(Part IV of a series. Go back to Part I, Part II, or Part III, or skip to Part V.)
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 concern is (as always) to organize and present the facts as I understand them to you, my readers, so you can draw useful conclusions about your own diet and life.
Furthermore, my diet at the moment contains roughly a Perfect Health Diet-compliant 15% of carbohydrate, plus whatever I need for intense physical activity (though I don’t count or track my intake), so I don’t believe I belong to either the high-carb or low-carb camps.
In previous installments, we’ve established the following:
- Hunger is not a singular motivation: it is the interaction of several different clinically measurable, provably distinct mental and physical processes.
- In a properly functioning human animal, likes and wants coincide; satiation is an accurate predictor of satiety; and the combination of hunger signals (likes and wants) and satisfaction signals (satiation and satiety) results in energy and nutrient balance at a healthy weight and body composition.
- Restrained eating requires the exercise of willpower to override likes, wants, and the lack of satiation or satiety; the exercise of willpower uses energy and causes stress; and stress makes you eat more. Therefore, a successful diet must minimize the role of willpower.
Now we can examine some of the ways that our hunger signals fail us.
It is important to remember that, by definition, all our hunger drives are in balance with our willpower at any moment in time! Otherwise we would be eating more or less than we are. The issue is that for many of us, this balance is only reached at an unhealthy weight or body composition—or it involves an excessively stressful amount of willpower. Part III explores this subject in detail.
Why Are We Ever Sated?
The desired result of eating is satiety: our body’s signal that it is replete with nutrients. But first, let’s ask a question: why are we ever sated? Since starvation is an animal’s primary concern, why didn’t Paleolithic humans simply eat themselves into obesity whenever possible?
We all know what happens if we eat a big meal just before intense exercise: at best, our performance suffers greatly, and at worst, we vomit. This is because digestion requires a meaningful amount of energy. Clearly it would be counterproductive to go hunting when our mental and physical performance is greatly impaired. Even foraging would be impaired, as gathering in the wild requires a keen eye and close attention, and the brain uses perhaps 20% of our energy at rest.
So it’s clear that we must wait until our body has either used or stored the energy and nutrients from our previous meal before we perform at our best. The fact that ghrelin is neurotrophic makes this clear: our brains only kick into high gear when it would be both possible and beneficial to acquire more food.
This suggests an obvious consequence: energy retrieval from storage is an important part of satiety. We don’t eat via a constant intravenous infusion of exactly the nutrients we need, at exactly the rate we are using them: we digest them and store them for use as needed. I’ll explore this in detail below.
Not so well suited to the African savanna.
Everything Flows Downhill From Satiety
As we previously established, satiety is our body’s signal that it is replete with nutrients. Therefore, it should be obvious that nothing can make up for a lack of satiety: no amount of tricks to achieve temporary satiation will make up for a nutritional deficiency.
Satiety Is Not Generic
As stated back in Part II, “hunger” is not a generic drive, satisfiable by a generic substance called “food”. A properly functioning animal is hungry for different foods, depending on its nutritional status: even butterfiles—insects!—are smart enough to lick water off of mineralized rocks, and every animal, from aardvark to zebra, is capable of finding and ingesting the myriad nutrients it needs to survive.
The Salt-Mining Elephants of Kitum Cave
There are caves in Mount Elgon National Park, Kenya, partway up the shield of the extinct volcano Mount Elgon. (The best-known is called Kitum Cave.) The soil in the park is of recent volcanic origin, and the high rainfall washes away many of its minerals, leaving animals throughout the reserve deficient in many things—most critically, sodium.
Kitum Cave reaches over 700 feet into the side of Mount Elgon, and the cave complex of which it is a part contains the only known salt deposits in the region. Consequently, nearly every herbivore in the park must make periodic pilgrimages to the cave—up the side of the mountain, and over a long, narrow, dangerous path with no escape—in order to lick sodium sulfate from the rocks of Kitum Cave. In fact, it is plausibly argued that Kitum Cave was primarily created by the mining actions of elephants scraping salt from its walls and floor!
