Why We Get Fat - G. Taubes
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I think Taubes has done a great job at presenting his research. I don't think he's trying to tell you "what" to think, he's just asking you to think.
I've never read anything indicating that he believes there is one diet that works for everyone, but I have read and seen him say numerous times "Not all of us get fat eating carbohydrates".
While i think he's a talented writer, he slanted his research and cherry picked studies. Then he proceeds to make ridiculous statements like;
""If you restrict only carbohydrates, you can always eat more protein and fat if you feel the urge, since they have no effect on fat accumulation"
Location 2519 Kindle edition of Why We Get Fat
"But protein and fat don't make us fat-only the carbohydrates do-so there is no reason to curtail them in any way"
location 3064 Why we Get Fat
and why does he say only CHO makes us fat? because it spikes insulin, as if protein doesn't do the exact same thing0 -
I'd break out the pop corn, but I don't have the calories for the butter to make it taste awesome....sooo...sipping water in amusement ....0
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When he says that the calories in/calories out model doesn't work is like saying "you can't see the forest for the trees" (don't focus on the details). Animals that are lean in nature, aren't lean because they count calories. My dog never gets fat. It's not from lack of food, her dish is always full. They eat when they're hungry, and stop when they're full. Shouldn't it be the same with humans?
YES!0 -
Acg67, we can both spend all day pulling published studies that prove the other wrong, but why? Don't we both agree that there is no "one size fits all" diet and lifestyle to suit us all?
I'd much rather be happy than right. :flowerforyou:
Here's a decent attempt at reconciling two opposing theories by Todd Becker. I really enjoy his approach and thoughtfulness in forming his opinions. http://gettingstronger.org/2011/02/does-insulin-make-you-fat/Does insulin make you fat?
55 Comments Tags: ASP, carbohydrate/insulin hypothesis, CarbSane, fat loss, HSL, insulin, insulin resistance, insulin sensitivity, intermittent fasting, Kitavans, Krieger, low carbohydrate, LPL, obesity, Okinawans, Taubes, weight loss
Posted 03 Feb 2011
Whether or not insulin is to blame for the obesity epidemic is one of the hot questions being debated on heath and diet blogs. On the surface, this seems like an arcane question that would mainly interest physiologists and diet researchers. After all, who really cares about the underlying mechanisms of fat storage and release? Most of us just want to know some practical steps we can take to lose excess weight and keep it off and, beyond that, to stay healthy.
It seems like a simple yes-or-no question of fact that you could settle by studying populations and doing lab studies. But it’s not so much a question about facts as one about causation. Questions of causation are often the thorniest ones. This particular question has taken on almost political or religious overtones, provoking emotion and acrimony in the diet blogosphere. On one side are defenders of the Carbohydrate/Insulin Hypothesis, like Gary Taubes and Michael Eades. This is laid out in detail in Taubes’ book Good Calories, Bad Calories (2007), and more compactly in “Why We Get Fat: And What To Do About It” (2010). On the other side are opponents such as James Krieger and CarbSane, who find the Carbohydrate/Insulin Hypothesis to be oversimplified and deeply flawed, citing recent scientific advances. People tend to chose up sides in this debate. I’ve been participating in this debate myself (while still learning a lot) on the websites of Jimmy Moore, James Krieger, and CarbSane. I won’t rehash all the technical details here. Instead, I’d like to propose a “frameshift” that recognizes and integrates the strong points from each side, attempting to overcome their shortcomings.
First, here’s an overview of what each side has to say:
Proponents of the Carbohydrate/Insulin Hypothesis, as articulated by Taubes, posit four main points:
Obesity is a disorder of excess fat accumulation, not voluntary overeating or inactivity, caused by an imbalance in hormonal regulation of adipose tissue and fat metabolism.
Insulin is the primary regulator of fat storage. When insulin levels are elevated–either chronically or after a meal–we accumulate fat in adopose tissue. When insulin levels fall, we release fat and oxidize it for fuel.
