I love nutrition science. So much so that I read a new book on it every week. The Alternative Hypothesis has a pretty old video on agriculture and evolution. I strongly disagree with his main thesis. I strongly disagree with his denigration of Gary Taubes. Most of all, I strongly disagree with what he says about the East Asian rice eaters because since that video has been made, the carbohydrate/insulin hypothesis of obesity has changed to the insulin hypothesis of obesity.
In the very beginning of the video he brings up Gary Taubes’s research on low-carb diets and how people tend to be healthier than those who eat higher carb diets. He brings up the East Asians who eat a lot of rice. However, it’s clear he doesn’t know that the percent of carbohydrate intake is nowhere near as important as the absolute amount of carbohydrate consumed:
- They consume a fraction of the sugar we do. More sugar consumption leads to greater insulin resistance, more fat creation, less fat breakdown, and more fat accumulation.
- They consume less total glucose, AND the glucose they consume is accompanied by less sugar (and less omega-6 PUFA, if it matters).
- They consume a ratio of omega-6 to omega-3 PUFA that is much lower than we do. This mayfurther reduce any insulin resistance brought on by the glucose they do consume (in smaller doses and with less sugar).
The fact that East Asians didn’t have high rates of diabesity (diabetes and obesity) was a big blow to the carbohydrate insulin hypothesis. However, the East Asian rice paradox is simply explained by low, if non-existent, consumption of refined carbohydrates. Those populations actually consume fewer total carbohydrates than Western diets, and have lower levels of glycemic load as a result. To quote Mark Sisson:
Before recently, Asians ate less refined sugar and used animal fats for cooking. Sugar intake is rising now, of course, and cooking oils made from corn and soybean have largely replaced lard and tallow, but rice in the context of a low-sugar, no-HFCS (remember, the oft-cited 55/45 fructose/glucose breakdown for HFCS is highly misleading and actually quite often incorrect), low-vegetable oil, nose-to-tail nutrient-dense diet is (or was) acceptable. You can’t reduce a food down to its constituent parts and focus on, say, the bit of fructose in a blueberry and then condemn the entire berry because of it. Similarly, you can’t reduce a diet down to a single constituent food and condemn – or praise – it based on that single food. You have to look at the entire picture, and the Asian diet is largely a nutritious one.
These paradoxes where one population seems to disprove a certain hypothesis are pretty easily explainable with the existing data. There are numerous reasons why East Asian rice eaters have lower rates of diabesity. Dr. Jason Fung also explains why:
Wheat, particularly in the modern iteration may be particularly fattening for numerous reasons. The high level of amylopectin means that most of the starch contained in flour is efficiently converted to glucose. This deadly combination of wheat and sugar has been introduced into the Chinese diet. The result is a Chinese diabetes catastrophe. The prevalence of diabetes in China has now even outstripped the USA.
This is the answer to the paradox of the Asian Rice eater puzzle. Why didn’t the Chinese have a diabetes epidemic in 1990 with all their white rice? Well, because they didn’t eat any sugar (fructose), they were not developing insulin resistance. Because they were not snacking all the time, they had periods of low insulin level that helped prevent the development of insulin resistance. So the high rice intake by itself was not enough to cause either of diabetes or obesity.
Then he says that whites intake more total carbs in comparison to blacks and ‘Hispanics’ (1:32 in the video). This is wrong.
Diaz et al (2005) showed that minority populations are more likely to be affected by diabetes mellitus which may be due to less healthy diets and/or genetic factors. Using the National Health and Nutrition Survey for 1999-2000, they analyzed overweight, healthy adults, calculating dietary intake variables and insulin sensitivity by ethnicity. They characterized insulin resistance with fasted insulin, as those who are more likely to become insulin resistant have higher fasted insulin levels (levels taken after waking, with the subject being told not to eat the night before as to get a better reading of fasted insulin levels). Non-‘Hispanic’ whites had higher energy and fat intake while ‘Hispanics’ had higher carb intake with blacks having lower fiber intake. Blacks and ‘Hispanics’ were more likely to have lower insulin sensitivity. However, ‘Hispanics’ were more likely to have lower insulin sensitivity even after controlling for diet, showing that metabolic differences exist between ethnicities that affect carbohydrate metabolism which leads to higher rates of diabetes in those populations.
