Unfortunately, we only got around to answering three of the questions I had selected:
- How does one lose fat?
- What do I (Stephan) eat?
- Why do many people gain fat with age, especially postmenopausal women?
What do you think about cutting carbohydrate for fat loss? Why does my weight increase after adding carbohydrate back to a low-carbohydrate diet?
As carbohydrate is a major factor in food reward, reducing it will allow fat loss in some people. Long-term studies of low-carbohydrate diets without deliberate calorie restriction indicate that the average person maintains a 5-10 pound weight loss at one year, mostly as a result of fat loss. Studies show similar trends for low-fat diets unrestricted in calories, although the fat loss is a bit less.
I think that an optimal diet for lean healthy people is probably not restricted in macronutrients, and if anything a diet biased toward carbohydrate is better for overall long-term health than one biased toward fat. However, obesity and diabetes are important factors in health, and if a person finds that reducing carbohydrate attenuates them, then it's worth considering.
In susceptible people, body fat increases after adding carbohydrate back to a low-carbohydrate diet because you're increasing the overall reward value of the diet, not because you're spiking insulin more. Carbohydrate is not inherently fattening, it just depends on the context. Replacing more fat with carbohydrate in the context of a low-fat diet will not increase the diet's reward value and will if anything accelerate fat loss. Conversely, while adding fat to a low-fat diet will increase its reward value and favor fat gain, replacing more carbohydrate with fat in a low-carbohydrate diet will if anything favor fat loss. But there will always be individual variation as the reward value of specific foods differs between individuals.
What is the role of insulin in body weight control?
Insulin has a role in body fat control, but it's the opposite of what many people believe it to be. In fact, insulin acts in a manner similar to leptin, although less potently:
- When injected into the brain, it reduces food intake and body weight in rodents and primates (1, 2)
- Knocking out the insulin receptor in the brain leads to increased fat mass (3)
- Foods that spike insulin the most in humans lead to the greatest satiety and lowest food intake at subsequent meals (4)
- Insulin is co-secreted with amylin, a hormone that reduces food intake and body weight, probably by increasing leptin sensitivity (5)
Insulin does act directly on fat cells to promote fat storage, but under normal circumstances, that's not a significant factor in 24 hour fat mass balance if you consider its effect in a whole, live organism (as opposed to cells in a dish). Type 1 diabetes is an exception, because insulin is completely lacking and fat can't get into fat cells at all, so people become very lean. Fat cells require some insulin to function normally. But T1DM isn't exactly a prescription for health!
Is fat mass controlled by a setpoint or a settling point?
There is no agreed-upon definition of what exactly a setpoint and settling point are, but here are two definitions that I find reasonable:
- A setpoint is regulated by an active, centralized system that measures the variable in question and defends against changes.
- A settling point is regulated by the passive confluence of many factors that influence the variable in question, and can also defend against changes.
One of the objections people have to the term "setpoint" is it sounds immutable and unresponsive to other factors. I believe the leptin system is modulated by food reward, and probably other factors to a lesser extent. So you could call it a setpoint that's responsive to other factors, especially food reward, or you could call it a settling point. I don't feel very dogmatic about it. Call it what you want.
In Peter's post re: Potato Diet and Weight Loss (http://high-fat-nutrition.blogspot.com/search/label/Potatoes%20and%20weight%20loss%20%281%29), he wrote the following - "The ultimate determinant of weight loss is fasting insulin"
Based on your post, would you disagree with Peter? If not, can you help connect the dots?
"...and if anything a diet biased toward carbohydrate is better for overall long-term health than one biased toward fat."
What causes you to say this, Stephan?
My understanding has always been that fat has been unfairly demonized in the mainstream media, and you've written extensively about the inaccuracy of the diet-heart hypothesis.
Since eliminating the "neolithic agents of disease" from my diet (sugar, grains, legumes, etc.), I've primarily replaced the lost calories from carbohydrates with calories from fat. This seems to be pretty widely endorsed in the paleo/ancestral eating blogosphere (e.g. Kurt Harris, Eades, etc). Would you say this is unhealthy?
I'm enjoying reading Seth Robert's work around the notion of a set-point (not set in stone, but specifically influenced by an average caloric intake over the previous n meals). He certainly has produced astonishing results with his Shangri-la diet. It's worth checking out:
Darin and Aravind,
My questions exactly!
I was referring to insulin spikes rather than fasting insulin. Still, I doubt fasting insulin plays much if any role in fat loss.
I don't think fat is inherently unhealthy, and I don't think saturated fat is unhealthy. I said "if anything" because I think there's still a lot of uncertainty. I'm not condemning fat or high-fat diets. A person can probably be perfectly healthy on a high fat diet if it's designed well. However, I think most of our ancestors have probably been eating more carb than fat for a very long time, so my default stance at this point is that if you're going to bias your diet toward a macronutrient, I'd go for carb.
Yes, I've read his book and we discussed his ideas in the podcast.
I wonder how you integrate these thoughts with the effects of liver damage from excess nut & seed oils + fructose. Is that meaningful, or are the negative effects just from the tasty reward of those foods?
Definite potential for a paradigm shift in the ancestral health community! I'm eager to see how these ideas develop.
With Dietary Fructose, would you say that it is fattening because it messes with leptin, or it is fattening because it compromises hepatic, and then systemic, insulin sensitivity? Or neither?
Are foods like refined vegetables a chief cause of leptin resistance?
And finally, is your main strategy in fat loss simply caloric restriction, or simply finding a way to decrease food reward?
If you answered these in the podcast, sorry! I'll listen soon.
I tried to repeat all-potato diet experiment, originally aiming at 2 weeks. My current BMI is ~24.5.
I was totally full at calorie intake of about ~1600kcal/day (~2.1kg potatoes), significantly lower than normal requirements of a healthy male. I was not hungry, or craving for anything, I even had to remind myself to eat.
But my energy levels were constantly very low (unlike in the original experiment), so low that I had to stop experiment after 5 days, as it was already interfering with my normal functioning.
Does it make sense? Lack of hunger strongly pointed one way, energy levels strongly pointed the opposite way.
I kept caffeine intake at the same levels as usual, and I had plenty of water all the time.
Do you have any explanation for this data point? Are you aware of anybody else having tried to eat only potatoes if only for much more limited time than in the original experiment?
In relation to your reponse to Darin regarding your default towards carbohydrate in terms of eating in line with what our ancestors ate, I presume here that you are talking about particular kinds of carbohydrate and perhaps not about grains or of course sugar? Do you think a major consideration here is also the degree of glucose intolerance such that the more glucose intolerant the more likely the person will be to benefit from a low carb approach? If this is the case then we can say a low carb approach would benefit a large section of the population as a large section are indeed glucose intolerant. A point to make here is that paleo could be either low carb or high carb.
you really post nice blog here..Its interesting and useful..keep posting ..I am going to follow your blog
Perhaps the health benefits of leaning towards a more balanced intake of carbs vs fats is lower frequency of ingesting oxidized lipid from the way we are preparing our foods????
