

Thank you for the references showing the differences between the non obese and the obesity damaged in the use of internal energy stores.

So yes! I found that portion of your article both interesting and illuminating.

In addition, it was no ordeal to read.

Slainte Mhaith - Good Health

JS,

Very thought-provoking stuff. That study of the formerly obese is particularly intriguing. I wonder if these were people who lost weight by sheer caloric restriction, which is the most popular route (lap band, anyone?) but presumably does little for metabolic flexibility. Perhaps it is possible to become formerly obese by developing met flex instead, via cycling macronutrient intake, intermittent fasting, etc.

You write that we have no storage depots for protein, but I wonder if surplus muscle tissue might fill this role in a human with a healthy hormonal balance.

Thanks for satiating my brain with this excellent series of articles.

I was looking forward ti this one! Will you have anything on how the formerly obese can regain better fat oxidation?

It is nice to see a well balanced article from someone without a dog in the fight. I have found that a whole lot of my former hunger was dealing with the first 2 issues of nutrient deprivation and malabsorption. I am not sure if the last one fit me or not, but it is certainly interesting food for thought.

[...] light on some of the recent nutritional conflicts in the community. Let me know what you think. When Satiety Fails: Why Are We Hungry? Part IV And there's much more to come in this series! Reply With Quote   + [...]

Hi Paul - thanks for pointing me to that post. Exercise is clearly the next thing I need to tackle. Increasing carbs for me is associated with gut problems, so it's a delicate balancing act that I think I'm winning at present. I guess IBS is my version of your sleep issues - there's always a new challenge in this road to health!

Just having a bit more of a think about it over a coffee, and I wonder how much we can decrease the reliance on glycolytic pathways in previously obese individuals by increasing their medium chain triglyceride intake rather than long-chain fatty acids? Certainly, going down the pathway of consuming more coconut products, for example, can bypass some of the digestive and mitochondrial short-comings in these people, and with a good dose of intermittent fasting and low level aerobic work, and perhaps some carnitine supplementation in the short term, one can re-establish sme more lipolytic capacity in the mitochondria?