Is the "calories in vs calories out" myth the reason why you are fat

[DoctwoB]

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The science of understanding caloric restriction is still very new, and thus any claims of its all about molecule "X" are likely overstated. IGF-1 likely does play a role, but is surely one of many factors.

 

[Spinietzschon]

Doesn't anyone remember that the post was about fat accumulation? I took the OP's comment as a purely cosmetic consideration, not going into life expectancy etc, just the science behind the cosmetics.

I mean we contort this into everything that adiposity entails and is implicated in and we can pretty much make it to STI transmission, health care costs or probably used car sales in only like 2 relationships like that game where you change your name in as few moves as possible to be related to a celebrity?

(or however you spell it)

 

[ToldYouSo]

lol dude sorry to rain on your parade but just about every putative explanation for WHY Calorie Restriction (CR) slows aging has to do with it limiting CARB metabolism!

See:

1. "How does calorie restriction work?" Or hell, even
2. the Wiki article on it will do:



Referenced article:



In fact, it was noticed years ago that feeding C. elegans sugar reduces their lifespan. And it has even scared some researchers on aging and calorie restriction to go low carb! Meet Cynthia Kenyon:



Anyways, as far as your dilemma is concerned, if being a vegan works for you, do you. More meat for the rest of us lmao. Health-wise, if you intend on eating carbs obviously your approach is the way to go!

Now you're talking about 2 different things, restricting total calories and composition of calories (ratio of fat/protein/carbs). Most people who are following a healthy diet aren't eating glucose straight up, their carbs are complex which limits their glycemic load along with fiber which lowers it even more. I regularly test my blood sugar and keep a log of it at home and it hasn't spiked significantly even after eating 5 bananas in one sitting. From the research I've done with CR, it sounds like downregulating IGF-1 by limiting protein intake is one of the most crucial things one needs to do. I'll find the paper later on, but casein (milk protein) was shown to upregulate IGF-1 production more so then other protein sources including soy (which I'm not a big fan of.) Besides that, the rhesus monkeys whose images are shown previously had the same composition of fats/proteins/carbs in their food, the only difference was the total amount of calories of food eaten. The results are striking and this study along with many others shows the physiological benefits of CR.

 

[CaptainSSO]

Meh regardless of whether meat was the driver of large brain sizes, it does not then follow that meat is necessarily the healthiest diet. I mean meat may be the best diet if you want to live to 26 (which is what the life expectancy would have been in those days if you were lucky) but it may not be the best if you wanted to live to 80. So it's not like the average person back then had remotely the variety and quality of fruits and vegetables available that we do now, definitely not pre-farming and even for the vast majority of people post-farming whereas meat would have given a LOT of calories (and lots of protein) quickly and efficiently. So it would be obvious why that would win out vs. a non meat foraging diet that would have consisted of a very few items around the area where you happened to be living - so it still wouldn't be a valid head to head comparison.

I mean meat makes up 90% of my diet (I'm pretty unhealthy) so I'm certainly not a vegetarian, let alone a vegan, but the evolution brain size argument is not really relevant to the question at hand.

Also, that's why I laugh at the 'cave man diet'. Yup, gimmie the diet that allowed these awesomely healthy cavemen to live to the ripe old age of 25 (obviously diet was just one factor in life expectancy but you could feed people twinkies and you would likely make it until 25 - that doesn't mean an all twinkie diet is healthy).

Shaggy, you remind me of myself about 6 months ago. I used the EXACT same arguments as you are, in regards to longevity, and I also thought the Paleo diet was a joke. It took me about 2 weeks of studying this stuff 8+ hours a day until my resistance to it finally cracked.

As far as longevity goes, the reason the life expectancy for paleolithic man was so short was due to several factors, but very rarely because of Western diseases that kill most people in America today. A huge factor was childbirth--infant mortality was extraordinarily high, and it doesn't take too many infant deaths to statistically lower the life expectancy of the entire population. The other main cause of death was accidents/infection, e.g., a man breaks his leg during a hunting accident, he is now screwed and almost certainly going to die. He cuts his arm and gets dirt in it, there's no antibacterial ointment to put on it. If it gets infected and turns gangrenous, he is ****ed. And so on and so forth. However, from bone studies, we know these men were actually very healthy--all the evidence points to them living long lives if they had some means of obtaining health care like we can.

Now, as far as the development of agriculture, this is the fascinating part. After we developed agriculture, we shrunk. Malnourishment was rampant, and we literally stopped growing as much as we had been. People's bones were weaker, diseases were seen for the first time that hadn't been present before (albeit part of this was due to the surge in population density). Here's an article by Jared Diamond, where he claims "agriculture was the worst mistake in the history of the human race." Now, I disagree with this, because w/o agriculture we wouldn't have the technology that we've come to know and love. However, he brings up interesting points.

Skeletons from Greece and Turkey show that the average height of hunger-gatherers toward the end of the ice ages was a generous 5' 9'' for men, 5' 5'' for women. With the adoption of agriculture, height crashed, and by 3000 B. C. had reached a low of only 5' 3'' for men, 5' for women. By classical times heights were very slowly on the rise again, but modern Greeks and Turks have still not regained the average height of their distant ancestors.

http://www.ditext.com/diamond/mistake.html

Your 90% meat-based diet is healthier than you think.