Joyce Lundberg and Donald A. McFarlane
Speleogenesis of the Mount Elgon elephant caves, Kenya
GSA Special Papers 2006, v. 404, p. 51-63
(fulltext, includes pictures and figures)From Lundberg and McFarlane’s overview article, “Mount Elgon’s Elephant Caves”:
“The caves, of which Kitum and Makingeny are the best known, have long been known to attract elephants and other animals. The herbivores enter the dark cave interiors to consume salts, mainly mirabalite and sodium sulphate (Glauber’s salt) that effloresce from the cave walls. The crystals are gouged out by elephant trunks and bushbuck teeth and licked off wall by buffalo.”
Elephants in Kitum Cave.
BBC 2 once aired an amazing documentary called “Elephant Cave”, which shows just how dangerous the round-trip to and from the cave is. Unfortunately it’s not available to watch online, but the enterprising web searcher can probably find a torrent of it.
Note that Kitum Cave is not the only example of a salt ingestion cave, just the largest known:
Lundquist Charles A., Varnedoe Jr. William W.
Salt ingestion caves
International Journal of Speleology, vol 35, issue 1, pp. 13-18, 2006.
(Note: containts link to fulltext PDF)
In conclusion, even small, skittish herbivores like bushbucks have instinctive hunger drives of sufficient discernment to motivate them to make a dangerous pilgrimage up a volcano to obtain just one of the many nutrients—sodium—they need to live.
We should not expect any worse from the hunger drives of a properly functioning human animal.
How Satiety Fails
Now we are ready to dig into the meat of this essay.
Satiety can fail in three ways:
- We fail to ingest the energy and/or nutrients our body requires.
- We fail to absorb the energy and/or nutrients our body requires.
- We cannot retrieve the energy and/or nutrients our bodies have stored.
Satiety Failure #1: Failing To Eat The Real Food We Require
We know from experience that no matter how many calories worth of Skittles or Oreos we eat, we won’t satisfy our hunger. Our stomachs might be full to bursting—but as soon as we have room to digest it, we’ll be hungry again, because Skittles and Oreos don’t give us the nutrients we need to live. And as I’ve explained above, satiety is not generic: if we’re short on any one of the hundreds of nutrients our body needs, we’ll keep eating until we get it.
I’ve linked this study before (hat tip to Fat Fiction), but since it’s so illustrative, I’ll link it again:
Y Li, C Wang, K Zhu, R N Feng and C H Sun
Effects of multivitamin and mineral supplementation on adiposity, energy expenditure and lipid profiles in obese Chinese women
International Journal of Obesity (2010) 34, 1070–1077“After 26 weeks, compared with the placebo group, the MMS group had significantly lower BW [body weight], BMI, FM [fat mass], TC and LDL-C, significantly higher REE [resting energy expenditure] and HDL-C, as well as a borderline significant trend of lower RQ [respiratory quotient] (P=0.053) and WC [waist circumference] (P=0.071). The calcium group also had significantly higher HDL-C and lower LDL-C levels compared with the placebo group.”
How much is “significant”? From the summary:
“…The multivitamin and mineral group lost an average of 3.6 kg (8 pounds) of body weight, compared to 0.9 kg (2 pounds) and 0.2 kg (0.44 pound) for the calcium and placebo groups, respectively.
Protein targeting is another very important issue (previously discussed here.) Our bodies have an absolute requirement for complete protein—but unlike carbohydrate or fat, we have no storage depots for it. So if we don’t get complete protein in our diet, we must disassemble our own tissues to get it. (Previously discussed here.)
“Protein” is just chains of amino acids. “Complete protein” is protein containing all the essential amino acids—the ones we must eat because our bodies can’t make them—roughly in the proportions our body needs them.
On the other hand, if we eat too much complete protein, our bodies have a limited capacity to convert it into glucose…so we tend to desire neither too much nor too little complete protein. For more on protein targeting, including links to the scientific literature, read Dr. Paul Jaminet’s excellent summary, “Protein, Satiety, and Body Composition.”
(This satiety mechanism can be extended to other essential nutrients—but this article is already far too long!)
In closing, I’ll note that a can of Pringles has the same number of calories as a dozen large hard-boiled eggs. Which will leave you sated hours later: 32 Pringles (300 calories), made of seed oil and potato slurry—or four hard-boiled eggs (300 calories), containing 12g of complete protein and a host of vitamins, minerals, and essential nutrients like choline and lutein?
