Ron Rosedale , Sunday, November 20, 2011

What’s the big deal about 100 grams of carbohydrate from starch? That’s 1 and 1/2 large baked potatoes, or 2 cups of cooked rice. Paul Jaminet, an astrophysicist from Harvard with a strong interest in health and diet, believes that these so-called “safe starches” are healthy, and that if these are not consumed, one might experience what he calls “a glucose deficiency”. I do not. We have been going back and forth on different blogs debating this.

I believe, quite simply, that all sugars, and foods that convert into sugar, will have a detrimental effect if eaten, and therefore the fewer non-fiber carbohydrates that a person has, the better, and that the difference should be made up by consuming more beneficial fats and oils. Besides that, our diets are fairly similar in that they are both, compared with a standard diet, higher in fat and lower in carbohydrates. My view is considered extreme by some, including many in the ‘safe starch’ camp who do not believe that glucose should be looked upon as that detrimental. I also realize that not eating any foods that can convert into glucose is, from a practical sense, impossible. I recommend that people have all the vegetables that they want, except for the overly sugary ones such as corn and beets. This makes our diets that much closer. Then why is this debate such a big deal?

One may think that a bowl of rice difference in carbohydrate per day in a diet is a small difference, and perhaps it is, but I also believe that that small difference can make a big difference, especially in those with overt diseases such as diabetes and heart disease. Furthermore, I believe that we all have, at least some degree, corruption in insulin and leptin signaling, that lie at the heart of the chronic diseases of aging such as (type 2) diabetes, cardiovascular disease, osteoporosis, obesity, and even many cancers, and therefore everyone can and should benefit from an optimal, not just better, diet. I had written a book a number of years back entitled The Rosedale Diet that talked about the connection between insulin, leptin, and the diseases of aging, especially obesity. I believe that diet to be the most scientifically advanced diet in the world, that has been shown to mimic the effects of calorie cutting on health and youthful life extension, without having to even think about cutting calories.

There are three major reasons why I believe it is very important to carry this discussion forward as far as possible. Firstly, I feel that what a person eats is instrumental in determining health. Secondly, I feel that it is extremely important for people to know the truth in science, whether or not it is “politically correct”, or, as Al Gore has stated “inconvenient”. This way they can make their own educated decisions about what to eat and whether it is “worth it”. This debate is about what constitutes an optimal or“perfect health diet” that is the name of Jaminet’s book. If one wants to deviate from that and have a few more likely subclinical ramifications such as glycated molecules, or resistant receptors, to enjoy a bowl of rice, that is up to them. I just do not want that person to think it is healthy to do so. It should be looked upon as we view a piece of chocolate cream pie; unhealthy, but we want it now anyway, and not that we are biologically better off for having eaten it. The point is that there is no such thing as a glucose deficiency or a healthy need to eat starches. If one wants to endure a bit of tolerable biological harm for some momentary pleasure, that’s great, but the person should know what he/she is doing. I drive occasionally without a seatbelt, but I do not want anyone telling me that this is safe. If there is some unbelievably great bread at a restaurant, I might have a small bit, and savor it, not because I am deluded into thinking it is healthy, but because I am willing to take the risk.

The third reason is less philosophical and more basic scientifically. I believe that many venues of science, from basic physiology to the biology and genetics of aging point to a simple, but very powerful statement concerning health, that I have stated for many years and has yet to be disproven. That is; one’s health and lifespan will be determined by the proportion of fat versus sugar that one burns over a lifetime. The more fatty acids and Keto OS from fat that you burn, the healthier you will be and the longer you will likely live. The more glucose that is burned as fuel, the more unhealthy you will be, the faster you will age, and the sooner you will likely die.. This, of course, is predicated on not getting hit by a semi truck. There are no absolutes. It is the chance of disease or health that I want to swing in our favor.

This brings us back to that bowl of rice that is the basis of the difference of Paul’s and my diet. That rice consumption spread throughout the day may, at least for a significant part of that day, prevent one from burning fat. Also, the biochemical and hormonal basis of the extreme health and longevity advantages of calorie restriction that has been shown for over 80 years is being uncovered, and it appears we can use that knowledge applied to diet without calorie restricting to experience the same or similar benefits (that is what I’ve done with The Rosedale Diet). Once again, eating that bowl of rice may undo that powerful effect.

There appears to me to be, not a point of diminishing returns by further reducing carbohydrate consumption (without increasing protein consumption, but by increasing beneficial fats and oils), but a point of accelerating returns the lower one goes below that 100 g of glucose consumption.

This debate started on Jimmy Moore’s fine blog where paleo and low-carb luminaries give their opinion for or against safe starches that was followed by a post on that blog by Jaminet, that was then followed by an even more extensive rebuttal on Jimmy’s blog by me. Jaminet then followed with a long reply on his blog and this was all summarized in Joe Mercola’s extremely popular newsletter just before Thanksgiving. I am now replying here to Jaminet’s last blog. Did you follow all that? No matter.

The debate continues. My rebuttal to Paul Jaminet’s last blog espousing the benefits of “safe starches” follows. Paul has been a gentleman throughout this discourse, and I only can hope to follow suit. I hope that no offense is taken, and that the effort at education for both the audience and myself is what shines through.

We very much wish to extend our appreciation to Joe Mercola, Jimmy Moore , and Paul Jaminet for their active participation, promotion and dissemination of the discussion from their websites. We hope you find this debate both enjoyable and educational. We Look forward to hearing your thoughts and opinions.

I start with Paul Jaminet; “Dr Rosedale argues that glucose is toxic, so we should want to have less of it in our bodies; and that low-carb diets deliver less of it. He cites a lot of papers on the relationship between blood glucose levels and health, and uses blood glucose levels as a proxy for the level of glucose in the body.”

The studies presented previously on glucose levels and health are to be taken as a whole to show that there is no threshold for a safe level of blood glucose that Paul has based his ‘safe starch’ recommendations on; no more, no less. That glucose can be toxic is very well known, however it is the effect of glucose on hormonal signals that is the most important.

Jaminet continues, “Two basic matters are at issue: (1) What blood glucose level is best for health? (2) Which diet will generate those optimal blood glucose levels?”

I have said often that we must get to the root of a problem, and that would certainly pertain to this discussion. I believe that the issues stated above are not the root issues that I have frequently referred to in the prior posts. The issue does not have much to do with blood glucose levels per se, but much more to do with the effects of glucose on nutrient signaling, in particular leptin and insulin.

As I have also so often stated, all disease is a disease of communication. This is particularly true with biological illness, but also happens with any form of communication, including written. There appears to have been a miscommunication resulting in a misunderstanding of what the primary issue(s) is (are). This must be clarified to arrive at appropriate answers.

The fundamental claim by Paul, as far as his diet is concerned, is that ‘safe starches’ are, well, safe, and do no harm and in fact are healthy to include to prevent what Paul terms a ‘glucose deficiency’.

So, we must keep that in mind as the major point of Jaminet’s argument. Paul’s new point above, “What blood glucose level is best for health?” circumvents the ‘safe starch’ threshold of damage issue, perhaps admitting that there is none, and now essentially asks, what levels of glucose might be the most ‘tolerably harmful’, that I had coined in the last post. This is not just a play on words. It rightfully acknowledges that glucose will cause some degree of damage at virtually any level, as I had previously maintained, and now puts the onus of health on the repair of that damage.

This is as it should be. In other words, the fundamental question should be stated as such;

Is there a diet (Rosedale’s or Jaminet’s) or glucose (starch) intake that can better maximize the repair/damage ratio that life, health, and youthful longevity depends on, admitting the inevitability of damage from glucose at any level? It is important to recognize that this is not just dependent on baseline levels of glucose, but more on the effects of the repeated glucose spikes that are known to occur from eating starches, ‘safe’ or otherwise, on critical hormones, particularly insulin and leptin, that ‘sense’ the amount of glucose and powerfully adjust the genetic expression of repair and the longevity phenotype depending on perceived nutritional circumstance.

I give a summary and conclusion near the end of this article that answers this very important question that is critical to determining an optimal diet. Those wanting the ‘Cliff Notes’ version of this rather long post can go directly there. Those wanting more details and my latest full rebuttal to Jaminet’s latest ‘safe starch’ arguments, read on.

Let’s see if Jaminet addresses this primary repair/damage ratio question.

From here I will comment (in black) after passages from Paul’s last blog (in red). Some links and more relevant statements from studies will be in blue.

Let’s look at what the evidence shows.

What Blood Glucose Level is Best for Health?

In my [Jaminet's] main reply I had written: What is a dangerous level of blood glucose?

In diabetics, there seems to be no detectable health risk from glucose levels up to 140 mg/dl, but higher levels have risks… In people not diagnosed with diabetes, there is also some evidence for risks above 140 mg/dl.

Dr Rosedale seemed to feel that this was the weakest point in my argument, and directed his fire here. My statement was a description of what the scientific literature shows, and the adjective “detectable” carries a lot of weight here. To refute my statement, you would have to find study subjects whose blood glucose never goes above 140 mg/dl, and yet show health impairments attributable to glucose.

… and many studies have been found that show that, at least for a short period of time, damage from glycation and other adverse molecular events occur with far lower blood glucose. Jaminet has admitted as much by stating below, “the number of glycation reactions may be proportional to the concentration of glucose, and if glycation products are health damaging toxins then toxicity may be proportional to glucose levels..”

