I was reminded the other day about the section in GCBC regarding Cynthia Kenyon's research linking carbohydrates and longevity (that is, at least for C. elegans). Adding glucose to C. elegans' diet significantly reduced its lifespan via an insulin-mediated pathway.
Is anyone aware of other research which could support or may contradict her results? Could a VLC diet be as effective at extending lifespan as a calorie-restricted diet? (For that matter, do CR diets really work for extending human's lifespans? We do know CR diets work great for extending the lifespan of rhesus monkeys.) Is there an article or paper with a good overview of the current state of longevity research?
I wonder if the longevity topic eventually ends up going in the same direction of the obesity topic: that is, newer research and insights will prove that it's not all about carbs nor calories, but rather a combination of several NADs.
asked bysmcdow (641)
Get FREE instant access to our Paleo For Beginners Guide & 15 FREE Recipes!
on August 28, 2011
at 01:16 PM
Aging, and health, are not related to caloric restriction per se. It is related to nutrient sensing hormones and pathways that caloric restriction effects that in turn greatly influences genetic expression towards a longevity phenotype. The same hormones may be affected the same way in a non-caloric restricted manner using a low non fiber carbohydrate, moderate protein, and relatively high-fat diet; the same diet that I have used to successfully treat many chronic diseases of aging including diabetes, cardiovascular disease, obesity, and even cancer for over two decades.
Below is a link to a research paper by myself and a couple of associates published finally a couple of years ago titled Clinical Experience of a Diet Designed to Reduce Aging along with the abstract of a related presentation to the American Aging Association given several years previously. They might shed some light on your question. See also my comments under Meredith's (much appreciated) answer??? My book,The Rosedale Diet, also largely addresses that question. http://www.jarcet.com/articles/Vol9Iss4/Kohnilias.pdf
The American Aging Association June 4-7, 2004
Clinical Experience of a Diet Designed to Reduce Aging
R Rosedale*, E Westman
Rosedale Center for Metabolic Medicine, Broomfield CO Department of Medicine, Duke University Medical Center
The neuroendocrine theory of aging is associated with elevated levels of glucose, insulin and leptin. The objective of this study is to describe the metabolic effects of a nutritional program designed to reduce these correlates of aging. A retrospective chart review was performed of patients attending an outpatient metabolic management program utilizing instruction in a high-fat, adequate-protein, low-carbohydrate diet, the use of nutritional supplements, and periodic individual visits. The general dietary recommendation was approximately 15% carbohydrate, 25% protein, and 60% fat. Recommended sources of fat included raw nuts, avocados, olives and olive oil, flax and cod liver oil. The intake of protein was limited to 1.0 - 1.25 grams/kg lean body mass per day (increased for exercise to 1.25 grams/day). Recommended sources of protein included sardines, fish, eggs, tofu, poultry, wild meats, non-fat cheeses (cottage, ricotta, cream), and seafood. Only non-starchy, fibrous vegetables were acceptable. Nutritional supplements recommended daily were: L-carnitine 2000mg, alpha-lipoic acid 400mg, coenzyme Q10 100 mg, 1 tbsp cod liver oil, magnesium 300mg, potassium 300mg, vitamin C 1000mg, vitamin E 800mg, and a multivitamin. Medications were adjusted if needed. The mean duration of follow-up was 91.5 days (range 36-211). Thirty-one patients were identified with baseline and follow-up body weight, and fasting laboratory tests. The mean age of patients was 57.6 years, 53% were female. Over a mean follow-up of 91.5 days, body weight decreased 8.2% (p<0.01), fasting serum glucose decreased 8.3% (p=0.001). There were approximate 50% reductions in insulin, leptin, fasting serum triglyceride, and triglyceride/HDL ratio (p<0.001). Free T3 decreased 7% (p<0.001), while TSH did not change significantly. We conclude that a high-fat, adequate-protein, low-carbohydrate diet with nutritional supplementation led to improvements in serum factors related to the aging process in adherent patients. Further research regarding this nutritional approach and its relationship to aging is in order.
on August 28, 2011
at 02:46 AM
I have the strong suspicion that a ketogenic diet is longevity producing, even more so than CR, and without the concomitant malnutrition. Here's a paper that shows they have common mechanisms: The Neuroprotective Properties Of Calorie Restriction, The Ketogenic Diet, And Ketone Bodies.
on August 27, 2011
at 08:53 PM
Actually Ron Rosedale has been talking about this for quite some time. A lot of what Nora Gedgaudas has to say on the MTor aspect of aging (which I understand NOT) has already been said by Rosedale years ago.
