“All truth passes through three stages: First, it is ridiculed; Second, it is violently opposed; and Third, it is accepted as self-evident.”

— Arthur Schopenhauer

A shorter summary is first, followed by a more complete version with additional comments about Kitavans, thyroid, nature, and more…

Short Summary…

Even in a state of starvation blood glucose is maintained right up until death. What this really shows is that even if you are starving, and eating no carbohydrates, or fat, or protein, there is no such thing as “glucose deficiency”. The body can easily make what it needs.

Question #1;

Is it better to eat the requisite glucose, or let the body make it?

The ‘safe starch’ debate boils down to whether it is better to eat the requisite glucose, or let the body make it when necessary. I believe strongly in the latter. We can never know exactly how much and when we will need extra glucose depending on environmental circumstances.

When you eat the glucose, there are different effects than if your liver makes it, namely it circulates for hours and leads to a spike in insulin and leptin, that circulates for hours, that over time will contribute to insulin and leptin resistance…that ultimately contributes to metabolic chaos resulting in chronic diseases of aging including obesity, diabetes, cardiovascular disease, osteoporosis, autoimmune disease, cancer, and others.

I have long summarized health by the ability to burn fat… or not.

Eating glucose i.e. “safe starches” will spike insulin and will, at least temporarily, prevent one from burning fat… in anyone… a worm, a mouse or any human. It will raise leptin that will prevent one from changing to the healthy calorie restriction phenotype (see below).

Glucose, like all parts, must be orchestrated; where, when, how it is used is what will determine health and life. When we talk about significance of starches, safe or otherwise, the most important factor is their effect on hormones and other biochemical pathways that affect the harmony of 15 trillion cells needing to act as one for life and health. And all starches raise insulin and leptin levels… a lot… having a long term adverse effect of insulin and leptin resistance; cells not being able to properly hear their life-giving messages.

Paul Jaminet and all the other safe starch advocates concentrate on blood glucose… and though it is unwise, to say the least, to eat glucose when one is trying to keep blood glucose down, diabetes is not a disease of blood glucose, but of insulin, and more importantly, leptin resistance. It is the effect of eating “safe starches” on insulin and leptin resistance that must be acknowledged and stressed.

Disease is not as much from the parts but much more from the misinformation given them.

It is not an excess of cholesterol that causes heart disease.

It is not a lack of calcium that causes osteoporosis.

Disease is not due to glucose, excess or deficiency, but the communication that tells it what to do…and sugars, more than most anything, by non-enzymatic glycation and insulin and leptin resistance, messes up that communication.

Question #2;

If the body can make all the glucose it needs from other biochemicals, called gluconeogenesis, are there potential adverse effects from this?

Any potential adverse effect of gluconeogenesis would be determined from the initial substrate; whether one is using amino acids to manufacture glucose or other precursors that are extremely benign such as from ketones, the glycerol backbone of fats, or from lactate and pyruvate recycling. Those latter sources of glucose substrates separate from amino acids, under adapted carbohydrate and protein restricted conditions, can virtually make up the entirety of precursors for whatever glucose might be necessary.

Most people on my diet actually gain lean mass without increasing exercise, via protein sparing and increased sensitivity to insulin. Therefore, one can’t be burning much of their lean mass/protein, if any. They are deriving their fuel from ketones, glycerol, recycled lactate and pyruvate. This is perfectly healthy, more so than burning glucose.

Fat is a great fuel, the best fuel, furnishing fatty acids, ketones, and glycerol (that can turn into glucose if necessary), to burn. However, one needs at least two weeks to adapt to properly burning fat, more if older or overtly metabolically challenged. I will maintain that the symptoms that people are experiencing occasionally and calling glucose deficiency are nothing but inadequate adaptation to properly burning fat by either consuming too much carbohydrate or eating excess protein.

Gluconeogenesis from protein requires deamination, and the nitrogen molecule is then used to manufacture ammonia and urea that are both poisonous. This is why urine is called urine. Burning protein is not healthy, but if you can’t burn fatty acids or ketones and you are limiting carbohydrates you will have no choice but to make glucose from protein, either from what you eat, or from your muscles, bone, or other protein sources. The trick then is to not eat more sugar, but adapt to burning ketones and fats…by eating less sugar, not eating too much protein, and eating fat if hungry. You learn to ski by skiing. You learn to burn fat by burning fat.