Indeed, glycation events have been shown to be very damaging to health. On the other hand, to support Jaminet’s claim, even if it were true that glucose must rise above 140 to cause damage and that therefore his higher carbohydrate diet is ‘safe’, one would have to show that in everyone eating Jaminet’s diet, blood sugar never went above 140. Obviously, this cannot feasibly be shown, so one has to use the best science available to extrapolate most accurately. All human studies pertaining to health and longevity are inferences and not proofs as, I’m sure Jaminet will agree, it is not feasible to carry these experiments out lifelong in people.

It is true that the word “detectable” carries a lot of weight when it comes to health risk. For instance, if one is just looking for a person to drop dead in the next couple of hours after consuming high glycemic starches, then in most cases the risk of glucose would not be detectable. But not in all;

When speaking of his research linking glucose spikes to endothelial dysfunction;

“The Acute Effect of Various Glycemic Index Dietary Carbohydrates on Endothelial Function in Nondiabetic Overweight and Obese Subjects”

J. Am. Coll. Cardiol. 2009;53;2283-2287

Dr. Shechter states, “..doctors know that high glycemic foods rapidly increase blood sugar. Those who binge on these foods have a greater chance of sudden death from heart attack. Our research connects the dots…”

However, as one looks deeper to detect adverse effects from raising insulin, leptin, or glycation, then yes, there would be detectable levels of health risk from even a single glucose excursion. In the last post I cited studies showing such risk.

Dr. Rosedale argues there is no threshold separating safe from harmful levels of glucose, because glucose acts as a toxin at all concentrations:

[Dr. Rosedale states]; “I will spend a fair amount of time and show a fair number of studies to show that there is no threshold. Very simply, the higher the blood sugar rise, the more damage is done in some linear upward slope.”

I emailed Ron to make sure that he really did mean there was no threshold, so that glycemic toxicity begins at 0 mg/dl. He replied:

[Dr. Rosedale]; “I mean the former; that glucose will cause some damage when above 0 mg/dl … obviously a moot point and theoretical when glucose very low and incompatible with life and likely a minute amount of damage when that low. At any level of glucose compatible with life some more meaningful degree of glycation, hormonal response and genetic expression will take place. We will always want/need to repair the damage done to stay alive, but with age the repair mechanisms become damaged also. Eventually damage outdoes repair and we “age”, acquire chronic disease, and die.”

Ron’s view can be graphed like this:

This view makes sense as a matter of molecular chemistry: the number of glycation reactions may be proportional to the concentration of glucose, and if glycation products are health damaging toxins then toxicity may be proportional to glucose levels. Good graph Paul; thanks.

The trouble with this is that it doesn’t really get at what we want to know: what blood glucose level optimizes human health?

Actually, what we really want to know is what level of glucose consumption optimizes human health. The consumption of glucose causes a much wider range of effects than just affecting baseline, fasting blood glucose. It causes large excursions in blood glucose temporarily at least. It effects nutrient signals that are perhaps the most powerful hormones in the body that detect nutrient levels, and have an extremely powerful effect on energy use and storage and genetic expression of health (or not), as I discuss more later.

If we change the y-axis so that it doesn’t measure glycemic toxicity, but rather overall health of the human organism, then the shape of the curve is going to change in two major ways:

First, in translating toxicity to its impact on health, we have to account for Paracelsus’s rule: “the dose makes the poison.” The body can readily repair small doses of a toxin with no ill effect – possibly even a hormetic benefit – but large doses of a toxin multiply damage exponentially and can prove fatal. So the impact of a toxin on health will not rise linearly, but non-linearly with a steeper slope as one moves to the right.

Second, we have to account for the fact that glucose has a role as a nutrient. As Ron himself says, having too little blood glucose is “incompatible with life.” So low blood glucose – depriving us of the benefits of normal levels of this nutrient – is a catastrophic negative for health. This means that the left side of the curve needs radical adjustment.

With these two changes, our graph becomes something like this:

It now has a U-shape.

I must point out, as Paul did, that it is not the previous graph that has changed. The prior graph remains unchanged. This is now a completely different graph with a totally different y-axis. The prior graph remains valid and shows detriment with increasing glucose.

Jaminet does bring up the matter of repair here, “The body can readily repair small doses of a toxin…” but I don’t believe this is discussed further by Jaminet, as he focuses, as we have done previously, on risk of damage. However, the issue of repair is paramount. Not only is the damage that life encounters somewhat variable, but the ability of a life to repair that damage is also quite variable, and depends to a large extent on genetic expression of repair mechanisms, such as intracellular (from within the cell; not from eating them) antioxidant manufacture, heat shock proteins, DNA repair mechanisms, waste removal (autophagy), and other tricks that nature has to keep a life alive, if nature believes that is beneficial. That genetic expression is, in turn, largely regulated by nutrient level detecting hormones, of which insulin, leptin and mTOR are primary, and they in turn are controlled by what you eat. Therefore, what a person eats can turn up repair, or lower it, and this arguably is the most important impact of diet on health and longevity, and must be primary when recommending a diet to promote health and longevity. That brings us back to how I had stated earlier the major issue here should be expressed; which diet, Jaminet’s or Rosedale’s best up-regulates the repair vs. damage equation. I discuss this more near the end of this post.

I’ve drawn the inflection point where toxicity starts rising rapidly at around 140 mg/dl, and the inflection point on the other side where hypoglycemia causes substantial health damage at around 60 mg/dl. But the precise numbers don’t matter much; the point is that there is a U-shape, and somewhere in that U is a bottom where health is optimized. [my emphasis]

I believe, that there is a very important clarification that needs to be made here, at least as it concerns this current post. Fasting glucose, and therefore this graph, will be pertinent in showing perhaps a correlation between fasting glucose and health, and perhaps more importantly if changing fasting glucose levels changes that correlation. The point of the studies that I cited previously pertaining to glucose levels was to show that there is no specific threshold for glucose above baseline that determines health or not, as Jaminet believes. I do not believe, nor might Jaminet, that fasting blood glucose is the sine qua non for health, and it should not be used as such. Again, it is the excursions in glucose and effects on corrupting insulin and leptin signaling that are much more significant. Therefore, most of the remainder of Jaminet’s post that deals only with potential risk to health of glucose levels takes on less significance, but let’s look further for more clarifications and explanations.

What do we know about the precise shape of that U, and the location of the bottom?

We can’t intuit the shape of the bottom of the U using theoretical speculations. Theory doesn’t allow us to balance risks of hypoglycemia against toxicity on such a fine scale.

Empirical evidence is limited. Most studies relating blood glucose levels to health have been done on diabetics eating high-carb diets. There are few studies on healthy people… Actually, most of the studies that I cited in my last response were on ‘healthy’ people.

His first cite is “Is there a glycemic threshold for mortality risk?” from Diabetes Care, May 1999,http://pmid.us/10332668.

For both fasting and 2-h postprandial blood glucose, the [relative risk of death was] lowest between about 4.5 and 6.0 mmol/l, which translates to 81 to 108 mg/dl. However, note that there is very little rise in mortality – only about 10% higher relative risk – in 2-h glucose levels of 7 mmol/l, which is 126 mg/dl. Since the postprandial peak is rarely at 2-h (45 min is a common peak), most of these people may well have been experiencing peak levels above 140 mg/dl. [emphasis mine]

That is a possibility but still speculative. In this study we do not know. Some people might have gone above 140, some might not have; just like the general population that might eat Jaminet’s diet. This is important, as Paul claims risk only above 140, not at or below.

I also find it quite doubtful that those following Pauls’s diet will consistently measure postprandial glucose after a “safe starch” meal to make sure that blood glucose has always stayed below 140. In fact, that likely will not happen in anyone all of the time given the variability in environmental circumstances such as daily stress and sleep.

I find it particularly interesting when Jaminet says above that “there is very little rise in mortality – only about 10% higher relative risk – in 2-h glucose levels of 7 mmol/l, which is 126 mg/dl.” Is he going from saying that keeping sugars under 140 is completely safe, to now saying that a 10% rise in risk is minimal and apparently acceptable for those whose 2 hr glucose is under 140, or saying that in all of these people their glucose must have risen above 140?

However, when one is looking only at glucose, one is looking only at the tip of an iceberg. It is what’s going on underneath (insulin, leptin) that is much more significant. If it was only blood sugar, than the initial graph would still hold, showing an increase in glycation correlating with an increase in glucose. Jaminet has even admitted as much. But we know there is more to the story.

My [Jaminet] interpretation: I would say that this study demonstrates that mortality is a U-shaped function of blood glucose levels, but it doesn’t tell us the shape of the bottom of the U. It is consistent with the idea that significant health impairment occurs only with excursions of blood glucose above 140 mg/dl or below 60 mg/dl.

That would depend what one’s definition of significant is. What the study illustrates is that there is a 10% additional risk of death at 126 mg, that is significant to me, and that is well below Paul’s safe limit of 140 mg and is at a level that most people would obtain after eating what Jaminet refers to as ‘safe starches’. There is added risk at any level above a relatively low baseline, and that was my point. The study does show a U-curve with 2 hr glucose, less so with fasting, with the bottom of the curve showing the mortality as stated in the conclusion of the paper; the lowest mortality is with glucose levels averaging approximately 90 fasting and 100 mg/dl 2 hrs after a glucose load. Does this study add support to the author’s premise, and mine, that there is no glycemic threshold above baseline (and above that which is overtly hypoglycemic) that is healthy and below which is not. Yes it does.