I have thousands of links if you want to read some more about the Paleo diet. Trust me, I was even more hostile than you are towards it. I thought it was a ridiculous idea. I guess, because, I was scared to let go of and admit something I had believed/followed my entire life was not accurate. 3 weeks after going on the Paleo diet, I was convinced. My body fat was lower than it ever was, when I went to the gym all my lifts skyrocketed, I was sleeeping better, concentrating better, feeling better. I got off it after a couple months, and started putting on fat right away, sleeping bad, feeling depressed. I finally realized a couple weeks ago I wanted to get back to feeling like that again, so I am once again back on the diet.

Edit: And my point about evolution and a meat-based diet was that eating meat is in our genes. Our bodies are "designed" (I use that word in a non-supernatural sense) to thrive on meat.

 

[Baron Samedi]

The agriculture vs hunter-gatherer argument is flawed. The change in mean height likely has a lot more to do with disease transmission than the fact that folks started eating rice nd broccoli. "Community-acquired disease" didn't exist in the form it does today prior to the dawn of agriculture - disease was instead largely restricted to zoonotics that spread much slower (LIKELY not at all m-2-m in most cases) and was restricted to small pockets of people rather than entire cities.

In fact, if it were the dietary switch that caused a decrease in mean height, you would expect that to be the rate-limiting process, but our mean height keeps increasing. Likely this is due to our better understanding and control of disease as our diet has remained relatively agriculture-based.

 

[mrwesticles]

The best advice is to keep a calorie log - even if you eat everything you ever want, just by looking at what you've eaten people tend to hold back.

The real reason so many people are fat is the convenience of diet, not necessarily the lack of knowledge.

 

[Asp]

Interesting thread. A few points.

I tend to agree with Aubrey de Grey's position that calorie restriction's life extension effect is only significant for short-lived species. It's an adaptation to get through a drought / time of famine. It might give you a year or two, a few years at most. So it makes a big impact on the lives of mice and rats, but unlikely to do so for humans.

I think it's fairly established that fructose is quite bad in large amounts. Chronic intake of soft drinks and processed foods with high fructose corn syrup led to the obesity epidemic. However, I tend to agree with Lustig over Taubes that there's really no conclusive evidence that carbs as a whole are bad. My personal feeling is that more processed carbs like bread are worse than rice or potatoes. I think a lot of the toxicity of carbs like potatoes go away when cooked, so I don't care much for the Paleolithic ideas. The value of the glycemic index is quite questionable. That said, my ideal diet is grass fed meats, wild fish in moderation, and organic vegetables and fruits, with plenty of sunshine for Vitamin D and maybe a cod liver oil supplement.

When you are more than 10% body fat or so, dieting is pretty much all calories in versus calories out. Below 10% I think you start getting into factors like macronutrient balance, insulin sensitivity, nutrient timing, resistant fat (too much alpha adrenergic receptors etc) but really this isn't an issue for the vast majority of people (who can't even see six pack under overhead lighting).

 

[facetguy]

New Lustig lecture on reducing sugar consumption. Recorded Friday.
http://www.youtube.com/watch?v=7OaD_ACer_g&feature=youtu.be

 

[facetguy]

Interesting thread. A few points.

I think it's fairly established that fructose is quite bad in large amounts. Chronic intake of soft drinks and processed foods with high fructose corn syrup led to the obesity epidemic. However, I tend to agree with Lustig over Taubes that there's really no conclusive evidence that carbs as a whole are bad. My personal feeling is that more processed carbs like bread are worse than rice or potatoes. I think a lot of the toxicity of carbs like potatoes go away when cooked, so I don't care much for the Paleolithic ideas. The value of the glycemic index is quite questionable. That said, my ideal diet is grass fed meats, wild fish in moderation, and organic vegetables and fruits, with plenty of sunshine for Vitamin D and maybe a cod liver oil supplement.

When you are more than 10% body fat or so, dieting is pretty much all calories in versus calories out. Below 10% I think you start getting into factors like macronutrient balance, insulin sensitivity, nutrient timing, resistant fat (too much alpha adrenergic receptors etc) but really this isn't an issue for the vast majority of people (who can't even see six pack under overhead lighting).

You lost me on that last part. The higher the % body fat, the higher the probability things like insulin sensitivity/resistance are at play. Addressing calories alone is unlikely to prove successful.

 

[CaptainSSO]

The agriculture vs hunter-gatherer argument is flawed. The change in mean height likely has a lot more to do with disease transmission than the fact that folks started eating rice nd broccoli. "Community-acquired disease" didn't exist in the form it does today prior to the dawn of agriculture - disease was instead largely restricted to zoonotics that spread much slower (LIKELY not at all m-2-m in most cases) and was restricted to small pockets of people rather than entire cities.

In fact, if it were the dietary switch that caused a decrease in mean height, you would expect that to be the rate-limiting process, but our mean height keeps increasing. Likely this is due to our better understanding and control of disease as our diet has remained relatively agriculture-based.