Satiety Failure #2: Failing To Absorb Nutrients
It doesn’t matter if we eat real food if we can’t absorb its nutrients.
Unfortunately, covering the various gut malabsorptions and dysbioses, such as celiac, IBS, Crohn’s, and SIBO, is well beyond the scope of this series. However, I must stop to point out that a diet low in simple sugars and high-GI simple starches, and that eliminates the antinutrients, enzyme inhibitors, and gut irritants found in grains and (to a lesser extent) beans and many nuts, is beneficial for almost all such issues.
Yes, I’m talking about a functional paleo diet.
(Those interested in digging more deeply into the subject might want to watch Dr. BG’s presentation at AHS 2011. Here’s the video, and here are the slides.)
Satiety Failure #3: Energy Stuck In Storage
We use energy continually throughout the day. And depending on how active we are, our energy usage can go from ‘minimal’ (sitting on couch watching TV) to ‘moderate’ (walking, intense mental activity) to ‘huge’ (sprinting at top speed, lifting heavy objects).
Yet we do not eat a constant stream of calories that corresponds exactly to our current degree of physical and mental effort. Our bodies must store the energy we eat for later usage. And as our storage capacity for glucose (as glycogen) is very limited, our body’s long-term energy storage is…fat.
Glycogen: A Short Explanation
A glycogen hairball.
Glycogen is a big hairball of glucose molecules connected to a protein called glycogenin, and it’s how our body prefers to store glucose. However, our body’s glycogen reserves are small: perhaps 70g in the liver and 200g in all our skeletal muscles, combined.* (The second capacity increases with muscle mass and training: a large, muscular, trained athlete can store perhaps 400g.) Furthermore, glycogen cannot be shuttled out of or between muscles: it’s only available to the muscle containing it.**This isn’t very much energy: about 1100 calories’ worth, of which only 240 are available to the brain via the liver. So our bodies store most excess energy as fat, which is more energy-dense (approximately 9 calories/gram vs. 4), and for which we have a basically infinite storage capacity in our adipose tissue (‘fat cells’).
* Figures cited for muscle glycogen storage vary widely, and I haven’t found an authoritative source. Furthermore, it’s not clear how deeply storage is or can be depleted by exercise: even running to exhaustion only depletes specific muscles by perhaps 40-60%.
** This study (hat tip to alert commenter Franco) appears to show that glycogen can move slowly between muscles (over the course of hours), but only after exercise and only when fasted. Transfer doesn’t appear to be significant during exercise.
But what if we had trouble using fat for energy—or using energy at all? Clearly we’d have a problem: we would eat food, and as soon as the energy was either used or stored, we’d be hungry again—even though we were gaining weight!
This is exactly what happens to many people.
I’ve previously discussed metabolic flexibility and the RER (“Respiratory Exchange Ratio”), also known as the RQ (“Respiratory Quotient”), at length in this article. Metabolic flexibility (“met flex”) is the ability of our cells (specifically, our mitochondria) to switch back and forth between glucose oxidation and fat oxidation for energy, and the RER/RQ is how we measure what proportion of glucose vs. fat we’re burning.
It turns out that:
- The obese have impaired metabolic flexibility.
- The obese have impaired mitochondrial capacity to turn nutrients into energy in the muscles.
- The obese have an impaired ability to oxidize fat for energy, which we can objectively measure.
- Both the formerly obese and the soon-to-be-obese also suffer these impairments.
Linda Bakkman, Maria Fernström, Peter Loogna, Olav Rooyackers, Lena Brandt, Ylva Trolle Lagerros
Reduced Respiratory Capacity in Muscle Mitochondria of Obese Subjects
Obes Facts 2010;3:371-375
(fulltext available as PDF)“Obese subjects had a decreased respiratory capacity per mitochondrial volume compared to the reference groups: this was evident in state 4 (65% and 35% of reference group A and B, respectively) and state 3 (53% and 29% of A and B, respectively) (p < 0.05)."
In other words, obese people have a greatly decreased ability to create energy from the nutrients they ingest.
The ability to oxidize fat is also impaired. How great is this impairment?