I will once again repeat the conclusion of the authors;

CONCLUSIONS: In the Paris Prospective Study, there were no clear thresholds for fasting or 2-h glucose concentrations above which mortality sharply increased; in the upper levels of the glucose distributions, the risk of death progressively increased with increasing fasting and 2-h glucose concentrations.

Jaminet saying that there was only a 10% increase in mortality at 126 mg supports their conclusion and mine… that there is a gradual increase in mortality above a baseline of approximately 90 mg/dl that Jaminet previously called safe. To fit his paradigm, he must assume that in all of these people, their blood glucose rose above 140 mg/dl at some point, and there is no evidence to support that, and indeed that is not feesible.

Dr Rosedale’s second cite is actually to a commentary: “‘Normal’ blood glucose and coronary risk” in the British Medical Journal, http://pmid.us/11141131, commenting on a paper by Khaw et al, “Glycated haemoglobin, diabetes, and mortality in men in Norfolk cohort of european prospective investigation of cancer and nutrition (EPIC-Norfolk),” http://pmid.us/11141143.

This study used glycated hemoglobin, HbA1c, which can serve as a measure of average blood glucose over the preceding ~3 weeks. (As a point of fact, HbA1C actually is meant to indicate blood glucose over 3 months.)

This supports the “blood sugar should be as low as possible” thesis, since lower HbA1c levels were associated with lower mortality. However, this study has a few flaws:

It includes diabetics. Diabetics have poor glycemic control, and episodes of hypoglycemia as well as hyperglycemia, so HbA1c levels (which represent average blood sugar levels) may be a poor proxy for the levels of glycemic toxicity. Also, diabetics are usually on blood-glucose lowering medication, which may distort the blood sugar – mortality relationship.

It lumps the population together in very large cohorts. Effectively there were only three cohorts, since the highest HbA1c cohort had only 2% of the sample; the other three cohorts contained 27%, 36%, and 36% of the study population respectively.

We can get a finer grip on what happens by looking at studies that lack these flaws. Here’s one: “Low hemoglobin A1c and risk of all-cause mortality among US adults without diabetes,”Circulation, 2010, http://pmid.us/20923991.

This study is an an analysis of NHANES III; it excludes diabetics and has 3 cohorts, not 1, with HbA1c below 5%. The U-shaped mortality curve is very clear. In raw data and all models, the lowest mortality is with HbA1c between 5.0 and 5.4. Mortality increases with every step down in HbA1c: in Model 1, mortality is 8% higher with HbA1c between 4.5 and 4.9, 31% higher between 4.0 and 4.4, and 273% higher below 4.0.

So the minimum mortality HbA1c range of 5.0 to 5.4 translates to an average blood glucose level of 96.8 to 108.3 mg/dl (5.36 to 6.00 mmol/l). This result is almost identical to the finding in Dr Rosedale’s first cite, from which Dr Rosedale quoted: “the lowest observed death rates were in the intervals centered on 5.5 mmol/l [99mg/dl] for fasting glucose.”

My interpretation: Once again, we find that there is a U-shaped mortality curve, and minimum mortality occurs with average or fasting blood glucose in the middle of the normal range – in the vicinity of 100 mg/dl or 5.5 mmol/l.

I’m really not sure what the point is that Jaminet is making. That too low of blood glucose can be detrimental? Certainly, especially under certain unhealthy circumstances that may or may not have anything directly to do with the glucose per se. Low average glucose can occur with adrenal insufficiency such that cortisol levels are inadequate, or growth hormone deficiency, etc. Certainly, just like with the thyroid studies that he has pointed out below and that I believe are misunderstood, the detrimental effects of lowering glucose would be determined by how and why it is being done; as part of illness, or as part of a physiological and “purposeful” regulation to extend longevity. Lower than typical blood glucose is found in almost all models of extended lifespan (and healthspan) including caloric restriction and centenarians. What this study once again shows is an incremental increase in mortality far below a glucose level that Paul has said is healthy. This study once again supports my contention that the increase in blood sugar brought about by eating ‘safe starches’ is anything but safe.

Let’s finish our examination of this issue with a quick look at Dr Rosedale’s third cite. (Does this mean that Paul is OK with the other 17 or so studies that I had cited previously showing a detriment of glucose at levels well below those that Jaminet had proposed were safe? That would be a pretty good batting average.) That paper, “Post-challenge blood glucose concentration and stroke mortality rates in non-diabetic men in London: 38-year follow-up of the original Whitehall prospective cohort study,”Diabetologia, http://pmid.us/18438641, is a familiar one; it was cited in our book (p 36, fn 35).

This study looked at blood glucose levels 2 hours after swallowing 50 grams of glucose, and then followed the men for 38 years to observe mortality rates. CarbSane makes an important observation: this study used whole blood rather than plasma to assay blood glucose. Whole blood has more volume (due to inclusion of cells) but the same glucose, and so less glucose per deciliter. According to this paper, standard (plasma) values are about 25 mg/dl higher, so 95 mg/dl in whole blood actually corresponds to a plasma value of about 120 mg/dl.

That was a 1965 paper. There have been considerable advances in the measurement of glucose since then, such that the differences are less, though still present. Actually, to convert from whole-blood glucose, multiplication by 1.10 (~10% difference) has been shown to generally give the serum/plasma level…

From the Joslin Diabetes Center at Harvard website; “The difference is that plasma numbers read about 10 – 12% higher than the older whole blood numbers. So if your fasting and pre-meal blood glucose target is 90 – 130 mg/dl plasma glucose, it would be 80 – 120 mg/dl if your meter reads whole blood.”

Though this is known among clinicians in the field, without having clinical experience, CarbSane would not know this. Furthermore, anyone checking glucose using a home monitor (other than perhaps some newer ones calculating serum glucose), is using whole blood.

The diagnosis of diabetes, by conventional standards, (though I believe that diabetes ought to be diagnosed by insulin and leptin values rather than blood glucose), is defined as a fasting plasma/serum measurement of 126. Using the conversion factor that Jaminet indicates would translate to a blood monitor level of 101. That, in turn, would translate to a whole lot more diabetics, that may benefit to a greater extent, as he mentioned in Jimmy Moore’s post, by using a more “diabetic” diet such as mine. My statement that we all should be treated as diabetics would start to ring true.

There is no significant difference in mortality among any group with post-challenge whole blood glucose up to 5.29 mmol/l (95 mg/dl), corresponding to 120 mg/dl or 6.7 mmol/l in standard measurements..

(…or 105 mg/dl if the correct conversion factor was used.)

My [Jaminet] interpretation: This study wasn’t designed to observe the lower end of the U. At the higher end, it is consistent with the other studies: mortality rises with 2-hr plasma glucose above 120 mg/dl.

Actually in this study, mortality correctly rises significantly above 95 mg/dl blood, but that correlates to 105 mg/dl plasma if the much more modern and accurate conversion of 10% is used. This again is far lower than the 140 mg/dl that Jaminet has deemed safe.

Summary: Optimal Blood Glucose Levels

All of the papers cited by Dr Rosedale are consistent with this story:

1. Mortality and health have a U-shaped relationship with blood glucose.

2. Optimum health occurs at blood glucose levels around 100 mg/dl – at normal levels, not exceptionally low levels.

It does not show this. It shows a correlation with lower mortality of fasting blood glucose at approximately 90-100 mg/dl. This is not the same. There is more to health than just fasting blood glucose. Excursions in blood glucose are at least as important.

3. The impaired health seen with fasting or 2-hr blood glucose levels of 110 or 120 mg/dl may be largely attributable to the portion of the day in which those people experience blood glucose levels over 140 mg/dl.

This is not indicated in any of these studies, or the many studies that I cited previously … It is possible, but so then is any speculation of impaired health. It could be due to that portion of the day in which people were in car accidents as they were texting on their phone… in other words, since other variables were not measured, we can speculate about any other cause other than the most likely and that all the studies cited here and in my last post point to; that elevations in glucose above baseline are not healthy.

I should note that Dr Rosedale acknowledges that high-normal blood glucose is better than low blood glucose for some aspects of health, like fertility:

[Rosedale said]; “Safe starch proponents say that raising blood glucose and raising insulin is a very natural phenomenon and needn’t be avoided. However, if we evolved in a certain way and with certain physiologic responses to the way we eat, it was not for a long, healthy, post-reproductive lifespan. It was for reproductive success. The two are not at all synonymous, in fact often antagonistic.”

He’s saying that higher blood glucose favors “reproductive success,” while lower blood glucose favors “post-reproductive lifespan.”

Not exactly, but partly correct never-the-less. Keeping blood glucose low even after eating does favor a longer and healthy post-reproductive life. What I did indicate was that ‘safe starch’ proponents should not use the proposition that since raising blood sugar is a natural phenomenon, that it is a reason for that being healthy. Nature’s concern for us only goes so far; namely for us to be healthy to have reproductive success, after which she loses interest. It is also natural to die, but we are reading this to avoid that natural event. I have no qualms about saying that what I’m doing and teaching to be healthy is quite unnatural, as it is the quest to be able to live a long, happy, and youthful life after making babies. Humans appear to be unique in that quest. This concern of nature and evolution began with the beginning of life to include single-celled organisms…like the 15 or so trillion cells that make you up. Increasing pressure to make more cells can increase risk of cancer, that elevations in glucose can promote. Many studies are now showing a correlation between glucose and insulin levels and cancer risk. However, large, multi-celled walking and talking organisms such as us can still reduce risk of cells multiplying in excess, while still even increasing our ability to make multi-celled babies. Insulin resistance, and especially leptin resistance is powerfully associated with infertility. One of the best ways to improve fertility is to improve leptin signaling that my diet has been shown to do.