Elevated blood insulin levels increase hunger and the drive to eat, while decreasing energy expenditure and activity
By stimulating insulin secretion, carbohydrates make us fat and ultimately cause obesity
In short: Carbohydrates drives insulin, which drives fat.
Opponents of the Carbohydrate Hypothesis challenge each of the above points. I’ve paraphrased four main counterpoints here:
Fat accumulation and obesity result from positive caloric balance (more calories consumed than expended), without regard to the macronutrient class of calorie (carbohydrate, protein, or fat).
Your body can store fat even when insulin is low, via the action of the hormone ASP (acylation stimulating protein)
Insulin doesn’t make you hungry; rather, it suppresses appetite. (The critics proffer that low carb diets may work because protein is more satiating than carbohydrates, but they merely report this observation and don’t attempt to explain it).
Carbohydrate doesn’t uniquely stimulate insulin; many proteins are equally or more insulinogenic.
In short: Calories in minus calories out drives fat.
On the surface of it, these two models of fat metabolism appear to be diametrically opposed. But are they really? There is at least one large point on which both sides appear to agree:
Obesity, particularly of the abdominal type, is associated with insulin resistance.
What that means is that people with abdominal obesity (the characteristic “apple” or pot belly shape, rather than those with “pear” shaped backsides or extra subcutaneous fat) tend to secrete more insulin after eating and have high basal insulin levels, ultimately leading to elevated blood glucose, triglycerides, elevated blood pressure, unfavorable cholesterol ratios, and a host of other issues associated with metabolic syndrome or “Syndrome X”. Nobody seems to deny this. Sometimes leptin resistance is also cited as an independent or alternative marker of obesity. But I’ll focus here primarily on insulin resistance, because it seems to be more closely involved with regulation of nutrient partitioning than is leptin.
Where the two sides disagree, however, is on the causal chain behind the association between obesity and insulin resistance. Advocates of the carbohydrate/insulin hypothesis tend to arrange the causal the order, from causes to effects, as:
carbohydrates > insulin spikes > hyperinsulinemia > insulin resistance > obesity
Whereas Krieger and CarbSane argue that the order of causality should be:
positive caloric balance > obesity > insulin resistance > hyerinsulinemia
When you look more deeply, however, there is acknoweldgement on both sides that insulin resistance is not a simple monocausal condition, but is likely multifactorial. There is evidence of many contributing factors, including:
specific dietary components: fructose, sucrose, saturated fats, gluten, lectins, dairy, allergens
micronutrient deficiencies: vitamin D, magnesium, omega-3 fatty acids
metabolites: triglycerides, free fatty acids (“FFA”, also called non-esterified fatty acids or “NEFA”)
inflammatory conditions
lack of physical activity and exercise (particularly strenuous exercise)
genetics
There is as yet no broad scientific consensus as to the relative importance of each of these factors in causing insulin resistance. But it is almost certain that there is no single cause. Regardless of the cause, however, it is important to understand what insulin resistance is on a cellular level: a reduction in the number and sensitivity of insulin receptors, such as GLUT4 receptors. Different tissues can experience different degrees of insulin resistance. Typically, muscle tissues are the first to become insulin resistance and fat tissue is one of the last. Insulin resistance in different organs like the brain or the skin can have different effects. Some have argued that certain pathologies such as Alzheimer’s disease and acne are associated with organ-specific insulin resistance. I’ve proposed elsewhere on this blog (“Change your receptors, change your set point“) that receptor number and sensitivity can serve as a kind of dynamic “set point” for weight and other physiogical states governed by hormone-receptor and neurotransmitter-receptor balances.
So here is where I think that a frameshift in the debate about insulin can reconcile the two sides, at least in good measure:
Insulin resistant (IR) individuals respond in a qualititatively different way to carbohydrates and fats in their diet.
