February 22, 2010
(Part IV of a series. Go back to , , or , or skip to .)
This is a long and detailed article, but it's very important. I believe the conclusions justify the length: we're done laying groundwork, and we're finally starting to build some answers to the original question: "Why are we hungry?"
I must emphasize that I have no stake in any of the current controversies. I have no diet books for sale and no research thesis to defend, and I began this series long before the AHS. My…
You are a genius. This explains so many things about me. Thanks.
I think I just swallowed this article whole. I feel like you have just taken ideas out of my head and then confirmed them with evidence (yes, I know you haven't but it's spooky anyway).I'll re-read this and will check out all the references. For now, thank you.
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
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).
Extremely interesting, as always. Thank you for taking the time to share. Be well.
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
I think I'm starting to get it!! JS, you have a magical ability to explain these concepts so that they are understandable, without "dumbing down" the truth!! I will re-read this article, as I do everything on the site, along with the intelligent comments by your readers, as I continue to seek the knowledge that will bring me back to health. Thank you so much!!
June 20, 2011
I'm pretty sure I'm with Anastasia on this one. You took exactly what I was thinking, and put it down on the page. Especially from my own experience I noticed that when I did take a multivitamin (with a little fat or food in general) I'd literally feel full forever.
Thanks again JS.
outstanding post! i'm with leonrover.... keep up like this, and i'll have to actually *buy* your book! ;-)
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'm loving this series! One question (since you didn't end this post with what, if anything, is next): where does the idea of reward tie in? I.e., Kessler's sugar, salt & fat combos certainly fit in with satiety failure #1, but in addition to lack of nutrients, these foods have substances that presumably increase hunger (or appetite) which implies reduction of satiety. Or?
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.
Where would MCT's (coconut oil) fit in on this discussion?
My limited understanding is that it functions unlike other sources of fat in how it is processed by the body.
February 22, 2010
Hey everybody! Help spread this one around! Twitter it, like it on Facebook, post it on forums...it's important.
Thank you. It certainly explains why some people can blithely chomp down junk and some people gain weight just from looking at a soda, doesn't it? And why losing weight doesn't solve all your problems?
You're welcome! It clears up a lot of fog to know that obesity is frequently caused by a lack of metabolic flexibility due to mitochondrial dysfunction. No, it isn't the patient's imagination that they are starving themselves and not losing fat mass, and it's not their imagination that carb-laden foods make them hungry.
And I know it's fashionable to bash on Taubes these days -- but even though he may be wrong as to the specific biochemical mechanism, the "greedy fat cells" theory of obesity is closer to useful truth than any theory that doesn't take mitochondrial dysfunction into account.
That's fascinating! It seems like the transfer is very slow (e.g. not significant during exercise), and only occurs while the subject remains fasted post-exercise. So I doubt the transfer is significant in most real-world cases, but it's a very informative study for many reasons...one being that it demonstrates that glycogen depletion is not the limiting factor in running (or, most likely, other types of exercise).
Thanks for bringing it to my attention.
Thank you. I'm doing very well, actually, after a recovery from AHS and an epic adventure I'll be recounting soon.
I'm glad you found it understandable. I'm seeing a lot of of fog blowing around lately, and I'm trying to help cut through the confusion.
Thank you! If so, I've succeeded. Anyone can give advice: it's much harder to explain. Hopefully this series will give you a sound foundation of knowledge from which to address your issues.
You're welcome. I noticed that when I take iodine supplements I don't crave seaweed salads anymore. It's instructive that our bodies understand nutrition even when our rational minds don't.
Buy it directly from 100 Watt Press and I'll sign it for you!
I'll get into proposed solutions later, once the problems have all been laid out. And you're absolutely correct: muscles end up being our storage depots for protein. (And fat...there is substantial fat content in muscle, as Paul Jaminet likes to point out.) This is why it's harder to lose fat than to just lose weight.
I'll get to 'food reward' as I explore the different ways in which the hunger motivations can fail: reward affects the eating end (wanting and liking), not the 'stop eating' end (satiation and satiety). Meanwhile, my earlier overview of the subject, which is still completely valid, is available here.
As I said to Timothy, proposed solutions will come later, once I've laid out all the problems. Part of the current controversy arises from a lack of seeing (or understanding) the big picture. If I present that correctly, the solutions should seem both reasonable and somewhat obvious.
Thank you! This series isn't really the right place to discuss fat digestion: we're on the hunger end of things right now. I'm not aware that the oxidation of MCTs in mitochondria is any different than the oxidation of LCTs (it's mainly the transport into circulation that's different) -- but if you or anyone knows of research to that effect, I'd be very interested in reading it!
Thanks, everyone, for your comments! I'm glad that you're finding these long, technical posts both understandable and of use.
I'm loving this series, thank you. I'm on my weight loss journey (10kg down, 20kg to go) and looking for sustainable and sensible answers to my questions about being hungry and exhausted. So far, you're delivering them right to my inbox. I'm very grateful, and stimulated and excited and reassured.
One of the fundamental questions at present relates to your section on the 'formerly obese' and their continued metabolic derangement. The article doesn't explain how they got to be non-obese, or what their metabolic markers re obesity are. In my more hopeful moments I expect that they got to be non-obese purely in terms of scale weight and BMI through the CW way of calorie restriction or low carb-low fat, which leaves you white-knuckling your way through hunger pangs and constant fears of regaining. Been there, done that.
Is it naivety to think that attending to cellular health via functional paleo might allow for weight regulation and restoration to healthy mitochondrial function? At present I'm doing VLC-HF, which seems to be the only thing that's working for sustained energy and weight loss.
Looking forward to the next instalments!
[...] 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 + [...]
June 5, 2011
Jacquie ... from a fellow who was obese and now rapidly falling from overweight back to normal, check out J's post on metabolic flexibility. I, too, went for the very low carb option and prolonged IF (eating 12 noon - 8 PM only 5 days and breakfasting at weekends) and lost a lot. Coupled with activity the weight dropped easily and fat reduced. I was in ketosis good an proper ... infact, waking up in the morning our bedroom smelled of acid! Not good in the long term!
It was not until I addressed my sleep, by not indulding in digital activity before going to bed, and increased my carb intake that I pushed through that little wall and started to lose more fat.
J's notion of 'Eat like a Predator' has been my biggest help - go from proper meal to proper meal, and if you feel hungry in the meantime ... address it at the next meal. After a while, it works itself out. I felt ravenously hungry between meals for a couple of weeks until I got back to the point that I felt full, satisfied and satiated without being bereft of energy. In fact, I like light walking after a meal. It will come ...
Do consider your activity, consider your sleep and consider when it is that you do that activity - use that period to de-stress, to wind down and to build yourself up for a really great evening or eating, fun, family and ... sleep.
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!
JS - Well said my friend. Love your work.
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?
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