But what seems to be the more likely culprit in this case? Disease affects only a subset of the population, whereas the switch to agriculture theoretically affects the entire population. To me, it seems more reasonable that the cause of this was diet.

As far as the mean height increasing over time, that could partly be explained by evolution--the ones who are most adversely impacted by agriculture do not live past reproductive age, or their progeny die, etc. Over time, humans could start compensating for this with import/export of food, and better disease control, as you said. However, this doesn't necessarily mean that diet wasn't the initial cause, just that we're compensating for it.

In the article, Jared Diamond stated that modern Greeks and Turks still haven't regained their previous, paleolithic stature, and with modern health care being what it is, leads me to believe that the underlying factor is food. (For what it's worth, I also believe a lot of the disease was caused by the switch to agriculture).

Anyway, I'm just speculating here, because I think this is an interesting subject, but the agriculture/height argument is just one tiny piece of the all the available evidence.

 

[ToldYouSo]

Interesting thread. A few points.

I tend to agree with Aubrey de Grey's position that calorie restriction's life extension effect is only significant for short-lived species. It's an adaptation to get through a drought / time of famine. It might give you a year or two, a few years at most. So it makes a big impact on the lives of mice and rats, but unlikely to do so for humans.

I think it's fairly established that fructose is quite bad in large amounts. Chronic intake of soft drinks and processed foods with high fructose corn syrup led to the obesity epidemic. However, I tend to agree with Lustig over Taubes that there's really no conclusive evidence that carbs as a whole are bad. My personal feeling is that more processed carbs like bread are worse than rice or potatoes. I think a lot of the toxicity of carbs like potatoes go away when cooked, so I don't care much for the Paleolithic ideas. The value of the glycemic index is quite questionable. That said, my ideal diet is grass fed meats, wild fish in moderation, and organic vegetables and fruits, with plenty of sunshine for Vitamin D and maybe a cod liver oil supplement.

When you are more than 10% body fat or so, dieting is pretty much all calories in versus calories out. Below 10% I think you start getting into factors like macronutrient balance, insulin sensitivity, nutrient timing, resistant fat (too much alpha adrenergic receptors etc) but really this isn't an issue for the vast majority of people (who can't even see six pack under overhead lighting).

I don't really agree with Aubrey's position about CR, the argument that it adds "only 1 or 2 more years" completely misses the fact that even if this is true (which I have no reason to believe given the massive benefit of CR to long lived species such as rhesus monkeys) that it extends the number of "healthy" years.

Most people who say they are afraid of getting old are actually afraid of having an old, frail and sick body. Take a look at the Okinawans, one of the longest living groups of people in the world who follow a mildly calorie restricted diet their entire life (eating until they are only 80% full), their physiological bio-markers are a complete opposite of the average overweight American in terms of weight, bmi, BP, bone density, cancer prevalence etc...

http://www.youtube.com/watch?v=ZwX9Ll19cX0

90 year old Okinawan woman who spends 8 hours a day climbing trees picking fruit...

Results from a CR study; The CR'd group of participants had drastic improvements in bio-markers indicative of good health.
The calorie-restricted group also fared much better than the control group in terms of average blood pressure (100/60 vs. 130/80 mm Hg), fasting glucose, fasting insulin (65% reduction), body mass index (19.6 ± 1.9 vs. 25.9 ± 3.2 kg/m2), body fat percentage (8.7% ± 7% vs. 24% ± 8%), C-reactive protein, carotid IMT (40% reduction), and platelet-derived growth factor AB.[7] The CR group had triglyceride levels as low as the lowest 5% of Americans in their 20s. (The CR group age-range was 35-82.) Both systolic and diastolic blood pressure levels in the CR group were about 100/60, a level more typical of 10-year-olds. Fasting plasma insulin concentration was 65% lower. Fasting plasma glucose concentration was also lower.

http://www.pnas.org/content/101/17/6659

 

[dozitgetchahi]

Interesting thread. A few points.

I tend to agree with Aubrey de Grey's position that calorie restriction's life extension effect is only significant for short-lived species. It's an adaptation to get through a drought / time of famine. It might give you a year or two, a few years at most. So it makes a big impact on the lives of mice and rats, but unlikely to do so for humans.

I think it's fairly established that fructose is quite bad in large amounts. Chronic intake of soft drinks and processed foods with high fructose corn syrup led to the obesity epidemic. However, I tend to agree with Lustig over Taubes that there's really no conclusive evidence that carbs as a whole are bad. My personal feeling is that more processed carbs like bread are worse than rice or potatoes. I think a lot of the toxicity of carbs like potatoes go away when cooked, so I don't care much for the Paleolithic ideas. The value of the glycemic index is quite questionable. That said, my ideal diet is grass fed meats, wild fish in moderation, and organic vegetables and fruits, with plenty of sunshine for Vitamin D and maybe a cod liver oil supplement.