Ranneries, C., Bulow, J., Buemann, B., Christensen, N. J.,
Madsen, J., & Astrup, A.
Fat metabolism in formerly obese women.
AJP – Endo January 1998 vol. 274 no. 1 E155-E161“…Fat mobilization both at rest and during exercise is intact in FO [formerly obese], whereas fat oxidation is subnormal despite higher circulation NEFA levels. The lower resting EE [energy expenditure] and the failure to use fat as fuel contribute to a positive fat balance and weight gain in FO subjects.”
The difference is remarkable. From Table 2 of Ranneries et.al., we find these startling facts:
- Normal subjects are burning 30% more calories at rest than the formerly obese.
- Normal subjects are burning 7% carbs and 78% fat at rest, whereas formerly obese subjects are burning 49% carbs and 34% fat at rest!
Let that sink in for a moment. These aren’t even the obese: they’re the formerly obese. So the theory that some people become “metabolically broken” has factual support.
Here’s the graph of fat oxidation before, during, and after an hour-long bout of exercise. The triangles are controls, the circles are the formerly obese:
Fraction of energy expenditure covered by fat oxidation (E%) during rest (t = 0 min), exercise (t = 0–60 min), and recovery (t = 75 min) in formerly obese subjects (FO, •) and matched controls (C, ▿). Values are means ± SD.
We can easily see that normal subjects have metabolic flexibility—the ability to switch back and forth between carb and fat oxidation—whereas the formerly obese are impaired. (Though exercise does increase metabolic flexibility, as I’ve previously noted.)
Continuing, we see that RER (= RQ) is predictive of future obesity:
F. Zurlo, S. Lillioja, A. Esposito-Del Puente, B. L. Nyomba, I. Raz, M. F. Saad, B. A. Swinburn, W. C. Knowler, C. Bogardus, and E. Ravussin
Low ratio of fat to carbohydrate oxidation as predictor of weight gain: study of 24-h RQ
AJP – Endo November 1990 vol. 259 no. 5 E650-E657“Subjects with higher 24-h RQ (90th percentile) independent of 24-h energy expenditure were at 2.5 times higher risk of gaining greater than or equal to 5 kg body weight than those with lower 24-h RQ (10th percentile).”
There are many more interesting papers I could cite and quote here—but if I do so, this article will expand to an unreadable size! So, instead of bombarding you with more citations, I’ll quote this excellent research review, which contains more citations for the above facts, and even more fascinating data for which space does not permit discussion.
Mary Madeline Rogge
The Role of Impaired Mitochondrial Lipid Oxidation in Obesity
Biol Res Nurs April 2009 vol. 10 no. 4 356-373
(fulltext available as PDF)“Figure 2. In obesity, impaired glucose tolerance, and type 2 diabetes, mitochondrial beta-oxidation is decreased in skeletal muscle cells.”
[Beta-oxidation is the process by which mitochondria produce energy from fat.]
“Carnitine palmitoyltransferase 1 (CPT1) activity, necessary for the transport of long-chain fatty acids into the cell, is diminished, leading to the accumulation of fatty acyl-CoA within the cytosol. Under the influence of the enzyme acetyl-CoA carboxylase (ACC), unmetabolized fatty acyl-CoA is converted to malonyl-CoA and committed to the re-synthesis of fatty acids, which can accumulate within the cell or be transported to other tissues as triglycerides. The reduced ability to use fatty acids for ATP production increases obese individuals’ reliance on glycolysis and decreases their exercise capacity.”
If you want to learn more, p. 361 of the full text and the subsection “Decreased Fat Oxidation” will be quite illuminating, and I strongly recommend reading it. For that matter, just read the whole paper, as it’s an excellent overview and summary.
These facts provide an explanation for the additional fact that some people, particularly the obese, do not find carbohydrate to be satiating:
Chambers L, Yeomans MR.
Individual differences in satiety response to carbohydrate and fat. Predictions from the Three Factor Eating Questionnaire (TFEQ).
Appetite. 2011 Apr;56(2):316-23. Epub 2011 Jan 8.“Those scoring high on the TFEQ-disinhibition scale consumed more energy at the snack test than those with low TFEQ-disinhibition, but this was only following the high carbohydrate breakfast. … In normal-weight females the tendency to overeat may be related to insensitivity to the satiating effects of carbohydrate.”