Diaz et al state in the results of the study:
Dietary differences are seen by ethnicity, with non-Hispanic whites having higherenergy, saturated fat and total fat intake, while Hispanics had higher carbohydrate intake and African-Americans had lower fibre intake.Both African-Americans and Hispanics had higher levels of fasting insulin, demonstrating lower insulin sensitivity in comparison with non-Hispanic whites.
So now that I’ve established that blacks and ‘Hispanics’ consume more total carbohydrates from refined foods, now I’ll show the physiologic effects of insulin.
Insulin inhibits the breakdown of fat in the adipose tissue by inhibiting the lipase that hydrolyzes (the chemical breakdown of a compound due to a reaction with water) the fat out of the cell. Since insulin facilitates the entry of glucose into the cell, when this occurs, the glucose is synthesized into glycerol. Along with the fatty acids in the liver, they both are synthesized into triglycerides in the liver. Due to these mechanisms, insulin is directly involved with the shuttling of more fat into the adipocyte. Since insulin has this effect on fat metabolism in the body, it has a fat-sparing effect. Insulin drives most cells to prefer carbohydrates for energy. Putting it all together, insulin indirectly stimulates the accumulation of fat into the adipose tissue.
Do you see why blacks and ‘Hispanics’ are more susceptible to obesity?
Another glaring error he commits is not separating refined carb consumption with natural carb consumption. Refined carbs spike insulin much more than those foods with natural carbohydrates. East Asians do not have a “higher carbohydrate tolerance than Europeans” (2:06 in the video). This one huge error he commits completely discredits his hypothesis.
He then goes on to talk about India’s diabetes rates. But why is it increasing? Because of Western diets. It’s not about a “lower carbohydrate tolerance” as he says at 3:07, it’s about consuming more refined carbohydrates.
Then at 5:05, he says that he’s “solved Gary Taubes’s race problem in regards to diet”. He did nothing of the sort.
I, of course, have no problem with his IQ data. I have a problem with the conclusions he jumps to in regards to carbohydrates and diabetes. He clearly didn’t look at other factors that would explain why East Asians have lower rates of diabesity (which is increasing as they adopt a Western lifestyle… Weird…). The same thing explains it with the Australian Aborigines.
I have absolutely no problem with the second half of his video. My problem is the first half of it–his denigration of Taubes, non-understanding of insulin spikes in comparison to the quality of carbohydrate ingested and not controlling for refined carbs– as it’s clear he didn’t do extensive research into these populations (which Taubes and others have) to show why they don’t have higher rates of diabesity.
What he doesn’t touch on are “obesogenic environments” which is defined as “the sum of influences that the surroundings, opportunities, or conditions of life have on promoting obesity in individuals or populations”. What a huge coincidence that most of the populations he cited today with higher rates of diabesity live in first-world nations, otherwise known as obesogenic environments.
He should have spoken about the Pima Indians and their rates of diabesity. They didn’t have rates of diabesity as high 100 years ago. Why? The introduction of the obesogenic environment. Prisancho (2003) in his study on the Pima and reduced fat oxidation in first-world countries showed how the Pima preferentially burn carbs and not body fat for energy. Fat-burning would account for 9 kcal lost and CHO for 4. Since they preferentially burn carbs for energy and not fat, this shows why they have higher rates of diabesity. It’s not that it’s a genetic susceptibility to burn CHO for energy over fat (there may be a small genetic component, but it doesn’t override the effects of the actual diet). I’ve shown insulin’s role in fat storage above, do you see why the Pima have this diabesity epidemic after the introduction of refined carbohydrates and the obesogenic environment?