Question #3;

Is it that important to eat less than 100 gm starch?

Answer; Yes; that is where the deeper benefits lie. That is when one gets into ketone burning and when one can get into the calorie restriction, longevity phenotype.

The worst diet to be on is high fat along with moderate and sometimes even “low” (as opposed to very low) carb. If you are going to eat fat, you have to be able to burn it, and as little as 100 gm non-fiber carb/day can prevent one from adequately burning fat.

According to George Cahill, perhaps the world’s foremost expert on the metabolism of ketones and starvation, 100 gms/day of sugar forming carbohydrates i.e. starches, is all it takes to prevent one from burning and therefore adapting to burning, ketones.

As one follows my diet more closely, meaning as little non fiber carbs as possible and avoiding excess protein (above 1 gm/day/kg lean mass for most), the beneficial returns not only increase, but accelerate.

Question #4;

Is the VLC diet only better for “sick” people?

What I said 20 years ago is just as true today; Carbohydrates should be defined as fiber or not fiber. Any carb that is not a fiber will turn to sugar and will cause harm…for any and everyone, males, females, monkeys and worms. The only difference among the sugars and non-fiber carbs is how fast and how much harm will be caused. ‘Safe starches’ is an oxymoron.

One should not discuss effects of starch only on blood glucose. What about intracellular glucose? If you eat that sugar and it’s not in the circulation, where is it? Much gets pushed inside cells causing intracellular glycation and cellular harm. Lots will turn into liver fat. It has to go somewhere, and wherever it goes it will do damage.

EVERYONE who eats starch will raise their glucose and/or insulin. Keeping glucose down by raising insulin is doing one no favors; just trading one evil, elevated glucose, by an even worse evil, high insulin. (See “Insulin and its Metabolic Effects“). This was shown clearly by the ACCORD study.

If diabetes were properly diagnosed as improper metabolic signals, especially from insulin and perhaps even more importantly from leptin, then we all have diabetes to one degree or another..

Life’s commonalities are much more critical to life than the differences, since life can’t live without them. (See my next blog, an essay I had written a few years back called “The Transcendence of Commonality Amongst Individuality”)

The basics of metabolism are true for all people, in fact virtually all life. This is why worm studies are important to us. Human insulin and glucose will work in a worm just as it does in a human, causing damage and shortening lifespan when elevated.

The major benefit of a very low carbohydrate, moderate protein, high-fat diet, and what will get you to the next level of health, is the adaptation to constantly burning fat and ketones and thus requiring less glucose. By forcing the intake of 100 gm or more/day of glucose into the body you would prevent that adaptation.

The lowering of free T3 is a sign of that adaptation, and, according to Paul Jaminet, when you follow his diet you prevent the lowering of free T3. That is powerful indication that following a “safe starch” diet is preventing one from changing into a calorie restriction phenotype and preventing the genetic expression and adaptation to deeper maintenance and repair that equates to health and longevity that a very low carbohydrate, high-fat diet would otherwise allow the opportunity for.

A Conclusion to the ‘Safe Starch’ Debate

Ron Rosedale M.D.

A more complete version with additional comments about Kitavans, thyroid, nature, and more…

I understand where Paul Jaminet, Chris Kresser and other ‘safe starch’ advocates are coming from, sort of; that if we have to maintain a certain level of blood glucose anyway, then why not eat it? I don’t need to hear more arguments that say that glucose is necessary for mucus; glucose is necessary for protein, etc. I could even add that glucose is needed much more importantly for self-recognition to help prevent autoimmunity (and I believe non-enzymatic glycation can mess that self recognition up), and many other purposes. I agree. I repeat; I agree that glucose is a necessary component of life. Few, I believe, deny that. However, this does not imply that glucose is an essential dietary nutrient or that we must, or even should, eat it. Being a necessary component of life and being a dietary necessity are far from the same. Cortisol is necessary for human life yet you don’t need to eat it, and rarely should. As with so many biomolecules, it’s far preferable to let the body adjust the levels depending on needs.

Paul Jaminet correctly states, as an example of glucose’s importance, that even in a state of starvation blood glucose is maintained right up until death. However, what this really shows is that even if you are starving, and eating no carbohydrates, or fat, or protein, there is no such thing as “glucose deficiency” (unless insulin toxic or relatively rare conditions where glucose cannot be made sufficiently, such as cortisol deficiency, but the ‘safe starch’ advocates are not referring to this). The body can easily make what it needs.

