A 20-year study of monkeys shows that a reduced-calorie diet pays off in less disease and longer life, U.S. researchers said on Thursday, a finding that could apply to humans.
They said rhesus monkeys on a strict, reduced-calorie diet were three times less likely to die from age-related diseases like heart disease, cancer and diabetes over the study period than monkeys that ate as they liked.
"We have been able to show that caloric restriction can slow the aging process in a primate species," Richard Weindruch of the University of Wisconsin in Madison, whose study appears in the journal Science, said in a statement.
"We observed that caloric restriction reduced the risk of developing an age-related disease by a factor of three and increased survival," Weindruch said.
Steenhuysen further reports:
The team found that half of the monkeys that were allowed to eat freely over the course of the 20-year study have survived, while 80 percent of the monkeys that ate 30 percent fewer calories over the same period are still alive.
While rhesus macaques have an average life span of about 27 years in captivity, the team said.
The animals that ate less had half the amount of heart disease and cancer, and there were no cases of diabetes in the low-calorie group.
Animals on a restricted diet also had more brain volume in some regions than the animals that ate freely, suggesting diet may affect brain health in aging as well.
Richard at Free the Animal has correctly pointed out that intermittent fasting without caloric restriction will very likely produce the same results. And Charles Washington at Zeroing In On Health pointed to what the scientists performing this study missed:
You’ll recall that aging is the work of advanced glycation end products, or AGE’s. AGEs can be thought of as aging accelerators. They are recognized as photosensitizers in the crystalline lens through crosslinking which has implications for cataract development. AGEs have been implicated in Alzheimer’s Disease, cardiovascular disease, and stroke. The mechanism by which AGEs induce damage is through a process called cross-linking that causes intracellular damage and apoptosis. Because AGEs are related to elevated blood sugar levels, a low calorie diet may reduce AGE body load.
Sharp readers of this blog will also recognize that if one can keep blood sugar low, this should also decrease aging. All of these maladies are included under the umbrella condition called “metabolic syndrome.” We can add obesity to that list as well. I argue that all of these conditions are merely symptoms of the metabolic disease of chronically-high insulin.
Charles goes on to remind us that
We all know that lowering calories has not been shown to reduce the symptom of obesity very well (beyond the short term), but at least in monkeys, some experts believe that lowering calories might work for that symptom, and indeed it seems to have in several species. But the astute observer will also recognize that when you lower calories, you automatically lower carbohydrates so any benefit to lowering calories may also be found with lowering carbohydrate consumption. And since low-carbohydrate diets consistently perform better in terms of obesity than low-fat, low-calorie diets, it’s safe to say that the same would be true in terms of longevity. The sad part of this is that the poor monkeys had to live their lives with less food when they could have eaten more fat and protein and just cut out the carbohydrates.[Emphasis added.]
Yes. As Gary Taubes discussed in Good Calories Bad Calories, Ronald Kanhn and his collaborators at the Joslin Diabetes Center have already published results of their research with mice that they had genetically engineered to lack the insulin receptor on fat cells. Let me quote Gary:
With their fat tissue immune to the effect of insulin, Kahn’s mice weighed 25 percent less than normal mice. These mice remained lean, even when forced to overeat. They were simply incapable of putting on fat. As Kahn later explained, this wasn’t surprising, since fat cells require insulin for fat synthesis. If they have no receptor to detect the insulin that’s present, then no fat can accumulate. The transgenic mice lived almost 20 percent longer than normal mice.[Emphasis Added.]
This study proved that high calorie intake does not shorten life, if the calories consumed don’t stimulate insulin receptors on fat cells. Ah, that would mean that calories from sugar and starch shorten your life, but eating fat doesn’t make you fat or shorten your life because fat does not stimulate insulin or receptors. Unfortunately, the people doing hungry monkey studies appear to have missed that memo. As Taubes notes, not even Kahn can make the logical deduction, he hopes for a drug to block insulin receptors on fat cells!