Added sugars and salts in foods causes us to want more of those foods. As I alluded to above, food scientists continuously work to find out which combinations of sugar, salt and fat will be more hyperpalatable to us and make us eat them more. Whites nor East Asians have a ‘higher carb tolerance’, they just eat different types of carbs (mostly unrefined, in comparison to blacks and ‘Hispanics’ anyway). If any individual were to overeat on high carb foods they would become diabetic and obese. Whites nor East Asians are exempt from that.
In sum, he didn’t look at where the carbs came from, only total carb intake. Refined carbs and unrefined carbs do different things in the body. The whiter a processed food is, the more it is refined. The more a food is processed, the more its natural nutrients such as fiber are taken out. These low-fat refined foods are one cause of obesity. However, it’s way too complicated to say that only refined carbohydrates cause diabesity.
I strongly recommend he read Taubes’s and Fung’s books. If he did, he wouldn’t have said what he said about Taubes’s theory and completely disregard the absolute total amount of carb intake and not the total amount of carbohydrates ingested.
This can be settled by looking at the ratio of processed to unprocessed carbs in the Japanese, French, and Indian diets circa 2012, because they are the same amount of carbs but had different diabesity rates. If the Indians were eating something equivalent to Wonderbread and the Japanese were eating something equivalent to oatmeal then you could chalk up diabesity rates purely to insulin theory. But if the Japanese were pounding down white rice in 2012 then there are likely racial differences, though perhaps not as much as Faulk said.
Nobody disagrees that carbs cause this – or that this happens to all races- but the Pima are evidence that some populations out there are slightly more susceptible. And steatopygia shows that there can be genes with globally varying frequencies that control how fat is stored.
Earlier I brought up lactase persistence and ability to digest alcohol varying globally… I also remember Eskimos having different genes related to fat digestion? I’ll try to dig up a source.
But yeah, carbs cause this and it happens to everyone. I’m also willing to accept that diabesity happens to blacks more because of overall proneness to obesity and less fiber in the diet. But I bet you $10 that minor but statistically significant differences in carb digestion are found globally and that the peoples with more exposure to carbs resist the negative effects a hair better.
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The Chinese eat less than 50 grams of sugar per day. Notice the carb consumption in comparison to overall sugar consumed per day in the Western countries. Along with other insulinogenic foods, this explains the East Asian paradox.
For more, read here.
For the French, their diets compared to ours were different 20 years ago, but as they switched to our Western diet, rates of obesity more than doubled. They eat more fresh, unrefined foods in France.
I showed the Indians increasingly are eating a Westernized diet. This explains their rise in diabesity.
Moreover, there are certain genes that predispose Indians to diabetes. With the introduction of the obesogenic, insulinogenic environment, their genetic susceptibility causes the rates of diabetes, and with it obesity as the two are strongly linked.
Chronic undernutrition in the womb causes one to not be able to oxidize fats as well as carbohydrates. When did the rates of diabesity explode in the Pima? The introduction to a Western diet. What the Pima prove is that increased adiposity is caused, to some extent, by their bodies burning carbohydrates for energy and not fat. The cause is high levels of insulin due to Westernized diets.
I can go more indepth on the Pima when I find my book with the references in it for the Pima.
To believe that body fat is not regulated by the body is ridiculous. Steatopygia is proof that the body regulates fat stores. Just eat less, you’ll get rid of that fat!!! Not.
Yep. I cited one study showing that fiber protects against obesity. Fiber reduces insulin, so since they intake less fiber then they’re more susceptible to diabetes. I showed that since they are more likely to be poor, they can only afford low-quality, refined foods and this is why they have lower intakes of fiber which manifests itself in their obesity and diabetes rates.
What do you mean? Do you mean those populations exposed to more carbs have less of a chance of becoming diabetic? This is not true. It’s the opposite. Refined carbs cause this. Sugar causes this. A whole slew of factors that raise insulin and decrease vitamins and minerals that protect against obesity cause this.
The introduction of Western, refined foods causes rates of diabesity to increase.