On a completely unrelated note: Stephan, have you researched the beta-casomorphine-7 epidemiology at all? Very interesting stuff.
Are you aware of anybody else having tried to eat only potatoes if only for much more limited time than in the original experiment?
My diet has been potato based for awhile now and I love it. I usually consume about 3k cals from potatoes and 1-2k from other stuff(butter, chocolate, milk etc.). I have an extremely active lifestyle and find potatoes give me a ton of energy but it can be rather hard to consume enough calories sometimes, my brother especially has problems with this but its not too hard for me most the time. If you plan to eat potatoes for the majority of your diet long term you should definitely make sure you at least getting bare minimum calorie reqs imo.
There is a study if you search around from the 1930s where they put volunteers on a potato and fat diet(about 50/50% calorie wise) and the volunteers were able to maintain nitrogen balance and gain some health improvements. One of the volunteers did start to lose a significant amount of weight a while into the expirement but they said it was because he took up a new exercise regimen.
Hi Stephan ,
I am a great admiror of your work, but I will have to disagree with you today.
Foods that spike insulin the most in humans lead to the greatest satiety and lowest food intake at subsequent meals (4)
I went for the reference, I found a paper about four protein meals... I saw that the whey protein had the greatest insulin response and the great satiety, but I think we cannot extrapolate and conclude it was the insulin that drove the satiety. It could be the glucagon response, the aminoacids composition , the peptide YY, or whatever other thing...
Would the injection of insulin have the same effect on satiety? I don´t think so...
Would you agree (at least partially) with me?
Note: excuse any misspellings, English is not my mother language.
I'm not an expert like Stephan, but I'd like to jump in here for a moment.
I think *many* people who are glucose intolerant find that restricting carbs helps them manage their glucose levels. But glucose intolerance can arise from a variety of factors, often a combination of factors. It also can change in an an individual in response to diet, but not necessarily just the amount of carbs eaten.
For instance, glucose intolerance can result from insulin resistance or problems in insulin response, or a combination. Impaired insulin response can result from beta cell dysfunction or death or from disruptions in glucose sensing or fatty acid sensing, and subsequent signaling to produce insulin. Beta cell dysfunction or death can result from gene mutations, autoimmune attacks, or mitochondrial dysfunction, or the toxic effects of chronically high glucose (usually subsequent to one of these). Similarly, insulin resistance can have more than one cause, although I'm not as familiar with that end of it.
Which is a long way of saying the solution to glucose intolerance may be as simple as carbohydrate restriction for some people, but it may not be for others. And because the body regulates circulating glucose based on a feedback system, a low-carb diet will itself cause relative glucose intolerance, as insulin response is adjusted downward, as will a high-fat diet. (This is all reversible.) Whether a low-carb, high-fat diet is, on the balance, beneficial to a person with glucose intolerance depends on the reasons a person is experiencing it in the first place.
Note that satiety is just post meal, not duration between meals. It is the space between meals that fat provides that allow us to use calories up. Note that when the C/t, calories divided by time to the next meal is less that your BMR, base metabolism rate, you are loosing weight. Satiety is at the end of the meal, your ability to push away from the table.
I totally concur here. The reason being is that I notice with the complete cutting of carbs you will find the weight gain from the reintroduction because of a rebound effect. That is, when you limit that one macro nutrient for so long, you become less insulin resistant. That's cool in the context of insulin, but the endocrine system is NOT all hinged on one hormone. Leptin, etc., are just now thrust into the picture.
As a type 1 diabetic, I learned fast about low carbing to get the blood sugars under control. I also learned about the swing later from introducing them back.
What has worked for me is allowing the carbs in the diet, adjusting for insulin needs, but also exercising at low-level intensity mixed with HIIT workouts 3 times a week. The walking/hiking is always at a fasted state, with recovery carbs and insulin injections to allow the carbs to replentish the glycogen levels. I am now at a stable weight, but I can still eat the carbs.
I know that in the short term I can go low carb to lose the weight, but then I can reach stasis later by reintroducing the carbs. In my books, that is far better.
I think too many people put too much weight on one diet, or WOE. It is a little more complex than that. The only thing that I insist is to eat REAL foods as much as possible.
Stephan, it is always nice to see someone challenge the conventional wisdom. In this case, I mean the paleo conventional wisdom.
Lutz challenged the conventional wisdom also, and he concluded that many health issues could be solved by limiting carbohydrates. His main thesis was that one should limit intake for health reasons, not as a way to regulate food reward or achieve fat loss. You have been very consistent about foods that can contribute to poor health outcomes and I wonder if you are softening on that as part of your hypothesis?
I think those of us who experienced improved health (like Peter at Hyperlipid), have different motivations about what is happening to us metabolically from a macronutrient intake perspective.
It is easy to imagine that many people will read your comments about macronutrients and add carbohydrates that will lead to poorer health outcomes, rather than understand the need to avoid those that contribute to inflammation, etc. I think you have been clear on this in the past, and I haven't seen that change. Obviously, anyone with compromised blood sugar regulation will experience damaging effects from diets that are more carbohydrate based than fat based.
It would be interesting to hear a podcast where you and Peter discuss some of these ideas!
Hi Tiago, are you form Portugal or from Brazil?
I'm from Portugal and it's very rare to see a portuguese name in this blog I think.
Thanks for sharing your experience with us. Did you eat fat with the potatoes, or potatoes only? Everyone I've heard of that did it successfully used fat, even if only in small amounts. Still, the diet is not that nourishing so I can imagine it might not work for everyone regardless.
I think we're well adapted to starch as a species, perhaps better from non-grain sources, but I think most grains can be fine for most people if prepared well.
I have looked into the A1/A2 issue a bit. I remain unconvinced that it's relevant, but I'm open to changing my position as I haven't gone through all the evidence in detail. I do find that goat dairy tends to agree with me better than cow dairy, but that may have nothing to do with BCM7.
Your point is well taken that other things are happening at the same time as insulin spikes in that study. Under normal circumstances, there is nothing you can do to spike insulin that won't change other factors as well. However, the result is consistent with the idea that insulin plays a role in satiety. You see the same thing with potatoes, which have a high insulin index and a high satiety rating.
Regarding your question, if you inject insulin into someone who's at fasting blood glucose, you can cause hunger, but only if it causes hypoglycemia. That's because of the "counterregulatory response" that tries to protect against dangerously low blood sugar, in part by strongly suggesting that you eat food.
