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By Tom Venuto
www.BurnTheFat.com
On a recent episode of the Oprah show, one of the guests was a 51 year old man with the heart of a 20 year old. He's been following a calorie restriction plan and they said he might be one of the first people to reach 120 years old by following this plan. There have been stories both in the lay press and scientific press about calorie restriction for years and it has been a frequent talk show topic on other many other TV shows. However, before you cut your calories in half in hopes of adding another decade onto your life, you'd better get the other half of the story they didn't talk about on Oprah.
I’ve seen a lot of strange things in the health field, and although calorie restriction (CR) is the subject of serious and legitimate scientific study, I consider CR to be one of those strange things. Of course, that’s because I choose a different lifestyle - the muscle-friendly Burn The fat, Feed The Muscle lifestyle - but there’s more than one reason why I’m not a CR advocate:
Hunger while dieting is almost always a challenge. There’s some hunger even with conservative calorie deficits of 15-20% under maintenance. Prolonged hunger is one of the biggest reasons people fall off the weight loss diet wagon because it’s unpleasant and difficult to resist. This is why pharmaceutical and supplement companies spend millions of dollars on researching, developing and marketing appetite suppressants. Yet CR advocates put themselves through 30-50% calorie restriction on a daily basis as a way of life in the hopes of extending life span or health.
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Practitioners of CR follow a low-calorie lifestyle, but technically, they are not in a chronic 30% calorie deficit. That would be impossible. What happens is their metabolisms get very slow (that’s part of the idea behind CR; if you slow down your metabolism, you allegedly slow down aging). So a 6 foot tall man who would normally require nearly 3,000 calories to maintain his weight, might eventually reach an energy balance at only 1800 or 1900 calories. This is not just due to a ‘starvation mode’ phenomenon, that’s only part of it. It’s primarily because he loses weight until he is very thin and his smaller body doesn’t need many calories any more.
Does caloric restriction really extend lifespan?
The biological mechanisms of lifespan extension through calorie restriction are not fully understood, but researchers say it may involve alterations in energy metabolism (as mentioned above), reduced oxidative damage, improvements in insulin sensitivity, reduction of glycation, modulation of protein metabolism, downregulation of pro-inflammatory genes and functional changes in both neuroendocrine and autonomic nervous systems.
Mouse studies on CR go back as far as 1935 and monkey studies began in the late 1980’s. So far the results are clear on one thing: caloric restriction does increase lifespan in rodents and other lower species (yeast, worms and flies). Studies suggest the life of the laboratory rat is 25% longer with CR (even longer with aggressive CR). Primate studies are still underway and humans have been experimenting with CR for some time. In primates and humans, biomarkers of aging show signs of slower aging with CR. This makes many proponents talk about this CR as if it were a sure-thing, already proven through double-blind randomized clinical human trials.
The truth is, there is NO direct experimental evidence that you will live longer from practicing CR. Due to the length of human lifespans, we will not have the necessary data for at least another generation and perhaps multiple generations. Even then, it will still be highly speculative whether CR will extend human life at all and if so how much. We can only estimate. I’ve seen guesses in the scientific literature ranging from 3 to 13 years, if CR is practiced for an entire adult lifetime.
Jay Phelan, a biologist at UCLA is skeptical. He says the potential life extension is on the lower end of that range and the increase is so small that it’s not worth the semi-starvation:
“There is no current evidence that lifelong caloric restriction leads to increased lifespan in primates. It’s certainly tantalizing that things like blood pressure or heart rate look as though they are a lot healthier and I believe they are. Whether or not this translates to a significantly increased lifespan, I don’t know. I predict that it doesn’t.”
I don’t quibble qualitatively with their results. Yes, it will increase lifespan, but it will not increase it by 50% or 60%, it won’t increase it by 20% or 10%, it might increase it by 2%. So if you tell me that I have to do something horrible for every day of my life for a 2% benefit - for an extra year of life - I say no thanks.”