Let’s see what that means specifically:
First, consider insulin resistant (IR) individuals, regardless of how they got that way. IR individuals have elevated basal insulin levels, usually defined as a fasting insulin of at least 15 μIU/mL, or perhaps higher. If you have a protruding belly, high triglycerides and a high blood pressure, you are probably in this category. Under these conditions, dietary carbohydrate, and to a lesser extent protein, add fuel to the fire by spiking an already elevated insulin level. And let us grant here the point of Krieger and CarbSane that ASP is a potent faciliator of fat storage. It is known than insulin significantly enhances the action of ASP. In addition, insulin upregulates lipoprotein lipase (LPL) a fat-storage promoting enzyme and inhibits the action of hormone sensitive lipase (HSL) an enzyme that favors hydrolysis of stored lipids to free fatty acids. Combine all three effects and we should expect that IR individuals store dietary fat easily, even with moderately low carbohydrate diets.
For these individuals, the elevated levels of basal insulin will tend to shift the balance of glucose and fatty acids from the blood stream into the tissues. (Krieger and CarbSane are correct that insulin may not play a big direct role in driving fat sequestration, but its indirect stimulatory effects on ASP and LPL and inhibitory effect on HSL are quite significant, reducing the concentration of fatty acids in the blood stream by shifting the equilibrium towards the adipocytes). This will also tend to stimulate appetite and eating, leading to more fat storage and a worsening IR condition. Sugarholics and those with carbohydrate cravings tend to be insulin resistant. Appetite has a large conditioned component, whereby preprandial levels of insulin, ghrelin, and other hormones are secreted based upon temporal cues and specific sensory cues. It has been found that this pre-prandial secretion is much more pronounced in overweight, IR individuals.
One of the best ways to break this cycle is to go on a very low carbohydrate diet, something like the Atkins induction diet. Since there is no insulin response to dietary fat, a high fat, very low carb, moderate protein diet will allow basal insulin level to gradually drift down. This will shift the balance, reducing (but not eliminating) the actions of ASP and LPL, and disinhibiting the action of HSL. This will increase release of glucose and fatty acids, supplying energy and providing satiety, further lessening the drive to eat. The vicious cycle is replaced by a virtuous one. Unfortunately, a reduced calorie, high carb diet will not work for IR individuals, because their appetite is so easily triggered by any increase in insulin, which leads to a faster than normal drop in blood glucose. Note that blood glucose does not have to be “low” to induce hunger. There is evidence that hunger is triggered merely by a rapid drop in glucose levels. On the Deconditioning Diet page of this blog, I describe a method for extinguishing this conditioned pre-prandial insulin response.
Claims that insulin suppresses appetite is based on studies involving central administration of insulin while artificially infusing glucose. Krieger is correct about the “central” effect of insulin within the hypothalamus and upon the vagal afferent fibers. However, as with many hormones, insulin can have opposing effects at different locations and times. We need to consider the important appetite-inducing effect of insulin secreted into the “periphery”, without the simultaneous supplementation of glucose or other nutrients. This is a particular issue for IR individuals who are vulnerable to insulin-induced cravings, and less of an issue for those with good blood sugar control.
Now let’s consider insulin sensitive (IS) individuals. These are people with less than 10 μIU/mL, ideally less than 5 μIU/mL insulin. The situation is quite different for these folks. As a result of much lower basal insulin levels, they have more stable blood glucose and fatty acid levels, because the lower insulin levels reduce inhibition of glucose and fatty acid release from glycogen and adipose tissue. So IS individuals are less prone to hunger cravings, because they can access their own energy stores more easily. They are much better able to tolerate higher levels of carbohydrate in the diet, because their insulin response is well controlled and glucose readily gets to the cells and brain after eating.
This may also provide a plausible explanation for why certain populations such as the Okinawans, the Kitavans, and other cultures remain lean on a relatively high carbohydrate diet: their low basal insulin levels and high insulin sensitivity permit them to handle carbohydrates easily. According to Stephan Guyunet’s Whole Health Source blog:
Grains, refined sugar, vegetable oils and other processed foods are virtually nonexistent on Kitava. They get an estimated 69% of their calories from carbohydrate, 21% from fat, 17% from saturated fat and 10% from protein. Most of their fat intake is saturated because it comes from coconuts. They have an omega-6 : omega-3 ratio of approximately 1:2. Average caloric intake is 2,200 calories per day (9,200 kJ). By Western standards, their diet is high in carbohydrate, high in saturated fat, low in total fat, a bit low in protein and high in calories.