I guess one has to choose one’s priorities. Not everyone will choose maximum lifespan.

They should…since extending maximal lifespan (as opposed to average lifespan) also entails extending “youthspan” and healthspan.

But suppose Dr Rosedale is right, and that low blood glucose levels are most desirable for at least some persons. I’m willing to stipulate, for the sake of argument, that optimal health for some persons may occur at below-normal blood glucose levels – say, 80 mg/dl. That brings us to the second issue: which diet will produce these low blood glucose levels?

Which Diet Minimizes Blood Glucose Levels?

If the key to health is achieving below-normal blood glucose levels, then low-carb diets are in trouble.

My low-carb diet is not, and that is far from the key to health.

In general, very low-carb diets tend to raise fasting blood glucose and 2-hr glucose levels in response to an oral glucose tolerance test.

This is a well-known phenomenon in the low-carb community. When I ate a very low-carb diet, my fasting blood glucose was typically 104 mg/dl. Peter Dobromylskyj of Hyperlipid has reported the same effect: his fasting blood glucose is over 100 mg/dl.

I don’t agree that low carb diets raise fasting BG (blood glucose) levels; perhaps certain kinds do, such as high-protein diets. I have never seen this in people following my diet; only in those perhaps who were following a high protein diet. I have treated many dozens of people, diabetics and otherwise, who have supposedly been on other low carbohydrate diets, and lowered their blood sugars considerably when I put them on my diet, that generally entailed reducing protein while increasing fat.

However a main point of my argument is that BG levels are only a small part of the story; What higher carb intake does to insulin and leptin is even more important; it raises them promoting insulin and leptin resistance.

From one of Peter’s posts:

Back in mid summer 2007 there was this thread on the Bernstein forum. Mark, posting as iwilsmar, asked about his gradual yet progressively rising fasting blood glucose (FBG) level over a 10 year period of paleolithic LC eating. Always eating less than 30g carbohydrate per day. Initially on LC his blood glucose was 83mg/dl but it has crept up, year by year, until now his FBG is up to 115mg/dl….

A high protein diet that many, if not most in the paleo community adopt by substituting protein for carbohydrates, is not healthy. I have noticed higher BG from higher protein diets many times, compared to my recommended higher (beneficial fat) diet with lower protein.

I’ve been thinking about this for some time as my own FBG is usually five point something mmol/l whole blood. Converting my whole blood values to Mark’s USA plasma values, this works out at about 100-120mg/dl.

Peter notes that low-carb dieters will generally perform poorly on glucose tolerance tests, but that increasing carb intake to about 30% of calories is sufficient to produce a normal response to a glucose challenge:

Again, a GTT is not at all sufficient to assess metabolic health. It is necessary to know the ihe insulin and leptin response. At the least, an insulin level measured concurrently with each glucose is necessary for any meaningful results pertaining to health. I must keep saying this; diabetes, and health, are not primarily a disease of glucose. They are a disease of improper signals being given to glucose, especially those coming from insulin and leptin. These need to be measured to have any meaningful idea about the roots of health. They effect many other, even more significant aspects of health, such as a massive shift in genetic expression. Though a mistake to focus on fasting blood glucose only as an index of diabetes or health as is conventionally being done, I must say that it is my experience that fasting glucose is uniformly reduced on my diet… as are insulin and leptin levels. I do not think that Paul can say the same.

The general opinion in LC circles is that you need 150g of carbohydrate per day for three days before an oral glucose tolerance test.

Not in the low carb circles that I have kept; in the low carb circles of those of us who helped found the field, or in those circles of clinicians who have regularly treated patients with glucose problems. You cite Jeff Volek’s work below. Let’s look at another of his papers;

Comparison of a Very Low-Carbohydrate and Low Fat Diet on Fasting Lipids, LDL Subclasses, Insulin Resistance, and Postprandial Lipemic Responses in Overweight Women

Journal of the American College of Nutrition, Vol.23, No.2, 177–184

Numbers given in order; baseline, very low carb, high carb;

Glucose(mg/dL) 86 83 88

Insulin(pmol/L) 41 37 50

InsulinResistanceHOMA 1.28 1.10 1.63

Please note that a very low 9%, 28 gm. carbohydrate diet did not raise blood glucose, in fact kept it in a healthy range. What’s more important is that it did so concurrent with lowering insulin, thus improving insulin sensitivity. The high carb diet also kept blood glucose low, and if this is all that was looked at, there would be little to conclude. However the real and big story is that the high carb diet kept the BG down at the expense of raising insulin significantly, and thus worsening insulin resistance, and this is a very detrimental effect to overall health, risk of virtually all chronic diseases of aging, and confers a high risk to shortened lifespan. I will emphasize again; only measuring blood glucose without knowing what insulin and leptin are doing gives very incomplete and often misleading information when it comes to effects of any intervention such as diet. Basing conclusions on this is fraught with danger. This is also why the standard of current medical care for diabetics generally makes them worse. (See results of the ACCORD study.)

Although I did show many studies showing the correlation of glucose on aspects of health and even mortality, it was done to disprove the notion that only glucose above 140 is detrimental, which they did, including in context of studies pertaining to insulin and leptin. The conclusion based on the totality of those studies was that detriments of glucose on various aspects of health are seen well below values that Jaminet claims are safe.

This is at the high end of the 20% to 30% of energy (400 to 600 calories on a 2000 calorie diet) that is the Perfect Health Diet recommendation for carbs.

The Kitavans eat more than 60% of calories as carbohydrate, mostly from starches. Their fasting blood glucose averages 3.7 mmol/l (67 mg/dl) (http://pmid.us/12817903).

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 is drawn that the high carbohydrate diet is causing the improved health.

Trying to draw conclusions from population groups is extremely difficult and can lead to very poor science. There are far too many variables to fully account for, and the best one can do is associate a particular variables such as a high carbohydrate diet with health. However, association does not mean cause, as I have talked so often about pertaining to cholesterol studies.

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.

How about this for a variable that I do not hear accounted for much pertaining to Kitavans;

“Should we be concerned over increasing body height and weight.”

Experimental Gerontology 44 (2009) 83–92

“Researchers have found that people in traditional societies have much lower rates of certain chronic diseases compared to developed populations . Virtually all of these populations are much shorter than northern Europeans…Kitavan males have averaged 163 cm (5’4″) and females 155 cm (5’1″) for several generations…The greater longevity of smaller animals within the same species became widely known when it was found that mice fed low calorie diets grew to be smaller than normal but had extended longevities.”

BMI and weight: their relation to diabetes, CVD, cancer and all cause mortality. In: Samaras, T. (Ed.), Human Body Size and The Laws of Scaling:

Physiological, Performance, Growth, Longevity and Ecological Ramifications.

Nova Science Publishers, New York, pp. 113–146.

“Shorter people experience lower BMI, lower levels of various risk factors for CHD, diabetes, and all-cause mortality, such as glucose, insulin, IGF-1, CRP, homocysteine, Apo B, total cholesterol, triglycerides, and LDL; however, they experience higher levels of desirable HDL, Apo A and SHBG.”

Why are they short? Kitavans eat less protein than in western societies, most of which is concentrated in 1 meal, further reducing IGF and mTOR, both of which have been shown to extend longevity.

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

All one can say is that Kitavans with their diet of far less junk food, lower protein, higher (cellulose) vegetables, high MCTs, that may help result in short and lean stature, with their less stressed lifestyle gives them low rates of heart disease and diabetes but with an approximately average lifespan with few centenarians. I don’t understand what the big deal is there.

I would not hang my hat on Kitavans as a reason to eat carbohydrates, as the hatrack is not secure. I don’t know about you, but I am striving for better health than revealed by the Kitavans.

Studies confirm that high-carb diets tend to lower fasting glucose and to lower the blood glucose response to a glucose challenge. CarbSane forwarded me some illustrative studies:

“High-carbohydrate, high-fiber diets increase peripheral insulin sensitivity in healthy young and old adults,” http://pmid.us/2168124. Switching healthy adults to a higher carb diet reduced fasting blood glucose from 5.3 to 5.1 mmol/L (95.5 to 91.9 mg/dl) and reduced fasting insulin from 66 to 49.5 pmol/l.

I will spend a bit of time going over this and the next study cited by CarbSane and presented here, as they are excellent examples of really bad science (if that word should even be used at all) that are very misleading, and they in no way support the position that increasing carbohydrate intake is healthy… at best perhaps only somewhat less unhealthy than worse diets.

In the prior study, let’s look at the feeding method;

“In the young subjects the usual ad libitum (control) diet composition was determined from a 2-wk dietary recall [that many studies have shown fail to 'remember' the unhealthiest foods. No one wants you to know that they downed a pizza chased by a hot fudge sunday as a midnight snack]. The HCF [high carbohydrate/fiber] diet was prepared in the metabolic kitchen at MIT and consumed by the subjects under supervision.”