If you increase circulating insulin without lowering blood glucose and thus without triggering the counterregulatory response (using the "glucose clamp" method), it does not cause hunger:
Yes, I didn't really use the term accurately there. Thanks for pointing it out.
"However, I think most of our ancestors have probably been eating more carb than fat for a very long time, so my default stance at this point is that if you're going to bias your diet toward a macronutrient, I'd go for carb."
Oh boy, now paleo is going high carb! I want to see how this goes on in the paleosphere.
to Gonçalo: I'm from Porto Velho, Brasil. U?
I see your point, thanks for the explanation.
However, I still have a doubt. In this other study, euglycemic insulin indeed had no effect on hunger, but it also had no effect on satiety, I mean, it had no effect at all on appetite. Is my interpretation correct?
I ate just potatoes, no fat. I usually used salt with them, sometimes ground pepper or herbs (but without much culinary success). They were mostly steamed, as that was most convenient.
I also took a multivitamin every day, but I doubt it makes much difference either way in less than a week.
My caffeine source of choice was Pepsi Max, which contains some sweeteners, and might have a minor influence on something, but I doubt it mattered much either. I drank only that and water iirc.
That's all. I meant to take more notes, but it ended very quickly.
Great points about insulin, Stephan. I think a great term would be the " settling point" as Dr. Linda Bacon suggests.
Scientists such as yourself understand it is not set absolute, and can be raised or lowered to some degree.
Thanks for the work you do.
In addition to industrially processed foods, perhaps any food that has been concentrated might serve as a superstimulus food. So, honey, butter, cream, nut butters?
Perhaps even most cooked foods, by way of being more palatable, or more easily eaten, e.g. cooked meat, mashed potatoes. Perhaps Denise Minger is on to something.
I do agree that paleo != high carb. i think it has to be the "safe carb" tho.
some carbs seems to spike my BG (1 hr postprandial) too much. (i'm not diabetic.)
my hunch is the (hidden) wheat in a lot of prepared food.
I really enjoy reading your blog. I would have to say it seems like you have the least idealized blog amongst the other astute dietary bloggers out there (hyperlipid, panu..etc). After reading the more mainstream books regarding this lower carb movement, it gets a bit confusing when you begin exonerating carbs, insulin..etc when so many have clearly convicted them as the reasons for poor health. Is there any chance you could clarify the reality of the situation, or at least give some direction towards how we should understand your ideas when compared with others adamant condemnation of carbs (such as hyperlipid).
It's been rewarding to watch your views evolve over time, in contrast to some of the staid dogma that persists on many of the "paleo" or "low-carb" sites. I fully agree with your newly arrived at positions and think you are on the brink of reaching real clarity, and dare I say it, something close to finality on certain issues.
Very well done and much appreciated. Keep up the great work.
Dr. Curmudgeon Gee,
I don't know if it would be hidden wheat spiking your blood glucose, but it may be something else about prepared foods.
The reason I say this is that for the past year I've been checking my blood glucose with a frequency that might warrant a diagnosis of OCD. I have mild diabetes. For this past year also, I've been on a gluten-free diet, but for the past three weeks I'd been doing a "gluten challenge" to prepare for a biopsy to check for celiac disease. (Results not in yet. I still won't eat it if I don't have it.)
The wheat I was eating wasn't hidden. Most days I ate a few wheat crackers. I didn't notice any change in my glucose readings.
On the other hand, my daughter's gastroenterologist, who has Type I diabetes, says that gluten makes her glucose control really whacky. I'm willing to believe that wheat in quantity (rather than hidden), or hidden wheat for people with celiac disease, could be particularly bad for glucose control. For people with celiac disease, I'd guess it would be a secondary effect - due to inflammation, disrupted CCK signaling, autoimmune reactions, or some other mechanism, and it would probably be more of a long-term effect, rather than being an obvious change from meal-to-meal.
Considering that insulin spikes increase satiety (i.e. potatoes), what interplay does fat have with carbohydrate? I have heard from diabetics that fat inhibits the mechanism of insulin. (I can't find a citation for this proposition, however.)
If true, doesn't this imply that consuming large amounts of fat with carbohydrates is dangerous in that it will prevent an insulin spike and perhaps lead to over-consumption of food?
thanks for your comment.
i have been 99% gluten free, i.e., i normally do not knowingly eat wheat anymore (only had small piece of sourdough bread in the last 3 months.)
the only time my 1-2 hr postprandial BG spiked (<~ 160 mg/dL!) was from curry beef + rice in Japanese restaurant. i felt chilled & horrible for 3 hours; no amount of heat & clothing could help. it was only after ~ 3 hour i felt better (my BG dropped to < 135).
when i eat rice @ home (w/ meat & vegi & SFA), it rarely rises
so i think the curry sauce has wheat. it was very saucy & thick.
my observation is when my BG >~ 135 (post-prandial), i feel cold.
FYI: my fasting glucose in morning is in the 90's. i'd like it to be lower. oh, well.
i probably should try plain white rice or potato challenge
Hi Peter, Thnx again for this food for thought. Since you seem to have a different opinion than Garry Taubes, it might be very interesting to have you and Gary together in one of Chris' next podcasts. VBR Hans Keer
I'm wondering about health effects of high insulin regarless of effects on weight gain. I have read that high insulin levels are linked to poor outcomes after a breast cancer diagnosis in both overweight and lean women(I was treated 4 yrs ago...). This is what brought me to Paleo- and low carb, higher fat.
I feel I might have had some blood sugar issues before changing to Paleo, but perhaps the improvement has been due to eliminating gluten or sugar and alchohol, not reducing carbs in general?? I have added back more carbs based on recent posts here and elsewhere (and not always feeling well when going too low on carbs) but I still worry about risk of a cancer recurrance if I am driving insulin w/carb consumption.
Also, you wrote:
"A person can probably be perfectly healthy on a high fat diet if it's designed well"
Could you expand on this to explain how you feel it should be designed?
Sorry for calling you Peter Stephan! I don't know what made me do this :).
Thanks Stephan, the distinction seems appropriate. So if I understand aright, leptin serves as a genuine set-point, but there is a distinct settling point, based on the confluence of other factors. For example, a room with a thermostat has a genuine setpoint, but independent factors (opening the window) might temporarily cause deviation from the setpoint, or completely overwhelm the thermostat's capacity to reach setpoint (setting the furniture on fire) or distort the setpoint itself (turning the switch up or down). There's therefore no need for a pseudo-debate about whether bodyweight is really a setpoint or a settling point, since there are both these things and they're importantly distinct.
Fwiw, from what you've said on the blog before, I still don't see why we'd think food reward influences the leptin setpoint, rather than being an influence on the settling point. i.e. if mice/people eat a lot more calories when the calories are high reward, why not just think that high reward food encourages ingestion of more food, quite apart from (and indeed against the work of) the setpoint, rather than thinking that food being high reward favour a higher level of fat and so eat more. This is, of course, quite separate from whether the setpoint must get distorted/negated somewhere down the line, since otherwise, as you say, it ought just to reduce weight (or reduce the rewardingness of food directly).