When you eat starch it is digested into glucose and before it goes anywhere it first enters the bloodstream. All you will accomplish then by eating starch is to raise the blood glucose further. Therefore, one cannot correctly talk about a glucose deficiency from not eating enough.

One needs to rephrase the question from, “Are ‘safe starches’ necessary to eat or even beneficial?” to…

Question #1;

Is it better to eat the requisite glucose, or let the body make it?

The ‘safe starch’ debate boils down to whether it is better to eat the requisite glucose, or let the body make it when necessary. I believe strongly in the latter. We can never know exactly how much and when we will need extra glucose depending on environmental circumstances.

Furthermore, when you eat the glucose, there are different effects than if your liver made it, namely it circulates for hours and leads to a spike in insulin and leptin, that circulates for hours, that over time will contribute to insulin and leptin resistance…that ultimately contributes to metabolic chaos and resulting chronic diseases of aging including obesity, diabetes, cardiovascular disease, osteoporosis, autoimmune disease, cancer, and others.

I have long summarized health by the ability to burn fat… or not.

Eating glucose i.e. “safe starches” will spike insulin and will, at least temporarily, prevent one from burning fat…anyone.. a worm, a mouse or any human. It will raise leptin and will remove one from the healthy calorie restriction phenotype (see below).

Glucose, like all parts, must be orchestrated; where, when, how it is used is what will determine health and life. The use of glucose, just like cholesterol and all biochemicals in our body, must be orchestrated. Let’s not mess that orchestration up by forcing that glucose on us at a time, place, or purpose that is likely not in tune with what the body, or brain, wants or needs. Let’s not mess with the orchestra unless we are absolutely sure that we totally know the score.

When we talk about significance of starches, safe or otherwise, the most important factor is their effect on hormones and other biochemical pathways that affect the harmony of 15 trillion cells needing to act as one for life and health, since there are many deceases which can disrupt health, being HIV or AIDS some of the worsts, that’s why getting more information on window period for HIV RNA test could be really good for taking care of health. And all starches raise insulin and leptin levels…a lot…having a long term adverse effect of insulin and leptin resistance; cells not being able to properly hear their life-giving messages.

Paul Jaminet and all the other safe starch advocates concentrate on blood sugar…and though it is unwise, to say the least, to eat glucose when one is trying to keep blood glucose down, diabetes is not a disease of BS, but of insulin, and more importantly, leptin resistance. It is the effect of eating “safe starches” on insulin and leptin resistance that must be acknowledged and stressed.

Disease is not as much from the parts but much more from the misinformation given them.

Life is in the instructions, not the parts. It is not a lack of substrates, parts, that is generally the problem, but the instructions of what to do with the part; the effect on hormones that tell the part what it needs to be doing to maintain the health of the republic of parts and cells..

It is not an excess of cholesterol that causes heart disease.

It is not a lack of calcium that causes osteoporosis.

Disease is not due to glucose, excess or deficiency, but the communication that tells it what to do…and sugars, more than most anything, by non-enzymatic glycation and insulin and leptin resistance, messes up that communication.

Question #2;

If the body can make all the glucose it needs from other biochemicals, called gluconeogenesis, are there potential adverse effects from this?

This is a whole different story than talking about glucose deficiency. Furthermore, any potential adverse effect of gluconeogenesis would be determined from the initial precursor; whether one is using amino acids to manufacture glucose or other substrates that are extremely benign such as from ketones, the glycerol backbone of fats, or from lactate recycling. Those latter sources of glucose substrates separate from amino acids, under adapted carbohydrate and protein restricted conditions, can virtually make up the entirety of precursors for whatever glucose might be necessary.

Most people on my diet actually gain lean mass without increasing exercise, via protein sparing and increased sensitivity to insulin. Therefore, one can’t be burning much of their lean mass/protein, if any. They are deriving their fuel from ketones, glycerol, recycled lactate and pyruvate. This is perfectly healthy, more so than burning glucose.

