Ron Rosedale says to keep your cells sensitive to leptin, insulin and other hormones for better health.
He gave this talk at the American Society of Bariatric Physicians (ASBP) meeting Oct 31, 2006. They’re medical experts who work to reduce obesity. As part of the 2006 presentations, the ASBP included a special segment that featured low-carb diets, researchers and scientists who are connected to the Nutrition and Metabolism Society. Special thanks to Instatapes for recording this presentation.
Listen to Ron Rosedale speech (60 minutes)
View PDF of keynote presentation that includes citations.
SPEAKER’S INTRODUCTION: Dr. Ronald Rosedale is an internationally renowned expert on the biology of aging. He was at the International Conference on Aging Medicine at Rio de Janiero, and the first European Conference on Longevity Medicine and many more. He is the author of The Rosedale Diet: Insulin and its metabolic effects. He will be speaking to us this morning on the detrimental effects of too much protein. Please welcome Dr. Ronald Rosedale.
We might give a different view on protein intake and nutrition and actually health in general. First, you hear a lot about paleolithic nutrition, the idea being that ancient man can tell us how to be healthy. That we need to go back to our ancient roots and eat like they did, and then we’ll be healthy. But you have to go back even further and understand what Nature is after. And there are two prime prerogatives of all life, since the beginning of life. And they both involve making more life.
How do you make more life? Reproduce. What do you do to reproduce? You have to eat. You have to eat and reproduce. It’s all life does, and we evolved with those dictums.
We can’t use Paleolithic Man. We evolved with a diet to not allow a man to live a long healthy life.
Nature does not care about us living a long healthy life, or any life, for that matter. Nature wants “Life” to live.
It’s like, you don’t care if there’s a little cell on your hand that dies, as long as the whole remains. Nature doesn’t care if you or I dies, or if all mankind dies. Nature wants life to live. The diet that ancient man grew up with was to maximize reproductive sense. Not necessarily the life of each individual.
We do know, there is a powerful connection between energy stores, reproduction and longevity. Certainly, we know that it takes a lot of energy to make babies. And if there was not a lot of energy around, Nature would put off reproduction, and it is that trick that we want to use. It puts off reproduction by allowing the organism to live longer. It appears that all organisms have genetic mechanisms to delay aging, to delay dying so that the organism can reproduce at a future more opportune time. And generally this is genetically controlled, and it’s controlled by the availability of nutrients, whether it’s good to reproduce now or put off reproduction into the future.
Because of this, we know now that there are nutrient sensors that tell the body and tell the genetics how much nutrition is available right now, and it is a liaison between nutrient stores and genetic expression that determines whether the body will move toward reproduction or maintenance and repair. This is on an organism level and on a cellular level. On a cellular level, increasing reproduction might not be such a good thing because when you push growth and reproduction too far, you stimulate cancer.
We’ll talk a little about diabetes because it’s the quintessential disease of nutrient stores. Ask anyone what is diabetes, and they’ll say it’s a disease of blood sugar. Diabetes is not a disease of blood sugar. If you get nothing else out of this talk today, realize that diabetes is not a disease of blood sugar. It is a disease of insulin signaling. What we have hear is a failure to communicate. Insulin tells the body a very vital message. Not how much sugar to have. The real purpose of insulin has to do with being a switch, a nutrient sensor, that is one of the pathways that will dictate whether a cell reproduces or whether it lives.
Caloric restriction, metabolism, IGF and insulin are integrated into this longevity pathway, and this pathway appears to be conserved through all of evolution.
It’s found in yeast and flies and worms. Everything down to yeast. Not bacteria. Bacteria has a different definition of life. In fact, it never dies. It just keeps reproducing. So you can’t throw bacteria in there. But yeast, flies, worms, rodents, primates, and certainly humans, it appears. Since the discovery of insulin, most studies have focused on the role of insulin in the metabolism of glucose, however a failure of insulin signaling is certainly associated with a shorter lifespan. What we’re seeing over the last decade is a central role of insulin signaling in lifespan. The discoveries indicate that aging is a programmed and well controlled process regulated by the same pathways that affect growth, metabolism and lifespan. It is an evolutionarily conserved process, so you can extrapolate, it appears, to humans, since it appears ubiquitous.
Calorie restriction also appears to ubiquitously extend lifespan in laboratory animals, and so far, it appears to extend lifespan in humans, too. It extends lifespan in yeast, flies, fish, worms, mice, rats, monkeys, and perhaps humans. Some common, consistent effects of caloric restriction include lower fat mass, particularly visceral fat–remember that–lower circulating insulin and IGF concentrations, increased insulin sensitivity, lower body temperature. Flowers live longer if you keep them cooler. It appears to be a universal truth. Lower fat free mass. Lower sedentary energy expenditure. Decreased levels of thyroid hormone and decreased oxidative stress. Reduced metabolism and therefore free radical production is another possible explanation. And there Other effects such as lower body temperature, decreased insulin, decreased IGF, decreased sympathetic nervous system activity, altered gene expression have all been suggested as mechanisms that explain the extended lifespan associated with calorie restriction.
There’s also a connection between calorie restriction and chromatin structure. Genes are wrapped around chromatin, and their expression is often dictated by how well they’re wrapped. Basically, you uncover the genes to read them. Genetic expression is really the importance of genetics. It’s not the genes you have. Every cell in your body other than your sperm and eggs have the same genes. What makes a heart cell a heart cell and a kidney cell a kidney cell depends on which genes are read. That depends on chromatin structure and other molecular mechanisms such as methylation and acetylation and things like that.
This is talking about an important part of genetic expression dictated by a gene called SIR-2 which in the humans, the homologue is SIRT-1, and research at MIT and Harvard has looked and determined this pathway is NAD and NAHD dependent, meaning energy stores, and when SIRT-1 in humans and SIRT 2 in so called lower forms of animals goes up, animals tend to live longer, and it appears it does this by turning off detrimental pathways that can accelerate aging and turns on maintenance and repair pathways that extend lifespan, and at least partially, you can up-regulate SIRT expression and therefore, by suggestion, lifespan, by amino acid restriction.
Interestingly also, SIRT-1 protein binds to and represses genes controlled by the fat regulator PPR. Where have you heard that before? That’s Avandia, Actos. The first one was Rezulun but they had to take it off the market because it killed too many people. They still kept the other drugs on the market. These are supposedly insulin sensitizers. They are NOT insulin sensitizers. That’s just marketing hype. These PPR agonist drugs such as Actos and Avandia actually work by increasing fat mass. They multiply fat cells. They give you a bigger dumping ground to put sugar. So yes, it lowers blood sugar. Only because you turn it into fat. But is that a healthy thing to do?
Okay? You have to ask the right questions.
Is reducing kidney disease a healthy thing to do?