Yup; an even playing field. The usual at home, unsupervised, ad-lib diet that could be recalled from 2 weeks prior, was compared to a very high fiber diet consumed under supervision containing on average 60 grams more fiber than the 15 gm “control” daily, the vast majority of which was insoluble and thus, though virtually totally excreted, is counted toward calorie intake. Have any of you tried to eat 75 grams of fiber daily? That’s 22 tablespoons of Metamucil a day.. Talk about in and out..

This study compared a standard high fat, high carb, low fiber diet to a diet much higher in fiber. I have stated innumerable times that the typical diet is so bad that making any changes to it leads to improvement. The worst diet to be on is a high fat, high carbohydrate diet, as the (non-fiber) carbs prevents the fats from being burned. In this case the high fat, high non-fiber carb diet was being compared to a low fat, very high fiber high carb diet.

Jaminet uses another study from CarbSane;

“Effect of high glucose and high sucrose diets on glucose tolerance of normal men,”http://pmid.us/4707966. On diets with glucose as the only carb source, 2-hr plasma glucose after a glucose challenge was 184 mg/dl on a 20% carb diet, 183 mg/dl on a 40% carb diet, 127 mg/dl on a 60% carb diet, and 116 mg/dl on an 80% carb diet. The 80% carb diet was the only one on which blood glucose never went above 140 mg/dl.

It is important to know the diets being talked about. These are the glucose diets being referred to in this above second study;

“The glucose diets contained 3,000 kcal with 15% of calories as calcium caseinate; 20, 40, 60, or 80% as glucose; and the remaining calories as corn oil.”

That’s right, 65% of the lowest carb diet was force fed corn oil…the ‘low-carb’ group was force fed high quantities of liquid corn oil to bring calories up to 3000 cal/day, and it’s not a revelation that these people didn’t do too well. Jaminet is attributing their poor relative results to their low carb intake that is, by the way, 20% glucose = 600 cal. that is exactly what Jaminet calls a ‘safe starch’ amount and type. I think there are other reasons; lucky for Jaminet.

Insulin was not measured. See my comments above. This is a usual and critical mistake. It is very possible that the very rapid and large spike in glucose secondary to eating carbs with a glycemic index of 100, caused an equally rapid spike in insulin that rapidly reduced the blood glucose. It is also well known that eating fat with sugar slows the absorption and “flattens” the blood glucose and insulin curve, resulting in perhaps higher 2 hour glucose values. But is this very rapid rise and decline i.e. high spike in blood glucose and insulin healthier? Quite the opposite.

Again, what I have said for decades is that lowering glucose by raising insulin is trading one evil for an even worse one. Spikes in glucose may even be worse than a high but steady BG (see studies below), and spikes in glucose and insulin may, and I believe do, bring about insulin and leptin resistance, and therefore a whole new realm of metabolic devastation.

Furthermore, in these studies, the low-carb group was not well adapted, and necessary nutrient supplementation was not given. It is well known that those people who are not adapted to a low carbohydrate diet may not fare well in the first few weeks following the initiation of this, especially if they have not supplemented with potassium and magnesium that will be lost as excess fluid is excreted in urine as insulin is reduced. Magnesium is also required for proper insulin signaling. Also, the almost infinitely high omega 6/omega 3 ratio seen in the first study would cause extreme inflammation that is known to damage islet cells and prevent proper insulin and leptin function while also impairing the metabolism of fatty acids and membrane function. I do not think that the authors were unaware of this.

Once again, what those two studies merely show is that eating carbs and fat (as pure corn oil !) together is very bad, that eating large amounts of pure glucose will rapidly spike blood glucose and therefore insulin that (at least for a while before insulin resistance kicks in) is known to rapidly lower the blood glucose, that force feeding copious amounts of corn oil to maintain high calorie intake might have deleterious effects, especially in conjunction with improper implementation and without proper supplementation of at least magnesium, potassium, and omega 3 oils.

The proper very low carbohydrate (higher beneficial fat, moderate only protein) diet, a few very simple precautions, and a little bit of time is necessary before significant benefits are realized,,,and they will be realized if this diet is properly implemented.

But wait; there’s more;

Medical and nutrition studies are now often (usually?) undertaken, not to discover some underlying truth, but rather designed to obtain a predetermined and biased outcome as part of a marketing effort.

Both of the previously cited studies, one from 1973, and the other from 1990, were authored by James Anderson, whom I am quite familiar with. Dr. James Anderson happens to be the chairman of the National Fiber Council, an organization that is funded by HCF [High Carbohydrates and Fiber] Nutrition Research Foundation (a nonprofit foundation reputedly funded by large carbohydrate containing food corporations and whose chairman happens to be Dr. Anderson), and other not very unbiased entities such as Procter & Gamble.

Furthermore, these studies are irrelevant to our discussion that ought to be comparing, as much as possible, a very low carb, high (healthy, not corn) fat and moderate protein diet in which the participants had enough time to become adapted, to a higher carb diet. The studies by CarbSane and Jaminet are like comparing a fat 40-year-old to a fat 50-year-old in the 100 yard dash, and assuming that the winner is fit for the Olympics.

This last study did not report fasting glucose, but did track blood glucose for 4 hours after the glucose challenge. If we take the 4-hr blood glucose reading as representative of fasting glucose, we find that dieters eating 60% or 80% carb diets had fasting glucose of 76 and 68 mg/dl, respectively.

With all due respect for Paul, he is taking way too much liberty here. Rarely do 4 hr post prandial glucose levels reflect fasting levels. They are often higher, sometimes lower depending on insulin response (i.e. reactive hypoglycemia). This is why fasting blood tests are done at least 8 hrs and usually 12 hrs after eating. Furthermore the inadequacy of testing may have covered up the rapid, and detrimental spikes in glucose (that Jaminet also alluded to earlier) and insulin that may have likely occurred, especially with the higher glucose diets. If Jaminet really believed in these studies, then why is he not recommending very high sugar diets? I believe that he knows them to be less than healthy.

interpretation of the evidence from multiple sources: A plausible conclusion is that a high-carb diet produces a low fasting glucose (let’s say, 80 mg/dl), a PHD type 20% carb diet an intermediate fasting glucose (95 mg/dl), and a very low-carb diet a high fasting glucose (say, 105 mg/dl).[my emphasis]

Let’s not just “say”. With all due respect, these are hypothetical numbers, and likely incorrect (see above). They appear designed to fit the following graph, based loosely on a couple of old and highly controversial studies and a couple of anecdotal reports. One cannot come to any conclusions, let alone what Paul is calling plausible, from those studies. There are a multitude of studies easily found that show the opposite; that eating a high carbohydrate diet is associated with raising fasting and post prandial glucose.

Just for fun, I decided to see where these fasting glucose levels show up on the mortality plot from Balkau et al:

The 20% carb diet lines up pretty well with the mortality minimum, and both high-carb and very low-carb diets wind up at bins with slightly elevated mortality.

…only when, shall we say, imaginative numbers are used.. and again, no insulin results. Also see my study cited also below that shows a resultant average fasting glucose of 99 mg/dl on my very low carb diet associated with great insulin and leptin results (cutting nearly in half!).

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2831640/

Now, I don’t believe we can infer from data on high-carb dieters what the relationship between blood glucose levels and mortality will be in low-carb dieters. It was Dr Rosedale, not me, who introduced this study into evidence.

But if we believe that lowest mortality really does occur with 2-hr post-challenge blood glucose around 100 mg/dl and fasting blood glucose below 100 mg/dl, as argued by the studies Dr Rosedale cited, and that this result applies to low-carb dieters, then I think the evidence is clear. One must eat some carbohydrates – at least 20-30% of energy.

…Whoa. That conclusion is hardly warranted. What the overwhelming preponderance of evidence had shown, and what the conclusions by the authors themselves had shown, is that there is no specific threshold for glucose below which is healthy. Raising glucose above baseline increases indexes of disease and mortality. That is all that can be concluded. More than that is speculation from using studies (a 65% corn oil diet?!) that I doubt Jaminet has faith in either. Regardless, there are way too many studies that show the opposite; that eating glucose and glucose forming foods impair glucose tolerance and insulin sensitivity, and worsens diabetes, if not being a major etiologic factor, to draw opposing conclusions.

This is the standard Perfect Health Diet recommendation. It seems that Dr Rosedale is supporting my diet, not his!

Oh No.. Keep me away from that Kool Aid!!

What About Diabetics?

Perhaps the boldest passage in Dr Rosedale’s reply was this:

“We are all metabolically damaged to some extent. None of us has perfect insulin and leptin sensitivity…. It is for that reason that I say that we all have diabetes, some more than others, and should all be treated as such.”

Well, if we all have diabetes, more or less, then I guess I have to consider whether our regular diet – which recommends about 20% of energy (400 calories) as carbs – is healthy for diabetics.

Now, before I begin this discussion, let me say that I don’t claim that this is optimal for diabetics. I think it is still an open question what the optimal diet for diabetics is, and different diabetics may experience a different optimum. I have often said that diabetics may benefit from going lower carb (and possibly higher protein) than our regular dietary recommendations. However, Dr Rosedale is here saying that even a healthy non-diabetic should eat a diet that is appropriate for diabetics. I want to see whether our regular diet meets that standard.