Taubes also reports the research of Cynthia Kenyon and colleagues at UCSF, who found that mutations that reduced activity in the insulin-IGF pathway in worms prolonged the worms’ lifespan significantly. Knowing that glucose stimulates that pathway, Kenyon and colleagues “began a series of experiments based on a single question: what would happened if she fed worms glucose, in addition to their preferred diet of bacteria?” Keep in mind that bacteria consist primarily of protein and fat, so a worm’s natural diet is low-carbohydrate. The results?
Kenyon added 2 percent glucose to the bacterial medium in which the worms lived, and the lifespan of the worms was reduced by a quarter.
Simple: High intake of glucose shortens life by 25 percent, via stimulating the insulin-IGF pathway. Solution? Reduce carbohydrate, not calories. Kenyon figured it couldn’t hurt to try it out herself – Taubes reports she decided to restrict her own carbohydrate intake to a bare minimum. She lost thirty pounds, and saw drops in blood pressure, triglycerides, and blood sugar, and an increase in her HDL. She’s on the way to a long life, hunger-free, while the monkeys go hungry.
This reminds me of a passage in the Histories, book 3, of Herodotus, to which Lutz refers in Life Without Bread. Herodotus (484 - c415 BCE) reported on an encounter between the king of Ethiopia and the king of Persia. The Persian king was showing the products of Persia to the Ethiopian, and:
“Finally he [the Ethiopian] came to the wine, and, having learnt the process of its manufacture, drank some and found it delicious; then, for a last question, he asked what the Persian king ate and what was the greatest age that Persians could attain. Getting in reply an account to the nature and cultivation of wheat, and hearing that the Persian king ate bread, and that people in Persia did not commonly live beyond eighty, he said he was not surprised that anyone who ate dung should die so soon, adding that Persians would doubtless die younger still, if they did not keep themselves going with that drink – and here he pointed to the wine, the one thing in which he admitted the superiority of the Persians.
“The Fish-Eaters, in their turn, asked the [Ethiopian] king how long the Ethiopians lived and what they ate, and were told that most of them lived to be a hundred and twenty, and some even more, and that they ate boiled meat and drank milk.”
[Herodotus, The Histories, book 3, trans by Aubrey De Sélincourt (New York, Penguin Books, 2003), pp 181-182.]
According to Charles, “ The federal government is funding a small study to see if some healthy normal-weight people could sustain a 25 percent calorie cut for two years and if doing so signals some changes that might, over a long enough time, reduce some age-related disease.”
I don't like this. This means some bureaucrats have decided to spend money they stole from me on a project to find the answer to a question they could get answered simply by reading GCBC or the voluminous research on caloric restriction done already to date. [BTW the "government" does not exist, what we call government consists of a gang of goons stealing money from us (taxes) and wasting it as they see fit.]
Assuming the typical caloric requirement is about 2000 calories, a 25 percent reduction would result in a 1500 calorie diet. As Taubes points out in his chapter 15 entitled “Hunger,” in October 1917, Francis Benedict, director of the Carnegie Institution of Washington’s Nutrition Laboratory “put twelve young men on diets of roughly fourteen hundred to twenty-one hundred calories a day with the intention of lowering their body weights by 10 percent in a month.”
Benedict hoped to find out whether humans could adapt to this level of caloric restriction and thrive. What happened? The men did lose weight, but they did not thrive. They complained of constant hunger, and of being constantly cold -- some found it almost impossible to stay warm regardless of amount of clothing worn. Their metabolic rates dropped by 30 percent, so that even their restricted diets now made them gain fat. They had drops in blood pressure and heart rate; they suffered from anemia, inability to concentrate, and “marked weakness” in physical activity. They had a decrease in sexual interest and expression, in some to “the point of obliteration.”
As Taubes points out in GCBC, these all are genetically conserved biologic responses to food restriction, occuring in all species so far studied, all minimizing energy output and maximizing energy retention under famine conditions, in order to extend life of the individual.