I donno about the potatoes bit (although many confounding factors are likely at play in this study).

http://www.nejm.org/doi/full/10.1056/NEJMoa1014296


Changes in Diet and Lifestyle and Long-Term Weight Gain in Women and Men

Dariush Mozaffarian, M.D., Dr.P.H., Tao Hao, M.P.H., Eric B. Rimm, Sc.D., Walter C. Willett, M.D., Dr.P.H., and Frank B. Hu, M.D., Ph.D.
N Engl J Med 2011; 364:2392-2404June 23, 2011

Background

Specific dietary and other lifestyle behaviors may affect the success of the straightforward-sounding strategy "eat less and exercise more" for preventing long-term weight gain.


Methods

We performed prospective investigations involving three separate cohorts that included 120,877 U.S. women and men who were free of chronic diseases and not obese at baseline, with follow-up periods from 1986 to 2006, 1991 to 2003, and 1986 to 2006. The relationships between changes in lifestyle factors and weight change were evaluated at 4-year intervals, with multivariable adjustments made for age, baseline body-mass index for each period, and all lifestyle factors simultaneously. Cohort-specific and sex-specific results were similar and were pooled with the use of an inverse-variance–weighted meta-analysis.


Results

Within each 4-year period, participants gained an average of 3.35 lb (5th to 95th percentile, &#8722;4.1 to 12.4). On the basis of increased daily servings of individual dietary components, 4-year weight change was most strongly associated with the intake of potato chips (1.69 lb), potatoes (1.28 lb), sugar-sweetened beverages (1.00 lb), unprocessed red meats (0.95 lb), and processed meats (0.93 lb) and was inversely associated with the intake of vegetables (&#8722;0.22 lb), whole grains (&#8722;0.37 lb), fruits (&#8722;0.49 lb), nuts (&#8722;0.57 lb), and yogurt (&#8722;0.82 lb) (P&#8804;0.005 for each comparison). Aggregate dietary changes were associated with substantial differences in weight change (3.93 lb across quintiles of dietary change). Other lifestyle factors were also independently associated with weight change (P<0.001), including physical activity (&#8722;1.76 lb across quintiles); alcohol use (0.41 lb per drink per day), smoking (new quitters, 5.17 lb; former smokers, 0.14 lb), sleep (more weight gain with <6 or >8 hours of sleep), and television watching (0.31 lb per hour per day).


Conclusions

Specific dietary and lifestyle factors are independently associated with long-term weight gain, with a substantial aggregate effect and implications for strategies to prevent obesity. (Funded by the National Institutes of Health and others.)

 

[Asp]

You lost me on that last part. The higher the % body fat, the higher the probability things like insulin sensitivity/resistance are at play. Addressing calories alone is unlikely to prove successful.

Why not? That's how bariatric surgery works -- addressing calorie intake first and foremost. And it's way more successful than any diet. Pretty sure most bariatric surgery patients are still on those pre-enlightenment low fat diets.

 

[Asp]

Most people who say they are afraid of getting old are actually afraid of having an old, frail and sick body. Take a look at the Okinawans, one of the longest living groups of people in the world who follow a mildly calorie restricted diet their entire life (eating until they are only 80% full), their physiological bio-markers are a complete opposite of the average overweight American in terms of weight, bmi, BP, bone density, cancer prevalence etc...

I think the jury's still out on whether those monkeys in Weindruch's study have a significant increase in lifespan especially when you look at all-cause mortality. If I remember correctly it wasn't statistically significant in 2009. The difference would have to be more than 2 years to be impressive. We may not know for another decade plus.

Sure the Okinawans are healthier than Americans. But they aren't calorie restricted. They may eat less than Americans, or eat better, but I'll bet you there's no cultural imperative to eat "20% less than you actually want to." They are human, and bear no resemblance to the emaciated, depressed looking creatures in the CR monkey group. You can reap the benefits of living well into your 80s and 90s without calorie restriction.

 

[Asp]

We performed prospective investigations involving three separate cohorts that included 120,877 U.S. women and men who were free of chronic diseases and not obese at baseline, with follow-up periods from 1986 to 2006, 1991 to 2003, and 1986 to 2006. The relationships between changes in lifestyle factors and weight change were evaluated at 4-year intervals, with multivariable adjustments made for age, baseline body-mass index for each period, and all lifestyle factors simultaneously. Cohort-specific and sex-specific results were similar and were pooled with the use of an inverse-variance–weighted meta-analysis.

Non-randomized controlled trials on diet are pretty much worthless.

 

[ToldYouSo]

I think the jury's still out on whether those monkeys in Weindruch's study have a significant increase in lifespan especially when you look at all-cause mortality. If I remember correctly it wasn't statistically significant in 2009. The difference would have to be more than 2 years to be impressive. We may not know for another decade plus.

Sure the Okinawans are healthier than Americans. But they aren't calorie restricted. They may eat less than Americans, or eat better, but I'll bet you there's no cultural imperative to eat "20% less than you actually want to." They are human, and bear no resemblance to the emaciated, depressed looking creatures in the CR monkey group. You can reap the benefits of living well into your 80s and 90s without calorie restriction.

"Generally, the traditional diet of the islanders was 20% lower in calories than the Japanese average and contained 300% of the green/yellow vegetables (particularly heavy on sweet potatoes). The Okinawan diet is low in fat and has only 25% of the sugar and 75% of the grains of the average Japanese dietary intake."