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The presence of carbs TODAY causes diabesity.
The presence of carbs in the last 10,000 years or so in some places has selected people for resistance to diabesity.
The Indians are an example of this. You say that their higher diabetes rate by comparison to the French diabetes rate is due to “the Western diet” and genetics. But France also eats that diet. This means that Indians- as you admit- are more prone to diabetes.
Carbs, particularly refined carbs, cause diabesity to everyone but by your own admission they do that more so to Indians for example.
Think about why that is. Why some populations are more prone and some are more resistant. What regional selective pressure could cause this?
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Incorrect. The East Asian rice eater paradox is explained. They don’t eat fructose. They intake more fiber. Their environment isn’t as obesogenic as ours is. As they adopt our lifestyle and way of life they will then incur higher rates of obesity.
It’s also worth noting that obesity rates won’t continue to increase. Contrary to those who push the CICO model, those who are genetically predisposed to get will will get fat. It’s no coincidence there are still thin people in obesogenic environments. And no moving more and eating less isn’t why. Individuals can have better lower CHO sensitivity, but as for racial groups I don’t see it. I do get the argument, but from what I know of nutrition science it does not make sense.
The Indians are interesting with this. They have multiple genes that predispose them to more abdominal fat and diabetes. However, as I showed in the link in my previous comment, the French obesity rate has double in a ten year period. Before the introduction to our diet (Standard American Diet, SAD), they ate more fresh whole foods. As our garbage lifestyle reaches around the world, more peoples who aren’t obesity will become obese.
Yes. The Pima, for instance, preferentially burn glucose over fat. Since fat is 9 kcal and chin is 4 kcal, their body is burning less kcal than if they’d have burned fat. I readily admit there is a small difference in carbohydrate metabolism with the Pima, but diet overrides small generic effects.
In my opinion everyone should go low carb. We have had no where near enough time to evolve to eat the refined trash we do. There are some populations that eat 70 to 80 grand of carbs in their diet but don’t have high rates of obesity nor diabetes. The Kitavans are a great example. The food they eat is fresh. It’s not refined, processed garbage. Refinement of food and obesogenic environments cause obesity.
When the East Asian obesity rate goes up will this guy’s theory change? Hell, even Africa’s obesity rate is climbing. Why? The introduction of the obesogenic environment. Cheap, garbage food.
Indian populations do have lower insulin sensitivity, but just because you have higher carbon sensitivity doesn’t mean you resist the negative effects of carbohydrates. There are multiple protective factors involved in regards to not acquiring diabetes or becoming obese, fiber is one huge one. Low insulin.
I really need to find my book that had the Pima references. Thatd settle this part of the discussion on them.
Differences in carb consumption. Type of carb consumed. Whether that food is high or low on the glycemic or insulin index. Check out this link.
Diet & insulin resistance: a review & Asian Indian perspective.
Especially with India, as these people adopt Western lifestyles, then the amount of “diseases of civilization” will increase. Why is diabesity almost unheard of in primitive populations? The rate of heart disease and diabesity are ridiculously low in those populations. I’ll check my book tomorrow for citations, but those populations also ate a diet somewhat high in carbs. But they were not refined. That’s the reason why they show almost nonexistent rates of these diseases of civilization.
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Haven’t gotten my grubby mitts on the primary research yet but this should give you an idea
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I know about that. I’ve written on it here and here.
The end of the article where it says ability to eat a high fat diet may depend on your genes, that’s ridiculous. We didn’t evolve eating processed carbs. That is the reason for the so-called “diseases of civilization”.
Peoples who don’t eat refined carbs have almost nonexistent rates of diabetes, obesity and early mortality.
But just because the Inuit evolved that way doesn’t mean you can make the leap to say that some populations digest carbs differently and that’s the reason for the differences in diabesity between populations.
Refined carbs and other insulinogenic and obesogenic factors are the cause.
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I’m not saying that differences in fat digestion necessitate differences in carb digestion.
