I recently had the opportunity to collaborate with Kevin Hall, PhD and Rudy Leibel, MD on a commentary in JAMA Internal Medicine (1). It was fun for me to work with two researchers who I respect tremendously. Hall’s energy balance modeling work has brought important new insights to the obesity research field and Leibel is, well, the co-discoverer of leptin. And he has done as much as anyone else to help us understand how this hormone works in humans.
Our commentary is titled “The Carbohydrate-Insulin Model of Obesity Is Difficult to Reconcile With Current Evidence”, and we wrote it in response to a review paper in the same issue written by David Ludwig, MD, PhD and Cara Ebbeling, PhD, titled “The Carbohydrate-Insulin Model of Obesity: Beyond ‘Calories In, Calories Out'” (2). In this paper, Ludwig and Ebbeling lay out their argument for the carbohydrate-insulin model (CIM), as they refer to it. This is nearly identical to the model Gary Taubes advocates: obesity is primarily caused by the ability of carbohydrate to increase insulin secretion, which reduces levels of circulating fuels (glucose and free fatty acids), shunts fat into fat cells, and makes us fat, hungry, and sluggish. According to this model, high calorie intake and low calorie expenditure are a result of expanding fat tissue, not its cause. Ludwig and Ebbeling focus particularly on glycemic load, which is the degree to which diet impacts blood glucose. In my view, this review paper is the strongest defense of the model currently available.
While Ludwig and Ebbeling had ample space to develop their arguments, we were limited to 1,200 words and 8 references. So I’m going to add to our commentary here, expanding on some points and adding others. This post reflects my views and not necessarily those of Hall and Leibel, who were not involved in writing it.
I don’t want to be on the wrong side of history, and one way to do that is to make overly confident and categorical predictions. I still think it’s plausible that some insulin-related variable could be involved in obesity and/or fat loss, particularly 1) insulin resistance in energy-regulating circuits in the brain, and/or 2) blood glucose levels between meals, or some other signal of glucose availability. What I think is very unlikely to be correct is the hypothesis articulated by Ludwig, Ebbeling, and Taubes: the primary cause of obesity is carbohydrate-stimulated insulin acting on fat cells.
That said, I want to be clear that I think certain forms of carbohydrate are part of the explanation for obesity, and low-carbohydrate diets do cause fat loss in most people, with greater carbohydrate restriction typically resulting in greater fat loss. Like most diets, low-carbohydrate diets aren’t very effective against obesity in the average person, but they do have some effectiveness and they are certainly a valid tool in the toolbox. They may also be particularly useful for managing diabetes, although long-term outcomes remain uncertain.
Mischaracterization of opposing viewpoints
Ebbeling and Ludwig begin their JAMA piece by citing a recent Endocrine Society scientific statement written by leading obesity researchers, including Rudy Leibel and my mentor Mike Schwartz, MD (3). Ebbeling and Ludwig present it as an example of something they call the “Conventional Model”, which holds that calorie intake, expenditure, and body fatness are not biologically regulated and all we have to do is fire up our willpower and “eat less, move more” to conquer obesity. This is the opposite of what the Endocrine Society paper actually says, and our first clue is the fact that it’s published on behalf of the Endocrine Society in the journal Endocrine Reviews– both organizations dedicated to the study of hormones.
Schwartz, and most of the other authors, have built their careers studying the mechanisms that regulate calorie intake, expenditure, and body fatness. Schwartz has been battling the “Conventional Model” since the 1980s, as I detail in my book The Hungry Brain. Here’s an illustrative quote from my interview with him (page 145):
I started my fellowship in 1987 and was immediately indoctrinated into the idea that there is an adiposity control system. What I was working on was considered way out of the mainstream at the time. Everyone just assumed that obesity is a problem where people eat too much, and if they could control their eating and be normal, they wouldn’t have this problem.
Schwartz and others in his field proceeded to spend 30 years debunking this assumption. This field is the very reason the Conventional Model has lost steam over the last three decades. This is the field that discovered leptin and satiety hormones, showed that hormones and specific brain circuits regulate appetite and body fatness, and overturned the notion that body fatness is just about how much we happen to decide to eat and move (note that this is perfectly compatible with the prevailing view that when calorie intake is held constant, all foods are similarly fattening in humans).
Here’s another illustrative quote, this time from the abstract of the Endocrine Society scientific statement (3):
Growing evidence suggests that obesity is a disorder of the energy homeostasis system, rather than simply arising from the passive accumulation of excess weight.
It’s beyond my understanding how a person could read this paper and interpret it as a defense of the Conventional Model, or continue to believe that the Conventional Model is the primary alternative to the CIM.
In fact, our choice of models is not between the CIM and the Conventional Model, and I’m starting to feel like a broken record pointing this out. The Endocrine Society statement presents a third model, not mentioned by Ludwig and Ebbeling, that is neither the naive and oversimplified Conventional Model nor the CIM. It happens to be widely supported within the scientific community. It acknowledges many influences on body fatness, particularly the brain circuits that regulate food intake, calorie expenditure, and body fatness in response to environmental and internal signals (3). If Ludwig and Ebbeling want to convince the scientific community that their model is better than what currently exists, they should be arguing against the prevailing model, not a straw man that has been obsolete for quite some time.
Dietary fat can be fattening
This is a simple observation that is hard to reconcile with the CIM. Researchers have known for decades that adding fat to food tends to increase body fatness in animals. I have seen Olympics-worthy intellectual gymnastics to try to rationalize away this fact, but as I will show, the conclusion is impossible to escape. Here is a quote from a review paper on this topic (4): “With few exceptions, obesity is induced by high-fat diets in monkeys, dogs, pigs, hamsters, squirrels, rats, and mice.” This paper reviews many studies in these species suggesting that higher fat, usually at the expense of carbohydrate, increases body fatness.
In my own research, we used refined diets that were 60 percent fat and 20 percent carbohydrate to induce obesity in normal rats and mice– and they were very effective! In my hands, these diets caused detectable fat gain in three days, more than doubled body fat content in two weeks, and increased body fat by sixfold in 20 weeks (5, 6). The weight and fat gain on these diets is rapid, massive, and unmistakable. In fact, fat gain on refined high-fat diets occurs even when calorie intake isn’t allowed to increase, suggesting that they impact both calorie intake and expenditure (7). In their paper, Ludwig and Ebbeling suggest that only the CIM can explain the phenomenon of fat gain without increased calorie intake in rodents, but this is clearly not the case– my field has been aware of this in the context of high-fat diets and brain lesions for a long time.
These diets aren’t just high in fat of course. They’re based on refined ingredients and they usually contain carbohydrate (e.g., 20% of calories) including sugar (e.g., 7% of calories). Aha, you may say! The refined carbohydrate is why the diet is fattening, not the fat! Researchers have already tested that supposition by comparing this diet to a low-fat version in which the fat is mostly replaced by refined carbohydrate. Although the low-fat version can be fattening under some conditions (8), it isn’t as fattening as the high-fat version, and often it isn’t fattening at all. Here is a graph from a recently published study by Matthew Dalby, PhD, and colleagues, comparing fat mass gains over 8 weeks of free access to unrefined low-fat (black), refined low-fat (blue), and refined high-fat (red) food in mice (9):
There was no difference between refined and unrefined low-fat diets, but the refined high-fat diet led to rapid and marked fat gain. This finding has been replicated independently, including in rats (10). [Update 7/18: a recent study using 29 diets and 5 strains of mice strongly supports the conclusion that dietary fat is much more fattening than carbohydrate, including sugar, in mice]
Refined carbohydrate and sugar are probably part of the reason why refined high-fat diets are fattening in animals, but there is no escaping the conclusion that the fat itself plays a key role. This simple observation is hard to reconcile with the CIM as articulated by Ludwig/Ebbeling/Taubes.