An impaired ability to burn fat for energy means that you will no longer be sated once your blood sugar drops, leaving you hungry again—even though most of the energy has been stored and you are in positive energy balance. In other words, the combination of impaired fat oxidation and a high-carbohydrate, low-fat diet is likely to leave you both hungry and gaining weight. (See this study for a real-world instrumented comparison.)
Impaired fat oxidation also causes the “low carb flu”. You’re forcing your body to adapt to burning fat by refusing to provide it with carbohydrate—but since your mitochondria don’t burn fat very well, you’ll have very little energy until you adapt.
I conclude this section with several thoughts:
First, this is not the “greedy fat cells” theory of obesity, which posits an inability of the obese to retrieve fat from fat cells into circulation. That ability appears to be intact. What is indisputably damaged is the mitochondrial function of the obese, the formerly obese, and the soon-to-be-obese, and their ability to oxidize fat for energy.
Second, any valid theory of obesity or its treatment must take the facts of these metabolic impairments into account.
Third, satiety is indeed a primary driver of hunger, and without satiety we will always be hungry—but as important as it is, this is only one part of the answer to “Why are we hungry?”
Conclusion
A lack of satiety will leave us hungry no matter what else we do to compensate.
We fail to achieve satiety in the following ways:
- By not ingesting the energy and/or nutrients our body requires.
- By not absorbing the energy and/or nutrients our body requires.
- By an inability to retrieve the energy and/or nutrients our bodies have stored, due to impaired metabolic flexibility caused by impaired mitochondrial function and, most importantly, impaired fat oxidation.
Thank you for reading all the way through this long but (I believe) rewarding article! The following installments explore failures of the other hunger drives—and once we understand the failures, we can finally begin to construct workable solutions.
Live in freedom, live in beauty.
JS
Continue to Part V: When Satiation Fails…Calorie Density, Oral Processing Time, and Rice Cakes vs. Prime Rib.
This is Part IV of an ongoing series. Go back to Part I, Part II, or Part III.
Did you find this article interesting or illuminating? I certainly hope so, because writing it was an ordeal. Use the buttons below to share it!
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
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).
Extremely interesting, as always. Thank you for taking the time to share. Be well.
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
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!!
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! 😉
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’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.
Great series!
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.
Hey everybody! Help spread this one around! Twitter it, like it on Facebook, post it on forums…it's important.
anand:
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?
Anastasia:
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.
Franco:
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.
Txomin:
Thank you. I'm doing very well, actually, after a recovery from AHS and an epic adventure I'll be recounting soon.
LeonRover:
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.
goddesslynne:
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.
chris:
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.
tess:
Buy it directly from 100 Watt Press and I'll sign it for you!
Timothy:
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.
Beth:
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.
JKC:
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.
Evan:
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.
JS
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 + […]
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?
“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).”
The transfer might be much more significant in higher intensity exercise (e.g. lifting) under anaerobic conditions.
I have other studies showing glycogen depletion is shifted towards fast twitch fibers during higher intensities. In any case, the depletion seems never more then ~1/3 of total glycogen stores in the worked muscles in all studies I have seen. So, maybe this “remaining glycogen storages just 2/3 wall” does indeed represent a limiting factor in (anaerobic) exercise.
Anecdotally, me and many others reported “loosing reps” from a given weightexercise(to failure) while on very low carb.
Most of the weightlifting world does agree that regular “carb ups” are required for lifting performance, especially while low carbing.
For me, a PHD with ~100g of safe carbs/day is enough to feel and perform well without the need of carb-induced comas once or twice per week.
Mmh…, somehow my posts here always wander off-topic, sorry for that!