Differences in fat, lactose, and ethanol digestion suggest that eating a given diet for 10,000 years will cause your allele frequencies to shift such that your body will fare better under that diet. It’s evolution.
The fact that Indians are more genetically prone to diabetes supports this.
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Yes you are. You’re arguing that since the Inuit et al live better on fat that there are intrinsic differences between populations in carbohydrate metabolism. This seems to be like Andrew Anglin’s “Europeans didn’t evolve to eat tropical fruit” argument. It’s ridiculous and makes no sense.
Also, it’s worth noting–and this is pretty big–only 23 percent of the variance in insulin spikes are caused by refined carbohydrates. There is still another 67 percent we need to account for
Is there any way to test this theory? What kind of study would need to be carried out to see who’s right? I’d assume all we need to do is look at existing data.
But I’m sure I gave enough evidence for my claims to disprove this hypothesis. Once the Pima were introduced to our diets, the percentage of people with those diseases exploded. Let me quote Gary Taubes from Good Calories, Bad Calories:
Then he talks about how over the next 25 years that the game was almost hunted to extinction and that the Gulf River got overtaken by Anglo settlements. So, he says, by the late 1890s, the Pima were relying on government rations to avoid starvation.
Researchers wondered whether their sedentary behavior was the cause of rising obesity rates, or, the logical explanation, diet. The same researchers even notice that obesity was rare among the Pueblo who were sedentary as well. Quoting Taubes:
Also give this a read.
The Pima, Sumo and Canine Diets – The Epiphenomenon of Obesity IV
Moreover, it was noticed that the Pima’s diet consisted of “mainly beans, tortillas, chili peppers and coffee while oatmeal and eggs are occasionally eaten for breakfast. Meat and vegetables are eaten only once or twice per week.” (Taubes, 2011: 238)
This section ends with the conclusion that excessive carbohydrate consumption was the cause for the obesity and diabetes rise in the Pima. It’s the only logical conclusion to draw. They were lean before the introduction of Western diets, obese and diabetic after.
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If my hypothesis were true- that it’s possible for diet to apply selective pressures – then we would expect populations with longer exposure to a given food source to be more resistant to its negative effects.
This is true. Europeans have had more exposure to alcohol and are more resistant to its negative effects. At least one allele has been identified to do this. This gene was selected for because Europeans had a greater need for it.
To test whether this applied to carb digestion you’d look at the Indian diet for the last few thousand years. If they ate less carbs- or less harmful carbs- then selective pressures for diabesity resistance would be less. This would explain why they have alleles associated with diabetes.
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Well the data the TAH gathered doesn’t take into account what type of carbs are eaten. I like the theory, it makes sense on the surface. But if you know anything about nutritional science, what he says is wrong. I explained the East Asian rice paradox. That’s a non-factor. The Indians are also a non-factor. The French are a non-factor. It seems that whenever people start eating our diets that these changes start occurring. As I showed in the quote from Mark Sisson, you can’t just take a look at one factor of the diet because as a whole the East Asian diet is extremely healthy. They consume tons of fresh foods, especially foods that protect against obesity and with it, diabetes.
Refer back to the Taubes quote in my previous comment. They were hunter-gatherers and agriculturalists. TAH’s theory says those populations that developed agriculture ‘have a higher carbohydrate tolerance’ (whatever that means). This is not true. It defies what we know about nutritional science and biochemistry.
It’s been extensively noted that hunter-gatherers don’t have these problems. The diseases that plague us are almost nonexistent. Hardly any diabetes cases, hardly any obesity or heart disease cases. Isn’t that weird? Hmmm I wonder why the cause could be…. Refined, cheap garbage. Notice how ‘Hispanics’ and blacks have higher rates of diabesity than American whites. Whites eat more protective foods, they eat more fat. These protect against obesity while the diets that the minorities consume cause their health problems.
I readily admit that there may be some differences between populations but they are extremely minute, not enough to cause any differences between populations in these diseases.