Fat is a great fuel, the best fuel, furnishing fatty acids, ketones, and glycerol (that can turn into glucose if necessary), to burn. I encourage you to see the fine summary of the great advantages of burning ketones at AHS 2012 by Nora Gedgaudas. However, one needs at least two weeks to adapt to properly burning fat, more if older or overtly metabolically challenged. I maintain that the symptoms that people are experiencing occasionally and calling glucose deficiency are nothing but inadequate adaptation to properly burn fat by either consuming too much carbohydrate or eating excess protein.

Gluconeogenesis from protein requires deamination (cutting off the nitrogen), and the nitrogen molecule is then used to manufacture ammonia and urea that are both poisonous. This is why urine is called urine. Burning protein is not healthy, but if you can’t burn fatty acids or ketones and you are limiting carbohydrates you will have no choice but to make glucose from protein, either from what you eat, or from your muscles, bone, or other protein sources. You will not be too happy. The trick then is to not eat more sugar/starch, but to adapt to burning ketones and fats…by eating less sugar, not eating too much protein, and eating fat if hungry. You learn to ski by skiing. You learn to burn fat by burning fat.

Question #3;

Is it that important to eat less than 100 gm starch?

Answer; Yes; that is where the deeper benefits lie. That is when one gets into ketone burning and when one can get into the calorie restriction, longevity phenotype.

The worst diet to be on is high fat along with moderate and sometimes even low (as opposed to very low) carb. If you are going to eat fat, you have to be able to burn it, and as little as 100 gm non-fiber carb/day can prevent one from adequately burning fat and ketones. If one is going to properly follow my high fat diet, one must go all the way; very low sugar forming carbohydrates, and no more than adequate protein.

According to George Cahill, perhaps the world’s foremost expert on the metabolism of ketones and starvation, 100 gms/day of sugar forming carbohydrates i.e. starches is all it takes to prevent one from burning and therefore adapting to burning, ketones.

The best diet allows for maximal burning of fat and ketones. This is also a high fat diet, but where non-fiber carbs are kept very low and protein is not consumed in excess. (For most, this is between 50-70 gm protein/day depending on lean mass, exercise, growth and pregnancy.) There is a tipping point where a high fat diet goes from not so good to great as non-fiber carbs and protein are further lowered.

As one follows my diet more closely, meaning as little non fiber carbs as possible and avoiding excess protein (above 1 gm/day/kg lean mass for most), the beneficial returns not only increase, but accelerate.

In a diabetic, as one lowers their sugar intake, one will generally lower their blood glucose, at least to some extent. But don’t get fooled into believing that the greatest results possible have been obtained. Do not confuse better with best or even good. It is easy to do better. The typical diet is so bad that most any change will lead to improvement.

You won’t see the really deep benefits of actually lowering the “glucostat” and reversing hormone signaling resistance in the hypothalamus and morphing into a longevity phenotype until you get into what the brain and body thinks is not necessarily starvation in general but glucose starvation, whereby genetic expression will be totally shifted towards maintenance, repair, and longevity that would relate to both disease prevention and reversal. This metabolic adaptation to nutritional availability was set during extremely ancient times shortly after life began around 4 billion years ago and long before fat was used as a fuel, long before paleolithic man, when glucose dominated the oceans and was what to eat.

Question #4;

Is the VLC diet only better for “sick” people?

What I said 20 years ago is just as true today; Carbohydrates should be defined as fiber or not fiber. Any carb that is not a fiber will turn to sugar and will cause harm…for any and everyone, males, females, monkeys and worms. The only difference among the sugars and non-fiber carbs is how fast and how much harm will be caused.

In everyone, when one eats starches it quickly turns to sugar, glucose, fructose, galactose, etc. that will circulate and glycate the collagen that lines the arteries causing inflammation and cardiovascular disease and all of the other adverse effects of glycation. This causes inflammation secondary to the AGE-RAGE reaction. Raising glucose raises insulin increasing risk of cancer. This is not safe and should not be called a safe starch. ‘Safe starches’ is an oxymoron.

One should not discuss effects of starch only on blood glucose. What about intracellular glucose? If you eat that sugar and it’s not in the circulation, where is it? Much gets pushed inside cells causing intracellular glycation and cellular harm. Lots will turn into liver fat. It has to go somewhere, and wherever it goes it will do damage. This is why it is better to talk about glycemic load than glycemic index. All sugar eaten will cause damage.