How about in humans? So far, two controlled overfeeding studies have compared diets rich in fat vs. carbohydrate and measured body fat gains (11, 12). Both studies reported that overfeeding with a high-fat diet produced the same, or even slightly greater, body fat gain than overfeeding with a high-carbohydrate diet of equal calories. Clearly, an excess calorie of fat gets into fat tissue as effectively as an excess calorie of carbohydrate, regardless of their effects on insulin.
How about when calorie intake isn’t controlled? Under these conditions, volunteers offered a high-fat diet tend to overeat and gain fat, just like in the animal studies discussed above (13, 14, 15, 16). Note that these studies didn’t use low-carbohydrate diets; they used high-fat diets that were unrestricted in carbohydrate, which is presumably why the results differ from low-carbohydrate diet studies in which people tend to eat fewer calories and lose fat.
Historically, many cultures ate high-carbohydrate (and high-glycemic-load) diets and were lean
This is another simple observation that is difficult to reconcile with the CIM. More precisely, it is a collection of many observations, because there have been, and continue to be, countless lean high-carbohydrate cultures. Ludwig has responded to this in the past, arguing that 1) the data are of insufficient quality to draw conclusions, 2) these people were lean because they were on the verge of starvation, and 3) they were protected by high levels of physical activity (17).
I’ll address these in turn, starting with the assertion that the data are of insufficient quality. The quality of data vary across observations, but some are quite high. For example, in 1990, Staffan Lindeberg, MD, PhD conducted a detailed survey of the diet, lifestyle, and health of the residents of Kitava, a Melanesian island scarcely touched by industrialization. He found a diet based on starchy plant foods (African yam, sweet potato, taro, cassava), fruit, vegetables, seafood, and coconut, with 69 percent of calories coming from carbohydrate (compared to ~49% in the US currently) (18).
Lindeberg described the Kitavans as “characterized by extreme leanness (despite food abundance)” (18). And the data back it up. Of the 247 Kitavans Lindeberg examined, none had obesity, and only a few were on the cusp of overweight (18). They did not gain weight with advancing age. There was no diabetes. Lindeberg described to me how the Kitavans had so much food they would let much of it rot or feed it to their animals. This is not to say that they never experienced food shortages– like all traditionally-living cultures, they probably did sometimes. However, they were not experiencing food shortage at the time of Lindeberg’s visit, and this is obvious in the photos he took of them (photos courtesy of Staffan Lindeberg):
Lindeberg actually did observe two Kitavan men who had borderline obesity. He describes them in his book Food and Western Disease (p. 119):
At the time of our survey in Kitava, we observed two cases of abdominal obesity, both in urbanised male migrants who had grown up in Kitavan and now came for a visit. We managed to examine one of them, a businessman aged 44 who differed in four variables from all other adults regardless of sex: he had the highest [body mass index], the highest waist-to-hip ratio, the highest diastolic blood pressure, and the highest PAI-1 in blood plasma… The most obvious difference in his lifestyle, as compared with non-migrant Kitavans, was the adoption of Western dietary habits.
This suggests that Kitavans were not genetically protected from fat gain and its metabolic consequences– they were protected by their diet/lifestyle, despite its high glycemic load. When they adopt an industrialized diet, which happens to be higher in fat and lower in carbohydrate, they become fat just like the rest of us.
Were the Kitavans protected from obesity by very high levels of physical activity? Lindeberg tested this hypothesis, and here’s what he found (18):
The amount of physical activity is estimated at 1.7 multiples of the basal metabolic rate, which is slightly higher than in sedentary Western populations.
In Food and Western Disease, he states that this corresponds to Westerners with “a moderate amount of physical activity on the job and during leisure time” (p. 84). I have little doubt that regular physical activity is part of the reason why Kitavans were lean and healthy, but their physical activity level was nothing extreme.
The book Western Diseases: Their Emergence and Prevention is primarily a collection of field studies from around the world that document the transition between traditional and modern lifestyles, and its health impacts. In most (not all) cases, the transition was from a very-low-fat, very-high-starch, high-glycemic-load diet to a more fatty diet, and this was invariably accompanied by increased rates of obesity and chronic disease. Certainly, the shift from carbohydrate to fat wasn’t the only change and we can’t attribute increasing body fatness to it exclusively. Concurrently, many of these cultures experienced increased consumption of sugar, salt, alcohol, and lower physical activity, among many other changes. These observations are nevertheless hard to reconcile with the idea that the CIM is the primary explanation for body fatness.
Just to ensure that there is no room to dispute the point I’m making here, I’ll discuss one more culture: Japan. Western Diseases contains historical data on the Japanese diet between 1950 and 1975, a time during which obesity was uncommon in Japan (p. 338). In 1975, long after postwar food shortages were over, the Japanese diet was 62 percent carbohydrate, with most of that carbohydrate coming from white rice. Furthermore, the predominant type of rice was high-amylopectin sticky rice, as it still is today (remember this word amylopectin, we’ll come back to it later). This type of rice has one of the highest glycemic loads of any food– precisely what Ludwig and Ebbeling argue is the most fattening. The Japanese ate it daily as their primary staple food, yet the prevalence of overweight and obesity were, and continue to be, lower than any other industrialized nation (19). As in many other cultures, over time the Japanese diet has become less reliant on rice and more reliant on fats, meats, sweets, and other foods, and obesity rates have increased, although they remain low compared to other countries.
Are Japanese people genetically resistant to obesity? Clearly not, because when they emigrate to the US they become much heavier (20, 21). Japanese people living in Japan are protected by their diet and lifestyle habits, despite the high glycemic load of their diet. What is different about the Japanese vs. Japanese-American diet? Many things, but here’s an obvious one: “Although total caloric intake was not greatly different between Japan and Hawaii, the percent caloric intake as fat was two times greater in Hawaii” (22). When they emigrate and their diets and lifestyles Americanize, they tend to develop overweight and obesity like people of European, African, and Native American descent, despite a reduction in dietary glycemic load.
To be clear, I’m not arguing that increased fat intake is the primary reason Japanese-Americans are heavier than Japanese, and Japanese today are heavier than in 1975– the point is to demonstrate that declining carbohydrate intake and glycemic load corresponded with an increase in body fatness. The CIM cannot be the primary explanation for obesity trends in this case, and I would argue, many other similar cases.
The genetics of common obesity argues against insulin and fat cells as the central mechanism of fat gain
Obesity has a strong genetic component, and geneticists are making great strides in cracking its code. As it turns out, the genetics of body fatness is incredibly complex, with differences at probably thousands of locations in the genome contributing to it. Each location only has a very small effect, but together they add up to a large effect. The latest and largest genome-wide analysis in 700,000 people has identified 716 places in the genome where genetic differences impact body fatness (23). By examining the functions of the implicated genes, we can gain insight into the mechanisms that determine body fatness. We know this method works: as expected, genes impacting type 2 diabetes risk tend to relate to insulin secretion, insulin sensitivity, and the pancreas, and genes impacting height tend to relate to skeletal and connective tissue growth (23, 24).
For our purposes, a key aspect of these studies is that they are unbiased (not hypothesis-driven). Researchers simply scan the entire genome looking for associations and report whatever they find, regardless of whether it conforms to our pre-existing beliefs about obesity. Whatever the mechanisms are that contribute to common obesity, they should turn up.