Hi Dr. Curmudgeon Gee,
That's interesting. I wonder if there was something particularly high GI in the sauce - either wheat starch or corn starch. Also, white rice is one of the highest GI things you can eat. Did you have white rice in the restaurant while eating brown rice at home? If so, that could account for the difference, but you probably know that.
It's also interesting how severe your reaction was. Maybe you were allergic to something. Or perhaps you are gluten-sensitive or even have celiac disease, although I'm not sure it usually manifests that way.
I'm not trying to exonerate gluten - just trying to make sense of it.
It's also interesting that you feel glucose spikes so strongly. I can't tell at all. Sometimes I've felt "low" when my glucose is high.
Your comment about helminths, iron status, and insulin resistance is fascinating. I know that helminth infection is protective against autoimmunity and allergy, but I had no idea of this effect.
It's interesting to think of all the different things that contribute to the contrast between "ancestral health" and the "diseases of civilization." Diet is only one factor, and here you've pointed out how it can be mediated by another.
I find it interesting that Stephan seems to be saying (as best as I can understand) pretty much what Don Matesz has been saying recently, and for which he (Don) has been receiving a tremendous amount of flack. I will be very interested to see where both of them go from here -
While I can follow your reasoning on insulin, body fat level and carb intake, my own n=1 experience is that eating low carb, high fat provides feelings of satiety that were absent in my pre-paleo diet.
I did a calorie restriction diet twice. The first time I successfully lost 8kg, but I originally wanted to lose 16kg. I was hungry all the time and could not muster the willpower to continue. It took me only 4 months on my regular food patterns to regain 7kg (feeling hungry a lot and not really getting satiety out of meals).
The second time I lost 10kg, mostly by limiting meals to 100-300kcal and grazing all day, limiting hunger. It was the twinkie diet and I ate mostly cookies, cakes and other highly rewarding foods, just not much of them.
In both diets, any social eating events would cause me to gain a few kg instantly, taking a week or more to recover from.
Near the end of that second diet, willpower almost depleted, I heard about paleo and low-carb, and I switched to that. I lost another kg and have been of steady weight ever since, without hunger or counting calories at all. I eat about 100g of carbs a day.
So for me at least, low-carb paleo has a dramatically different satiety response than my previous highly-in-refined-carbs diet. Was it the fructose? The total amount of carbs? The wheat? I don't know. All I know is that I have dramatically more energy and feel much better than before.
If you want to state it in terms of reward value, eating cookies and other sweets is highly rewarding but it doesn't give me satiety at all. I end up feeling bloated and hungry-ish.
Eating paleo food is also highly rewarding, but I feel satiated at appropriate times. Even when I pass the point where I'm satiated and eat just for the reward value (e.g. nibbling cheeses, macadamia nuts and deli meats), I just feel full and happy.
So I don't think food reward is the full story although it does play a role.
Another interesting take on low-fat/low-carb is from http://www.inherenthealth.com/our-tests/weight-management.aspx : They claim that certain genes will predispose you to responding better to one or the other.
I know you've addressed why you haven't hosted your blog before, but as I can't find all of your comments and would like to read your work more diligently, would you consider having a blog where you copy and paste your comments from blogs where you participate with a link to the original post?
As omnivores living in widely varying climates, cultures and cultivation practices, I'm interpreting your higher carb recommendations as serving as an integral piece of following a "tri-c" approach, thereby allowing for variation but still optimizing nutritional availability and promoting healthy metabolism and immune status. Is that fairly accurate? Or are you aiming at more specificity and universality of approach? Plenty to think about here - thanks.
So you're implying that the glucose intolerance induced by low carb is actually negative and that excess iron is causing this?
Cutting out store-bought grains removes a significant amount of iron from diet; I eat more dairy protein than "red meat;" certain foods and combinations reduce iron absorption; some donate blood. What are we aiming toward though? ..."paleo" starches have significant amounts of iron. Is absorption simply less? Is it mostly in the skin (which is discarded)? Can you even make the general statement that low fat dieters eat low iron while high fat eat high iron--I know the Inuit had a very high iron intake?
Yes, that study does not support the idea that insulin plays a role in short-term satiety. However, the studies I liked to in the post still demonstrate that it plays a role in long-term food intake and body weight.
Yes, I think there are natural foods that can be superstimuli if they're overconsumed.
Sorry if I'm misrepresenting Peter's views, but I don't recall him adamantly condemning carbohydrate. He acknowledges that there are healthy high-carb cultures. I don't like addressing the views of specific authors, because I don't want it to turn personal. However, I will remark that many LC authors are way off base in their understanding of insulin biology. The most common errors I see are failing to distinguish between post-meal insulin spikes and chronically high fasting insulin, or saying that the former leads to the latter.
Thanks. I also feel like I've reached a point of some clarity. The food reward hypothesis is a big piece of the puzzle.
I don't see any reason to avoid eating fat with carb at this point.
Keep in mind that high fasting insulin indicates a metabolic problem (insulin resistance), whereas the insulin spike after eating a meal does not. High fasting insulin associates with a variety of health problems.
Hi David M,
My hypothesis is that food reward alters the level of fat mass defended by the hypothalamus, which is the central long-term regulator of body fatness as far as we know. I have my reasons for thinking that. However, other plausible hypotheses are 1) that reward systems are simply overriding the homeostatic mechanism; 2) that they are "competing" against one another, and reach a sort of equilibrium (settling point) that's between what each system would prefer on its own.
I can't conclusively demonstrate that my favorite hypothesis is correct, and it's mostly based on indirect lines of evidence. So it's possible that some other related explanation will eventually predominate. Only time will tell. Fortunately, the practical implications of all three versions are pretty similar.
I don't doubt your experience at all, and I think it actually fits pretty well with the hypothesis. Carbohydrate is a major palatability factor and removing it reduces food reward, and therefore often reduces hunger and total food intake.
Stephan talks a bit about it in his post, "Glucose Tolerance in Non-Industrial Cultures." Peter of Hyperlipid has several posts with titles "Physiological Insulin Resistance..." Both authors talk about the observation that long term carb restriction leads to a [short term] glucose intolerance and "insulin resistance."
* A setpoint is regulated by an active, centralized system that measures the variable in question and defends against changes.
Why impose the extra limitation of "central"?
IMHO this un-necessarily restricts a search for a mechanism.
Could a set point not be maintained by a body-wide distributed neural net or something similar - and the reason it's not been found is people are looking for one clump of cells that do it all, when in fact it's several such clumps, maybe many more.