Sounds like a great way to extend life -- not. Actually, I'd call it torture. But the monkeys can't fight back.
After the experiment, the men “almost invariably over-ate.” They managed to regain all the lost weight and body fat in less than two weeks, and within another three weeks, they had gained, on average, eight pounds more. As a result, the men came out of this exercise heavier and fatter than they were when they started.
Yep, that's what happens when people restrict calories. They get fatter in the interim and the long run.
This 1917 experiment documented all the ill effects people experience from caloric restriction, and you can also find them all online by just checking out the Risks page of the Caloric Restriction Society.
So, for only $16.95 spent on Good Calories Bad Calories, or, by spending a few minutes online, or even by trying it yourself, you can find the answer to the question of whether people can sustain a 25 percent caloric restriction for two years in good health. But the goons will take millions of dollars stolen from us at gunpoint and throw it at this question to make it look like they are serving us. Bullshit.
So, the authors of this hungry monkey study appear ignorant of the research in their own field, which shows that the villain is excessive glucose, not excessive calories, and that we can get all the benefits of caloric restriction by reduction of glucose intake and insulin activity, which you can obtain without caloric restriction by two routes 1) reducing your carbohydrate intake, and 2) intermittent fasting.
So you don't have to suffer deprivation your entire life to get to "heaven," always depicted as a pleasant life without end.
You can enjoy yourself NOW. When else? You can't enjoy in the past, nor in the future, you can only enjoy NOW.
But if you did, that wouldn't work for priests and "government" authorities, including the enviro-nazis and veg-heads, who promise a future of eternal life and bliss if only you pay taxes and tithes, sacrifice your self and health, avoid meat, and obey them NOW.
If you follow your primal wisdom, they won't get a cut of your life, will they?
Addendum: More on the Hungry Monkey Study
Surprise, surprise! The "scientists" who published the hungry monkey study didn't tell the whole story. Sandy Szwarc at Junkfood Science did a lot more digging than I did and found that the media report didn't fit the facts.
Sandy reports:
1) "The lower mortality claimed among the monkeys on the calorie restricted diet were achieved only after eliminating 37% of the monkey deaths. They defined mortality as “age-associated deaths” and eliminated any cause of death they didn’t believe was associated with aging. As the supplemental data explains, 16 deaths from “non-age-associated causes were censored and their age of death used as the time variable in the regression.”"
She found in the New York Times report this nugget:
"If caloric restriction can delay aging, then there should have been significantly fewer deaths in the dieting group of monkeys than in the normally fed comparison group. But this is not the case. Though a smaller number of dieting monkeys have died, the difference is not statistically significant, the Wisconsin team reports."
No statistical difference in overall mortality between the hungry monkeys and the others.
Sandy goes on:
"The non-aging-related causes of death included monkeys who died while taking blood samples under anesthesia, from injuries or from infections, such as gastritis and endometriosis. These causes may not be aging-related as defined by the researchers, but they could realistically be adverse effects of prolonged calorie restrictions on the animals’ health, their immune system, ability to handle stress, physical agility, cognition or behavior."
2) Control monkeys were overfed by 20%. So this study compared underfed with overfed animals, not underfed with normal eating. The methods were discussed in Attenuation of Sarcopenia by Dietary Restriction in Rhesus Monkeys.
3) "Most interesting, calorie restriction doesn’t extend average lifespans in wild-derived mice, but only in certain laboratory mice bred to be adapted to specific conditions and which may not be representative of the species. “The inability of CR to extend lifespan of wild-derived mice, which were not adapted to laboratory conditions like typical laboratory mouse strains, may suggest that CR is in part an artifact of breeding animals specifically for laboratory studies,” said João Pedro de Magalhães at the Integrative Genomics of Ageing Group at the University of Liverpool."
4) The researchers have conflicts of interest.
For the full story, read Sandy's full post Calorie restrictive eating for longer life? The story we didn’t hear in the news.
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