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Amazing scientific blog entry on why the carbohydrate hypothesis of we


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#1 TheFountain

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Posted 19 August 2011 - 07:47 PM


I really am compelled by this blog entry by Stephan Guyenet, in which he outlines all the reasons it is likely the carbohydrate hypothesis of weight gain is simply wrong, with a special eye on the premature insulinogenic theories of Gary Taubes.

Some excerpts:

'While we're on the subject, let's address the idea of "internal starvation". Taubes suggests that people overeat because they can't access their fat stores due to elevated insulin. However, obese people have equal or higher circulating free fatty acids and glucose (22, 23), so how is that possible? It's not. The internal starvation model was interesting at the time it was proposed, however the evidence has refuted it since then. If anything, obesity is a condition of "internal excess". This information is readily available in the scientific literature, and I'm sure the numerous obesity researchers he interviewed would have been happy to explain it to him, so it doesn't make sense that he instead relied on his own speculation here.

Let's also address the claim that obese people don't necessarily eat more than lean people. Food records are notoriously inaccurate, however there is at least one way to measure total energy intake in a precise and unbiased manner. It is called the "doubly labeled water method" (DLW). DLW studies have shown that after controlling for confounding factors, obese people almost invariably expend more, and consume more calories than lean people (24, 25). Weight stable obese people have a higher energy flux out of fat cells, and a higher metabolic rate, but it is not enough to overcome the higher calorie intake that is also observed (26, 27). That has been repeatedly confirmed and it is simply a fact at this point.

Therefore, the insulin hypothesis is not consistent with basic thermodynamics, and it's not consistent with research on the biological functions of insulin. Obese people do not have a defect in the ability to release fat from fat cells and burn it, to the contrary. They release more fat from fat cells than lean people, and burn more of it. However, this is compensated for by a higher energy intake, and a higher rate of fat incorporation into fat cells that counterbalances the increased expenditure. The fat cells of obese people do not suffer from excessive insulin signaling, to the contrary, the evidence suggests that their fat cells are insulin resistant and therefore insulin signaling is reduced. This shows that insulin does not cause obesity by acting directly on fat cells to cause fat storage. To understand obesity, we have to understand what causes increased food intake, and that factor is not insulin.'

Also:

I've already demonstrated that Taubes's conception of the effects of insulin are badly misguided, therefore it makes no sense to invoke insulin as a mechanism between carbohydrate consumption and body fatness, unless your hypothesis is that carbohydrate lowers body fatness by increasing insulin secretion.

Another problem with the hypothesis is a thing called the insulinogenic index (II). The II is simply a measure of how much eating a food increases insulin, per unit calorie (28). It turns out, it doesn't correspond with the carbohydrate content of the food very well. In particular, protein-rich foods such as beef can increase insulin secretion as much as certain starch foods such as pasta, or more. High-protein diets, as many of you know, aid with weight loss. The other problem is that refined and unrefined carbohydrates often have a similar II. Pasta made from white and whole-grain wheat have the same II, and the same goes for white and whole-grain bread (29). Doughnuts and cookies are on par with whole grain bread. So post-meal insulin is not a compelling explanation for the potentially different effects of protein, unrefined carbohydrate, refined carbohydrate and sugar on body fatness.

I think it's likely that refined carbohydrate and sugar can contribute to obesity, but by what mechanism? Insulin is not a compelling explanation. Food reward/palatability is an alternative possibility that fits the evidence better. Another plausible hypothesis is reduced fiber and micronutrient density.

Also:

Northern Cameroon, 1980s. The Massas tribe (also spelled Massa) is known for its overfeeding ritual called Guru Walla, which Taubes describes in GCBC:

The Massa tribe of northern Cameroon fattens their males using both milk and a porridge made from sorghum, a corn-like grain that provides sweet syrup from the stalk. One man gained seventy-five pounds on a ceremonial binge. The average weight gain tends to be fifteen to twenty pounds using milk and porridge. The Massa are cattle herders and their staple diet is primarily milk. This fattening comes about by the addition of carbohydrates (sorghum) almost exclusively.