They did eat less refined carbs. Of course they did. Before the 1900s the Pima had nowhere near these levels of obesity. As I quoted, they had a ton of food stored yet they did not have the rates of diabesity they do today.
The Pima Indians and the Obesity Epidemic
There is some evidence for the assertion, but I highly highly doubt it. It defies everything I’ve learned about nutrition science. These so-called paradoxes are easily explained once one looks into it deeper and if TAH would have looked into this debate more, they’d see that all of the populations cited have one thing in common: consumption of refined carbohydrates.
Is it any coincidence that once the Pima were introduced to diets high in refined carbohydrates and sugar from the government rations that their rates of disease increased? No. There is numerous data out there to explain these differences.
And I’ll stress again: the percent of carbohydrate intake is nowhere near as important as the absolute amount of carbohydrate consumed. Diet quality matters, which high-quality diets protect against obesity. Fiber and vinegar are two protectants (Fung, 2016).
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Nice blog, just found this.
I don’t have anything directly relevant on the subject on hand, but if you’re interested in nutrition science, you should read this blog: http://high-fat-nutrition.blogspot.com/
Written by a (white) British veterinarian, it is one (if not the) best resources of knowledge on how different energetic substrates feed into the mitochondria, and how this systemically effects the body as a whole.
Seriously, this man has done more for nutritional science in the last 9 years of blogging, than the whole of the scientific community has in the past 100 years.
I will give you some tl;drs, without sources, if you are intrigued I might dig up the studies.
-The reason ‘sugar’ (sucrose/HFCS) is bad is because of fructose. Glucose has absolutely nothing to do with it. Fructose is almost completely metabolized by the liver, it cannot be metabolized/used to any large extent by anything else in the body.
When a cell consumes too much energy, ROS are produced and major problems occur, including insulin resistance (which is an effort by the cell to stop energy influx).
Say you consumed 100g of glucose too many, more than your body needed. What would happen is that your 1) FFAs/triglycerides would enter your tissues, mostly your adipocytes, because of insulin (which forces them to be stored). This is a way for the body to balance the energy supply of the cells, to avoid “overfeeding”. This would also cause fat storage everywhere. 2) glycogen reserves would be filled to the brim. 3) the rest of the glucose that cannot possibly be stored would be simply be fermented into lactate (this is a defense against energy overload). De novo lipogenesis requires a lot more glucose overload than 100g, studies say 500g are required for de novo lipogenesis.
But say you consumed 100g of fructose. Even if you hadn’t met your carbohydrate needs that day, this could still be a huge problem.
Here’s an example: the high end average weight of the liver is around 1.5kg. Compared to, lets say, a full bodyweight of around 70kg, this means the liver is around 1/46 the weight of the body.
100g of carbs being metabolized solely by the liver is then equivalent to 4600g of carbs being metabolized by the entire body. Think about that.
When consuming glucose, there’s multiple layers of regulation, and the body can soak up any excess. 100g of carbs over is nothing for the entire body, comparatively. The liver has ways of dealing with excess glucose.
Fructose however HAS to be metabolized by the liver. There’s no other option. And there’s far less regulation.
And think about fat gain. Eating a little bit of carbs over your daily need could result in a couple grams of fat being stored over your entire body, which is nothing. A couple grams of fat locally stored in your liver every day, however, is less than a year away from fatty liver.
-Circadian rhythm has a yuge effect on metabolism. For billions of years life has evolved to yoke the metabolic processes around the day/night cycle. Billions of years of uninterrupted evolution and rhythm. With the widespread use of technology, this rhythm has been destroyed. Blue light exposure at night, a completely foreign stimulus, is certainly very bad for humans, and is likely a huge contributing factor in the health crisis that is happening right now. We know from studies that circadian dis-regulation is bad for glucose tolerance.
-Read the protons series on Hyperlipid. Long chain saturated fat causes reverse electron flow, which causes superoxide to be released, which causes insulin resistance. PUFA and carbohydrate does the opposite.
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