How do diabetics do on a 20% carb diet? Here’s some data that I found in a post by Stephan Guyenet at Whole Health Source. It’s from a 2004 study by Gannon & Nuttall (http://pmid.us/15331548) and the graph is from a later paper by Volek & Feinman (http://pmid.us/16288655/). Over a 24 hour period, blood glucose levels were tracked in Type II diabetics on their usual diets (blue and grey triangles) and after 5 weeks on a 55% carb – 15% protein – 30% fat (yellow circles) or 20% carb – 30% protein – 50% fat diet (blue circles):

The low-carb diet was a little higher in protein and lower in fat than we would recommend, but very close overall to our recommendations and spot-on in carbs.

What happened to blood glucose? It came close to non-diabetic levels. Fasting blood glucose dropped to 7 mmol/l (126 mg/dl), roughly the level at which diabetes is diagnosed. Postprandial blood glucose elevations were modest – peaking below 160 mg/dl which is about 20 mg/dl higher than in normal persons. Average daily blood glucose looks to be around 125 mg/dl.

What would have happened on a zero-carb diet? Fasting blood glucose probably would still have been elevated, near 126 mg/dl;

That’s fairly fanciful, and I don’t agree that lowering carbs further would start raising blood glucose. The opposite will typically happen. See Cahill cited below and in my Jimmy Moore post. Starvation (0 carb) lowers glucose dramatically. Properly implemented, lowering carbohydrates leads to further improvements. Regardless, no one is really recommending a 0 carbohydrate diet, as this would have to be laboratory fabricated. However, what my experience has been with my VLC (very low carb) and higher fat diet, is that fasting and post prandial glucose become further improved, into completely healthy, non-diabetic, non impaired glucose tolerant ranges. I do not and have not disputed that Paul’s diet may lead to (much) better results than the french fries (whoops, potatoes allowed by Paul) and coke diet that the average person may eat. But to make it “perfect”, the starch consumption would need to be reduced.

It is interesting that Jaminet would use Jeff Volek for support. I am quite familiar with Jeff and his work through Eric Westman who has collaborated with Jeff often and me previously; he is a co-author on my paper cited here. It is extremely unlikely that Jeff (or Eric) would agree with that statement or Jaminet’s conclusions about a very low carbohydrate diet raising blood glucose.

Let’s see what Jeff Volek has to say;

Cardiovascular and Hormonal Aspects of Very-Low-Carbohydrate Ketogenic Diets [VLCKD]

Jeff S. Volek and Matthew J. Sharman

Obesity Research Vol. 12 Supplement November 2004

The studies were conducted on healthy volunteers.

Aside from having higher protein than I would recommend, this is close to my diet..

Volek’s VLCD; Protein ~28%, Carbohydrate 7% (39 gms), Fat (%) 64

“…there were significant decreases in insulin (28%) and leptin (64%) concentration after the VLCKD [very low carbohydrate ketogenic diet]. Postprandial insulin responses immediately after the fat-rich meal were significantly lower after the VLCKD.

…Another consistent effect we have seen in our studies is a reduction in fasting glucose and insulin [on a VLCD]… Fasting glucose, insulin, and insulin resistance were all significantly lower after the VLCKD compared with the low-fat diet…we propose that VLCKD may be particularly suitable for preventing and treating metabolic syndrome.”

And in;

Lipids 2009 Apr;44(4):297-309. Epub 2008 Dec 12.

Carbohydrate restriction has a more favorable impact on the metabolic syndrome than a low fat diet.

Volek, JS, Phinney SD

CRD (carbohydrate restricted diet; % carbohydrate:fat:protein = 12:59:28) vs. a low-fat diet (LFD) (56:24:20)

“…subjects following the CRD [12% carbs] had consistently reduced glucose (-12%) and insulin (-50%) concentrations, insulin sensitivity (-55%), weight loss (-10%), decreased adiposity (-14%), and more favorable triacylglycerol”

…this is common in diabetics because the loss of pancreatic beta cells creates a glucagon/insulin imbalance that leads to elevated fasting blood glucose. This blood glucose level would have been maintained throughout most of the day, with the postprandial peaks and troughs flattening. Average daily blood glucose level would have been similar to that on the 20% carb diet.

There are too many “would have” speculations (likely false) in this argument. I believe that I was the first person to use a low carbohydrate, relatively high-fat diet to treat diabetics and taught most of the others in one way or another who are doing this today, And I will emphatically say that lowering carbohydrates as much as possible, without the consumption of excess protein, is by far the best way to lower glucose and insulin (and leptin), i.e. to reverse insulin (and leptin) resistance, and in fact to frequently totally reverse the disease of T2 diabetes (or impaired glucose tolerance). Any additional carbohydrate or protein will adversely affect these results. I do believe that if Paul were to treat diabetics and compare results, his ideas would be quite different.

So the big benefit, in terms of glycemic control for diabetics, comes from reducing carbs from 55% to 20%. Further reductions in carb intake do not reduce average 24 hour blood glucose levels, but may reduce postprandial glucose spikes.[my emphasis]

I am happy that Jaminet said that, since reducing glucose spikes may be even more important than reducing fasting glucose. There are in fact quite a few articles that are now showing that spikes in glucose are worse than steady high glucose. Here’s one;

Glucose oscillations, more than constant high glucose, induce p53 activation and a metabolic memory in human endothelial cells

Schisano, Diabetologia, Volume 54, Number 5, 1219-1226

“Conclusions/interpretation; Exposure to oscillating glucose was more deleterious than constant high glucose and induced a metabolic memory after glucose normalisation. Hyperactivation of p53 during glucose oscillation might be due to the absence of consistent feedback inhibition during each glucose spike and might account for the worse outcome of this condition.”

And another;

Effects of intermittent high glucose on oxidative stress in endothelial cells.

Qin-Min Ge, Acta Diabetologica, Volume 47, Supplement 1, 97-103

“Intermittent high glucose induced a greater over-production of ROS [reactive oxygen species] than constant high glucose…and may be involved in the development of vascular complications.”

…and I do not think that I need to show studies that eating ‘safe starches’ such as rice and potatoes will spike and oscillate blood glucose…The glycemic index again shows that well.

In fact, we have some Type II diabetics eating Perfect Health Diet style. Newell Wright reports good results:

I am a type II diabetic and a Perfect Health Diet follower, so I want to chime in with my experience….

I switched from the Atkins Induction diet to the Perfect Health Diet. I have been eating rice, potatoes, bananas, and other safe starches ever since, as well as fermented dairy products, such as plain, whole milk yogurt. I have also slowly lost another seven pounds. I enthusiastically recommend the book, Perfect Health Diet by Paul and Shou-Ching Jaminet.

Today, my fasting blood glucose reading was 105. Note that since following the Perfect Health Diet, my fasting blood glucose reading has gone down. Previously, I was suffering from the “dawn phenomenon.” My blood glucose levels overall were well below 140 one hour after a meal and 120 two hours after a meal. Only my fasting BG reading was out of whack, usually between 120 and 130, first thing in the morning.

For dinner tonight, I had a fatty pork rib, green beans, and a small baked potato with butter and sour cream. For dessert, I had a half cup of vanilla ice cream. One hour after eating, my blood glucose level was 128 and two hours after, it was 112.

So not only am I losing weight on the Perfect Health Diet, my blood glucose levels have actually improved, thanks to the increased carbs counteracting the dawn phenomenon, just as Dr. Kurt Harris (another proponent of safe starches) said it would.

So for me, as a type II diabetic, this “safe starches” exclusion is pointless…. [D]espite the type II diabetes, I am doing just fine on the Perfect Health Diet, thank you. I reject the diabetic exclusion of safe starches.

Note that Newell’s fasting blood glucose went down from 125 to 105 mg/dl when he raised his carb intake from Atkins Induction to Perfect Health Diet levels, and postprandial glucose levels on PHD were no higher than his fasting levels on Atkins Induction. It looks like he reduced blood glucose levels by adding starches to his diet.

Mine is not the Atkins diet. Furthermore Newell’s blood sugar is still not healthy. It appears likely he is talking about his home measurement of glucose being 105. Using Jaminet’s conversion, that would equate to a laboratory serum value of 130 mg/dl, that would still place him very much in the diabetic range; not such a great result. Using a more accurate conversion, it would be 118; still very unhealthy and considered impaired glucose tolerant. It is extremely unfortunate that this is being touted as healthy by Newell himself, who will have to suffer the consequences of being misinformed. Also, do we know what his insulin is? Has it ever even been measured? As I have stated so often; lowering glucose at the expense of raising insulin is doing someone no favors. Newell may be doing better than bad on the surface (only in-so-far as blood glucose levels go), but I consider it a failure if a type II diabetic of mine is not completely reversed, such that healthy blood sugars are obtained without medication and associated with lower insulin. It is so important, that I have to keep repeating it; diabetes is not a disease of blood glucose, but a disease of the signals being given to glucose. These are what need to be treated and measured. Giving only glucose measurements tells me little about the health of a “diabetic”.

To repeat: I’m not claiming that our regular diet, providing 20% of energy from “safe starches,” is optimal for diabetics. I don’t know what the optimal diabetes diet is, and it may be different for different diabetics. But I think there is plentiful evidence that even for diabetics, our “regular” diet is not a bad diet. And for some, it might be optimal.