Generally, the traditional diet of the islanders was 20% lower in calories than the Japanese average and contained 300% of the green/yellow vegetables (particularly heavy on sweet potatoes). The Okinawan diet is low in fat and has only 25% of the sugar and 75% of the grains of the average Japanese dietary intake.
Walford, Roy; Walford, Lisa (2005), "The Caloric Limitation Principle", Review: The Anti-Aging Plan: The Nutrient-Rich, Low-Calorie Way of Eating for a Longer Life--The Only Diet Scientifically Proven to Extend Your Healthy Years

My BMI is on the low end of normal, and the average BMI of participants in the WUSTL CALERIE study was closer to 20, FAR from emaciated. This same study also showed drastic improvements in patients hearts, who diastolic function was on levels 15 years younger then their actual age "norms".

http://news.wustl.edu/news/Pages/6362.aspx

 

[facetguy]

Why not? That's how bariatric surgery works -- addressing calorie intake first and foremost. And it's way more successful than any diet. Pretty sure most bariatric surgery patients are still on those pre-enlightenment low fat diets.

The effects of gastric bypass surgery are more complex than that. The metabolic impact of this surgery is often almost immediate, way quicker than any weight/fat loss can occur. There's been a good discussion happening at this blog over the past week or so on this topic:
http://wholehealthsource.blogspot.com/2011/07/how-does-gastric-bypass-surgery-cause.html

From International Journal of Obesity 2009:
http://www.ncbi.nlm.nih.gov/pubmed/19363506
"Increasing evidence indicates that the impact of RYGB on T2DM cannot be explained by the effects of weight loss and reduced energy intake alone. "

 

[CaptainSSO]

This thread needs to stay alive. This is actually quite important stuff.

I just picked up Good Calories, Bad Calories by Gary Taubes.

Reminding me what bologna the Fat Cholesterol Hypothesis is. A series of blunders and stubbornness led to our current understanding of healthy diets.

 

[celkon]

exercise > nutrition brb going for a run

 

[plsfoldthx]

I did an experiment on fruit flies in college. We put samples of flies of varying species of same species on a all sucrose, all yeast, or 50-50. The all yeast diet flies consistently lived about 4-5 days over the all sugar with the half-half diet in between. It was never published because I realized I hate research with the passion of a thousand suns and quit my MS

 

[CaptainSSO]

I did an experiment on fruit flies in college. We put samples of flies of varying species of same species on a all sucrose, all yeast, or 50-50. The all yeast diet flies consistently lived about 4-5 days over the all sugar with the half-half diet in between. It was never published because I realized I hate research with the passion of a thousand suns and quit my MS

There's an interesting point here--we can't compare animals with naturally differing diets from humans.

For example, in 1913, a Russian pathologist did an experiment with rabbits wherein he was able to induce atherosclerotic lesions in their arteries by feeding them a diet of olive oil and cholesterol.

The key problem with this is that rabbits are herbivores and wouldn't ever naturally eat cholesterol (as evidence of this, cholesterol was found in their tendons and connective tissues, as if they couldn't metabolize it).

Animal experiments like this were part of what kept the cholesterol hypothesis alive long enough for it to gain broader influence.

From Good Calories, Bad Calories.

 

[facetguy]

http://www.nature.com/ejcn/journal/vaop/ncurrent/full/ejcn2011132a.html

In other words, it's not just about 'eat less and exercise'. "Dietary composition rather than energy balance", as the authors say.

 

[CaptainSSO]

http://www.nature.com/ejcn/journal/vaop/ncurrent/full/ejcn2011132a.html

In other words, it's not just about 'eat less and exercise'. "Dietary composition rather than energy balance", as the authors say.

Do you have the full article, facetguy? I would love to read it.

 

[facetguy]

Do you have the full article, facetguy? I would love to read it.

I don't have access to it from here. Someone had forwarded it to me and mentioned how thorough the full article was, and then I couldn't access it.😡

 

[mTOR]

Now you're talking about 2 different things, restricting total calories and composition of calories (ratio of fat/protein/carbs). Most people who are following a healthy diet aren't eating glucose straight up, their carbs are complex which limits their glycemic load along with fiber which lowers it even more. I regularly test my blood sugar and keep a log of it at home and it hasn't spiked significantly even after eating 5 bananas in one sitting. From the research I've done with CR, it sounds like downregulating IGF-1 by limiting protein intake is one of the most crucial things one needs to do. I'll find the paper later on, but casein (milk protein) was shown to upregulate IGF-1 production more so then other protein sources including soy (which I'm not a big fan of.) Besides that, the rhesus monkeys whose images are shown previously had the same composition of fats/proteins/carbs in their food, the only difference was the total amount of calories of food eaten. The results are striking and this study along with many others shows the physiological benefits of CR.