Beautifully written! You certainly are a natural and gifted writer. I’ve always suspected that specific cravings are the body’s wisdom to goad you to seek out missing nutrients.
great write up. i think from personal experience the following is a good way to cut back on bodyfat:
very low carb for a short period: i did atkins induction level so 20g carbs but i kept functional paleo in mind with my food choices.
after that full paleo (plus dairy if you tolerate) with lots of veg and some fruit (keep that low if fat loss is goal but no need to go mental with it)
this has twice this year enabled me to lose considerable fat mass while continuing to improve body composition and weights progression.
my wife is starting on this now and lost the following:
week one, 3 pounds
week two, one pound (time of month)
week three, 6 pounds!
i think the difference between women and men is quite significant though, i got 10 pounds in my first two weeks on both times this year (but i train 3 times a week, my wife has just started training properly this week).
longterm i think functional paleo is where i will live diet-wise. right now i’m focussing on muscle gain/retention and fat loss so not cheating at all.
my future definitely involves dark chocolate though 😀
Amazing article!
optimalhealthsource.blogspot.com
Jacquie:
I'm sure it's the case that most of the “formerly obese” were on Weight Watchers or some other standard diet plan.
Eating low-carb paleo certainly helps — but there is clear evidence that some people have permanently altered metabolisms that simply can't tolerate carbs like they did before. Jack Kruse can probably talk about the role of leptin and hypocretin neurons…I don't want to get into that because there is still a lot of argument about exactly what leads to this state and how (or if) it can be recovered from. However, there are a few suggestive leads which I'll be investigating and reporting on once the series gets to the point of offering proposed solutions.
Meanwhile, any intense exercise that depletes glycogen will definitely help you, as seen in my article which Paul pointed out. You don't have to exercise for long durations, and lifting heavy things is a great glycogen depleter: pushups (wall pushups or knee pushups if you can't do normal ones) are great, as are air squats…anything that makes you breathe hard will do.
Jamie:
Great to hear from you! I was disappointed we didn't have any time to converse at AHS…too much to do, too little time.
Anyway, your suggestions are good. I'm looking into MCTs right now…the chemistry seems sound, because the implication is that transport is the biggest bottleneck (though function in general is also impaired). And we know about the beneficial effect of glycogen-depleting exercise on met flex and IR…
If you have any other ideas or suggestions, leave a comment or email me directly (through the “Contact” link)…of course I'll acknowledge and plug all contributions. (This holds true for everyone, btw, not just Jamie.)
Thanks for stopping by! I've been plugging your site for a while, and am glad to see you getting recognized for it.
Franco:
No, please post links to references if you have them. It's always been an article of faith that glycogen can't move out of muscles, only in…so if it can be transferred, even if only at a slow rate and under certain limited circumstances, that has direct relevance to what we're talking about.
Aaron:
Thank you! I work hard on these articles, and I appreciate it when people notice.
As far as cravings (note: cravings for actual food, not Oreos), particularly for random vegetables, I think you're right. Why would I suddenly crave seaweed salads and sushi handrolls? Answer: I need iodine. And so on.
eddie:
I think you're right: many people notice that they can dial their bodyweight by altering carb intake and nothing else. I actually get too skinny on VLC unless I force myself to drink protein/heavy cream shakes and other artificial calorie bombs.
Functional paleo is a good place to be…it lets us worry less about doubtful anthropology and more about biochemistry.
Rafael:
Thank you!
JS
JS,
I have the most relevant of the glycogen-depletion studies saved on my pc. Don’t want to spend again the time to search the net for days. I can send you some by mail if you want. Just tell me.
The full text of the one I quoted above, by the way shows that the amount of depletion from the forearm is not so trival like the abstract implies. And that’s the depletion happens after the exercise isn’t so important in my view. Some studies anyway show that depletion continues after exercise in the worked muscles, especially with higher intensities (sprinting/lifting).
[…] posts: JS Stanton of gnolls.org has been doing a great series on satiety, hunger, and obesity. Part IV went up this week. JS points out that the obese have damaged mitochondria and reduced ability to […]
Franco:
Yes, please email them to me! You should have my email address now.
JS
Hey JS,
There's been a lot of dissention among the ranks; and it's making it hard to make clear what is and is not bad based on *one* person's interpreation of the science. Recently Stephan has been making some headways into this, as long as some others. One of the most disconcerting posts was this one: http://wholehealthsource.blogspot.com/2011/08/seed-oils-and-body-fatness-problematic.html
I wonder what your take on it is?
Chris:
I'm puzzled at the post you reference for several reasons, not the least of which is that he seems to be directly confronting Paul Jaminet's recent post “Low-Carb High-Fat Diets and the Thyroid”, which referenced Stephan's earlier work, and which I find to be very well reasoned.