The body seeks to control so much of itself, so many of its operating parameters in such minute and varied ways that Taubes' settling point theory makes almost ZERO sense to me, cohering with no overarching principles.
body seeks to control ... settling point theory makes almost ZERO sense to me, cohering with no overarching principles
meant to illustrate heuristics:
definitely NOT meant as a logical or scientific argument (in which case it would be an invalid "argument from personal incredulity")
The mechanism behind the setpoint has been found. It's a negative feedback loop between fat tissue and the brain. The hypothalamus is the area that appears to contain the setpoint, but it receives input about leptin status from other parts of the brain as well as by detecting it directly.
I have to disagree.
First, in the context of modern foods. If we go back to the Paleo premise that we are evolved to be 'hunter -gatherers' - there is no doubt that early man hunted and fished - year round. We also gathered food WHEN AVAILABLE - vegetables that contained carbs BUT the amount of carbs is unlike modern foods and the amount of fiber and protein was significantly higher.
As an example, my first hand experience eating rice on farms in the Philippines - it is not the rice that we - including Asian immigrants eat here. It is much harder - fails to turn sweet in the mouth and has a lower carbohydrate content. Even the rice the common people eat there is not natural food - it contains much more carbohydrates than the earlier rice. The point is that any food that is farmed has been selected into a food unlike any paleo version and thus the natural amount of carbs in a paleo diet was lower than you assume.
On the insulin levels - post postprandial blood sugar levels are quite different in people that tend towards obesity - so I think what you are saying is over simplifying the subject.
Eating carbohydrates is not unrelated to health risk - we know quite well that it raises triglycerides - as was rigorously shown in the synthetic diet studies for the Appolo program.
Eating lots of carbohydrates causes higher blood sugars - both peak and average, which are directly related to many cancers, kidney disease, glaucoma, cataracts, brain plaques, and elevated oxLDL - the only LDL that appears to cause cardiovascular disease.
I don't think that low-fat vs low-carb is the whole story, but low carb diets - if actually followed long term - greatly help a subset of people with less than ideal postprandial BG control.
We also know that carbohydrates increase serotonin in the brain - post synaptic receptors down regulate over time and thus carbohydrates act as a comfort food that appears to be a sort of addiction cycle. (Not that leptin isn't important - it is just MUCH more complex than that).
I am quit humbled and frustrated by what I've read about diets - we know just a little - but many claims are not based rigorous science (to many need the result to be something to ensure the next grant) - my take is we need to remember how much we really don't know.
Hi, Helen & Mighty Al,
thanks for your comments.
although most of what Mighty Al's says is beyond me. (methink he should have a blog too!)
so my electrons do not "de-couple" easily that's why the chill comes from inside.
actually, i was feeling cold & bloated a lot more in my old diet (low fat + lot's of whole wheat).
I appreciate all the great advice you have given, but I have a question regarding low carb diets. I was just recently browsing through an interview of Loren Cordain when I managed to scroll through the comments section and find your name (http://www.meandmydiabetes.com/2010/03/24/loren-cordain-caution-on-saturated-fats-disaster-with-grains-will-be-public-after-march-25th/). While I have read numerous articles and books regarding the benefits of reducing carb intake, it still brings about some uncomfortable and unsettling feelings when I find a source that exposes one of the so called paragon's of the low carb world to have atherosclerotic plaques (i.e. the inuit). Sorry to ramble on but my main question revolves around the fact that most foods suggested on low carb diets involve meat products, and those are the sources of both saturated fats and cholesterol; something you have not laid to rest as harmless (your only calming words were in regards to discrediting a study where inordinate amounts of cholesterol were added to monkey subjects).I know this post is a bit jumbled, but any response would be much appreciated .
In terms of the consumption of carbohydrates, what about the standard belief that the cultivation of grains led to cramped cities where average height shrunk, life expectancies were lowered, and general health, including teeth, worsened. Every society increases the amount of meat that they eat as they gain income. This would tend to suggest that meat is a highly valued -- and expensive -- part of the diet that people would prefer to have in their diet if they could afford it. And none of this relates to the issues you have discussed about modern, manufactured foods.
I guess I meant that I didn't see the harm in having skeletal muscle insulin resistance (enough to fail an oral glucose tolerance test) in the context of a low glucose intake...
...Assuming two people eat low carb every meal, what's the difference between person A, who would pass and OGTT, and person B, who wouldn't? To be clear, I'm not asking what happens when they take a glucose tolerance test, but how they are different during & between their typical low carb meals. All else equal, does low iron absorption/intake in person A contribute to his/her ability to pass?
Scientists find "master switch" gene for obesity
Reuters – Subway commuters walk through the turnstiles while leaving the U.S. Open in New York September 4, 2007. …
Play VideoWeight Loss Video:Valley woman says gym gave her bank account a workout KTVK 3TV Phoenix
Play VideoWeight Loss Video:Schools Criticized for Methods to Fight Obesity ABC News
– Sun May 15, 1:12 pm ET
LONDON (Reuters) – Scientists have found that a gene linked to diabetes and cholesterol is a "master switch" that controls other genes found in fat in the body, and say it should help in the search for treatments for obesity-related diseases.
In a study published in the journal Nature Genetics, the British researchers said that since fat plays an important role in peoples' susceptibility to metabolic diseases like obesity, heart disease and diabetes, the regulating gene could be target for drugs to treat such illnesses.
"This is the first major study that shows how small changes in one master regulator gene can cause a cascade of other metabolic effects in other genes," said Tim Spector of King's College London, who led the study.
More than half a billion people, or one in 10 adults worldwide, are obese and the numbers have doubled since the 1980s as the obesity epidemic has spilled over from wealthy into poorer nations.
In the United States, obesity-related diseases already account for nearly 10 percent of medical spending -- an estimated $147 billion a year.
This is all very interesting, and I'm trying to figure out how to synthesize this with the rest of the knowledge I have acquired since my quest for nutrition understanding began.
So my question: How does food reward alter the setpoint?
In one of the comments, you mention that you believe that this is what is going on. I find it quite hard to believe that food reward, which is inherently short term, would influence a setpoint, which is inherently long term. This sounds quite a lot like the claim that short term insulin spikes can cause elevated fasting insulin, which you dismissed earlier in the comments.
Of your three competing theories, the third one about the two competing makes the most sense to me, but I still don't think that this hypothesis would be sufficient to explain all of the observed phenomena. Somehow marrying the food reward theory with the inflammation theory of leptin resistance may though.