In fact, according to Luigi Fontana, you don't even have to calorie restrict (CR) at all! Just don't eat protein! As he states:

In conclusion, our findings demonstrate that, unlike in rodents, long-term severe CR does not reduce total and free IGF-1 levels in healthy humans if protein intake is high. In addition, our data suggest that chronic protein intake is more powerful than calorie intake in modulating circulating IGF-1 concentration in humans.

http://onlinelibrary.wiley.com/doi/10.1111/j.1474-9726.2008.00417.x/full

And

However, there are major differences in effects of dietary restriction between rodents and humans. Dietary restriction decreases serum IGF-1 concentration
by ~30 to 40% in rodents but does not reduce IGF-1 levels in humans, unless protein intake is also reduced (68) (Fig. 4B), raising the possibility that protein restriction alone may provide some benefits, as in Drosophila (38).

[-- snip --]

Can protein restriction mimic the effects of dietary restriction and limit cancer growth?

Protein restriction is much less difficult to maintain than dietary restriction and may be more powerful than dietary restriction in reducing the serum IGF-1 concentration in humans. Moreover, protein restriction, by lowering intracellular amino acid levels, reduces mTOR activity and stimulates autophagy, two key processes involved in aging and cancer. Randomized clinical trials of healthy volunteers and patients with cancer are needed to understand the long-term metabolic and clinical effects of protein restriction in humans.

http://www.sciencemag.org/content/328/5976/321.short

Other recent review articles on calorie restriction highlight that, based on several rodent studies, the finger may be pointed more narrowly at certain amino acids -- namely the essential amino acids tryptophan and methionine. However, they acknowledge more research in humans are needed. I agree. (lulz, Inb4 epidemic kwashiorkor)

Both of the above quoted articles were written by our buddy Luigi. Luigi Fontana. And it's funny, when you look at the first paper, while it shows PR > CR when it comes to lowering IGF-1 levels, CR > PR when it comes to reducing insulin levels:

In effect, it would seem that without a concomitant effort to PR, CR's effects = Carb Restricting's effects! The authors, however, did not include a low carb experimental group as they had already decided to focus very narrowly on the IGF-1 effects and not insulin levels (or perhaps, more importantly, levels of insulin resistance).

Why?

In fact, paper after paper, Fontana seems to minimize the importance of insulin. He wholly neglects to say a word about it even for his 2010 Science magazine comprehensive review of longevity mechanisms!

So, one begins to wonder, Who is Luigi? What's his deal?


Well, after a brief google search I have come to the conclusion this WashU physician scientist is some one who desperately wants you to believe the only solution to the plague of obesity and metabolic syndrome is to become a raw-food vegan (lulz and after looking at a couple of his videos I think it's safe to say he probably practices what he studies).

[YOUTUBE]Bfw3RQ64arQ[/YOUTUBE]
*Warning: this lecture is narcogenic

Fontana points out in his papers that part of IGF-1's putative life-shortening effects is due to it's known promotion of tumorigenesis. However, so is insulin. And let's be honest, the epidemic rise in cancers and other diseases associated with Western diets probably isn't due to the carnivorous elements of it (as the PR-reduces-IGF-1 association might imply). As Taubes touches on in his book, GCBC:

Burkitt and Trowell called their fiber hypothesis a "major modification" of Cleave's ideas, but the never actually addressed the reasons why Cleave had identified refined carbohydrates as the problem to begin with: How to explain the absence of these chronic diseases in cultures whose traditional diets contained predominantly fat and protein and little or no plant foods and thus little or no fiber - the Masai and the Samburu, the Native Americans of the Great Plains, the Inuit? And why did chronic diseases begin appearing in these populations only with the availability of Western diets, if they weren't eating copious fiber prior to this nutrition transition? Trowell did suggest, as Keys had, that the experience of these populations might be irrelevant to the rest of the world. "Special ethnic groups like the Eskimos," he wrote, "adapted many millenia ago to special diets, which in other groups, not adapted to these diets, might induce disease." Trowell spent three decades in Kenya and Uganda administering to the Masai and other nomadic tribes, Burkitt had spent two decades there, and yet that was extent of the discussion.

Intredasting indeed.


In this paper published in PNAS last year, researcher Ulanet et. al. addressed the issue of focusing too much attention on IGF-1 and its receptor while neglecting to consider insulin's role:

Compared with the IGF-1 [receptor], the [insulin receptor] has received relatively little attention in regard to its potential cancer promoting properties, likely reflecting recognition of its important role in maintaining glucose homeostasis with consequent concerns about toxicity upon therapeutic intervention; there is, however, mounting evidence that the IR may also contribute significantly in transducing protumorigenic effects of IGFs, including a complementary study recently published by Zhang et al. demonstrating a role for IR in growth and metastasis of breast cancer cells in vivo.