So what mechanisms do these studies report as being most intimately linked to obesity? Are they genes related to fat cell function? Insulin signaling? In fact, these studies consistently report that obesity-linked genes relate primarily to brain development and function: “[body mass index]-associated genes are mostly enriched among genes involved in neurogenesis and more generally involved in the development of the central nervous system” (25). This is consistent with the prevailing view in my field that the brain is in the driver’s seat, not insulin or the fat cell. That doesn’t mean the brain is the only thing that matters– probably a lot of things matter to some degree– but the brain appears to be the most important driver of common obesity. This is why my book is titled The Hungry Brain and not The Hungry Fat Cell.
I can’t overstate the importance of these genetic findings for evaluating hypotheses about obesity. They offer a rare and valuable, unbiased, 10,000-foot view of the mechanisms that drive excess body fat accumulation in the general population. We should be calibrating to these findings and asking ourselves hard questions if our hypotheses are inconsistent with them.
Circulating free fatty acids are not reduced during active fat gain in rodent models of dietary obesity
Another serious problem for the CIM is that people with obesity have circulating levels of glucose and free fatty acids (the two main circulating fuels) that are normal or elevated– not reduced as the CIM predicts (26, 27, 28, 29). Despite high levels of circulating insulin in most people with obesity, neither insulin nor anything else is preventing the release of fat from fat cells. To address this problem, Ebbeling and Ludwig conceive of a novel concept they call the “dynamic stage of obesity development”. According to this concept, during the “dynamic stage”, people are actively gaining weight because insulin is shunting fat into their fat cells, suppressing circulating fatty acids levels. But after the dynamic stage is over, weight plateaus and circulating glucose and fatty acid levels normalize or increase, which is presumably why, despite countless studies, the dynamic stage has never been observed.
Thus the CIM hinges on a phenomenon proposed by Ludwig and Ebbeling that has never been observed, and that honestly I find a bit too convenient. But has it been disproven? Let’s see if we can find any data. What we want are time course studies where researchers measure circulating free fatty acid levels at regular intervals in humans or animals that are actively gaining fat. I found two studies in rats, both of which report that circulating free fatty acids were normal or elevated at all points during active fat gain resulting from a fattening diet (30, 31). In this model of obesity at least, there is no “dynamic stage of obesity development” that supports the predictions of the CIM. Importantly, obesity was caused by a fattening diet in these studies. This is more pertinent to common human obesity than studies that involve brain lesions, leptin deficiency, or excess insulin injections, which tend to be cited by Ludwig and Ebbeling.
Reducing the flow of fatty acids out of fat cells doesn’t reduce energy expenditure, increase food intake, or increase body weight in humans
The cornerstone of the CIM is the idea that insulin suppresses fat release from fat cells, reducing energy levels in the blood, which reduces metabolic rate (energy expenditure), increases hunger, and causes fat gain. What if there were a way to experimentally restrict the flow of fatty acids out of fat cells, independently of insulin? If the CIM is correct, we should see a decrease in energy expenditure, an increase in food intake, and fat gain.
Fortunately for us, there is a way to do this: a drug called acipimox. Acipimox inhibits lipolysis, or the release of fatty acids from fat cells, mimicking the effect of insulin (32). As a consequence, free fatty acid levels in circulation decline. Acipimox has been used in humans many times, but of particular interest to us is a six-month randomized controlled trial that reported the impact of acipimox vs. placebo on energy expenditure, food intake, and body composition (33). The (preregistered) primary goal of this study was to examine the effects of acipimox on mitochondrial function, but it reported a number of other outcomes (34).
Researchers randomly assigned 39 men and women with obesity to acipimox or placebo for six months. 31 continued for the whole 6-month period (16 in acipimox and 15 in placebo) and compliance was excellent. Acipimox robustly and consistently inhibited lipolysis and at the six-month time point fasting free fatty acids in circulation were reduced by 38 percent.
How did energy expenditure change? “No significant effects of acipimox compared to placebo on [resting energy expenditure] or [respiratory quotient] were observed during either the fasting state or the hyperinsulinemic clamp.” And: “Changes in physical activity over 6 months were not different between groups”
How about food intake? According to 4-day food records: “Caloric and relative macronutrient intake did not change significantly between groups”.
Body composition? To measure this, they used the accurate DEXA technique: “There were no significant effects of acipimox vs placebo on measures of body composition, including [body mass index], [visceral adipose tissue], or lean body mass”.
Acipimox simulated the effect of insulin on fat cells that is supposed to make us hungry and fat according to the CIM, but it had no effect on food intake or body composition. Furthermore, this study suggests that the brain doesn’t respond to low free fatty acid levels by increasing food intake, which is another unproven assumption that underlies the CIM. These findings are very hard to reconcile with the CIM.
Animal studies cited by Ebbeling and Ludwig are not as supportive as suggested
Ludwig and Ebbeling cite rodent studies their team and others conducted in which they placed rats and mice on low-glycemic/insulinemic vs. high-glycemic/insulinemic diets. Since they rely heavily on these rodent studies in their arguments, and ostensibly believe rodents are useful animal models for human obesity, let’s take a closer look at them.
Let’s start with a series of studies, conducted by Gerard Slama and colleagues between 1996 and 1998, cited by Ludwig and Ebbeling. These compared diets based on mung bean noodles (low glycemic) or ground-up toast (high glycemic) in rats. You read that correctly: mung bean noodles vs. powdered toast. According to the authors, mung bean noodle starch is 8 percent indigestible fiber (resistant starch) while ground-up toast starch is only 2 percent indigestible fiber (35). So right off the bat, these diets were not isolating the glycemic index as a variable– they also differed substantially in fiber content, somewhat in calorie density, and probably in many other ways. Furthermore, resistant starch is a type of fiber that is actively under study for its potential weight and health benefits.
In the first study, published in 1996, the researchers put diabetic and nondiabetic rats on the two diets for five weeks (36). I’ll let them share the results in their own words: “Body weight was significantly lower in rats (normal and diabetic) fed on the mung-bean starch diet until the fourth week. However, body weight was comparable for both diets at the end of the 5-week period.” I don’t see how this supports the CIM.
Onward to the second study, published in 1998 (37). Again, they put diabetic and nondiabetic rats on the noodles vs. toast diets, this time for three weeks. The abstract says what we want to know: “After 3 wk, food intake, epididymal fat pad weights, and plasma glucose, insulin and triglyceride concentrations did not differ between diet groups.” Again, I don’t see how this supports the CIM.
The third study was published later in 1998 (38). Same design and the previous study, same findings: “After 3 wk, neither body weights nor relative epididymal fat pad weights differed.” None of the three studies cited by Ludwig and Ebbeling found that noodles vs. toast meaningfully impacts weight or body fatness in rats, despite other differences in diet composition that should have favored the low-glycemic noodle diet.
Let’s move on to a study conducted by Ludwig’s group and published in 2004 (39). It’s much better controlled than the noodles-vs.-toast studies, as the only difference between the two diets was the type of starch: fast-digesting amylopectin vs. slow-digesting amylose. In the first experiment, the researchers began by removing 60 percent of the rats’ pancreas to impair their insulin secretion. I don’t buy the rationale for doing this (wouldn’t reducing insulin secretion make carbohydrate less fattening according to the CIM?); they say it’s to make the rats more similar to people with prediabetes. Rats were fed the diets for 18 weeks. The amylopectin group began gaining weight halfway through and the researchers had to restrict their food intake to keep their weight similar to the amylose group. Despite no differences in weight and a lower calorie intake, the amylopectin group ended up fatter than the amylose group at the end, although neither group was especially fat (18 vs. 10 percent body fat).