While this is a “high carbohydrate” diet, the carbohydrates are not typical western foods: The Kitavan diet consists mainly of foods like tubers, fruit, coconut, fish and vegetables. Even with the high carbohydrate levels, their insulin levels are much lower than that of typical Westerners. One could argue that these foods have low levels of fructose and sugars, and are generally quite non-inflammatory, so they should promote insulin sensitivity. According to Lindeberg, their fasting insulin levels averaged 3.12 and 3.29 IU/ml for males and females, respectively. This is about half the basal insulin levels of Swedes: 6.98 and 6.65 IU/ml for males and females, respectively. Fasting blood glucose levels for the Kitavan’s were about 27% lower than that of the Swedes.
Furthermore, IS individuals should be able to lose fat quite easily by restricting carbohydrate, intermittent fasting and/or exercise. With resulting very low basal insulin levels, it should be even easier to release fat from adipose tissue and oxidize it for energy, or to go into ketosis. It is known that Type 1 diabetics, who have no insulin, shed fat readily and have trouble holding onto it without injections. But someone with low basal insulin can achieve a naturally lean state easily, while also being able to handle insulinogenic meals without difficulty. Based on my own experience over time, as my fasting insulin level has dropped, intermittent fasting and even fasted workouts become easy, and this does not preclude a reasonable level of carbohydrates in my diet.
Now let’s ask the question of whether insulin sensitive (IS) individuals can accumulate body fat on a high-fat, low carb diet. According to Krieger and CarbSane, this should be no more difficult than on a high-carb diet. You just have to eat a “caloric surplus” of fat, with no or little carbohydrate, and ASP will do the job, even without insulin. But will this really have the predicted effect? Without doing the study, it is hard to know for sure. But my prediction would be that it is unlikely to play out as they suggest, for several reasons:
Despite the claims that ASP works without any insulin, the primary sources don’t show this. For example in the paper by Saleh et al., which CarbSane cites in support, there is still some insulin and carbohydrate present to stimulate ASP, with or without the action of chylomicrons.
Even assuming that the ASP could drive fat accumulation without insulin present, the lack of insulin would also favor downregulation of LPL and activation of HSL, which will tend to balance ASP’s action by liberating fatty acids from the adipocyte.
Under low insulin conditions, even with excess fatty acids being fixed within the adipocytes, one would expect a reasonably high equilibrium level of free fatty acids in the blood stream. This would favor satiety, so that eating the fat meal would be self-limiting. This contrasts with the action of insulin which, when elevated, will tend to deplete the blood stream of glucose and fatty acids.
I will conclude with the following synthesis between the above opposing positions:
Obesity is a disorder of excess fat accumulation resulting from insulin resistance (and leptin resistance), which stimulates appetite and naturally leads to caloric imbalance, including overconsumption of both carbohydrates and fats.
Insulin and ASP together regulate fat storage and release. While ASP acts directly to transport and fix fatty acids within fat cells, insulin acts to induce fat storage via ASP and LPL, and to inhibit fat release via HSL and epinephrine and norepinephrine. Reduced levels of both insulin and ASP favor lipolysis and fat loss. The synergy of insulin and ASP further explain why the combination of dietary carbohydrate and fat is particularly fattening.
In insulin resistant individuals, elevated blood insulin levels stimulate hunger and the drive to eat; this effect is largely absent for insulin senstive individuals due to superior blood glucose control
In insulin resistant individuals, the pancreas compensates for reduced receptor sensitivity by secreting more insulin, leading to hyperinsulinemia.
So the answer to the question is to shift the blame from the hormone insulin to the condition of the insulin receptors. Insulin spikes at meal time are no problem, so long as basal insulin remains low. Restriction of dietary carbohydrate is one very effective strategy, which should be chosen not for the short term benefits in weight loss, so much as the longer term benefits in improving insulin sensitivity and reducing basal insulin. With the focus on “regrowing” and “reconditioning” insulin receptors, we should look at the full arsenal of tools, including intermittent fasting, nutrients such as vitamin D, magnesium and fish oil, and high intensity interval training.