EVERYONE who eats starch will raise their glucose and/or insulin…a lot. Keeping glucose down by raising insulin is doing one no favors; just trading one evil, elevated glucose, by an even worse evil, high insulin. (See “Insulin and its Metabolic Effects“). This was shown clearly by the ACCORD study.

.

If diabetes were properly diagnosed as improper metabolic signals, especially from insulin and perhaps even more importantly from leptin, then we all have diabetes to one degree or another..

Paul Jaminet and Chris Kresser have stated that maybe a very low carb diet is better for those who are sick with metabolic diseases, but not for ‘healthy’ people. However, we all are in various stages of metabolic disease. We all have some degree of insulin and leptin resistance. Most wake up recovering from their dietary insults and are the most insulin sensitive they will be the whole day. In other words, we all have some degree of diabetes, if it were diagnosed properly.

When you eat a so-called ‘safe starch’ meal, many people’s blood glucose, if not most, will go above 126 mg/dl, meaning that if they were fasting, they would by definition be called a diabetic. The fact that they were not fasting does not mean that the glucose does not do the same harm as if they were fasted. Eating several such meals/day would mean that the supposed ‘healthy’ person was ‘diabetic’ most of the day and perhaps only upon awakening was the BS at a healthier range…and this is saying nothing about insulin and leptin levels and resistance, where the underlying disease actually resides.

Life’s commonalities are much more critical to life than the differences, since life can’t live without them. (See my next blog, an essay I had written a few years back called “The Transcendence of Commonality Amongst Individuality”.)

The basics of metabolism are true for all people, in fact virtually all life. This is why worm studies are important to us. Human insulin and glucose will work in a worm just as it does in a human, causing damage and shortening lifespan when elevated.

Starches, “safe” or otherwise turn quickly to glucose in any animal that can digest them and all will get the same side effects; it will cause glycation, AGEs, raise insulin, leptin, whether you have blue eyes, brown eyes, are a mouse or a worm… This is the advantage of getting further down, closer to the roots of disease; differences fade away and the commonalities are left to see…and treat.

Yes people are different, but the basics that we are talking about here are not only true for all people but transcends humans and are true for virtually all animal life. It is worth repeating; if you eat a non-fiber carbohydrate (sugar or starch), it will raise your blood sugar, as it would your neighbor’s blood sugar, and it will raise virtually every person’s blood sugar in the world…and every dog’s, and every worm’s blood sugar… In turn, raising glucose raises insulin and leptin and accelerates the rate of aging, and the symptoms of aging, including cardiovascular disease, diabetes, obesity, osteoporosis, and cancer.

OTHER POINTS

Kitavans and Okinawans are poor examples to use in defense of carbohydrates.

I have consistently heard those in the Paleo, higher carbohydrate camp refer to the Kitavans as an example of a population eating a high carbohydrate diet and supposedly being much healthier, and the conclusion often made is that their high carbohydrate diet is causing the improved health of Kitavans.

It’s interesting to look at small subpopulations such as the Kitavans, but not more. Basing dietary recommendations on that is fraught with error. They are a very small, isolated group of people that easily could have certain genetic anomalies that might allow for longevity (even though they don’t particularly live a long life). Kitavans also mostly eat one major meal a day and that offers benefits in spite of any starches since most of the day they are calorie and protein restricting. Both are highly correlated with longevity in many animal studies. Partly because of this they’re much smaller than the average Western population, the average male being 5’4″ tall and female being 5’1″. It is known that smaller members of a species such as dogs live longer, and there is evidence that this may also apply to humans. This is likely related to lower IGF-I levels, a well studied longevity factor in animals. Was this measured in the Kitavans? How about mTOR, also associated with lower protein intake and strongly associated with longevity?

Little mentioned of the Kitavans is their high intake of coconut oil. This is very high in medium chain triglycerides that have been shown to have numerous and powerful metabolic advantages. That is the trouble with population studies. It is impossible to control all of the variables in diet and lifestyle.

But do Kitavans have extended longevity? That’s quite debatable. They do not have a higher number than average of centenarians (if any) and do not apparently have higher than (even post 50 year old to account for high infant death rate) average lifespans.