I’m going to skip over the second experiment because it isn’t very relevant here. In the third experiment, they fed normal obesity-prone mice (C57BL/6J strain) the two diets for 9 weeks without restricting their intake. Body weight didn’t differ at the end, but body fatness was meaningfully higher in the amylopectin group (25 vs. 14 percent body fat). A longer-term study by Ludwig’s group also showed that an amylopectin-based diet leads to a meaningfully higher level of body fatness than an amylose-based diet in mice (40).
Together, these experiments do suggest that amylopectin is more fattening than amylose in rodents, although amylopectin-fed rodents look like runway models next to those fed refined high-fat diets (as described above). However, it’s strange to me that they only reported results from rats that had 60 percent of their pancreas removed. No matter, because I was able to find another study that put normal rats on amylose or amylopectin diets for 16 weeks (41).
This study is really interesting because it not only included amylose and amylopectin-based diets, it also included a third glucose-based diet. Glucose is digested and absorbed even more quickly than amylopectin, and stimulates insulin to a correspondingly greater degree. So if the glycemic index is what really matters, we should see the most weight gain in the glucose group, followed by the amylopectin group, followed by the amylose group. Here’s what happened: “There was no significant difference in body weight between the [amylose] or [amylopectin] groups at any of the testing points. The [glucose]-fed animals gained weight at a slightly lower rate than the [amylose] or [amylopectin]-fed animals. The [glucose]-fed animals had a significantly lower body weight than [amylose]- or [amylopectin]-fed animals at both the 8- and 16-wk testing points.” This is despite elevated insulin secretion in the glucose group.
The highest-glycemic diet caused the least weight gain, and there was no difference between the amylopectin and amylose groups eating ad libitum, in contrast to Ludwig’s study where they had to restrain the amylopectin-fed rats’ food intake to rein in body weight. It’s worth repeating that 16 weeks of a refined high-fat diet causes severe, unmistakable obesity in rodents (42, 43).
This leads me to question whether glycemic/insulinemic index is the relevant difference between amylose and amylopectin-based diets. If that were the case, wouldn’t a glucose-based diet be the most fattening of all? Another thing that leads me to question the relevance of these findings is the human evidence. Low-glycemic/insulinemic diets are not very effective for fat loss in humans, including in Ludwig and Ebbeling’s randomized controlled trial where their low-glycemic diet caused weight loss nearly identical to a low-fat diet (44). Then there are the Japanese data I discussed above, where the consumption of amylopectin-rich sticky white rice as the primary staple food did not lead to obesity (Western Diseases: Their Emergence and Prevention).
Is the CIM well-enough supported to justify diet advice?
Ludwig and Ebbeling state that “high-quality research will be needed to resolve the debate”, yet their paper contains a panel titled “Dietary Recommendations Based on the Carbohydrate-Insulin Model”. As I recall, one of the favorite pastimes of CIM advocates is criticizing the USDA for prematurely dispensing low-fat diet advice in the 1980s. If the science isn’t settled yet, perhaps it’s not the right time for bestselling books that confidently promote the CIM and a diet based on it to the public?
Conclusions
The question we must answer is not “can we find evidence that supports the CIM”, but rather “does the CIM provide the best fit for the totality of the evidence”. Although it is certainly possible to collect observations that seem to support the CIM, the CIM does not provide a good fit for the totality of the evidence. It is hard to reconcile with basic observations, has failed several key hypothesis tests, and currently does not integrate existing knowledge of the neuroendocrine regulation of body fatness.
Certain forms of carbohydrate probably do contribute to obesity, among other factors, but I don’t think the CIM provides a compelling explanation for common obesity.
Thanks Stephan. I wanted to read this but it was behind a paywall.
The Insulin Index is more informative than the Glycemia Index or Glycemia Load. When either fat or amino acids are ingested with carbohydrates, the insulin response increases, though the response to fat alone is negligible, and the response to amino acids alone is balanced somewhat by glucagon. Recall that longer dietary fats enter the circulation via the thoracic duct & vena cava, with distribution first to the coronary arteries and the rest of the body, while shorter volatile fats and enter via the portal vein for hepatic processing. Dietary composition is sensed from lips to jejunum, with the hypothalamus playing a role in insulin secretion, along with the incretins & portal vein glucosemia.
What is the result? The brain senses that energy rich chylomicrons are available to the body, so glucose can be directed to filling hepatic glycogen stores (for fasting glucosemia maintenance) and muscle glycogen stores (for glycolysis when sprinting away from carnivores), and the remainder to become Triglycerides for export in VLDLs.
Recall also that insulin both suppresses lipolysis and promotes TG synthesis and storage – which are independent processes. In insulin resistance, these processes don’t respond with normal, healthy precision. Lipolysis and fatty acidemia is not appropriately suppressed, and glycerinemia results in hepatic glucose genesis and hyperglycemia, which may stimulate further hyperinsulinemia. That fatty acids are being released doesn’t tell anything about the rate at which new Triglycerides are being added to adipocytes, in the same way the diameter of a bathtub drain is somewhat irrelevant when filling the tub from a larger diameter hose.
Finally, most large mammals, whether carnivores or fermenative microbivores, feed on fats and proteins, whether from flesh, or volatile short fats from fermentation and the cell membranes and organelles of the intestinal microbes which produced them.
The organisms that thrive on carbohydrate are microbes, and small birds and mammals. When grazers are fed starchy grains they become fat for slaughter. Perhaps a study into the insulinemia variations between grass fed and grain fed cattle are in order.
Chimpanzees, our closest relatives, are largely fruit eaters (and 2% small animals and insects). Bonobos too, and orangutans and many monkeys. Anthropological evidence proves humans have been eating starchy tubers since before we could cook, and grains and legumes after that. We may be the most carb-ivorous species of all.
LOL Nic. We are not a carnivore. Nor are we a microbe. The above anthropomorphisms are inaccurate.
We are opportunistic scavengers, cracking left-behind bones, eating roots and fruits. If something has calories we can digest we eat it.
Great article. The carbohydrate model has never made any sense (at least to me), as there are so many traditional, healthy and lean high-carb societies around the globe.
The one thing that did change with ‘western food’ is an increase in sugar/fructose consumption by several thousand percent, which has had a huge impact in terms of metabolism and energy homeostasis (not to speak of dental health and digestive issues).
Interestingly, the NuSI studies have shown exactly this: both high-carb and high-fat is fine as long as it’s low-sugar (excluding, as always, whole fruit).
Not just low sugar but also very low n-6 fats
btw keep in mind that rodent studies of sugar/fructose won’t work as rodents metabolize fructose very differently from humans (they still possess an active uricase enzyme). If you knock out their uricase gene, sugar/fructose becomes as fattening in rodents as in humans.
Moreover, human studies with pure fructose won’t work either as it is poorly absorbed in the intestine. Only if combined with glucose (as in sugar/sucrose or HFCS) does fructose reach the liver in large amounts and wrecks metabolic havoc.
Meanwhile, salt is no problem at all (see recent work by James DiNicolantonio), while alcohol is basically metabolized in the same way as fructose, thus causing similar metabolic problems (though you get drunk only after two beers, not two soft drinks).
Hi Thomas,
I’m not convinced that uricase is as important for body fatness as Johnson suggests. In a quick search the only relevant study of his I found reported that inhibiting uricase had no effect on body weight following exposure to sugar-sweetened beverage in rats. He speculates that this is the mechanism by which sugar is fattening, but in his review papers I skimmed he didn’t cite evidence that convincingly supports that position. Furthermore, if this were a major mechanism of obesity then uric acid-related genes should turn up prominently in genome-wide association studies of body mass index, but to my knowledge they haven’t.