Taubes states here that the typical diet is "primarily milk", therefore by inference, low in carbohydrate. Let's follow his reference and see what it says. It leads to a freely accessible paper by Drs. Igor de Garine and Georgius J.A. Koppert titled "Guru Fattening Sessions Among the Massa" (30). The Massas indeed herd cattle, but "their main use is not as food." The typical diet (not during overfeeding) is described as containing 516 grams of carbohydrate per day, and only 32 grams of fat (Table VIII). The typical diet is 81% carbohydrate, and primarily based on sorghum, according to Taubes's own reference. This account is consistent with other freely accessible references in respected peer-reviewed journals (31). These people are lean on their typical high-carbohydrate fare until they deliberately overconsume a mixture of sorghum and milk.

Most of Asia, 20th century. Many Asian countries, including China, Japan, Taiwan and India, have a traditional diet that is very high in carbohydrate. In many cases, the dominant carbohydrate was white rice, a refined carbohydrate. Yet traditional Japanese, Chinese and Southern Indians eating mostly white rice were renowned for their leanness. Any plausible hypothesis of obesity needs to account for these observations.

Kitava, 1990s. Dr. Staffan Lindeberg showed that the Kitavan diet is 69% carbohydrate, mostly from taro, breadfruit, sweet potatoes and cassava (32). Thus, their diet would have had a high glycemic load and high II. They also obtain 50 g/day of carbohydrate from fruit, most of which would presumably been sugar (unrefined). Yet there was no obesity on the island, and only a few individuals that were slightly overweight (33). Fasting serum insulin was low, consistent with other high-carbohydrate cultures. Dietary carbohydrate does not cause insulin resistance.

Pima, 20th century. The Pima of New Mexico currently have one of the highest obesity rates in the world, on par with Nauru. It is rather ironic that Taubes uses them as an example in GCBC, when they are at odds with his hypothesis. The Pima were first contacted in 1539 by the Spanish, who apparently found them to be lean and healthy. At the time, they were eating a high-carbohydrate, low-fat diet based on corn, beans, starchy squash, and a modest amount of gathered animal and plant foods from the forest and rivers in the area. In 1869, the Gila river went dry for the first time, and 1886 was the last year water flowed onto their land, due to upstream river diversion by settlers. They suffered famine, and were rescued by government rations consisting of white flour, sugar, lard, canned meats, salt and other canned and processed goods. They subsequently became obese and have remained that way ever since. Their diet consisted mostly of bread cooked in lard, sweetened beverages and canned goods, and they also received salt. More recently, their diet has modernized but still relies heavily on processed food (34, 35).

http://wholehealthso...esity.html#more

Edited by TheFountain, 19 August 2011 - 07:50 PM.

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#2 rwac

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Posted 22 August 2011 - 12:15 AM

I agree with you that low-carb is not the panacea it is made out to be. For instance, I have never been able to go low-carb for any length of time, it just makes me feel sick.I didn't even lose weight.

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#3 Lufega

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Posted 22 August 2011 - 12:27 AM

I think there's a lot more to this low-carb movement that we haven't seen. I never really believed the mechanism to be mediated by insulin. Because proteins (especially BCAA's) increase insulin and so does butter. But keep in mind that these do not increase blood glucose. In the populations he reviews that ate a lot of carbs, they were in the form of starchy, fibrious tubers like sweet potatos. No one in these groups ate refined grains and excess sugars. I follow a low carb, grain/sugar free diet but I still eat sweet potatoes, satsumaimo (we call it Batata), squash and other tubers with a good nutritional profile, that are traditional in my culture. These however, I keep these to a minimum. I think the fiber content of these different foods is probably why they can gorge on carby foods without enduring metabolic problems.

edit: When I say sugar free, that doesn't include fruits. I eat tons of fruits and berries. In fact, in the past, I've been able to loose weight by getting most of my calories from fruits.

Edited by Lufega, 22 August 2011 - 12:30 AM.


#4 TheFountain

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Posted 22 August 2011 - 01:58 AM

I like what he said about the reward centers of the brain being the biggest contributors to weight gain. A line of reason not seen very much in dietary circles. He also demonstrates well how non-diabetic obese people have even faster metabolisms than normal weight, healthy people! So how could insulin be the driver of weight gain in the non-diabetic average populace?