Here I am happy to finally agree, and it feels good to be able to do so. Jaminet’s diet is certainly not a bad diet, and I hope that I have never given the impression that it is. It is better than most other diets generally being touted. Optimal for some? I can’t say.

I truly believe that the closer that any diet comes to mine, the better it is. This has been shown to me over the last 2 decades of patient experience, the continual outpouring of supporting science, first pertaining to insulin, then leptin, then mTOR and the now very robust science over the last decade pertaining to the biology of aging…and also by the numerous well known low carb diets that have ultimately modified their original programs to try to morph into mine.

Summary: Putting It All Together

It looks like 20% of energy is a sort of magic number for carbs. It:

Averts glucose deficiency symptoms while achieving normal insulin sensitivity and glycemic control on oral glucose tolerance tests;

Avoids significant hyperglycemic toxicity even in diabetics.

Why does this magic number, which happens to be the Perfect Health Diet recommendation for carb intake, do so well?

Perhaps a chart will make the science a little clearer.

“Dietary glucose in” (blue) represents the amount of carbs obtained from diet. “The body’s glucose utilization” (maroon) is how much glucose will be put to useful purposes at a given daily carb consumption. Glucose utilization does not vary as strongly as glucose intake.

Actually, glucose utilization can vary tremendously depending on the activity of many hormone levels, including insulin, leptin and their level of sensitivity, cortisol, thyroid, growth hormone. When one eats glucose there will be glucose spikes of varying amplitude, and as shown above, this is particularly detrimental.

At low intakes a deficit is made up by gluconeogenesis (manufacture of glucose from protein) and at high intakes an excess of glucose is destroyed by thermogenesis or conversion of glucose to fat. Where the blue and maroon lines cross, dietary glucose in matches the body’s glucose utilization.

But 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 on Paul’s behalf, “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 then 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 outthink it by forcing 400 cal. glucose daily [or even 600 cal.]

For most sedentary adults, this level will be around 600 carb calories per day.

Not so. A VLC well adapted person has a glucose requirement closer to 300 cal, all of which can easily come from non carbohydrate sources, including glycerol from fat and recycled lactose. See Cahill and my entire last post on Jimmy’s site.

We recommend eating close to or slightly below this point (“PHD Recommendation”).

There are dangers in straying too far from this intersection point:

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.

Eating too many carbs results in unnecessary exercise of glucose disposal pathways, and possible unhealthy fluctuations in blood glucose levels if those disposal pathways fail.

I totally agree. That’s twice in one day…on a roll… though I would argue that consistently eating 600 cal. glucose forming carbs and even less will at least sometimes, if not nearly always, cause unhealthy fluctuations in blood glucose.

Hitting just below the intersection is a safe, low-stress point which will work well for most people.

I would move that intersection considerably to the left.

For diabetics, the excess glucose disposal pathways are broken. However, this is not a major problem if you have no excess glucose to dispose of. Eating up to 20% of calories from carbs doesn’t require the use of disposal pathways – glucose can be stored as glycogen and then released as needed, so the effect of dietary glucose is primarily to reduce the amount of gluconeogenesis. Suppressing gluconeogenesis requires some residual insulin secretion ability, so Type I diabetics cannot achieve this, but most Type IIs can.

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…

The Issue of Thyroid Hormones and Anti-Aging

The most distinctive element of Dr. Rosedale’s diet is its emphasis on longevity as the supreme measure of health, and its emphasis on calorie restriction (especially, carb and protein restriction) and metabolic suppression as the means to long life.

Our book, Perfect Health Diet, relied strongly on evidence from evolutionary selection to guide us toward the optimal diet.

Dr. Rosedale rejects evolutionary selection as a helpful criterion, since evolution did not necessarily select for longevity:

[Rosedale says], “If we evolved in a certain way and with certain physiologic responses to the way we eat, it was not for a long, healthy, post-reproductive lifespan. It was for reproductive success. The two are not at all synonymous, in fact often antagonistic. We have no footsteps to follow as far as the best way to eat for long healthy post reproductive life. We can only use the best science pertaining to the biology of aging and apply it to proper nutrition. That is what I feel I am doing.”

We actually share much of Dr Rosedale’s perspective on what influences longevity; it is for longevity that we recommend slightly under-eating carb and protein compared to what evolution selects for. However, we don’t go as far in that direction as Dr Rosedale does.

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”.

Note that Dr Rosedale acknowledges that his glucose-scarce diet reduces body temperature. Many Rosedale dieters have had this experience. Darrin didn’t like it:

This comment from Rosedale support may be of interest to you;

“The best place to measure is under the tongue. Ideal basal temperature is what you have when you first wake up in the morning, and on the Rosedale diet should be upper 96′s lower 97′s. We have found that when someone starts our diet, their basal temperature will go down about 1-2 degrees Fahrenheit which is a great improvement”.

Personally, i did not feel good on a lower body temp when i was low carb (sub 50g) & have been working hard (following phd diet & supps) to get my body temp back up. i would say my basal/morning oral temp is now around the 97.5F on average (up from around 96.5F average pre PHD).

As far as Darrin; I have not known anyone who had difficulty in maintaining my diet because of low body temperature that was not hypothyroid (from disease) or had deficient adrenal function. The fact that he had to work hard to get his temperature up leads me to believe that there were/are other problems involved, as getting temperature higher is typically extremely easy and can happen in as short as one day by eating more carbs. This should be looked into.

As stated before, single anecdotal stories are not very good science. I have literally hundreds of testimonies indicating extreme benefit when switching to my diet from many other diets.

Low body temperatures are associated with a variety of negative health outcomes. For instance,low body temperature is immunosuppressive, leads to poor outcomes in infections, and is a significant independent predictor for death in medical patients. Fever is curative for most infections, low body temperature is a risk factor for infections.

Again, I am not talking about a sick thyroid. I am not talking about a thyroid that is low because it has to be, or a body temperature that is low because the body does not have enough lean mass or proper physiology to maintain a higher temperature, which is all that the above examples and studies indicate. I am not talking about hypothyroidism. I am talking about a thyroid that is purposefully being lowered to enhance the wellness and survivability of that life. Please understand that this is very different. One is very healthy; one is very not.

This is analogous to fasting insulin. Almost always, a high fasting insulin indicates insulin resistance and poor health. Properly treated, fasting insulin goes down and the person is healthier. You don’t say that that person now has a sick pancreas. The same is true for thyroid. As part and parcel of making that person healthier, fasting insulin is reduced, fasting leptin is reduced, and so is free T3 reduced.

Also, as in my previous post, temperature must be orchestrated for maximal health. As we age, one of the major problems is that our temperature does not go as high with infection as it did when we were children. This is what can predispose to serious infection. My diet does not relegate people to low temperature. It keeps temperature a little bit lower when that is healthiest, but does not prevent a rise in temperature, a fever, when necessary as with infection, but instead would promote it. This is very healthy. Having a “fever” when not necessary, and is promoted by the thermogenesis of burning ‘healthy starches’ and excess protein is what is not.

Readers of our book know that we think infections are a major factor in aging and premature death. Whether a diet so restricted in carbs that it significantly lowers body temperature is really optimal for longevity is, I think, open to question.

it is extremely important to have the confusion and misunderstanding by many if not most in the medical and health community of the true meaning of free T3 and body temperature being lowered, resolved.

In caloric restricted animals where body temperature and free T3 goes down, the immune response is markedly increased, and their mortality rate is well known to be significantly reduced while lifespan significantly increased. There is also a huge reduction in autoimmune diseases, secondary to improving immune function, not lowering it. The reason for the difference between the sick thyroid in the above-cited studies and the healthy thyroid in CR and my diet, is the reason that T-3 and body temperature is being lowered. In the former, it is being lowered because of sickness not because it generally is causing the sickness (though it may also). Certainly I can give the more extreme example that body temperature is lower when one is dead. In calorie restricted animals and in those on my diet, on the other hand, free T3 and body temperature are reduced as part and parcel of a shift in genetic expression towards maintenance, repair, and longevity, in the same way that the temperature of your car is reduced when it is functioning best; when it is getting the best mileage, has the best acceleration, and where the engine will live longest. In both cases, it is making the best use of available resources, and wanting to reduce waste. In the former, thyroid is low because it is sick. In the latter, and with my diet, thyroid goes lower to keep one healthy. If the car is running hotter, you know that is sick. It does so because it must and perhaps better than not running at all.

Furthermore, it is now a fairly well stablished finding that free T3 is reduced in centenarians. One example;

“A cross-section analysis of FT3 age-related changes in a group of old and oldest-old subjects, including centenarians’ relatives, shows that a down-regulated thyroid function has a familial component and is related to longevity”

Andrea Corsonello, et al

Age and Ageing 2010; 39: 723–727

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

The key is that we can reset our thyroid function to be that of centenarians, even if we were not so genetically predisposed. We can make our own luck, but not by adding carbohydrates..

If ketosis is an indication of fatty acid utilization as fuel, and if this is a marker of a shift in metabolism towards that seen in caloric restriction that has been shown to confer tremendous health benefits including longevity, then what Cahill states in his previously cited paper must be strongly noted; as little as 100 grms. of carbohydrate (that Jaminet recommends) will prevent this.

Fuel Metabolism in Starvation

Annu. Rev. Nutr. 2006.26:1-22.

George F. Cahill, Jr.