“Furthermore, rodents are relatively resistant to fructose in part because they generate less uric acid in response to fructose due to the presence of the uricase gene in their liver (38). Uricase degrades uric acid to allantoin, and as a consequence, rats degrade uric acid rapidly after it is formed in their liver. When uricase is inhibited, rats show a greater metabolic response to fructose with worse fatty liver and higher blood pressure (79).”
https://www.hindawi.com/journals/jnme/2013/682673/
Of course, uric acid is just one of the unique effects of fructose. It’s also converted into fat much more rapidly than glucose, especially in the liver (via the KHK pathway).
The human uricase gene is silenced, so there is nothing to show up in association studies.
Also, keep in mind the recent trial study with obese kids by Lustig et al., where they replaced a high-carb high-sugar diet with a high-carb low-sugar diet and got highly significant results within just two weeks.
Hi Thomas,
There are probably many genes that impact circulating uric acid levels, just as there are many genes besides the insulin-coding genes that impact circulating insulin levels. The lack of active uricase should not prevent these genes from turning up in GWAS if uric acid is important. My view of Johnson’s hypothesis about the uric-acid/obesity link is that it relies heavily on speculative arguments and not much on data.
I did see Lustig’s paper but I didn’t find it very convincing. Most of the weight loss appears to have come out of lean mass.
The Lustig study actually was isocaloric, and it did improve several metabolic parameters, including blood pressure, triglycerides, LDL, glucose tolerance and hyperinsulinemia within just 9 days. It wasn’t about weight loss, in fact it was adjusted for weight maintenance. https://onlinelibrary.wiley.com/doi/abs/10.1002/oby.21371
Regarding uric acid, the point is that 1) the effect of fructose in rodents is only seen once uricase is silenced, and 2) uric acid in humans is an independent predictor of metabolic syndrome. Both of these points are established, as is accelerated de-novo lipogenesis due to fructose.
Moreover, Johnson noted already back in 2013 that it’s no so much about the effects of serum/circulating uric acid (which are often beneficial), but intracellular uric acid, which also explains the GWAS results. http://hyper.ahajournals.org/content/hypertensionaha/61/5/948.full.pdf
Thank you, Mr Guyenet! You do an excellent job of describing the scientific problems involved in this debate, as well as that of explaining difficult concepts clearly in a manner that allows us general readers/mere mortals to obtain a better understanding of these issues without having to tackle the many difficult intricacies of the scientific literature, which I have found are too often beyond my powers (and training).
Absolutely first rate. I’m not surprised Hall and Leibel wanted to collaborate with you.
Ludwig doesn’t understand how insulin works. Here’s what he said to you in 2016:
“In animals, insulin administration causes weight gain. Even when food intake is restricted to prevent weight gain, the animals still become excessively fat, showing that insulin redirects metabolic fuels to adipose tissue at the expense of lean body mass.”
https://medium.com/@davidludwigmd/ludwig-responds-to-whole-health-source-article-93d8e1667477
He refers to a 1985 paper in which the animals were injected with long-acting insulin. Here it is.
Insulin Increases Body Fat Despite Control of Food Intake and Physical Activity https://www.ncbi.nlm.nih.gov/pubmed/3881983
Long-acting insulin is non-physiological. Insulin is supposed to oscillate, and target cells need periodic absence or near-absence of insulin if they are to work properly.
Here is the crux: prolonged exposure to insulin suppresses mitochondrial biogenesis, according to this paper.
Prolonged Exposure to Insulin Suppresses Mitochondrial Production in Primary Hepatocytes
http://www.jbc.org/content/284/21/14087.full
Short-term insulin exposure is expected to do the opposite, by this pathway:
Insulin -> Akt -> eNOS -> mitochondrial biogenesis.
In other words, the only evidence Ludwig has for what he is claiming is a paper from 1985 which does not show what he thinks it shows. If mitochondrial biogenesis is suppressed all bets are off.
Thanks for this, I have been confused about the explanation for what is portrayed as a biological law that injected insulin -> fat gain. Are there any other papers on this? Or anything in humans? Stephan?
A couple of thoughts in reading this.
The carbohydrate insulin theory doesn’t explain enough to be of any relevance. I feel that its proponents distract relevant discussions by always going back to their intellectual insulin well to dredge up new challenges to “conventional wisdom”. A number of useless and potentially harmful ideas have resulted. The salt sideshow is a good example.
https://www.nytimes.com/2012/06/03/opinion/sunday/we-only-think-we-know-the-truth-about-salt.html
This journalistic hubris gains credibility only because of the pseudo-scientific conceits of the author.
The other thought relates to sedentarism. Physical activity allows us to eat more without becoming obese, without regard to macronutrient ratios. The historic levels of activity that Cordain et al observe (https://www.ncbi.nlm.nih.gov/pubmed/21545934) are more critical to our human existence than dietary considerations. In the past this level of activity – ca 900 kcal/day – was obligatory. Wonking diets will not compensate for inactivity IMO.
Hi Stephan,
What’s your steel-man version of the CIM?
Thanks!
Hi Raphi,
Great question. This will be a good exercise for me. I think the first thing I would do is alter it so that it’s not claiming to be the primary explanation for obesity. In other words, I would have it be a contributing factor rather than THE cause of obesity. Right off the bat that would make it much more plausible, because it wouldn’t be inconsistent with data from animal models, traditional cultures, and diet trials.
Second, I wouldn’t restrict its possible mechanism to direct impacts on adipocytes. I think if the hypothesis included the possibility that excess insulin was acting via other tissues such as the brain, it would also be more plausible.
Third, I would alter it so it’s consistent with our current knowledge of energy balance. Rather than insisting against all evidence that calories are irrelevant, I would hypothesize that it operates primarily via the calorie intake side of the energy balance equation, and perhaps impacts brain circuits that regulate calorie intake and body fatness.
Thoughts?
Stephan, excellent clarification of some important details
Taubes’ advice (avoid sugar and flour) has been extremely helpful to me since it’s relatively easy to sustain, whereas.strategies for eating less overall seem to only work in the short run. And it fits with your and Taubes’s observation that many high carb cultures are very healthy till they start eating flour and sugar,
Link to your commentary is broken
I am not sure I understand what you mean with
“””
Weight loss and obesity prevention are not
simply a matter of willpower, and any accurate model of obe-
sity must include the known physiological processes that re-
sist weight loss and promote weight gain.
“””
It was my understanding that the hormones like leptin more or less act on willpower.
Are you saying, that if people restrict calories, while somehow managing to not lower their expanditure, there might be cases where they would not lose weight / bodyfat?
Could you point me to a writeup of your current best guess on how obesity works and in particular the role of Caloires In Vs Caloires Out on obesity?
Hi Rene,
The point we were making is that willpower isn’t the only factor– we have to contend with our impulses, such as hunger and cravings. Conscious intentions aren’t the only influence on our energy intake and expenditure.
My model is not that hormones act on willpower. It’s that nonconscious brain systems generate impulses in response to internal and external cues (including but not limited to hormones), and willpower is a filter we can use to influence how those impulses are expressed as behavior. So for example, if we’re hungry that’s an impulse. We can then either let ourselves eat, or apply willpower to prevent ourselves from eating.
Willpower is part of the picture but the problem is that it’s a limited tool. Most people can’t fight themselves forever.
Willpower has worked for me for 11 years and counting. The alternative is obesity and diabetes. That’s my motivation to keep doing it.