Note that Paul's post references only human studies, which I find much more convincing than rodent studies, especially mouse studies — since mice are herbivores, any study that feeds fat to mice (especially animal fat) isn't going to tell you much.
(Rat studies are more relevant, since rats are at least omnivores — although since seeds and grains are a significant part of their diet, they are likely to have better adaptation to grains and grain products than humans. Also consider the relative time and reproductive capacity of rat vs. human generations, and the consequent speed of environmental adaptation, specifically to agricultural diets.)
Also note that Stephan has taken down two of his old posts, “Omega-6 Linoleic Acid Suppresses Thyroid Signaling” as well as “Vegetable Oil and Weight Gain”. I recommend saving a copy of each out of Google's cache while they're still there, so you can see for yourself how his thinking on the matter has changed, and whether you find the change convincing.
My take on that post: Stephan's conclusion seems to state that there is still a strong correlation between n-6 intake and obesity — but he believes it's purely due to n-6 intake increasing the reward value of modern foods. First, see my note above about mouse studies. Most importantly, given that high n-6 intake has known metabolic effects that have nothing to do with dopamine signaling pathways, such as disrupting liver function (e.g. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1797607/), I don't find the conclusion convincing.
Future articles in this series will address the role of food reward in hunger signaling.
JS
[…] is a fact that they do, but people disagree on the reason why.[Update 22/8: I was notified of a great article on the causes of hunger and weight gain over at gnolls.org, I highly recommend that you read […]
Thanks for opting in JS. I left my personal belief out of it; but you've mimicked and as always, added more to my thought process than what I originally had.
I whole-heartedly agree that I had trouble agreeing with the conclusions since most of the studies were about rodents; I'll also take a more detailed look at Stephan's original posts.
Thanks again for your input!
[…] a great series on satiety, hunger, and obesity. Part IV went up this week. JS points out that the obese […]
JS
As someone who has read everything you’ve written herein, plus the Gnoll Credo, plus the books you’ve recommended, and a considerable number of the papers, I must again add my voice to the choir of appreciation for what you’ve done here! This piece is another wonder of clarity and concision, despite its length (which isn’t much, actually, considering the volume of information it contains).
A shout-out to the commenters who have contributed, too.
I’m in the process of preparing a series of small nutrition talks to give at the gym where I work and I’m basically going to paraphrase your entire blog! (with due attributions, of course)
Thanks again for the fine work.
Juan
Indeed! Thanks, man!
Chris:
Sure! I'll be addressing reward more directly as the series continues.
Juan:
This post was an ordeal to write, so I'm glad you find it useful…and I'm honored that you find my work to be a credible source of information. I only request that if you're going to paraphrase me, that you plug me at some point, too 🙂
Paul:
You're welcome!
JS
Great series. I’m excited to see what’s next – while I’ve never been obese, I was “skinny fat” and have a surprisingly high body fat %, although eating paleo and doing lots of strength training is bringing it down. I imagine I have trouble using my fat for energy too, so I’m curious about what you’ll discuss!
Alta:
Welcome! There are a lot of skinny people who are diabetic or pre-diabetic, and undiagnosed…and they tend to be “skinny-fat” because of the mitochondrial dysfunction.
Congratulations on your progress!
JS
[…] When Satiety Fails: Why Are We Hungry? Part IV September 8, 2011By: J. Stanton Read the Full Post at: GNOLLS.ORG […]
[…] I deeply thank J Staton for doing all of the work for me, reading Hyperlipid and taking the trouble to get the key cut then posting it to me via the comments. Go read. […]
Still haven’t found “the answer.” I lost 100 lbs on a low-carb diet in 1999 (actually 130, but re-gained 30). Having low-fat-dieted myself all the way to 350 lbs, losing that much and keeping most of it off for a dozen years has been relatively easy. What has *not* been easy is getting rid of the remaining 50+ lbs I need to lose (for several reasons, including Obstructive Sleep Apnea). I can struggle my way down to around 240, and then the weight seems to just re-attach itself despite my almost religious avoidance of carbohydrate. I’m down close to eating only meat (and some supplements, mostly minerals, but including Vitamin C, D, & K), yet the weight will not budge below 240.