For instance, maybe food reward value overrides the leptin setpoint in the short term, and so if you're only feeding someone extremely rewarding food (like the chocolate ensure experiment in rats), they will become obese in the long term since they are overeating at every meal, but since most people don't live entirely on these foods, there have to be other elements in their diet that are influencing the leptin resistance. Since many of the super rewarding foods contain toxic substances like wheat and excess PUFA/artificial trans fats, maybe the inflammatory response to the damage done by these foods is causing some kind of interference with leptin receptors (or some other inflammation-leptin resistance mechanism). The beauty of this marrying is that you have short term upregulation of the setpoint causing the overeating of the toxic foods that cause the long term upregulation of the setpoint, a positive feedback loop. Any thoughts on this armchair conjecture?
In response to the question, "Why does my weight increase after adding carbohydrates back to a low-carbohydrate diet?" I suggest that the initial spike has less to do with reward systems and could be simply an effect of an increase in muscle and liver glycogen levels. An increase in glycogen in the cells (which, by the way, comes with up-regulation of enzymes associated with glucose metabolism) creates an osmotic gradient that increases water absorption by those cells. Initial low-carb diets can come with weight loss due to the diuretic effect of decreased muscle and liver glycogen stores. Neurons have even been shown to change size as levels of carbs are changed. It would be important to understand changes in the individual's composition in order to determine the source of the weight gain/loss.
I suspect if you looked at what they ate traditionally in the Philippines, it would have been very high carb just like nearly all Pacific island cultures. Even if traditional rices have a lower carbohydrate content, if that's all you have to eat, you just eat more of it to make up for it. Rice is inherently high in carb and low in protein and fat. There is no type of rice that is low in carbohydrate.
Eating carbohydrate primarily raises trigs if it's refined carb or simple sugars. Unrefined, fiber-rich carbs do not raise trigs much if at all.
Although restricting carbohydrate can be useful for people who have glucose intolerance or diabetes, those problems are not caused by carbohydrate in the first place. In fact, there are several studies that used low-fat, high-fiber, high-carb diets to successfully treat glucose intolerance and even improve mild T2 diabetes. In that sense, they resemble the studies showing that you can have a similar effect by restricting carb.
I have written extensively about the connection between saturated fat consumption and heart disease. I find it unlikely that it plays a significant role. The Inuit had a very unusual diet and you can't attribute their atherosclerosis to saturated fat. Also, keep in mind that their heart attack rate was exceptionally low despite the athero.
Food reward is heavily intertwined with the dopamine-secreting regions of the brain, the VTA and substantia nigra. These regions project to the hypothalamus, the region that seems to encode the setpoint, and we know that dopamine modulates the activity of that region. Reward is not inherently short term, although it has a short term component. Reward-related behaviors change over time as an animal becomes habituated to highly palatable food, and they end up resembling a drug addiction state in some ways.
I agree with you that food reward doesn't need to be the only mechanism. I'm not trying to imply that the food reward hypothesis should replace all other hypotheses-- such as hypothalamic inflammation. I think they both probably contribute.
I agree 100%. I usually tell people not to pay attention to the weight change that occurs in the first 2-3 days after changing the amount of dietary carbohydrate. Glycogen may actually explain some of the difference in weight loss between low-fat and low-carb diets, making them seem even more similar to one another in effectiveness.
One more question if I may...
In your response to a question from me, you wrote "I doubt fasting insulin plays much if any role in fat loss."
In a response to Sandra, you wrote "High fasting insulin associates with a variety of health problems".
I am trying to reconcile these two statements and perhaps my paradigm of health is getting in the way.
Vanity and aesthetics notwithstanding, I view being lean as a marker for health. To be clear, I am not stating that if one is lean that he/she is automatically healthy! My dad was rail thin his entire life until age 52 when he died with a myriad of diseases of civilization (lymphoma, T2 diabetic, etc).
But if you are "healthy" (whatever that means), I assume that you will tend to be lean as an ancillary benefit of your health. I am not debating the minutia of whether 10, 12, 15% bodyfat (for males) is the right number. 25-30% is likely not healthy. 5-6% for a competitive bodybuilder at the other end is irrelevant since that is about performance, not health.
For several months now, I have followed an "ancestral" style of eating, largely based on your writings - avoiding gluten, avoiding vegetable oils, minimal fructose, and other modern foods that you have discussed previously. The motivation was health. In the process, I have lost a significant amount of weight. I have not been carb restricting and so I have come to realize that macronutrient ratio seems to be less of the issue than avoiding neolithic agents of disease.
I could go on, but to cut to the chase, could you please explain the importance of fasting insulin as a marker for health while having limited importance for weight loss?
In terms of food reward I would use the following inequality to represent my system's hedonic pathways.
Refined Carbs >> Cooked Fat >>>>> Seasoned Carbs >>>>>>>> unseasoned carbs >>>>> raw fat
I find raw fats to be the least pleasurable (though not unpalatable).
You wrote "However, I think most of our ancestors have probably been eating more carb than fat for a very long time,..."
For over a million years we have been eating mainly meat and a fatty one at that. It is deducted from piles of bone, most of them with cut marks and smashed to extract marrow and most of the of larger animals. Isotope analysis of bones until the dawn of agriculture indicate high consumption of meat in relation to plants.
Recent active regions in the gnome found to be concentrated in areas associated with glucose metabolism.
Yes, we are getting adapted to process large quantities of carbohydrate but the basic genome is still probably better built for meat and fat. Also we shouldn't forget that animals were also domesticated. Domesticated animals are normally more fatty.
References can be supplied upon request.
@ Psychic24 - I'm guessing that the Inuit used indoor cooking fires or stoves, which can increase the risk of atherosclerosis, as well as lung disease. (So can other forms of air pollution.) Maybe their diet actually protected them from this effect in some way. Some have hypothesized that too much PUFA from marine animals (even if omega-3) accelerated their aging. I'm not sure, but I think the air pollution factor gets overlooked in comparisons of different groups' diets and health outcomes. Other factors get overlooked as well.
@ Paleo diets and iron. Men and post-menopausal women concerned with iron overload from a diet high in organ meats and low in iron-blocking phytic acid could donate blood as an alternative to helminth infection. More convenient and maybe less oogly to a Westerner. Whether or not high iron causes insulin resistance, it is suspected to play a role in heart disease and cancer. Then again, too low iron isn't good either.
@ High-carb diets and trigs. Glad to know that about high-fiber diets, Stephan. I've switched to such a diet myself and it's good for my blood sugars and my weight. I had been wondering if it's affected my triglycerides, which were previously low (44-47) on various diets (semi-veg, WAPF, and low-carb/high-fat), but it's not quite time for my annual test yet. We will see. What you say about the difference between refined carbs and carbs with fiber (especially soluble, I assume) is reassuring.
Miki - There was an article in Scientific American in the late 80s, I think, on how archeological research bias (based on assumptions about sex roles and the lives of "cavemen") miscalculated how much of Ice Age Europeans' diet was meat-based. Bones and hunting and carving tools survive the ages longer than baskets and nets made from, and containing, vegetable matter, but when sites were carefully examined, the imprints of gathering nets and baskets in the clay floors of dwellings were found, as were remnants of gathered tubers.