A serious mistake so frequently made in health and medical studies is confusing correlation with causation. This is well illustrated with virtually all of the studies that correlate cholesterol with heart disease. But even here, in the Kitavan study, the most one can say is that their health and longevity, if indeed they have increased longevity, is correlated with a diet and not caused by it. It could be that the diet is an innocent bystander and that the real cause of their enhanced health is from their short stature and the possibly related low IGF-1 and mTOR. They may even be healthier in spite of their diet.

Being short and thin, with likely low IGF-1 levels, eating a somewhat protein restricted diet high in MCT’s, the Kitavans have several known reasons to live long, healthy lives. Even so, they do not have remarkably long lifespans. It is this that needs to be explained. Why not? Perhaps because they are eating high amounts of starches. In other words, rather than the notion that is being perpetuated by starch proponents that Kitavans live a long, healthy life secondary to eating starches, it could be that whatever health benefits that are being experienced by Kitavans are in spite of the starches rather than because of them. It is very possible, in fact probable, that they would live even longer and healthier lives if they ate a high-fat, very low carbohydrate diet in addition to their other advantages, thus keeping glucose and insulin lower to go along with their likely lower IGF and mTOR.

All one can say is that Kitavans, with their diet of far less junk food, higher (cellulose) vegetables, high MCTs, lower protein, that may help result in short and lean stature likely secondary to lower IGF-1and mTOR (known longevity factors in animals), with their less stressed lifestyle gives them low rates of heart disease and diabetes but with only an average lifespan with few centenarians, that may likely be despite eating starches than because of it. And this is the best example that ‘safe starch’ advocates can come up with??

As far as the Okinawans; simple. They are calorie restricted, eating a diet higher in fish and vegetables, and lower in rice than their mainland counterparts. In the most comprehensive study pertaining to the Okinawan diet and longevity, the following was found;

“Findings include low caloric intake and negative energy balance at younger ages, little weight gain with age, life-long low BMI…and survival patterns consistent with extended mean and maximum life span.”

The study concluded…

“This study lends epidemiologic support for phenotypic benefits of CR in humans and is consistent with the well-known literature on animals with regard to CR phenotypes and healthy aging.”

I have not seen a breakdown of the calories eaten, but since they eat more fish and fibrous vegetables than their mainland counterparts and lower calories, simple logic could conclude that they eat fewer non-fiber carbohydrates, which, along with reduced stress, may account for their increased average lifespan.

Caloric Restriction, the Traditional Okinawan Diet, and Healthy Aging, Annals of the New York Academy of Sciences, Volume 1114, Healthy Aging and Longevity: 3rd International Conference, p 434–455, October 2007

We must understand the limited information allowed by laboratory tests to interpret them properly.

Lowering thyroid (or raising rT3) is not hypothyroidism.

Lowering WBC does not mean impaired immunity, but perhaps less stress on the immune system, or stronger WBCs as far as phagocytic activity, therefore requiring fewer of them. Lowering insulin does not necessarily mean T1 diabetes.

Centenarians and CR (calorie restricted) animals including humans have lower free T3.

I don’t doubt that Paul’s diet is a good one. There lots of good diets and virtually any diet that is different than the typical American diet will be better. But we are not just talking about better. We’re not talking about improving diabetes but reversing diabetes, heart disease, and slowing down the aging process itself. The major benefit of a very low carbohydrate, moderate protein, high-fat diet, and what will get you to the next level of health, is the adaptation to constantly burning fat and ketones and thus requiring less glucose. By forcing the intake of 100 gm or more of glucose into the body you would prevent that adaptation (according to George Cahill) and would prevent experiencing the truly deep benefits of a very low carbohydrate, high-fat diet.

The lowering of free T3 is a sign of that deep adaptation, and, according to Paul, when you follow his diet you prevent the lowering of free T3. That is powerful indication that following a “safe starch” diet is preventing one from changing into a calorie restriction phenotype and preventing the genetic expression and adaptation to deeper maintenance and repair that equates to health and longevity that a very low carbohydrate, high-fat diet would otherwise allow the opportunity for.

Age and Ageing 2010; 39: 723–727

“Down-regulation of thyroid hormones, due to either genetic predisposition or resetting of thyroid function favours longevity.” [emphasis mine]

It is important to understand nature, and to understand what its primary directive is…and its primary directive is not longevity, and certainly not post reproductive health and longevity. For that we have no footsteps to follow. As far as I know, no other species is purposely trying to live a long, healthy post reproductive lifespan. For that we only have the best science go by.

