Insulin/Low-Cal

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Wedgewod

New Member
Interesting study off of Mercola's website...

Low Insulin Not Calorie Restriction Lengthens Your Life

A lean body devoid of fat may be more significant in determining lifespan than a calorie-restricted diet, according to a new study of genetically altered mice.

The mice in the study were able to eat whatever they wanted and still stay slim because their fat tissue had been altered so it could not respond to the hormone insulin. Insulin helps to move sugar from the blood into the body’s cells and also helps fat cells to store fat.

Researchers altered the insulin receptor gene in the fat cells of lab mice, and since insulin is needed to help cells store fat the mice had less fat and were protected against obesity.

The altered mice ate 55 percent more food per gram of body weight than normal mice, yet had 70 percent less body fat by the time they reached 3 months of age.

Moreover, the altered mice lived 18 percent longer than normal mice, and after three years all of the normal mice had died, but one-quarter of the altered mice were still alive.

Previous studies have shown that a calorie-restricted diet can extend the lifespan of everything from yeast to mammals. One theory for why this occurs is that eating less produces fewer chemical by-products, known as free radicals, which can damage cells. However, the current study suggests that leanness may also play a role in promoting longevity.

The findings could open the possibility of a new drug that would fight obesity, and related illnesses like type 2 diabetes, by blocking insulin receptors in fat tissue. The drug would need to be targeted to fat only, however, as a loss of insulin sensitivity through out the body results in type 2 diabetes, researchers noted.

Science January 24, 2003;299:572-574
 
This is definitly one more point in favour of low carb diets. Lower body temperature and low insulin leves were already thought to be the two most relevant factors in what concerned the life extending properties of calorie restriction, but I always suspected insulin would probably be the biggest culrpit.
 
It's an interesting finding, all right, but the title added to the article for Dr. Mercola's site gets the point all wrong. These mice don't have low insulin at all; they have fat which does not respond to the insulin they have.

The original study is in Science Online, but your can read the abstract here: Extended longevity in mice lacking the insulin receptor in adipose tissue.

This study does NOT find that "Low Insulin Not Calorie Restriction Lengthens Your Life" at all. Rather, it finds that low bodyfat is more important than calorie restriction

From the abstract: "Thus, a reduction of fat mass without caloric restriction can be associated with increased longevity in mice, possibly through effects on insulin signaling."

If this finding bears out, then it's great news for bodybuilders. It implies that keeping really lean is great for your long-term health. (Of course, bearing all that extra muscle mass may not be so easy on your system, but that's another matter. . .)
 
And it also comes back around to once again showing exercise (increasing muscle insulin sensitivity) is great.
 
Well, but anyway, the only way I can think of to significantly lower insulin levels without calorie restriction or some kind of drug would be going lowish carb, or at least get most from vegetables.

This one is also interesting:

Insulin exposure and aging theory.

Parr T.

The underlying mechanism of calorie restriction (CR) extension of mammalian life spans operates by altering the rate of decline in reserve capacity (with time) as well as the exposure to growth stimulus, two mechanisms that seem to be related to the central genetically determined mechanism that controls mammalian life span over a 50-fold range. While genetic control is principally exerted at the level of metabolic rate and entrained protective defenses, CR appears to alter the rate of decline in reserve capacity and the exposure to growth stimulus without appreciable alteration of metabolic rate. CR accomplishes this by lowering the nutritionally driven level of insulin exposure, which in turn lowers overall growth factor exposure, improves age-declining maintenance of mitochondrial maximal function, and maintains a longer-term favorable balance of the insulin:growth hormone antagonism. Obtaining the 'halved' insulin exposure in calorie-restricted animals (relative to ad libitum fed) can be specifically targeted in non-obese ad libitum fed humans by multiple techniques, a situation that may confer most of the life span extension of CR without restricting calories. The prospect for even further extension of the human life span is considered.

Gerontology 1997;43(3):182-200
 
And this one, though it's old news:

A glucose-rich diet shortens longevity of mice.

Mlekusch W, Lamprecht M, Ottl K, Tillian M, Reibnegger G.

Institute of Medical Chemistry and Pregl Laboratory, Karl-Franzens-Universitat-Graz, Austria.

High plasma levels of glucose and insulin over long-time periods play an important role in the genesis of diabetic complications. There is evidence that the long term consumption of glucose-rich diet by rats is detrimental to insulin sensitivity. We investigated the effect of a glucose-rich diet on longevity of 70 female mice which were compared to 70 mice on a control diet. The average age of death of the control group was 568 +/- 139 days compared to 511 +/- 170 for the glucose group and the seven oldest mice of the control group died at age 890 +/- 52 days, while the seven oldest mice of the glucose group died at 833 +/- 49 days. These differences are statistically significant (P < or = 0.05). Our work shows that a life-long intake of a diet with 20% of total energy derived from glucose leads to a significant reduction of the average and maximal life-span in female mice and thus, supports previous observations of detrimental effects of high glucose intake over long periods.