In addition, big kills might have been pictured more in cave paintings because they were more rare and lead to a feast. Furthermore, many of the knife-marked bones of large animals were found near watering holes, suggesting that humans often scavenged from animals that were already dead.
The claim of the article was that the diet of Ice Age Europeans was more plant-based than previously thought, that women and children participated in incidental (while gathering) hunting of smaller animals and that whole communities hunted smaller game as groups by scaring it into nets.
Another point to keep in mind is that the conditions for relying primarily on meat as a food source were hardly universal among Paleolithic peoples, but rather represent the experiences of small subsets of people in very specific places and times.
Don Matesz at Primal Wisdom has written about this in more detail recently.
Insects are completely left out of this discussion, including the 'women and children mostly gathered plants, CLEARLY' mythos.
Human Doing - Agreed! I predict insects to be the next health food craze.
Given the pleiotrophic effects of leptin, it is unreasonable to expect that a single neural circuit (such as the POMC/AgRP circuit) or a single nucleus (like the ARC) could mediate all- or even the majority- of leptin action. There is little evidence for a set point in neurobiology found to date. Again your hypothesis may be true.....but you need to really back it up by better biologic plausiblity. Each region and subregion of the brain contains neurons with specific functional properties that dictate the physiological outputs they control. You have to do more here to support your premise.
@ Helen, Psychic 24
Inuit Community has a history of high exposure to heavy metals. That can't be too good for their health either.
I found a big bug (1cm long!) with my steamed kale the other day. Tempted to eat it since it might be nutritious, just couldn't bring myself to do so.
If you look at the nutritional content of animal foods versus plant foods, overwhelmingly the animal foods have more of what we need and with much less introduction of sugars into the body. I see no reason the diet should be biased toward carbohydrate at all. Yes, add it in if you like it, if it doesn't contribute to metabolic problems and if you can't seem to get enough energy without it. And certain carbohydrate foods (i.e., certain fruits and vegetables) are useful for people who can't or won't eat organ meats. But as someone whose diet has been biased toward carbohydrate for most of her life, I can say with some authority that eating that way is not a prescription for long-term health. I really feel the indigenous groups who got away with all the carb-eating did so because (1) the carb foods were high in fiber relative to sugar or starch content; (2) they engaged in enough physical activity to burn off the extra glucose and maintain insulin sensitivity [though I don't agree they "worked out" to the degree, that, say, a Crossfitter does]; and (3) they ate a lot more saturated fat than Americans typically eat today, even if a majority of their calories did not come from fats.
Someone who's not willing to do the work to learn proper plant preparation techniques in the kitchen should probably not get too invested in plant foods. Someone who's not willing to do the work to learn which plant foods have the most nutritional bang for the buck, definitely should not get too invested in plant foods. There are too many people who've had successful weight loss by cutting back on carbohydrate because at the end of the day, whatever carbs were doing to their insulin and whatever influence the insulin had on their fat excess, the carbohydrate foods themselves were diluting any good nutrition these people were managing to obtain.
I.e., I can look back on my childhood and understand that the period in which my family life fell apart and everyone began needing mental health intervention just happened to coincide with the period in which we replaced a significant portion of animal foods with grain foods--and dropped liver entirely.
Word to the wise.
I think you are quite incorrect with respect to Paleo diets and carbs. The Northwest Indians were viewed as a perfect example of a Paleo tribe, one which did not cultivate plants. Their diet had some tubers and berries. The rest was primarily fish, especially Salmon, and shellfish. By drying their fish (one type was pemmican)they were able to have plenty of food year-round. There's no reason that European caveman couldn't dry his food, too. When the Paleo had a choice, animal protein was his overwhelming favorite.
I agree that the arcuate nucleus and POMC/AgRP neurons don't mediate all of leptin's actions. Leptin has direct actions in many parts of the brain, including the reward centers. In addition, Tamas Horvath's group showed that hypothalamic energy balance circuits detect leptin in part though an indirect route involving serotonergic neurons in the brainstem.
However, it appears fairly clear to me that the hypothalamus is the primary site that is responsible for the long-term regulation of fat mass, in the same way that it is the primary site regulating a number of other homeostatic functions. I don't understand why you think it needs more biological plausibility. The body clearly defends fat mass, and many studies suggest the hypothalamus is the main determinant of that process.
The Scientific American 80's paper was written prior to the availability of isotope tracing technologies. It is clearly outdated.
I was referring to pile of actual bones with actual cut marks and of prime adults that carnivores usually don't hunt so could not represent scavenging. The bones are of prime parts of the animal so not what are likely to be left to scavengers.
The phenomena was indeed universal until the beginning of agriculture. Another point that I didn't mention is dental size and morphology. Our molars are half and less the predicted size predicted in comparison with Australopithecans and H. habilis who relied on savanna type plant nutrition. The shape of our teeth is adapted to shearing (meat)rather than grinding (plants).
Might o' - Increase in the number of copies of AMY1 (amylase producing gene) occurred about 200kya indicating that until than there was no need for it. Even today the number of copies is not high in all populations.
David L -
I'm wondering what you think I'm "quite wrong" about? I didn't make any claims about what proportions of plants to meat or carbs to protein to fat that Paleolithic Europeans ate (which I don't feel that I can make an educated comment on), but that one theory about the slant of the diet was challenged by a later theory, based on a new look at archeological sites by different researchers. The main point of the article is that Ice Age European "cave women" weren't as passive as they were initially thought to be. The previous theories underestimated women's role in food procurement, which in hunter-gatherer groups is closely linked with status.
My point in raising this is that I've seen similar biases on paleo/primal blogs leading to vast over-generalizations about what Paleolithic peoples ate. They seem to favor speculation on the diet and health of Ice Age Europeans, backed by actual research on Inuits still eating traditional diets. Both these groups lived in a colder climate than most people have throughout history, so why the focus on them?
Again, I'm no expert, but the peoples of the American Pacific Northwest are known to be a pretty special group, with such food abundance that they were able to be settled without agriculture. They do seem to have had a wonderful diet. Hunter-gatherers from a little lower down in coastal California, however, had acorns as a staple of their diet.
I'm not married to any particular theory about diet. If a high-fat diet based on current knowledge of a certain paleolithic dietary pattern makes you healthier, go for it, I say. I tried it and it made me less healthy (the high-fat part, anyway), but I'm not bitter about it, nor am I beating a low-fat drum.
Miki - I've heard so many things over the years about what our teeth (and intestines) prove about what we're supposed to eat that I'm a bit jaded at this point. I find that my teeth (and intestines) work well for both plants and meat.
My belief is that we're highly adaptable omnivores.