Whether you call it willpower or sensible eating it amounts to the same thing, no matter whose diet you follow. Following any plan is a conscious act opposing the involuntary effect of a hormone.
http://www.nwcr.ws/Research/default.htm
Great read. I know this wasn’t the grunt of your post, but it perplexes me that we even consider obesity as a disease. People can exist and be healthy at various shapes and sizes. As a dietitian, I find it hard to advocate that someone lose weight because they may be in a larger body with more fat tissue. Does this really make someone unhealthy? Weight stigma is related to a higher risk for disease and then we add on our own weight biases and that makes the situation even more difficult for the person we might be treating. While I don’t do research, I find that chronic dieting and the inability to adequately self monitor (understand hunger and fullness cues) can really impede one’s ability to allow their body to settle into its natural set point.
https://www.health.harvard.edu/staying-healthy/big-thighs-may-be-wise
If there is a golden ratio for health, waist to thigh ratio may be it. It’s harder for men to achieve than women.
I’m puzzled why the Kitawans and Japanese in the 1950 are an example why the CIM is not correct. I don’t think the Kitawan food was very palatable, nor the Japanese. Also, in Japan the whole culture is built on not overindulging in anything. Portions are small and eating food is like a ritual.
But in the western world, where carbohydrates are things like doughnuts, french fries, ice cream and candy, I think CIM becomes more valid. High glycemic load carbs cause high insulin and in turn more palatable foods become more irresistible to eat.
I do agree that if one would be able to eat only boiled sweet potatoes without much salt or spices or sushi in a culture where overindulging is highly shunned, it would be more likely to not eat too much. But in the current western culture where overeating is almost encouraged and foods are very palatable, it is better to stick with LCHF, as it is more satiating and one does not tendo overeat meat, vegetables and fat so readily as things like ice cream.
On a related note to this, you Stephan said in an earlier post that fat has been found to affect dopamine the same way as carbohydrates and protein. (This is what I understood). I have been wondering this: When I’m hungry on either high carb diet or low carb diet (finding myself hungry on a low carb tends to happen very seldom), I tend to crave things like ice cream or maybe just plain rice. When I eat even plain rice when really hungry, I get the dopamine response and the almost euphoria like feeling where my body is telling me “Ah, I’ve finally eaten something”. But in either diet scenario, if I take even several spoonfuls of coconut oil, I do not seem to get any dopamine response. The hunger just gradually moves away and after a while I find that I don’t have such a need to eat something. But this takes quite a long time and I never have a craving for fat. Thus I think that in a low carb setting, I at least don’t have any craving for fat, thus when I don’t allow myself to eat carbs, I do not overeat fat either. But in a high carb diet, when there is the possibility to eat carbs, I tend to overeat carbs. In ketosis, the hunger is almost totally gone, thus I have no desire to eat anything and I can easily have intermittent fasting for 36h, which I’ve tried and found to be impossible with high carb.
The junk foods you listed are all about 50% fat, 50 % carb. They do not have high glycemic indices compared to potatoes, bread and rice. Fat is an important factor in their palatability, and contributes a lot to their calorie density.
It is of interest to compare the Kitavans with the Pukapukans and the Tokelauans when they were all eating the traditional diet composed mainly of tubers, coconut (mostly milk), fruits and fish, but in various amounts/proportions. See: https://www.ncbi.nlm.nih.gov/m/pubmed/7270479/ The Kitavans (as per Lindeberg’s research) consumed the least amount of fat, around 21E% (eq approx 3 tbsp coconut fat) and were very slim, but also short statured (males age 40-59 were 161 cm). The Tokelauans obtained about 53% fats and were much fatter, but also taller and consumed more calories. The females had BMI’s of close to 30. Despite this and the enormously high intake of coconut (saturated) fat, they appeared to be free of vascular disease. The Pukapukans had about 35% fat with BMI’s in between.
So it’s not clear that coconut really helps much with weight loss. It may perhaps do so in the short term. At least a study showed this to be the case with MCT oil when compared to olive oil over 16 weeks. But towards the end of the period the olive oil group did slightly better.
Or maybe coconut oil works better than coconut milk for weight loss because it more easily gives nausea.
It is also worth considering that the Tokelauans ate twice as much fish as the Kitavans, and meat/fish may also play a role in driving obesity. The Japanese ate very little such proteins in the 1950’s. The Sumo wrestlers are known to eat a very high protein-high carb-low fat diet and this is obviously very fattening. In the Japanese movie Spirited Away from 2001 it is all the (fatty) meat/seafoods, coupled with greed, lack of moderatation, loneliness etc that results in the overeating.
The average diet in the UK 50 years ago seems to have been what most experts would consider highly obesogenic: At least according to this report https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/549212/Domestic_Food_Consumption_and_Expenditure_1968.pdf it appears almost all the calories came from refined grains, sucrose, butter, lard and margarine. And yet only 1% of women and 2% of men were obese, compared to almost 30% today. Page 155 in the document suggests the average diet at the time supplied 2560 kcal, 11.8% protein, 41.6% fat and 46.6% carbs. Animal protein was just 46 grams, probably around 35 grams from meat/fish (far less than in the US at the time where rates of obesity were much higher). It’s even suggested that sugar intake was significantly higher in the UK 50 years ago than today (https://www.czarnikow.com/sites/default/files/uk_per_capita_online_0.jpg).
Another example of low protein high fat high carb diet could be Crete in the 1960’s (studied by Ancel Keys and others). In Crete they were obtaining about 35-40% of energy as fats, mainly olive oil, but some places as much as 45%. Animal protein intake was very low, most of the carbs came from whole grain bread, which typically has a much higher GI than refined flour pasta. Yet estimated BMI among middle aged farmers of Crete was just around 23. By 2005, this had risen to 30 (and 43% were obese). https://www.ncbi.nlm.nih.gov/m/pubmed/19176283/ Greece still has the highest per capita olive oil intake (in Italy and Spain more sunflower oil is now consumed). But they now also eat more animal fat and protein, more sugar, more refined flours and less vegetables.
—
Earlier this year Gary Taubes tweeted «if only we had listened to Yudkin in the 1960’s».
This I agree with if he talks about Yudkin’s paper published in 1960 (https://www.ncbi.nlm.nih.gov/m/pubmed/13787548/) with the title
«The treatment of obesity by the «high fat» diet. The inevitability of calories»
which says among other things in the introduction:
«… It seems fairly certain that, apart from these initial differences, a calorically restricted diet leads to weight loss in the obese which is independent of the sources of calories. This makes it unlikely that the «high fat» diet recommended for the treatment of obesity owes its effectiveness to some peculiarity in metabolism.
The alternative explanation is that the «high fat» diet leads to weight loss because, in spite of its unrestrictrd allowance of fat and protein, it is in fact a low calorie diet. This was the explanation that one of us had alteady put forward (Yudkin 1958). Such a view is simple and orthodox, and therefore unspectacular. This is probably a reason why many have preferred to accept the more exciting theories based on some postulated but unproven defect in metabolism. Yudkin (1958) pointed out that a diet severely restricted in carbohydrates, would if anything also be restricted in fat. Thus, restriction of bread is also likely to lead to a lower intake of butter. This restriction of ice cream, cookies and most biscuits restricts not only the carbohydrate they contain but also the fat.»
The study then aims to prove this. The normal caloric intake of six individuals (four females, two males) were first measured over two weeks – and on average was found to be about 2400 kcal/day (but with huge variations). Then they were instructed to limit carbohydrates to 50 grams per day for another two weeks but eat as much protein and fat as they liked. This resulted in an average caloric intake of 1400/day. Protein and fat intake was roughly the same as before, but the carb restriction resulted in a significant reduction in calories, and hence weight loss.