Several reports have documented the overexpression of IR, and in particular the IR-A isoform, in human cancers. We hereby provide evidence that up-regulated IR expression can be functionally relevant to tumor progression.

http://www.pnas.org/content/early/2010/05/04/0914076107.short

Building on the idea that insulin and its receptor may play a huge role in cancer, using a murine model, researchers in Canada set out to investigate whether a low carb diet could indeed slow or prevent tumorigenesis. They published their results this past June in the journal of Cancer Research:

A Low Carbohydrate, High Protein Diet Slows Tumor Growth and Prevents Cancer Initiation
Victor W. Ho1, Kelvin Leung1, Anderson Hsu1, Beryl Luk1, June Lai1, Sung Yuan Shen1, Andrew I. Minchinton3, Dawn Waterhouse4, Marcel B. Bally4, Wendy Lin5, Brad H. Nelson5, Laura M. Sly2, and Gerald Krystal1

Since cancer cells depend on glucose more than normal cells, we compared the effects of low carbohydrate (CHO) diets to a Western diet on the growth rate of tumors in mice. To avoid caloric restriction&#8211;induced effects, we designed the low CHO diets isocaloric with the Western diet by increasing protein rather than fat levels because of the reported tumor-promoting effects of high fat and the immune-stimulating effects of high protein. We found that both murine and human carcinomas grew slower in mice on diets containing low amylose CHO and high protein compared with a Western diet characterized by relatively high CHO and low protein. There was no weight difference between the tumor-bearing mice on the low CHO or Western diets.

Additionally, the low CHO-fed mice exhibited lower blood glucose, insulin, and lactate levels. Additive antitumor effects with the low CHO diets were observed with the mTOR inhibitor CCI-779 and especially with the COX-2 inhibitor Celebrex, a potent anti-inflammatory drug. Strikingly, in a genetically engineered mouse model of HER-2/neu&#8211;induced mammary cancer, tumor penetrance in mice on a Western diet was nearly 50% by the age of 1 year whereas no tumors were detected in mice on the low CHO diet. This difference was associated with weight gains in mice on the Western diet not observed in mice on the low CHO diet. Moreover, whereas only 1 mouse on the Western diet achieved a normal life span, due to cancer-associated deaths, more than 50% of the mice on the low CHO diet reached or exceeded the normal life span. Taken together, our findings offer a compelling preclinical illustration of the ability of a low CHO diet in not only restricting weight gain but also cancer development and progression.


[-- snip --]

Low CHO diets cause a drop in plasma insulin and lactate

To gain some insight into how the low CHO diets were reducing tumor growth rates, we measured plasma insulin levels and found that all the low CHO diets reduced plasma insulin, with the 8% and 10% CHO having a more marked effect than the 15% CHO diet (Fig. 4A). As high BG triggers insulin release from pancreatic b-cells, and the released insulin then enhances cellular uptake of BG via insulin receptor-mediated upregulation and activation of glucose transporters (25), these insulin results suggest that low CHO diets can reduce insulin-mediated glucose uptake into tumor cells. Consistent with this and our hypothesis that glucose supply is related to tumor growth, we found a positive correlation between plasma insulin levels and tumor size (Fig. 4B).

[-- snip --]

Interestingly, we detected no changes in IGF-I levels in mice on our low CHO diets, unless there was CR (e.g., with our 8% CHO diet; data not shown). Our findings suggest that although IGF-I reduction may be a relevant mechanism in some models, low CHO diets may also slow tumor growth in an IGF-I&#8211;independent manner.

Cancer Res; 71(13); 4484&#8211;93. ©2011 AACR.
http://cancerres.aacrjournals.org/content/early/2011/06/10/0008-5472.CAN-10-3973.abstract

More relevant to the longevity argument as derived from mouse models, Fontana's overemphasis of the importance of the somatotropic axis (GH/IGF-1) remains a willful oversight of the importance of the insulin axis. This recent paper reviews the data of what we know on longevity from murine models. Of particular note, is Taubes's favorite mouse (discussed in both of his recent books on the adiposity) -- the FIRKO mouse, or rather, the Fat-specific Insulin-receptor Knock-out mouse. This mouse, created by researchers at Harvard's Joslin Diabetes Center, has NO insulin receptors on its adipocytes and lives on average 18% longer than normal mice:

Extended Longevity in Mice Lacking the Insulin Receptor in Adipose
Matthias Blüher1, Barbara B. Kahn2 and C. Ronald Kahn1,*

Caloric restriction has been shown to increase longevity in organisms ranging from yeast to mammals. In some organisms, this has been associated with a decreased fat mass and alterations in insulin/insulin-like growth factor 1 (IGF-1) pathways. To further explore these associations with enhanced longevity, we studied mice with a fat-specific insulin receptor knockout (FIRKO). These animals have reduced fat mass and are protected against age-related obesity and its subsequent metabolic abnormalities, although their food intake is normal. Both male and female FIRKO mice were found to have an increase in mean life-span of &#8764;134 days (18%), with parallel increases in median and maximum life-spans. Thus, a reduction of fat mass without caloric restriction can be associated with increased longevity in mice, possibly through effects on insulin signaling.

http://www.sciencemag.org/content/299/5606/572.abstract

And

Extended longevity and insulin signaling in adipose tissue
Nora Klötingb and Matthias Blüher