What, or even whom, is evolution selecting for? Evolution does not select for (somatic) longevity. However it wants to keep the genome immortal. If one looks at an individual human or any animal or any life, it can be broken down into the soma, the body, and the germline. The soma is there to take care of the germline and see it through to the next generation. The soma is taking the chromosomal baton that had been handed to it and passing it to the next soma to take care of that chromosomal information so that it too can do the same to the next generation. As such, our germline has stayed immortal since the beginning of life. The soma becomes expendable and takes the environmental hits, the oxidation and glycation and other insults. It is the shield that protects your genetic information from that damage. It is why we even age. Therefore, the only longevity that can be talked about is the immortal longevity of our germline and the “expendableness” of our soma. The longevity of the soma becomes, at least for nature, irrelevant outside of that.

Until we understand that nature cares little for us living a long and healthy life and until we go beyond what is typically “natural”, we will continue to do what is very natural, and it is inevitably natural to get sick and die soon after our children can stand on their own two legs, as it were.

Any discussion of health and medicine should at least take into account the biology of aging.

Life is a constant battle between damage and repair. It is repair that we have the most control over, and is therefore the most important.

As far as damage; there are at least 2 major sources. We have only limited control over oxidation. This, by definition is from oxygen. However, you shouldn’t stop breathing.

Glycation. Don’t eat glucose. Any excursion increases glycation.

Repair; The biology of aging convincingly shows nutrient sensors including insulin for glucose and mTOR for protein, control a genetic pathway that is almost universally conserved among all animal life from single celled yeast onward to humans. Science also is showing that leptin controls the healthy phenotype imparted by calorie restriction in so-called higher organisms that use fat as a primary fuel.

It appears that nature has all sorts of tricks up her sleeve to allow the members of the species to live as long as necessary to impart a reasonable chance of reproductive success. Tricks such as intracellular antioxidant up regulation, DNA repair, increased autophagy (cellular garbage collection), are all enhanced when nature believes this is necessary, including times of hardship such as perceived famine. Those nutrient sensors are controlled by the amount of macronutrients in each meal, sugars and proteins raising all of them…but not fat. When these nutrient pathways are raised, cells are told to multiply and repair is diminished, accelerating aging and increasing risk of cancer in complex multi-celled people.

Paul Jaminet and the other ‘safe starch’ advocates seem to be concentrating only on the on potential damage, or lack thereof, secondary to glucose, including mitochondrial damage. I, along with many biology of aging experts, believe strongly that glucose is a major cause of molecular damage in all life and that it contributes to aging. However, the “accumulated damage” school of aging, especially as it pertains to reactive oxygen species is really quite archaic today. Being ignored is the effect of eating glucose on the above extremely important nutrient sensing pathways that help regulate the genetic expression of extremely powerful repair mechanisms. To dig into this ancient health-promoting pathway, one must simulate glucose deprivation and eat far less glucose forming carbs than recommended by ‘safe starch’ advocates.

Controlling intake of protein is very important. I believe that I was the first low carb advocate to disavow high protein and instead recommend higher fat. I was then and am now extremely confident that I am right. I had plenty of friendly disagreements with the Eades about protein when we worked together, as they believed high was good as did almost all low carb advocates. My public talk/debate with the Eades at ASBP (American Society of Bariatric Physicians) in 2006 that is posted on my site – Protein: The Good, The Bad and The Ugly and several others, where I introduced the science of mTOR and the relationship between protein, cancer, and aging changed a lot of minds about high protein including apparently Jeff Volek and Steve Phinney who are now embracing the lower protein and higher fat diet in their books.

A quote by Oscar Wilde that is very apt, “Everything popular is wrong”…

A low fat diet to lose weight and treat diabetes and even that diabetes is a disease of blood sugar…

Take calcium to strengthen bones…

Cholesterol causes heart disease…

Even low carb advocates pushing high protein…

I have long said these were all wrong, and I have argued against them all for 2 decades…and I will be shown ultimately to be correct on all counts…

I have used my diet to save many lives. I have been fighting for my VLC, high fat and no more than adequate protein diet and the importance of insulin, leptin and mTOR to be accepted, since I am certain this can save millions more. No offense, but comparatively ‘safe starches’ is just a speed bump.

© Copyright 2012 Ron Rosedale, M.D.