Let me emphasize here that my proposed explanation is meant as a tentative conceptual framework rather than a conclusive scientific analysis. I’m still learning about the details and I fully expect that our understanding of the underlying mechanisms of fat metabolism will continue to be revised and evolve. But I do think that there has been too much emphasis placed on hormones and neurotransmitters, which fluctuate every day, and not enough on receptor health, which is something we can can influence over the long term by commitment to scientifically informed practices.
His site usually contains many interesting comments from readers if you're interested.0 -
Acg67, we can both spend all day pulling published studies that prove the other wrong, but why? Don't we both agree that there is no "one size fits all" diet and lifestyle to suit us all?
I'd much rather be happy than right. :flowerforyou:
that was an interesting read, thanks for posting it.
while there is no one size fits all diet per say, they all work because of a caloric deficit. It doesn't matter how you arrive at it, be it cutting carbs, exercising more etc, that is how everyone loses weight, short of surgery. To single out a single macronutrient and blame that for obesity is ridiculous.
I have no issues with ketogenic/low carb diets, it's only when it's adherents start proclaiming it is the best or only way to lose weight do i take issue with it0 -
I have no issues with ketogenic/low carb diets, it's only when it's adherents start proclaiming it is the best or only way to lose weight do i take issue with it
yeah, it can be annoying, at best.
So many members attacking each other's beliefs. I'd like to think they're so passionate about it because they found something that works well for themselves, and want to share it.
I'm glad you found the Getting Stronger post interesting! There's some good stuff on that site.
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I'd like to think they're so passionate about it because they found something that works well for themselves, and want to share it.
that's all well and good but they should not be ignorant of basic nutritional facts0 -
I have no issues with ketogenic/low carb diets, it's only when it's adherents start proclaiming it is the best or only way to lose weight do i take issue with it
So, what you really have a problem with is other people's opinions.0 -
Simplest answer is calories vs. calories out. that's it. eat less cals and exercise or get fat.:drinker:0
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Going through this book now. Have already read Good Calories / Bad Calories.
If you believe what he has researched and argues........it makes a big part of this site irrelevant.
Agree?
Conversely, if you believe in this site and how it works (and I do), it makes a big part of what Taubes writes irrelevant. 0 -
A website with a "makes sense" approach and the tools to use that approach doesn't make scientific research irrelevant.0
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A website with a "makes sense" approach and the tools to use that approach doesn't make scientific research irrelevant.
What about all the research Taubes ignored?0 -
A website with a "makes sense" approach and the tools to use that approach doesn't make scientific research irrelevant.
What about all the research Taubes ignored?
Starting a subjective argument brings no added value to the table.
This thread is about whether or not taube's ideas (if you agree with them) make this site irrelevant.
Ive seen on one occasion where a moderator here locked a post because of this type of discussion. How's that for myfitnesspal looking out for everyone's best interest?
I'm not here for cals in cals out. I'm using this site to help control moderation.0 -
I have no issues with ketogenic/low carb diets, it's only when it's adherents start proclaiming it is the best or only way to lose weight do i take issue with it
So, what you really have a problem with is other people's opinions.
This is your first post on the forums?
Did you come here to contribute? Learn something new? Share something? Or just poke at something Acg said 6 months ago?
Come on... start a new thread if you have something to say. 0 -
Having read Good Calories, Bad Calories, I think Taubes' hypothesis makes a lot of sense, even though it is flawed.
First thing to make clear is that Taubes' hypothesis is completely consistent with the laws of thermodynamics.
Anyways even if you set the science aside, I have a hard time believing that humans are the only species incapable of regulating their own fat metabolism, such that when presented with an abundance of food, they will end up obese. That whole notion seems absurd to me. Now people can find flaws in Taubes' hypothesis, but I can't rule it out especially when a HUGE proportion of the obese population has insulin resistance. And we all know insulin resistance can cause further weight gains.