About the Author:
Tom Venuto is a fat loss expert, lifetime natural (steroid-free) bodybuilder, independent nutrition researcher, freelance writer, and author of the #1 best selling diet e-book, Burn The Fat, Feed The Muscle: Fat-Burning Secrets of The World’s Best Bodybuilders & Fitness Models (e-book) which teaches you how to get lean without drugs or supplements using secrets of the world's best bodybuilders and fitness models. Learn how to get rid of stubborn fat and increase your metabolism by visiting: www.burnthefat.com
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Here's a bit from a paper on drosophilia, which is the small fly commonly referred to as a "fruit fly" ( a favorite for this type of research).
I'll provide the absract, conclusion and then a link to the full article.
Calories Do Not Explain Extension of Life Span by Dietary Restriction in Drosophila
William Mair, Matthew D. W. Piper, Linda Partridge
Centre for Research on Ageing, University College London, Department of Biology, London, United Kingdom
Abstract
Dietary restriction (DR) extends life span in diverse organisms, including mammals, and common mechanisms may be at work. DR is often known as calorie restriction, because it has been suggested that reduction of calories, rather than of particular nutrients in the diet, mediates extension of life span in rodents. We here demonstrate that extension of life span by DR in Drosophila is not attributable to the reduction in calorie intake. Reduction of either dietary yeast or sugar can reduce mortality and extend life span, but by an amount that is unrelated to the calorie content of the food, and with yeast having a much greater effect per calorie than does sugar. Calorie intake is therefore not the key factor in the reduction of mortality rate by DR in this species.
Conclusions
The response of Drosophila life span to nutrition is not governed by calories, but rather by specific nutritional components of the food. This finding represents a departure from the generally accepted model in rodents, where it has been suggested that the level of calorie intake per se, not the source of calories, is critical for life-span extension [1]. The apparent disparity between the factors in the diet that affect life span in fruit flies and rodents leads to two possible conclusions. First, the mechanisms by which these organisms respond to food shortage could be different. Second, the long-held view that calorie intake is the critical variable in the response of mammalian life span to DR may require further evaluation.
Despite some reports in the literature that DR did not extend life span [38,41,42], the overwhelming majority of data support the idea that DR in some form extends life span across diverse taxa. However, it is still unknown if life-span extension under DR is achieved through common mechanisms in different species. A case for conservation of the mechanisms by which DR extends life span can be made from evolutionary considerations. It has been suggested that, during times of famine, diversion of resources away from reproduction towards somatic maintenance will increase the chances of an organism surviving to more plentiful times and thus increase long-term reproductive success [43–46]. The selective advantage of shifting resources from reproduction to maintenance when food is restricted could be the “public” factor shared between diverse organisms. However, the mechanisms by which extension of life span is achieved could be an example of convergent evolution, producing the same plasticity of life span in response to food shortage through mechanisms at least to some extent specific to different organisms, dependent upon their diet, experience of food shortages, and life history. More work is needed to elucidate the precise relationship between the composition of the diet and life span in different organisms, including mammals. Our results suggest that it may be possible to obtain the full extension of life span by DR by reducing critical nutrients in the food without any reduction in overall calorie intake.
http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.0030223
The author supplies this information in good faith. The reader is responsible for his or her own neuroses.
I had forgotten to point something out in that previous post. That is that DR - dietary restriction is acually the major field of study not CR - calorie restriction. They are not the same thing, of course becasue DR could entail restriction in other ways, such as of certain macronutrients such as protein, fat, or carbohydrate. OR just sugar, etc. In fact rat and mice experiments were carried out invlolving dietary restriction of just ONE amino acid, methionine, which showed increased lifespan in both the rats and the mice.[1]
DR is often called calorie restriction or "CR" because calorie intake has been so often implicated as the primary factor, regardless of where the calories come from but it is far from clear that calories is always the key and increased life-span has been shown is isocaloric diets with things like protein restriction etc. So like Tom says in the article, things are far from clear.
1. 20. Zimmerman JA, Malloy V, Krajcik R, Orentreich N (2003) Nutritional control of aging. Exp Gerontol 38: 47–52
2. Calories Do Not Explain Extension of Life Span by Dietary Restriction in Drosophila." PLoS Biology : Publishing Science, Accelerating Research. Web. 24 Nov. 2010. <http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0030223>.
The author supplies this information in good faith. The reader is responsible for his or her own neuroses.
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