I don't know if glucose could be the cause either, since I often splurge on carbs and they don't make me fat. I do cyclical dieting of course, but the two or so weeks I do high carb low fat should still demonstrate changes in metabolic function and corresponding weight fluctuations if there is anything to the carbs=weight gain theory. Of course there is always gene mutation to consider too. Different epigenetic expressions could be as modern as agriculture! Some adapt, some don't. But then, I don't even know if we can say adaptation (or lack thereof) is the issue. What clear evidence is there of that?
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#5 Rick Moranis

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Posted 22 August 2011 - 11:40 PM

http://wholehealthsource.blogspot.com/2011/08/carbohydrate-hypothesis-of-obesity.html
I hope you can see by now that the carbohydrate hypothesis of obesity is not only incorrect on a number of levels, but may even be backward. The reason why obesity and metabolism researchers don't take Taubes's idea seriously is that it is contradicted by a large body of evidence from multiple fields. I understand that people like ideas that "challenge conventional wisdom" as the GCBC book cover states, but the fact is that obesity is a complex problem and it will not be shoehorned into simplistic hypotheses.

----
I wonder how Guyenet explains role in fat-loss of all of these other catabolic and anabolic hormones Taubes cites in GCBC book:

http://paste2.org/p/1430577
[line 118]
Hormones that promote fat mobilization
Epinephrine
Norepinephrine
Adrenocorticotropic hormone (ACTH)
Glucagon
Thyroid-stimulating hormone Insulin
Melanocyte-stimulating hormone
Vasopressin
Growth hormone

Hormones that promote fat accumulation
Insulin

...
[line 309]
These various fat deposits are also regulated over time by the changing flux of sex hormones, so LPL can be
considered the point at which insulin and sex hormones interact to determine how and when we fatten. The male sex
hormone testosterone, for instance, suppresses LPL activity in the abdominal fat, but has little or no effect on the LPL
in the fat of the hips and buttocks. Increasing fat accumulation in the abdomen as men age may therefore be a product
of both increasing insulin and decreasing testosterone. The female sex hormone progesterone increases the activity of
LPL, particularly in the hips and buttocks, but estrogen, another female sex hormone, decreases LPL activity.*120 It’s
the decrease in estrogen secretion during menopause—and so the increase in LPL activity—that may explain why
women frequently gain weight as they pass through menopause. The effect of decreasing estrogen secretion on LPL
activity would also explain why women typically fatten after the removal of the uterus in a hysterectomy. The change
in hormonal regulation of LPL also explains how and why fat deposition changes during pregnancy and, after birth,
with nursing.


And Robbwolf from ThePaleoSolution cited hormones:

Hormones: for Digestion and Fun or Can You Hear Me Now?
Now that we know the players (protein, carbohydrate, and fat), let’s see how they fit into digestion, hormonal release, and eventually health and disease.
How does your body know it’s “hungry”? What does “hunger” really mean? You likely have a much better social life and get out more than I do, so you
have never pondered these riveting topics, but since we are here, we might as well ask the important questions—and they are important.
Understanding how our body normally regulates hunger will give us insight into the development of obesity, cancer, diabetes, and a number of other
nasty problems we would all do well to avoid. Similar to the fuel gauge of an automobile, our sense of hunger tells us when our body is running out of
stored energy. But when we eat, we need to know when we have had enough. Hunger lets us know when we are “running on empty” and the sense of
satiety tells us when the fuel tanks are full.
All of this information is communicated throughout the body by chemical messengers called hormones. Before you are finished with this book, you will
“meet” quite a number of hormones and you will understand a good bit of what they do in critters such as yourself. In simple terms, hormones are
messengers that communicate information throughout the body. How we age, burn fat, think, and reproduce are largely controlled by hormones.
Each hormone has a very specific way of interacting with the cells in our bodies. They interact through a molecule called a receptor site. A common
analogy for hormones and receptors is the picture of a lock and key. The key would be the hormone, which fits snuggly into the specific “lock” (receptor).
This analogy is helpful in that it describes accurately the physical interaction of a hormone and receptor based on shape, but it is a bit odd to imagine
keys floating about your body.
I like the additional analogy of hormones acting like radio signals and receptors acting like receivers tuned to specific hormones. The combination
describes both the physical interaction of the hormone and receptor, but also the fact that information can be transmitted across vast distances by the
hormone, which is then received by the receptor site. Hormonal communication in the body controls our levels of body fat, our thinking, our hunger, and
just about anything you can think of.
Now let’s look at the main hormone players, beginning with insulin.
____________________________
Insulin is critical in regulating blood sugar, body fat, and aging. To live long, look good, and keep our marbles, we would do well to keep our insulin on the
low side by controlling carbs and certain lifestyle factors.
____________________________
Geek-Speak
Insulin acts as a nutrient-storage hormone that maintains blood glucose levels. In simple terms, insulin puts nutrients into our cells. What we will find,
however, is that insulin plays a key role in a staggering number of critical processes completely unrelated to blood sugar management.
____________________________
Why Is Blood Glucose Important?
So, I mention blood glucose (sugar) levels quite a few times in this book. Why is it important? Well, the red blood cells and certain parts of the brain can
run on no other fuel besides glucose. In certain situations like insulin resistance, blood sugar levels can fall and the result can range from dizziness and
hunger to unconsciousness and death. So, we should eat lots of carbs then, right? Uh, no. As you will see we are better served if we can encourage most
of the body to run on fat and just provide enough carbohydrate to meet the needs of these truly glucose-dependent tissues. By reducing the body’s total
need for carbohydrate, we actually protect ourselves from blood sugar crashes.
____________________________
Insulin is relevant not only in glucose storage, but also in fat and protein (amino acid) storage. Insulin is released from the beta cells of the pancreas
primarily in response to increasing blood levels of glucose and amino acids and plays a significant role in micronutrient storage and conversions. Insulin’s
primary role as a nutrient sensor (when you ingest food, insulin tells those nutrients where to be stored) greatly influences genetic expression surrounding
aging by up or down regulating maintenance and repair at the cellular level. If you are interested in aging, your level of body fat, when or if you will lose your
marbles, and whether or not your “reproductive machinery” works, you will want to keep an eye on insulin.
____________________________
Glucagon helps normalize blood sugar and energy levels between meals by releasing energy from the liver and allowing us to better access our body fat
for energy.
____________________________
Geek-Speak
Glucagon is the counter-hormone to insulin and prompts the release of glucose from the liver, as well as free fatty acids from fat stores, by a process
called lipolysis. Glucagon secretion is stimulated by decreased blood glucose levels (hunger), increased blood amino acid levels, and the hormone
cholecystokinin (CCK). High levels of insulin, free fatty acids, ketone bodies, or urea in the bloodstream will inhibit glucagon release. Insulin and glucagon
play complementary roles of helping us to manage energy levels by storing and releasing nutrients at the right time. Insulin facilitates the passage of
nutrients into cells, while glucagon tends to release stored nutrients to be used for energy.
____________________________
Leptin tells our body how much fuel we have in storage, and when we are “full.” If we lose the ability to sense leptin, appetite control is lost.
____________________________
Geek-Speak