What is less clear to me is what will happen in the long term on such a low carb diet with unrestricted intake of fat and protein. Could it be that a reason people didn’t eat more fat and protein was the fact that their bodies (i.e liver, kidneys etc ) was not adapted to it and responded with a satiety/nausea signal? At the same time we know that hunter gatherers can eat astonishingly large amounts of meat in one sitting, which must then involve weight gain. Or like the wolf that can eat 20 pounds of meat in one day and then go 10 days without food. So to me there’s something counter intuitive that meat and fat should not lead to weight gain. Instead what could be happening is some exploitation of the unaccustomedness-effect, or as Yudkin mentions that the body simply will not tolerate too much fat when carb intake is low and then it’s not really possible to gain weight. However, I suspect that over time the body will adjust to a higher protein intake and use this similar as carbs making it possible/desirable to eat very large amounts of fat.
Taubes was probably off on his current evil sugar tangent with his tweet.
Yudkin firmly believed in CICO. He added carb counting on top of that, counting them in 5 gram units and limiting to 10-15 units a day for weight loss. It’s a very effective weight loss diet in my experience. It was harder to follow than simple calorie counting because you have to deconstruct all your foods. And we have SO many now. Yudkin’s 1958 tables don’t include pho and tacos….mmmmmm
My old Paleohacks post on this is still intact!
https://www.paleohacks.com/fat/has-anyone-read-any-john-yudkin-2100
It’s not true that sumo wrestlers eat a low-carb diet as a quick search in Japanese will tell you. (e.g. http://www.futoru.com/article/14832061.html 『炭水化物』を大量に食べる『ご飯をたくさん食べる』 (eat lots of “carbohidrates”, lots of rice); or look at the first bit of this video: https://youtu.be/Wu8oF0pf44U
PeterL,
I wrote that the Sumo wrestlers eat «a very high protein-high carb-low fat diet». But I’m not quite sure what is the typical macronutrient balance for the Sumo wrestler today. A study from 1976 suggested 5000-5500 kcal/day of which 13-27% of energy as protein (165-365 gram), 57-78% carbs and 9-16% fats https://www.ncbi.nlm.nih.gov/m/pubmed/973605/ My point anyway is that animal protein intake has gone up significantly over the past 50-60 years worldwide and this correlates with higher prevalence of obesity, and it may have been a contributing factor. According to https://www.nationalgeographic.com/what-the-world-eats/, average combined meat and fish intake globally went from 93 grams in 1961 to 173 grams in 2011. In the 1950’s animal protein intake was relatively low in Japan, and although it has gone up considerably it is still low by western standards.
Sorry for mis-reading your comment.
Do fish count as “animal protein”? The National Geographic graphic doesn’t seem to have a category for fish, only “meat”.
No problem, Peter.
Try and click on the «meat» icon. «Meat» includes beef, pork, poultry, seafoods and «other meat».
Thank you for taking time to write this. Your communication style is very much appreciated.
i was lowcarber 4 years ago. the lowcarb theory is entierly bullshit. it’s obvious in many, many, MANY ways
The CIM may be dead, but the RCIM is almost universally accepted (refined). Of course after metabolism normalization one goes back to carbs, otherwise K and Mg depletion, not to mention lower SCFA from lower fiber intake, will take their toll. And it does not take much experimentation to arrive at an optimal combination of legumes, tubers, roots, nuts, and perhaps Mg-rich, light grains such as buckwheat.
But being fat adapted has some advantages. First, you use all your digestive channels, in particular you spare your liver the extra work from fructose. Some supposedly healthy carbs, such as apples, will tax your liver. Second, it is much easier to fast. Third, good amounts of fat induce satiety, allowing you to use your limited amount of free will on other endeavors.
Hi glib,
If you mean the idea that refined carbohydrate contributes to obesity, then yes that is widely accepted. If you mean the idea that refined carbohydrate contributes to obesity by increasing insulin levels, trapping fat in fat cells, increasing calorie intake and decreasing energy expenditure, that mechanism is not widely accepted.
As for the Japanese diet, which both you and Taubes have mentioned (Taubes claimed that sugar isn’t eaten much in Japan and you’ve mentioned that Japanese eat a lot of high-amylopectin sticky rice), maybe I can dispel a few untruths from having lived in Japan for a few years (things that tourists might not experience) and also having a somewhat “traditional” Japanese wife (who’s a good cook) [yes, I know the plural of “anecdote” isn’t “data”]:
The so-called traditional Japanese diet is fairly low-fat, low-sugar, high-carbohydrate (rice), high-protein (fish, tofu, beans). I’d describe it as non-vegetarian with lots of veggies. I suppose this makes it “low palatability”, at least on the high fat/sugar scale, although Japanese cooking often emphasizes “umami” which is another kind of palatability; and there’s a fair bit of salt/sodium (e.g., in soy sauce or MSG).
If I eat a “traditional” Japanese diet for a while, I don’t like the taste of American food because it’s too sweet and too greasy. For me, the typical American diet requires habituation.
Japanese cooking has some deep-fried/fatty food (tempura, ton-katsu, ramen, etc.) but usually with vegetables (vegetable tempura, ton-katsu with raw cabbage salad). Fatty fish also, of course.
The traditional Japanese breakfast is savory, not sweet (no sweetened cereals or jam on toast); e.g., miso soup, rice, fish or egg, natto, pickles, green tea. A westernized breakfast tends to be something like toast, salad, egg, coffee (you can see examples by doing an image search for モーニングセット).
The traditional way of describing a meal is “things that go with rice” (o-kazu). The word for “meal” is identical with the word for “cooked rice” (go-han). It’s normal to ask for seconds of rice (o-kawari) – often at no charge in a restaurant. Traditionally, one doesn’t eat rice while drinking saké (if drinking, rice and pickles would be served at the end of the meal rather than rice throughout the meal), although this “rule” isn’t followed very strictly.
It’s not true (as someone claimed) that sumo wrestlers eat a low-carb diet as a quick search in Japanese will tell you. (e.g. http://www.futoru.com/article/14832061.html 『炭水化物』を大量に食べる『ご飯をたくさん食べる』or look at the first bit of this video: https://youtu.be/Wu8oF0pf44U
There’s probably a lot of fiber in the Japanese diet (vegetables, beans, seaweed, mushrooms). The relative amount of vegetables is much higher (and has more variety) compared to typical American. Vegetables are usually cooked, which can make their bulk deceptive (e.g. ohitashi)
Desert is not traditional in Japan and if provided, it’s often a small amount of fruit. But a meal often ends with rice and pickles.
Treats or snacks tend to be small (home baking is uncommon). Traditional snacks have little fat and often have fiber (e.g., made from adzuki beans + sugar).
Portion sizes tend to be small (but sufficient for even a large person like me) and a meal will have quite a bit of variety (e.g., 10 kinds of vegetables and mushrooms).
Sweetened drinks are relatively uncommon (easily observed by looking at vending machines).
Most meals have some kind of fermented food (miso, pickles, natto, umeboshi, katsuobushi, etc.)
Fruit tends to be a bit of a luxury (with a few exceptions, such as oranges) and is usually eaten raw (pies are uncommon). Apples, pears, grapes tend to be peeled.
“Eat until you’re 80% full” (“hara hachi-bu”) is a common proverb.
Japan is definitely a “foodie” country. There are lots of cooking shows on TV and tourism TV shows often emphasize the food. Different regions of the country advertise their specialty foods (e.g., Kyoto is known for its vegetables — often served in a minimalist way that brings out the subtle flavor).
People are more physically active than in the US (walking, bicycling, using public transit rather than driving).
Also, an observation from when I was a kid in Canada in the 1960s: whenever we visited the US, we were all amazed at the portion sizes in restaurants – and Canadians are not exactly small eaters.
Hi PeterL,
Thanks for this additional context.