With more research in his grasp, however, Stephan has beaten me to the punch in this argument with his current post.
Miki - Not to beat a dead mastodon, but I didn't say that the meat had been scavenged from animals killed by other animals. It was from animals that died a natural death.
In the article, this is presented as part of an argument that community hunting with nets and scavenging were previously unrecognized sources of meat - with implications for interpreting Upper Paleolithic sex roles.
I found the article - well worth a read. I was wrong about where and when I read it - it was 1998 in Discover, but my memory of the information within was pretty sound.
"New Women of the Ice Age," Discover, April 1998.
Helen, what were the health effects of your high-fat diet for you?
If you go to the link I mentioned earlier you can find a paper on the effects of various genes to your metabolism, and perhaps you have the geneset that makes low-fat a better choice for you?
I must say I learned a lot from these comments. I had no idea our mitochondrial DNA varied so much between populations for example.
I read the very nice article at Discover but see nothing there that will support Stephan's assertion that we have consumed mainly carbs for a long time. If man or women or both together hunt they still don't hunt carbs. That people ate carbs is no news. They did, just not most of the diet as isotope studies have shown. For example:
Richards, M. P. (2009). Stable Isotope Evidence for European Upper Paleolithic Human Diets. In J.-J. Hublin & M. P. Richards (Eds.), The Evolution of Hominin Diets Integrating Approaches to the Study of Palaeolithic Subsistence (pp. 251-257).
Regarding teeth here is a reference for a paper whose conclusion is: "meat seems more likely to have been a key tough-food for early Homo than would have USOs (underground storage organs)"
Ungar, P., 2004, Dental topography and diets of Australopithecus afarensis and early Homo, Journal of Human Evolution 46 (2004) 605–622
I will be very interested to see a scientific paper with a dental analysis that comes up with different conclusion.
I realize this is incredibly late but reading down the comments, I realized I did have a couple thoughts I would like to share. I do, however, completely understand if you cannot post this comment as it has been several months since the last comment on this post. If you decide not to post this but want to answer my questions you can e-mail me at firstname.lastname@example.org or message me on facebook where we're friends. My name is Sam Phillips.
From what I've read of Vilhajmur Stefannson, the Inuit only cooked one meal a day, granted, indoors, and that was dinner. For breakfast and lunch they ate raw or fermented fish. Knowing how much Kitavans smoke cigarettes while maintaining an undetectable risk of heart disease, it seems unlikely to me that the oxidative stress caused by the smoke from cooking once a day would be enough to cause death by heart disease in the Inuit.
The thing that came to my mind after reading your comment about Inuit atherosclerosis is that in traditional cultures, atherosclerosis doesn't always mean CHD disease risk. It certainly doesn't for the Masai. We know that the Kitavans have an undetectable risk of heart disease, but do we know if they have any atherosclerosis? That would be an interesting check for Helen's theory about atherosclerosis in the Inuit. I have not yet read Food and Western Disease but it seems unlikely to me that Lindeberg had many corpses to examine for atherosclerosis on Kitava.
From a source I could not verify, I read at one point that the Inuit's premature deaths were due to stroke. Regardless of whether or not that claim has any validity, is it possible that the Inuit's shortened life span was partially due to extreme PUFA imbalance in the opposite direction of westeren society (N3>>N6)? Could this theoretically carry with it ill health effects?
The other comment I had was in regard to your book recommendations. Thinking of Stefansson reminded me that you mentioned you were reading Cancer: disease of civilization? at some point. It would be great to hear your thoughts on that book and other pieces of scientific literature that you've read but haven't made your recommended books list. I've thoroughly enjoyed what I've read so far from your list. I get the impression that you're very careful not to steer anyone in the wrong direction with your recommended books and that might restrict you from placing certain books there that have interesting information, but are partially incorrect. I enjoyed Good Calories, Bad Calories despite being unable to agree with its thesis, because of its brilliant investigative journalism in clearly exposing every facet of the rise of the diet-heart hypothesis. I would greatly appreciate any suggestions about more good books to read regardless of whether or not the information contained within is partially or fully correct.
I don't think you should be so quick to dismiss the possibility of indoor or outdoor air pollution as contributive to disease - cardiovascular and pulmonary, and possibly other kinds - based on the reported low incidence of heart disease among smoking Kitavans.
Try Googling air pollution and heart disease, cooking stoves or cooking fires and disease/health. I've even seen articles linking obesity to inflammation caused by air pollution.
Most diseases are multifactoral. It could be that some groups are protected from some risk factors by other factors - dietary, genetic, or other. But this doesn't mean that they aren't risk factors.
There's a lot of romanticization of certain storied groups - Inuits, Kitavans, Maasai, the French - on come these traditional health and paleo blogs. Seventh Day Adventists, Cretes, and the Japanese are revered in other diet/health camps. I'm getting a little skeptical of all this!
I know that no group was absolutely in perfect health including the Inuit or the Masai; they both had atherosclerosis. I was even suggesting that the Kitavans might have atherosclerosis as well (maybe from smoking) and we might not know about it because atherosclerosis does not seem to necessarily indicate dying of heart disease in traditional groups. I'm not saying I think the atherosclerosis or the air pollution were healthy, but they are not enough to make me think that coronary heart disease was what the Inuit died of. I would still lean towards the opinion that coronary heart disease is a pretty unnatural disease of civilization that is tied to high n6 and a poor n6:n3 ratio. I know the older Inuit tended to die suddenly around the age of seventy, but someone is going to have to show me more evidence than atherosclerotic plaques to convince me that it was CHD that they died of. I don't feel that the Japanese diet is particularly healthy today, but they do have a much lower rate of CHD deaths than most industrialized countries. I feel this can be pretty easily linked to high seafood consumption balancing the n6:n3 ratio as the Japanese now also consume plenty of industrial seed oils just like everyone else. Indeed, there are good and bad things about every culture's diet, even traditional cultures' diets. I would argue that the amount of the Inuit ate too much seafood, the French ate too much bread, the Masai consumed too much milk sugar, and the Japanese traditionally ate too much rice and soy, not to mention their current sugar consumption. That said I do feel it's possible to draw plausible connections between different traditional groups without glorifying them. The Masai had extensive atherosclerosis without having a detectable risk of CHD death; I don't see why this isn't likely the same for the Inuit. CHD deaths and atherosclerosis are not synonymous. Heart disease was pretty damn uncommon at the turn of the 20th century, but grew in prevalence as industrial seed oils grew in prevalence. Until I see some pretty strong evidence otherwise, my working hypothethis is that CHD deaths were triggered by the introduction of seed oils and other risk factors for CHD death are negligent in the context of healthy n6-n3 ratio and levels. I have yet to see evidence of a group that is higher in n3 than n6 or balanced in them dying of CHD.
Post a Comment