Dr Rosedale's Rebuttal of Paul Jaminet Safe Starch Theory - Extract

B ut it is critical to note that this point, where the body’s glucose utilization and needs meet, are a constantly moving target that a person can never consciously know, and therefore one cannot eat accordingly. This is a major point I made in my last response and post on Jimmy’s blog in answer to my question that I had asked, “Is it healthier to consume the required glucose (though much less required than Paul had assumed) or is it better to let the body manufacture its own needs?” I will repost my answer;

Is it healthier to get the glucose, any glucose, from the diet, or from gluconeogenesis? Is it healthier to eat starches, and in fact go out of one’s way to do it, for the necessary glucose, or is it better to let the body make its own from other sources, i.e. gluconeogenesis via glycerol from fat or from lactate and amino acids.

It first needs to be pointed out that in reality one cannot eat a zero carbohydrate/sugar diet. Although not necessary, one will always eat some sugar or sugar forming carbohydrate even on a good very low carbohydrate (VLC) diet. Even plain green vegetables will have some sugar, as will nuts. However, for purposes of this discussion we will assume that a VLC diet has almost no non-fiber, sugar forming carbohydrates.

Eating rice or potatoes or any bolus of starch will result in at least three adverse consequences in everyone.

#1. They will be quickly converted into glucose that will spill into the circulation in a relatively uncontrolled way raising blood glucose as a bolus…in some more than others, but will raise blood glucose significantly in everyone.

#2. This will raise insulin (if one still has functioning islet cells) and it will raise leptin. This is meant for relatively short-term survival, but not so good and has not evolved for a long, post-reproductive and healthy lifespan. The immediate physiological consequences of raising insulin are well known, are in every medical physiology textbook, and was the topic of a talk that I gave 15 years ago “Insulin and its Metabolic Effects“ that is easily found all over the internet. It reduces if not prevents one’s ability to burn fat. This also reduces production of glycerol substrates to make glucose.. It causes fluid retention and sodium retention. It causes vasoconstriction, both increasing blood pressure, etc.

#3. Repeated elevations and insulin and leptin cause insulin and leptin resistance. Now we are into a whole new realm of poor health. Now insulin and leptin are not staying high for a few hours a day, but staying high throughout the entire day…and night, whether one eats or not… Causing more and more insulin and leptin resistance in a vicious cycle until, at least for insulin, the islet cells start burning out…lowering insulin but further raising glucose…and now we are into full-blown diabetes. Raising insulin and leptin repeatedly has extremely adverse consequences that I feel are instrumental in the early onset of virtually all of the chronic diseases of aging and in fact accelerating aging itself..

When glucose is consumed, that bolus of glucose circulates, potentially doing damage before being picked up by the liver for metabolism and controlled redistribution. Eating starch and therefore a bolus of glucose will, at least to some extent, by spiking blood glucose, insulin, and leptin, mimic the stress response.  I, for one, do not need any help with that.

When, however, the liver makes the requisite glucose, the amount and distribution is immediately regulated. The liver will only make what is necessary…unless it has become resistant to signals that tell it what to do, as in insulin and leptin resistance brought about from spiking those hormones by constantly eating boluses of glucose/starch.

Under typical, non stressed conditions, there is far less of an insulin and leptin excursion if glucose is made via gluconeogenesis than if taken by diet. In fact, one of the major signals to shut off gluconeogenesis is elevated insulin.

The ancient, deep brain (as opposed to cortex) and body knows its constantly changing, biologically complex needs far better than ‘thinking’ we do and if kept healthy, will only make the glucose that is necessary. I would far prefer to keep my liver sensitive to the bodies’ signals and let it do its thing, than to think for one minute that I could out-think it by forcing 400 cal. glucose daily [or even 600 cal.]

Eating too few carbs creates a risk of health impairment due to insufficient glucose or protein.

Jaminet is speaking here I assume about what he had previously referred to as “glucose deficiency”. I had refuted the existence of this quite thoroughly in that last post on Jimmy Moore’s blog. There is no such entity in a non clinically hypoglycemic individual. As opposed to my repeating this here, those interested should refer back to that last response.

As far as too few carbs creating insufficient protein; I don’t get the connection there.

The upshot: A 20% carb diet meets the body’s glucose needs without much risk of hyperglycemic toxicity even in diabetics.

I see the shift starting to happen…from a 20% carb diet being healthiest, to now resulting in not too much risk. Just a little more time may be needed for Paul to come over to my camp. As I’ve said, it takes a little time to adapt to my diet; even conceptually…

We have written of the suppression of T3 thyroid hormone levels which is part of the body’s strategy for conserving glucose in times of scarcity, and how this is a risk factor for “euthyroid sick syndrome.” See Carbohydrates and the Thyroid, Aug 24, 2011.

Dr Rosedale acknowledges this (I am not acknowledging that this leads to euthyroid sick thyroid syndrome; quite the opposite) and believes it to be beneficial:

[Rosedale says], “I believe that Jaminet and most others misunderstand the physiologic response to low glucose, and the true meaning of low thyroid. Glucose scarcity (deficiency may be a misnomer) elicits an evolutionary response to perceived low fuel availability. This results in a shift in genetic expression to allow that organism to better survive the perceived famine…. As part of this genetic expression, and as part and parcel of nature’s mechanism to allow the maintenance of health and actually reduce the rate of aging, certain events will take place as seen in caloric restricted animals. These include a reduction in serum glucose, insulin, leptin, and free T3…The reduction in free T3 is of great benefit, reducing temperature, metabolic damage and decreasing catabolism…. We are not talking about a hypothyroid condition. It is a purposeful reduction in thyroid activity to elicit health. Yes, reverse T3 is increased, as this is a normal, healthy, physiologic mechanism to reduce thyroid activity.”

This is an explanation of why this is not “sick thyroid”.