The big question is whether Taubes is right, that excess refined carbohydrate consumption CAUSES insulin resistance and obesity.
Here is one doctor's opinion:
http://www.carbohydratescankill.com/402/carbohydraterich-diet-likely-culprit-for-insulin-resistance-20 -
Going through this book now. Have already read Good Calories / Bad Calories.
If you believe what he has researched and argues........it makes a big part of this site irrelevant.
Agree?
Conversely, if you believe in this site and how it works (and I do), it makes a big part of what Taubes writes irrelevant.
What's cool is that both this site and Taubes' books lead to weight loss.0 -
Going through this book now. Have already read Good Calories / Bad Calories.
If you believe what he has researched and argues........it makes a big part of this site irrelevant.
Agree?
Conversely, if you believe in this site and how it works (and I do), it makes a big part of what Taubes writes irrelevant.
What's cool is that both this site and Taubes' books lead to weight loss.
and guess what is also cool? they work exactly the same way, a caloric deficit0 -
*takes front row seat for fireworks*
Save me a spot!
Popcorn?0 -
*takes front row seat for fireworks*
Save me a spot!
Snuggles in between y'all.0 -
Going through this book now. Have already read Good Calories / Bad Calories.
If you believe what he has researched and argues........it makes a big part of this site irrelevant.
Agree?
Conversely, if you believe in this site and how it works (and I do), it makes a big part of what Taubes writes irrelevant.
What's cool is that both this site and Taubes' books lead to weight loss.
and guess what is also cool? they work exactly the same way, a caloric deficit
Even Taubes will admit that.0 -
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Nice. :laugh:0 -
I haven't read it but I've seen it discussed on here several times. My thoughts on in are the same as my thoughts on anyone that says they know why "we" get fat, and that is that I don't need to read it. I already know why I got fat, and I know that it is not for the same reason as many others.
One of the few things that I am certain of is that there is no one reason 'we' get fat, which is why there is no one way 'we' get thin.0 -
I can't stop watching this.0 -
It's whatever works for you. Different diets work for different folks. However any diet that makes your body rely on it's own fat stores is going to work! Whether it's Atkins or MFP or using both simultaneously. You could using MFP and have a quite healthy diet without junk, lots of healthy veg protein and complex carbs. Or you could be doing Atkins and eating lots of healthy veg, protein and lotsa fat. As long as your body is put in a position where it's eating into it's own fat reserves, you'll lose weight.0
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There is nothing complex about this topic what so ever.
Humans eat food with poor nutritional value, and too much of it, while moving around too little. It's quite simply, as easy as that.
LOVE THIS! This is EXACTLY true!!0 -
Overconsumption of food in general causes insulin resistance, not carbs on their own and diet is only 1 factor that contributes to insulin resistance and why people think it's all that matters is just lack on information.. Anyone can eat all the carbs they want and if it's at a maintenance level, it gets used as energy, or stored as glycogen. If that same person is eating a lot of carbs in a deficit then they become more insulin sensitive, every time. Saying carbs causes obesity is no different than saying saturated fat causes heart disease. The big question, or the big equation that is hard to figure out is that all metabolic dysfuction and the difficulties trying to figure out how we the individual burn calories is enormous, and has everyone saying and thinking everyone is different. In reality all factors that make it difficult to figure out why and how we burn calories are automatically accounted for on the outside of the energy balance equation, even though people don't know what they are, and calories in vs out always works, the problem like i said is people don't know much about the out side of the EBE, as opposed to the in side where it's just calories from food.Having read Good Calories, Bad Calories, I think Taubes' hypothesis makes a lot of sense, even though it is flawed.
First thing to make clear is that Taubes' hypothesis is completely consistent with the laws of thermodynamics.
Anyways even if you set the science aside, I have a hard time believing that humans are the only species incapable of regulating their own fat metabolism, such that when presented with an abundance of food, they will end up obese. That whole notion seems absurd to me. Now people can find flaws in Taubes' hypothesis, but I can't rule it out especially when a HUGE proportion of the obese population has insulin resistance. And we all know insulin resistance can cause further weight gains.