Leptin regulates both appetite and metabolism. Leptin enters the central nervous system where it acts on receptors in the brain that control energy intake
and expenditure. Leptin is produced by white adipose tissue (fat cells), as well as the cells lining the wall of the stomach. The leptin produced by the cells
in the stomach is responsible for controlling appetite. When Leptin is working correctly, it’s very effective at telling us we are “full” after eating a meal. As
we will see, when leptin signaling (how a hormone “talks to a receptor”) breaks, it is the beginning of problems ranging from cancer to accelerated aging
to neurological degeneration.
____________________________
Ghrelin tells us we are hungry or low on energy. We would like this to be an accurate message, but it is important to note that stress and lack of sleep can
alter ghrelin levels and unfavorably increase our sense of hunger.
____________________________
Geek-Speak
Ghrelin is a hormone that stimulates hunger, increases food intake, and increases fat mass. It is produced by cells in the lining of the stomach, as well as
epsilon cells of the pancreas. Ghrelin is also produced in the hypothalamic arcuate nucleus, where it stimulates the secretion of growth hormone.
Inadequate sleep is associated with high levels of ghrelin. A little down the road, you will discover just how important sleep is to maintaining a lean, healthy
body. Since sleep deprivation increases ghrelin, and since ghrelin increases appetite, this is one of the reasons why sleep disturbance leads to
increased food intake.
____________________________
Adiponectin is another of several satiety hormones. Not only does it tell us when we’ve had enough food, but it also protects our arteries from oxidative
damage.
____________________________
Geek-Speak
Adiponectin is a protein hormone that is secreted by adipose tissue and has the following effects: decreases gluconeogenesis (the conversion of protein
into glucose), increases glucose uptake, and protects from endothelial dysfunction (a common feature of atherosclerosis). Although released by adipose
tissue, levels of adiponectin in the bloodstream of adults is inversely correlated with percentage of body fat (folks with low body fat have high adiponectin).
Adiponectin is an independent risk factor for metabolic syndrome and plays a role in the suppression of the metabolic derangements that may result in
type 2 diabetes, obesity, atherosclerosis, and nonalcoholic fatty liver disease.
____________________________
Peptide YY (a.k.a. PYY) is yet another hormone trying to tell us when to stop eating. Protein and fat release a lot of PYY and are thus very satisfying.
Carbohydrate, by contrast, releases relatively little PYY, which is why your breakfast of bran muffins and juice leave you ravenous in a few hours.
____________________________
Geek-Speak
PYY is a gut hormone that reduces hunger while simultaneously improving central nervous system sensitivity to leptin. PYY is released by neuroendocrine
cells in the ileum and colon in response to feeding. Protein causes greater PYY secretion than fat, which causes greater PYY secretion than carbohydrate.
PYY plays a synergistic role with leptin in helping us feel satisfied after a meal.
____________________________
Cortisol raises blood sugar levels, which can cause fat gain. Although many people don’t know this, cortisol release from stress and a lack of sleep
factors prominently in body fat gain, leading to that pesky spare tire around the midsection. Cortisol shouldn’t be feared, because it is a crucial antiinflamatory—
we just don’t want too much of it.
____________________________
Geek-Speak
Cortisol is often referred to as a “stress hormone,” given that it is released in response to stress and anxiety. Cortisol increases blood pressure and acts
as an anti-inflammatory by lowering the activity of the immune system. It will trigger the breakdown of muscle mass by converting protein (amino acids)
into glucose via gluconeogenesis. Cortisol decreases insulin sensitivity, lowers the rate of bone formation, and causes a loss of collagen in the skin and
other connective tissues. The following increase cortisol levels: intense or prolonged physical activity, caffeine, sleep deprivation, stress, subcutaneous fat
tissue, and certain contraceptives.
____________________________
Insulin-like Growth Factor-1 (IGF-1) is another hormone we want “just the right amount” of. It aids in physical recovery, but poor diet can abnormally
raise IGF levels, which in turn increases both our likelihood for cancer and our rate of aging.
____________________________
Geek-Speak
IGF-1 is critical to the growth of children and has an anabolic effect in adults. IGF-1 activates the insulin receptor but generates a response that is only 10
percent of that observed for insulin. Low IGF-1 promotes cell maintenance and stress resistance. IGF-1 levels are highest during pubescent growth
spurts. Exercise, stress, and nutrition can affect IGF-1 levels. Increased levels of IGF-1 stimulates both growth and aging.
Now that you have met the players in this digestion/endocrinology orchestra, you likely understand a little about the chemistry of our food and “who” the
primary hormones are that we must consider in digestion, health, and disease. Gold star for you. This is a nice start, but we have some more work to do.
Next, we need to consider what actually happens to both our food and our hormones during various conditions like fasting and overeating. With this
knowledge we will be in a position to understand Type 2 diabetes, various types of cancer, Alzheimer’s, Parkinson’s, infertility, cardiovascular disease,
and osteoporosis.


Edited by Rick Moranis, 23 August 2011 - 12:40 AM.

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