Here’s James Fallow’s article “No Fat City”, about his American family living in Japan in the 80’s.
https://www.google.com/amp/s/www.theatlantic.com/amp/article/306107/
The family spent a lot of time eating tonkatsu to get their accustomed fat fix.
I ate a lot of wheat noodles in Japan too. Particularly on Shikoku, where we ate a lot of udon.
Fallows forgot to mention that the Japanese “fatty [Chicken-fried] pork cutlet” also came with a mound of raw cabbage salad, rice, green tea, and maybe miso soup (and refills on the cabbage and rice). As compared to the American hamburger, which comes with a single piece of lettuce and tomato, fries, and a soft drink.
e.g. https://tabelog.com/en/tokyo/A1314/A131401/13190933/
He also probably walked to and from the local ton-katsu outlet.
I’ve used that Fallows article for years, for a number of reasons. It’s based on real observations made by an ordinary American living in Japan for an extended period.
I’ve found personally that it’s very difficult to change dietary habits. Americans are conditioned to eating a macronutrient mix of about 45% carb, 43% fat and 12% protein (USDA, 2010 if I recall correctly). The Japanese are accustomed to eating something more on the order of 65% carb, 25% fat, 10% protein. If an average American is suddenly dropped into that dietary pattern, they will seek fat the way Fallows did with the tonkatsu.
Sedentarism is something that has bothered me for the last 20 years. I first noticed it living in France, when I lived in downtown Bordeaux and walked everywhere for everything instead of driving. I dropped 15-20 pounds in a few months, yet ate all I wanted of every food offered. A lot of that was fatty carby foods, like American junk food only much more rewarding. When I went back to the US and started driving everywhere again, the weight came right back, to the point of obesity and diabetes.
A diet that contains high energy density carby/fatty foods needs exercise to go with it. It’s not surprising that the Japanese invented the concept of 10,000 Steps as an antidote to the problem of the sedentary salaryman.
https://bigthink.com/ideafeed/the-origin-of-the-10000-steps-per-day-goal
It was key for my weight loss in France, though I didn’t recognize it at the time. I’ve used it for the last 11 years, for weight loss and maintenance, and so that I can continue to eat any food I like so long as I don’t regain the weight. I estimate I put in an equivalent of 25,000 steps a day walking and biking.
It takes a very long time to walk 25,000 steps. Definitely not compatible with any kind of normal desk job unfortunately. Even 10,000 is almost impossible during a work day, unless you have some sort of treadmill desk (which wouldn’t work for me, because I do artwork, and need a stable surface). I stand at my desk most of the time, which is better than nothing, but nowhere near as good as walking. Modern life makes it terribly inconvenient to function as a healthy human.
I’m semi retired so have more time than most people Robin. But even when I was doing a sedentary desk job I got in at least 10,000 steps. One of my French habits was walking to and from work. That’s tougher in the US suburbs, but it set a pattern for me of walking early in the morning to get coffee, walking to lunch and walking on breaks.
I’ve been rereading Joyce’s Ulysses, about downtown Dublin on June 16, 1904. Everyone is walking, all the time. In the stream of consciousness, the ravening hunger that walking generates is evident, as noon approaches and Bloom is seeking food. Here’s a longer summary.
https://www.researchgate.net/profile/Petru_Golban/publication/273382491_James_Joyce_and_the_Condition_of_Modern_Man_Hunger_Food_and_Eating_Revealing_Self-Identity_and_Inter-Human_Relationship_in_Lestrygonians/links/54ffe8e30cf2741b69fa06af/James-Joyce-and-the-Condition-of-Modern-Man-Hunger-Food-and-Eating-Revealing-Self-Identity-and-Inter-Human-Relationship-in-Lestrygonians.pdf
I am currently in Japan for 2 months. One thing that amazes me is that no one here intakes more K than Na. At the very best they have a Na/K ratio of 1.5, although few go as high as 2.5. They are nutritionally very homogeneous. I would cite the paper(s) but I do not have a proper connection now. This is generally true across East Asia, as white rice is really poor in K. Generally, K intake is about half of what Europeans take. Mg is similarly on the low side.
And all that Na surely supports insulin response to a high carb diet, so I think high salt intake is something they evolved into to tolerate all that rice.
Re Europe I think there are huge variations in the Na/K ratio depending on what foods are consumed in each country. Cheeses and commercial white bread are major sources of salt which lacks potassium, while boiled potatoes and milk are high potassium-low sodium. Modern pizza can have a particularly high Na/K ratio.
A study found that among Italian children the Na/K was about 2 (3000 mg Na and 1500 mg K), compared to 1 in France (2500 mg each). The prevalence of overweight or obesity in Italian children is a whopping 35% (as of 2014), the second highest in the OECD countries listed here after Greece where it’s 41%: http://www.oecd.org/italy/Obesity-Update-2014-ITALY.pdf
A study in the elderly mediterranean population found that cheese consumption significantly increased risk of metabolic syndrome, while it was opposite for milk/yogurt: https://www.ncbi.nlm.nih.gov/m/pubmed/26290009/
It’s pretty simple, really. The only way you can get fat is to at fat (for humans). The CIM hypothesis of de novo lipognesis is clearly incorrect.
More supporting evidence:
http://www.dailymail.co.uk/health/article-5958463/Fat-consumption-cause-weight-gain.html
Thanks for the article. The author points out the “fat won’t make you fat” books like GCBC. The expression is true in the context of HFLC dieting with restricted calories, but outside that it is false. The “fat calories don’t count” mantra perpetuates the obesity crisis in the general population.
The latest winner in the Food Reward sweepstakes:
Reese’s and Hershey’s whipped cream is here and it looks delicious
https://www.facebook.com/uniladmag/videos/5098341853522166/
Some concerns with very high protein diets though. In pigs it does appear to help body composition in the short term, but not long term and then additionally leads to kidney damage. Note that pigs are more similar to humans than mice. 4 months for a pig may be equivalent to 20 months for a human.
Long-term high intake of whole proteins results in renal damage in pigs.
Randomized controlled trial
Jia Y, et al. J Nutr. 2010.
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Abstract
Despite evidence of potential antiobesity effects of high-protein (HP) diets, the impact of consuming diets with protein levels at the upper limit of the acceptable macronutrient distribution range (AMDR) on kidney health is unknown. To test whether HP diets affect renal health, whole plant and animal proteins in proportions that mimicked human diets were given to pigs, because their kidneys have a similar anatomy and function to those of humans. Adult female pigs received either normal-protein (NP) or HP (15 or 35% of energy from protein, respectively) isocaloric diets for either 4 or 8 mo. The higher protein in the HP diet was achieved by increasing egg and dairy proteins. Although there were initial differences in body weight and composition, after 8 mo these were similar in pigs consuming the NP and HP diets. The HP compared with NP diet, however, resulted in enlarged kidneys at both 4 and 8 mo. Renal and glomerular volumes were 60-70% higher by the end of the study. These enlarged kidneys had greater evidence of histological damage, with 55% more fibrosis and 30% more glomerulosclerosis. Renal monocyte chemoattractant protein-1 levels also were 22% higher in pigs given the HP diet. Plasma homocysteine levels were higher in the HP pigs at 4 mo and continued to be elevated by 35% at 8 mo of feeding. These findings suggest that long-term intakes of protein at the upper limit of the AMDR from whole protein sources may compromise renal health.
https://www.ncbi.nlm.nih.gov/m/pubmed/20668252/
I really appreciate this.
Thanks, Stephan, for this article. You serve the public well by digging deep and sharing what you find in language even I can understand. You seem to distill as much science as you can find and present it without a bias that taints what you publish. Good on you.