Caloric restriction and leanness have been shown to increase longevity in organisms ranging from yeast to mammals. Adipose tissue seems to be a pivotal organ in the aging process and in determination of lifespan. We have recently shown that fat-specific disruption of the insulin receptor gene is sufficient to increase lifespan in FIRKO mice, suggesting that reduced adiposity, even in the presence of normal or increased food intake, can extend lifespan. The model also suggests a special role for the insulin-signaling pathway in adipose tissue in the longevity process. Reduced fat mass has an impact on the duration of life in several other model organisms. In Drosophila, a specific reduction in the fat body through overexpression of forkhead type transcription factor (dFOXO) extends lifespan. Furthermore, sirtuin1 (SIRT1), the mammalian ortholog of the life-extending yeast gene silent information regulator 2 (SIR2), was proposed to be involved in the molecular mechanisms linking lifespan to adipose tissue. In the control of human aging and longevity, one of the striking physiological characteristics identified in centenarians is their greatly increased insulin sensitivity even compared with younger individuals. The effect of reduced adipose tissue mass on lifespan could be due to the prevention of obesity-related metabolic disorders including type 2 diabetes and atherosclerosis.

http://www.sciencedirect.com/science/article/pii/S0531556505001464

Cliffs:

-Western diet carbs chronically drives insulin WAY up, among other things (= definitively bad)
-Western diet protein doesn't lower IGF-1 (bad????)
- maintain diet of 100% lard to stay healthy, lulz.

 

[mTOR]

http://www.nature.com/ejcn/journal/vaop/ncurrent/full/ejcn2011132a.html

In other words, it's not just about 'eat less and exercise'. "Dietary composition rather than energy balance", as the authors say.

Awesome paper! Basically a formally submitted version of Lustig and Taubes's argument (with appropriate crediting) with further elaboration on other "paradoxes" their paradigm can explain.

 

[Lubeckd]

thanks for posting this up!

 

[ToldYouSo]

In fact, according to Luigi Fontana, you don't even have to calorie restrict (CR) at all! Just don't eat protein! As he states:



And



Other recent review articles on calorie restriction highlight that, based on several rodent studies, the finger may be pointed more narrowly at certain amino acids -- namely the essential amino acids tryptophan and methionine. However, they acknowledge more research in humans are needed. I agree. (lulz, Inb4 epidemic kwashiorkor)

Both of the above quoted articles were written by our buddy Luigi. Luigi Fontana. And it's funny, when you look at the first paper, while it shows PR > CR when it comes to lowering IGF-1 levels, CR > PR when it comes to reducing insulin levels:

In effect, it would seem that without a concomitant effort to PR, CR's effects = Carb Restricting's effects! The authors, however, did not include a low carb experimental group as they had already decided to focus very narrowly on the IGF-1 effects and not insulin levels (or perhaps, more importantly, levels of insulin resistance).

Why?

In fact, paper after paper, Fontana seems to minimize the importance of insulin. He wholly neglects to say a word about it even for his 2010 Science magazine comprehensive review of longevity mechanisms!

So, one begins to wonder, Who is Luigi? What's his deal?


Well, after a brief google search I have come to the conclusion this WashU physician scientist is some one who desperately wants you to believe the only solution to the plague of obesity and metabolic syndrome is to become a raw-food vegan (lulz and after looking at a couple of his videos I think it's safe to say he probably practices what he studies).



Fontana points out in his papers that part of IGF-1's putative life-shortening effects is due to it's known promotion of tumorigenesis. However, so is insulin. And let's be honest, the epidemic rise in cancers and other diseases associated with Western diets probably isn't due to the carnivorous elements of it (as the PR-reduces-IGF-1 association might imply). As Taubes touches on in his book, GCBC:



Intredasting indeed.


In this paper published in PNAS last year, researcher Ulanet et. al. addressed the issue of focusing too much attention on IGF-1 and its receptor while neglecting to consider insulin's role:



Building on the idea that insulin and its receptor may play a huge role in cancer, using a murine model, researchers in Canada set out to investigate whether a low carb diet could indeed slow or prevent tumorigenesis. They published their results this past June in the journal of Cancer Research:



More relevant to the longevity argument as derived from mouse models, Fontana's overemphasis of the importance of the somatotropic axis (GH/IGF-1) remains a willful oversight of the importance of the insulin axis. This recent paper reviews the data of what we know on longevity from murine models. Of particular note, is Taubes's favorite mouse (discussed in both of his recent books on the adiposity) -- the FIRKO mouse, or rather, the Fat-specific Insulin-receptor Knock-out mouse. This mouse, created by researchers at Harvard's Joslin Diabetes Center, has NO insulin receptors on its adipocytes and lives on average 18% longer than normal mice:



And



Cliffs:

-Western diet carbs chronically drives insulin WAY up, among other things (= definitively bad)
-Western diet protein doesn't lower IGF-1 (bad????)
- maintain diet of 100% lard to stay healthy, lulz.

Wow, thanks so much for those articles and the detailed analysis, these are really useful reads. Paul McGlothin, a noted CR advocates eating a calorie restricted diet that's low in protein which according to these papers seems like the ideal setup in terms of keeping IGF-1 and insulin levels low.

 

[goldenwest]

In fact, according to Luigi Fontana, you don't even have to calorie restrict (CR) at all! Just don't eat protein! As he states:
- maintain diet of 100% lard to stay healthy, lulz.

 

[mrwesticles]

Another note: I'm seeing more and more sodas being manufactured with cane sugar instead of HFCS, but it's still a metric crap-ton of sugar.

At least we're addressing the source and type, though. Baby steps.