I keep reading all of this talk about leptin, and impaired metabolism of former fatties. That’s all good information, but what I’m looking for is HOW DO I FIX IT?
Howard, I appreciate your comment as I am having a similar experience. Can I have your contact information? I have as of yet to find a solution. I need to lose an additional 30 (maybe even 40) pounds to achieve “ideal” weight and it seems that no matter what I try the weight will not budge!
Fascinating article! (found it through Peter’s blog). I have to add a comment from a different angle: our ability to oxidize stored and dietary fat is limited not only for people with metabolic syndrome but for everyone – except those limits are vastly different! Chris Masterjohn posted a very interesting article touching this aspect (read also my comment there underneath). One of the limiting factors seems to be the cellular and immune system’s ability to handle metabolic byproducts, involving glutathione.
An upper limit on fat on a high animal fat LC diet (like the one I am on since 1999) could be an important factor preventing some people from effectively using such a diet for healing themselves. For most people such limit is well below satiety threshold, that is you would first stop eating fat (i.e. try overeating butter!) before you manage to overeat it, but for some this limit is so small (initially) that overeating may happen.
It would be very interesting and useful (if you have means) conduct more thorough study on what that limit exactly is for different groups of patients and what is a typical time-frame for the limit to increase. For example in my case it was 2 months (I was 43 at the time with some metabolic syndrome). I knew of people (very rarely) who had to abandon a high fat diet after several months to a couple of years due to that effect.
Regards,
Stan (Heretic)
Howard, Stephen:
This series isn't complete yet. After I define and explain all of the hunger motivations, the Big Picture should allow us to start drawing some useful conclusions.
One thing to keep in mind is that hunger is multifactorial. Your low-carb eating has most likely addressed the satiety/energy storage issue, and now you're running into a different limiting factor caused by something else. But without knowing your current diet and eating habits, I can't possibly make any suggestions.
Stan:
The dysfunction discussed here (and in Rogge et.al.) is a defect in the carnitine shuttle that decreases the effective “bandwidth” available for oxidizing long-chain fats (including palmitic acid) in the mitochondria. This would cause the “overload” referred to in Masterjohn's article to occur more quickly and at a lower threshold.
So it appears that the two mechanisms are complementary. I'd seen the article but hadn't related it to this one…thanks for pointing that out!
As far as studies, I'm not involved in academia and am in no position to conduct a formal study. I'm happy to accumulate and present others' experiences, though!
JS
[…] Debattens vågor fortsätter att gå höga om vad som egentligen gör oss feta (typ debatten mellan Taubes och Guyenet) och flera kunniga personer har kommit med intressanta inlägg. Ett av de senaste, av J Stanton på gnolls.org, är mycket intressant: When Satiety Fails: Why Are We Hungry? Part IV. […]
[…] Re: Cubbie's Low/No Carb Log Referenced by Peter at hyperlipid and an excellenbt read. It plays into all the recent controversy… When Satiety Fails: Why Are We Hungry? Part IV - GNOLLS.ORG […]
[…] steps forward in the obesity discussion: Peter at Hyperlipid is following up on JS Stanton’s lead regarding mitochondrial dysfunction in obesity. CarbSane chips in with evidence for metabolic […]
[…] Part VI which explains key concepts relating to food reward, and has links to Parts I through V. Part IV was my […]
[…] When Satiety Fails: Why Are We Hungry? Part IV […]
Hello form Greece.
Excelent and full digestible article.
Thank your brain cells for exchanging glucose to usefull thoughts.
George:
Thank you! It's always good to hear that I've succesfully communicated to my readers.
I'm sure ketones were involved, too.
JS
[…] for Maximum Nutrient Density One proposed reason behind eating in excess is that our bodies are not getting the base nutrition it needs from our […]
[…] has a clear relationship to how much energy storage we carry in our bodies, or to our health. The changes to our diet that have correlated with the obesity epidemic have not been in how much meat we eat, but in how cheap and highly available vegetable oil and high […]
[…] high-carbers and ab-libitum low-carbers? Somehow people eating more carbs might eat more and be hungrier? What carbs are we comparing here? A diet of steamed chicken breast, whole grain pasta and […]
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