The big question is whether Taubes is right, that excess refined carbohydrate consumption CAUSES insulin resistance and obesity.
Here is one doctor's opinion:
http://www.carbohydratescankill.com/402/carbohydraterich-diet-likely-culprit-for-insulin-resistance-20 -
One other thing I've noticed is that almost all the MFP posts I've seen raving about this book are from people with some type of hormone/metabolic disorder.
Is there anyone having better results with the methods in this book that has no diagnosed disorders (i.e. as far as you know you are healthy other than your weight)? What other methods did try?0 -
Since I started to use this site, I loose weigth by cutting carbs (and other stuffs), like pastas. I did not do it because of funny theories, but because those kind of carbs had much more calories that I could imagine. Nothing more complicated than that.
I read a study that show that with a high fat and high protein diet, during a long time, you reduces your life time. I can post it there but it is in french, my mother tongue...
That pisses me off with all these theories, is that a lot of people imagine they will continue to eat like pigs and loose weight by cutting some sort of food and keeping some others. They are just lazy, and miracle doctors that write those kind of books know that.
Eat everything and learn to eat less, to listen to your body and to decorrelate emotions from food, and you will loose weigth.
I did it the MFP (and the conventional way) for the first six months and lost 10lbs (my goal). But I never lost my belly (even after two months of P90X). I was eating every couple of hours and that consisted of counting calories, weighing and logging food each time. My day was spent thinking about or preparing food. So yes MFP is successful but you will have to count calories the rest of your life to keep from gaining the weight back.
I started Primal Blueprint (no grains, legumes, milk, sugar and real, whole foods) as an experiement and dropped another 10lbs and LOST MY BELLY. With less exercise I maintained my lean muscle mass. And I hit a weight I haven't been since before puberty (I'm 41). This was in four months. And the majority of it was in the first 6 weeks (carbs make your body retain sodium and therefore retain water so I dropped more water retention and now I don't even retain water during TOM). And I don't have to eat every couple of hours because I get hungry maybe a couple of times a day.
Sugar travels the same brain pathways as opiate drugs (i.e. heroin). Grains contain morphine-like compounds called exorphins.
The Need for Steady Fuel: Where fueling the fire of our brain and body's metabolism is concerned, carbohydrates can best be described as kindling. Whole grains and legumes are somewhat like twigs; starch, such as cereals and potatoes, and simple sugars are like paper on the fire; and alcohol might best be described as gasoline on the fire. If you're relying on carbohydrates as your primary source of fuel, you need to feed that fire often, regularly, and consistently. You will be craving that fuel. Unfortunately, most people today have forcibly adapted their bodies to this sort of an unnatural dependence by over-consuming carbohydrates in their diet. (Most - if not all alcoholics have - for instance - severe issues with dysglycemia and sugar addiction. Alcoholics are dependent on and regularly seek fast sources of sugar - alcohol being the fastest...because the problem in alcoholism, in fact, isn't really alcohol, per se, but severe carbohydrate addiction (this is interesting to me because most people I know that have completely stopped drinking develop sweet tooths.)...One might get a burst or a ball of flame with respect to energy from many carbohydrate sources, but no one can get long-term, sustainable energy. As soon as the flame starts to die out, which doesn't take long, you're stuck with cravings for fuel or stimulants again. It can be quite a roller coaster ride. This is why dome dietary experts are always telling you to eat every two hours or to eat "numerous small meals throughout the day". If you're sugar dependent - and almost everyone in this culture is victim to that unnecessary reality - then frequent small meals become necessary to maintain an even keel. If you have ever heated your home with a wood stove using paper, twigs and lighter fluid all day, you'd be a slave to that fire and you'd need a mountain of fuel to constantly feed that hungry beast. You'd be forever preoccupied with keeping that fire going, and you'd have little other life...Nature would never have intended for us to constantly live this way. It is a terribly impractical state to maintain, particularly if you view this from the primitive perspective of ongoing survival in a less certain world where food wasn't constantly available. Our primitive (particularly ice-age) ancestors would never have made it this far if carbohydrates were essential to the diet or if glucose were necessary as a primary source of energy. Nature isn't that crazy or stupid...Mind you, it is possible to live in a state of primary glucose dependence. The idea that we are necessarily dependent on sugar as our primary source of fuel is true only conditionally, only if we've metabolically adapted ourselves to that unnatural dependence....It isn't necessary at all and it will age you faster (and cost you much more in grocery bills and health care). Dietary fat, in the absence of carbohydrates, is like putting a nice big log on the fire. Fat's flame burns as a regular, even rate, and is easily dept going, Protein, consumed in moderate quantities, is mainly diverted toward repair and maintenance. Only in excess does it convert to sugar. Fat's even flame keeps the hormone leptin under control, keeps insulin quiet, and keeps our appetite satisfied...One can go many, many hours on this longer-burning type of fuel without experiencing any discomfort or cravings at all. You may eventually get hungry if you really go a long time without eating, which is normal, bu you are far less likely to experience irritability, dizziness, brain fog, cravings, fatigue, jitteriness, or mood swings because of it. That's the say it's supposed to be!