Mech Ageing Dev 1996 Nov 29;92(1):43-51
 
And while we're at it....


Caloric restriction in primates and relevance to humans.

Roth GS, Ingram DK, Lane MA.

Laboratory of Neurosciences, Gerontology Research Center, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA. [email protected]

Dietary caloric restriction (CR) is the only intervention conclusively and reproducibly shown to slow aging and maintain health and vitality in mammals. Although this paradigm has been known for over 60 years, its precise biological mechanisms and applicability to humans remain unknown. We began addressing the latter question in 1987 with the first controlled study of CR in primates (rhesus and squirrel monkeys, which are evolutionarily much closer to humans than the rodents most frequently employed in CR studies). To date, our results strongly suggest that the same beneficial "antiaging" and/or "antidisease" effects observed in CR rodents also occur in primates. These include lower plasma insulin levels and greater sensitivity; lower body temperatures; reduced cholesterol, triglycerides, blood pressure, and arterial stiffness; elevated HDL; and slower age-related decline in circulating levels of DHEAS. Collectively, these biomarkers suggest that CR primates will be less likely to incur diabetes, cardiovascular problems, and other age-related diseases and may in fact be aging more slowly than fully fed counterparts. Despite these very encouraging results, it is unlikely that most humans would be willing to maintain a 30% reduced diet for the bulk of their adult life span, even if it meant more healthy years. For this reason, we have begun to explore CR mimetics, agents that might elicit the same beneficial effects as CR, without the necessity of dieting. Our initial studies have focused on 2-deoxyglucose (2DG), a sugar analogue with a limited metabolism that actually reduces glucose/energy flux without decreasing food intake in rats. In a six-month pilot study, 2DG lowered plasma insulin and body temperature in a manner analagous to that of CR. Thus, metabolic effects that mediate the CR mechanism can be attained pharmacologically. Doses were titrated to eliminate toxicity; a long-term longevity study is now under way. In addition, data from other laboratories suggest that at least some of the same physiological/metabolic end points that are associated with the beneficial effects of underfeeding may be obtained from other potential CR mimetic agents, some naturally occurring in food products. Much work remains to be done, but taken together, our successful results with CR in primates and 2DG administration to rats suggest that it may indeed be possible to obtain the health- and longevity-promoting effects of the former intervention without actually decreasing food intake.

Ann N Y Acad Sci 2001 Apr;928:305-15
 
I remember metformin being marketed as an anti-aging drug because it keeps insulin levels low. Does anyone take this?
 
Metformin increases insulin sensitivity, in adipose and muscle, so it shouldnt increase lifespan like it was done in the origonal study.
The origonal study made them absolutely insulin insentive (no receptors) in adipose. This meant that they lost fat and this increased lifespan. Not a reduction in glucose, not a reduction in insulin, a reduction in adipose
In the studies above
A glucose-rich diet shortens longevity of mice. a diet with 20% energy as glucose decreases lifespan, they dont state in the abstract if the diets were hypocaloric, but even then, it shows that eating lots of glucose isnt good for mice.
Insulin exposure and aging theory.
Even tho its a theory, it could be that insulin exposure is being confounded by adiposity, and that once removing the adipose out of the equation, insulin means nothing? (as the recent study showed)
 
Exactly, Aaron. The changes in insulin levels are certainly an effect of Calorie Restriction. There is not yet enough evidence to conclude that the changes in insulin levels are the cause of the life extension.

Studies like the one quoted at the beginning of this thread provide evidence that insulin by itself is NOT the primary cause. . .

The most frustrating thing to me is when people like this Dr. Mercola take a study and tack a title onto it which is contradictory, or at best, irrelevant, to the study it is quoting.
 
Sears' comments:

[b said:
Quote[/b] ]New research published in Science from the Joslin Diabetes Center has provided a powerful insight into the relationship of excess body fat and longevity. The scientists at Joslin (part of Harvard Medical School) developed genetically altered mice that had no insulin receptors on their fat cells. As a result they could not accumulate fat. (Remember that insulin is the storage hormone that drives fat into the fat cells.) When compared to normal control mice, these genetically altered cousins had 70 percent lower fat levels and lived 18 percent longer even through both groups of mice ate the same amounts of food. Of course the 18 percent in lifespan pales compared to the usual 40 percent longevity increase found in calorie-restricted mice.

But what does this all mean for humans, since we can't genetically re-engineer ourselves? First, increased body fat is a constant generator of inflammation caused by increased secretion of tumor necrosis factor (TNF) and IL-6. The more inflammation to which you subject the body , the shorter your lifespan. So decreasing body fat is great way to reduce inflammation throughout your body. However, eating too many calories increases the production of free radicals that will damage your DNA. This explains why the increase in longevity in the genetically altered mice was not as great as you might expect if they simply ate fewer calories. So how do you restrict calories and lose excess body fat, all without hunger and deprivation? The answer is the Zone Diet. If you want maximum longevity without dietary suffering, then simply stay in the Zone.
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