There are some great interviews on this site with Rosedale - http://www.meandmydiabetes.com/2010/05/07/ron-rosedale-insulin-leptin-and-the-control-of-aging/
on August 30, 2011
at 12:04 PM
Good point below, Travis. In fact, that is the point. It is not caloric restriction per se that mediates longevity; it is a change in, specifically down regulating, particular metabolic pathways that elicits the shift in genetic expression towards a longevity phenotype. These pathways must be intact as they are in non-genetically modified people for CR to have significant benefit. The latest science is showing that these pathways likely pertain to insulin and mTOR that are conserved in virtually all animal species, and I suspect the leptin pathway will be shown to be very significant in mammals including humans. This places (non-fiber) carbohydrates and excessive protein in the middle of the fray.
The calorie restriction protocol has been shown to extend lifespan in the vast majority of species studied. In many of these species, obesity is a non issue such as flies, worms, spiders, and many others. DBA2 mice are being studied as in the paper cited by Travis precisely because they are a known exception to the CR extending lifespan rule. But for every exception, you could likely find hundreds of studies since the 1930s that show caloric restriction extends lifespan in other strains and species. Research is being done to try to find out why exceptions exist.
The DBA 2 mice are quite weird aside from their well known non response to caloric restriction. CR increases their blood glucose rather than decreasing it as in almost all other species, including humans. This can hardly be called an insignificant difference. They also die of unusual diseases and also have some strange genetic defects affecting their brain manifested as hearing impairments and epilepsy I believe.
It is known that if you dietary restrict any animal too much it will tip the scale beyond hormesis and decrease lifespan. A 30% reduction in calories may be too much for this strain.
Attributing the lack of effect of caloric restriction on lifespan extension in this strain of mice to their being thin and non obese is far from conclusive and a hugh scientific leap, as these mice have many other genetic and metabolically relevant differences other than being thin. I would not sing the death knell to CR just yet.
It is quite possible and I would say probable that the lack of lifespan extension in this mouse strain is due to its inability to burn fat as opposed to glucose, secondary to the strange genetic abnormalities that the strain possesses including the maintenance of elevated glucose and therefore the likelihood and necessity of constantly burning it.
To summarize, the advantage to health and lifespan that caloric restriction elicits is not due to CR per se, but to changes in metabolic hormone signaling. Part and parcel of that change is the increased ability to effectively burn fat.
To quote from p 18 of my book, "I am often asked to briefly summarize what it is that establishes health. I can do this in a single sentence. 'Health and life span is determined by the proportion of fat versus sugar people burn throughout their lifetime'. The more fat you burn as fuel, the healthier you will be. The more sugar you burn as fuel, the more disease-ridden you will be, and the shorter will likely be your life."
on August 29, 2011
at 07:16 PM
Regarding caloric restriction, I was under the impression that it only extended the life of animals with a strong genetic predisposition (due to our engineering) toward obesity. In those cases, caloric restriction was necessary to fend off obesity, and all of the longevity-reducing things that come with it:
It seems like caloric restriction is a ham-handed way to reduce oxidative stress.
on August 27, 2011
at 08:49 PM
Igf 1 pathways can be bad if there is back round cellular inflammation. This depletes the stem cell supple and the organ become senescent. When a cell is senescent it has two options apoptosis or cancer. The more inflammatory the terroir is the more likely your develop cancer. High protein diets with inflammation do thensame thing to the mTor pathway
on August 28, 2011
at 01:32 AM
First, of course, there's no proof, but it is illogical that primates would be the exception to the rule.
Second is my observation. Regardless of its origin, I consider the bible to be an historical account. In the earliest parts, closer to hunter-gatherer times, people were living several hundred years. As time passes, moving well into agriculture, lifespans decrease. I've never heard an explanation that makes sense. Cynthia Kenyon's research produces the missing puzzle piece IMO. It also explains why we didn't breed like rabbits during H-G times.