You are one of two things: you are either a "fat burner" or a "sugar burner". If you are overweight, crave carbohydrates (and stimulants), or are insulin or leptin resistant, then you are a sugar burner. It's that simple. It also should be noted that stress, food sensitivity issues, caffeine and other stimulants, alcohol, sleep deprivation, aspartame, tobacco, and drugs of all types further aggravate and exacerbate excess insulin production (Schwarzbein and Deville 1999). For people who are unconcerned about dietary carbohydrates from a weight-gain perspective because of higher metabolic levels or athletic activity, the caution is this: Although it is possible to burn off the excess glucose, one cannot burn off the excess insulin. Excess insulin production, no matter how thin you are, wreaks metabolic havoc and invariably yields unhealthy consequences over time and accelerates again. It is also possible to be thin and diabetic.
The only thing in the body that needs glucose is red blood cells. Everything else can run on fat and/or ketones. Excess protein can be converted into glucose (and it takes more energy to do this than to just consume carbs/sugar and have that convert to glucose - i.e. burns more calories!!).0 -
Overconsumption of food in general causes insulin resistance, not carbs on their own and diet is only 1 factor that contributes to insulin resistance and why people think it's all that matters is just lack on information.. Anyone can eat all the carbs they want and if it's at a maintenance level, it gets used as energy, or stored as glycogen. If that same person is eating a lot of carbs in a deficit then they become more insulin sensitive, every time. Saying carbs causes obesity is no different than saying saturated fat causes heart disease. The big question, or the big equation that is hard to figure out is that all metabolic dysfuction and the difficulties trying to figure out how we the individual burn calories is enormous, and has everyone saying and thinking everyone is different. In reality all factors that make it difficult to figure out why and how we burn calories are automatically accounted for on the outside of the energy balance equation, even though people don't know what they are, and calories in vs out always works, the problem like i said is people don't know much about the out side of the EBE, as opposed to the in side where it's just calories from food.Having read Good Calories, Bad Calories, I think Taubes' hypothesis makes a lot of sense, even though it is flawed.
First thing to make clear is that Taubes' hypothesis is completely consistent with the laws of thermodynamics.
Anyways even if you set the science aside, I have a hard time believing that humans are the only species incapable of regulating their own fat metabolism, such that when presented with an abundance of food, they will end up obese. That whole notion seems absurd to me. Now people can find flaws in Taubes' hypothesis, but I can't rule it out especially when a HUGE proportion of the obese population has insulin resistance. And we all know insulin resistance can cause further weight gains.
The big question is whether Taubes is right, that excess refined carbohydrate consumption CAUSES insulin resistance and obesity.
Here is one doctor's opinion:
http://www.carbohydratescankill.com/402/carbohydraterich-diet-likely-culprit-for-insulin-resistance-2
Are we all really that different in caloric expenditure? I don't think we are. I think people who are sedentary burn less than people who are active all day long, and that difference is pretty significant but predictable. But I think the individual activities' expenditures are probably comparable from person to person.0
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