Department of Medicine, Harvard Medical School

There is a plausible case to be made for the Rosedale diet as a diet that sacrifices certain aspects of current health in the hope of extending lifespan. It cannot however claim to be the optimal diet for everyone. It is certainly not optimized for fertility, athleticism, or immunity against infections.

I suppose my diet may not be optimized for every single person, but not for the reasons that Jaminet states. Those with impaired digestive function, that produce insufficient lipase or bile, may have difficulty with a high fat diet, but this would pertain to Paul’s diet also. As far as the fertility, immunity, and athletic performance; ‘The Rosedale Diet’ actually improves fertility and immunity compared to a higher carbohydrate diet, and can be excellent for sports, with certain adjustments, depending on the type. The control of leptin is essential for immune function and fertility, and many studies show this.

Both Paul and I are asking people to sacrifice a little for the reward of better health. I may be asking for a little bit more (and that is debatable as ones addiction and desire areas of the brain become rewired as leptin is lowered), but I believe that the reward is exponential as one follows a diet that I have recommended, lowering non-fiber carbs as much as possible.

After all, we are not talking about a better health diet. We are talking about an optimal diet, a “Perfect Health” diet, as it were. That diet, as far as promoting a long, healthy and happy life would be as I have recommended for so many years, and would entail reducing consumption of sugars and starch as much as possible.

Jaminet Conclusion;

I am sympathetic to the broad perspective that underlies Dr Rosedale’s diet. Both our diets are low-carb, low-protein, and high-fat, and studies of longevity are the biggest factor motivating the recommendation to eat a fat-rich diet.

Thank you, and I agree…and ultimately, when this ‘debate’ settles down, we should join to fight the much larger battle against those recommending and even prescribing a low fat, high carbohydrate diet to the masses, that I think we both believe is largely contributory to the epidemic of chronic disease worldwide.

However, Dr Rosedale takes low-carb and low-protein dieting to an extreme that I think is not well supported by the evidence.

Dr Rosedale’s direct attempt at refuting our diet consists mainly of two claims:

Lower blood glucose is better than higher blood glucose.

The way to lower blood glucose is by eating fewer carbs.

Not exactly. As often previously stated, the major detriment of Jaminet’s diet are the spikes in glucose, insulin, and leptin that his diet results in, and the resultant contribution to insulin and leptin resistance. Unfortunately, this has been addressed only to a minor degree. I do agree, that this would happen less on Paul’s diet then the typical American diet, but considerably more than with the diet I recommend.

Neither claim is supported. Mortality is a U-shaped function of blood glucose and blood glucose levels around 90 to 100 mg/dl are healthiest, not low blood glucose levels. Moreover, the diet that delivers the lowest blood glucose levels is a high-carb, insulin-sensitizing diet, such as the Kitavans eat, not a low-carb diet.

This last statement is highly debatable, likely false, and disputed by many researchers and studies, some of which I have previously cited. A high carb diet only appears to be insulin sensitizing if compared to an even worse diet. Otherwise the phrase, “a high carb, insulin sensitizing diet”, is an oxymoron.

Calorie restriction results in very low blood glucose… and enhanced health and longevity. Furthermore,… Paul has just told us that the lowest blood glucose levels are not healthy, and yet cites the Kitivans with very low fasting BG for being so healthy. I’m confused.

If I truly believed Dr Rosedale’s argument for lower blood glucose, he would have persuaded me to eat a high-carb Kitavan-style diet. However, I am not persuaded.

I believe that:

Optimal blood glucose levels are in the 90 to 100 mg/dl range. High-carb diets cause below-optimal levels of blood glucose, especially during fasts. (Indeed, high-carb dieters routinely experience hunger and irritability during long fasts.) Very low-carb diets cause elevated blood glucose due to the body’s efforts to conserve glucose by suppressing utilization. Excessive suppression of glucose utilization is unhealthy.

A 20% carb diet, while not optimal for every single person, is healthy for nearly everyone. Twenty percent may be the best single prediction of the optimal carb intake for the population as a whole. Even diabetics can do well eating 20% carbs.

And that is why we recommend moderate consumption of safe starches.

While I maintain that fasting glucose is a much poorer index compared to measuring glucose excursions and insulin and leptin resistance, I must again show results from my own study;

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2831640/

Here the fasting glucose on my diet fell to 99 mg/dl or that value that Jaminet says indicates the healthiest of diets, but here this occurs concurrent with lowering insulin and leptin, indicating much improved insulin and leptin sensitivity.

Rosedale Summary and Conclusions;

The studies and statements presented in my Jimmy Moore post and here should be understood by what they altogether point to.

1) The requirement for glucose is much less, even half of what Paul has indicated.

2) These requirements can easily be met without the consumption of a single gram of glucose in a very low carbohydrate adapted individual.

3) There is no such thing as a glucose deficiency.

4) Any excursion of glucose above baseline will result in some increment of damage and/or mortality. There is no threshold.

5) Repeated excursions of glucose above baseline cause excursions of insulin and leptin, and repeated excursions of these contribute to, if not cause insulin and leptin resistance, and this results in a significant acceleration of the chronic diseases of aging and aging itself. This is the major significance and detriment of eating a food that raises blood glucose.

6) One can’t pin one’s hope on only doing what is natural. Post reproductive death is extremely natural. We can only rely on science, especially the science of the biology of aging, to show how to live a long, post-reproductive lifespan. We have no footsteps to follow. Not the Kitavans, not the Okinawans.

7) We all have some degree of metabolic derangements including insulin and leptin resistance, and this really should be considered the hallmark of diabetes. We should therefore all be treated as such, especially with a diet known to improve those parameters as much as possible. That would be my Rosedale diet, as revealed in the only research paper that I am aware of (cited previously here) that correlates a particular diet with nearly all of the laboratory parameters associated with and perhaps causative of enhanced health and lifespan in a well known model of this, caloric restriction, though without having to caloric restrict.

8 ) I talked considerably about the meaning of the purposeful genetic expression of reduced thyroid levels that my Rosedale Diet accomplishes, particularly reduced free T3, and especially as it relates to point 7 above.

Jaminet’s major emphasis in this blog is the significance of fasting and 2 hr post prandial glucose. Unfortunately, that is likely the least important variable pertaining to glucose, insulin, leptin that is influenced by diet. There are many determinants of fasting blood glucose; sleep patterns, cortisol, sympathetic overdrive, growth hormone, to name but a few, that not only raise blood glucose but may increase mortality irrespective of blood glucose. I had used some studies of glucose levels to merely show a lack of toxic threshold.

Furthermore, I have shown that oscillations in glucose that undeniably occur after the consumption of ‘safe starches’, as any table of glycemic index would show, may result in damage to a more significant extent than even elevated fasting glucose.

Much of Jaminet’s argument is illustrated by his statement,

“Studies confirm that high-carb diets tend to lower fasting glucose and to lower the blood glucose response to a glucose challenge.”

Studies do not confirm anything of the sort. One study cited by Paul supports only that if a person eats a very high carbohydrate diet containing the equivalent of 22 tablespoons of Metamucil made up by a lab and eaten under supervision, that it can lead to some improvement over a standard American diet eaten at home, especially if that study is funded by large corporations with a huge financial interest in the outcome. This only serves as an example of the very poor science that permeates medicine and nutrition that unfortunately often is not realized…as does the other study that Jaminet uses to illustrate his point, where a high carbohydrate diet is compared to a low carbohydrate diet, and where the difference in calories is made up by force feeding 65% calories from corn oil. Moreover, it is confusing that this statement is made to support Jaminet’s diet, since he does not recommend a high carbohydrate diet, but a diet containing only a moderate consumption of ‘safe starches’ that these studies did not come close to following.

Furthermore, the support that Jaminet is able to muster from other articles he presents, is only derived by his improbable assumption that, since glucose spikes were not measured, that they mustn’t have ever gone above 140 mg/dl. Further ‘support’ was only secondary to a large error in conversion between blood and plasma glucose.

I believe the only conclusion that can be drawn from these and related studies that were presented, is the same as the authors’ conclusions; that fasting and 2 hr. glucose above some number, 100 mg/dl?, 105 mg/dl?, is correlated with some incremental degree of damage and/or mortality, and this is considerably less than 140 mg/dL that Jaminet has said is safe.

Little argument is given about the detrimental effects of eating ‘safe starches’ and glucose spikes on raising insulin, and resultant insulin resistance, with the exception of the (very poor) study that compared people eating a standard American diet to those eating a controlled, very high fiber (22 tablespoons!) diet, in which the latter did predictably better. I’m still not sure what the relevance of that study is.

Nothing was mentioned about leptin.

I believe that all of the 8 points that I have stated above are still standing strong, with little evidence to the contrary.

Further arguments given by Jaminet misinterpret the concept I had presented of the natural selection of reproductive success over a long post reproductive lifespan. He assumes that my diet would impair fertility, when, in fact proper leptin signaling, that my diet has been shown to promote, is essential to fertility. However the concept that nature doesn’t much care whether we live a long, healthy (post-reproductive) life is important, in that it tells us that we should not necessarily copy what we perceive to be natural. After all, hemlock is natural. So is dying.

So now, let’s take this debate deeper, and where it belongs.

Though nature doesn’t care whether we live a long, healthy life, nature does want us to live long enough to make (and raise) babies. We can use nature’s secrets about how to stay alive and healthy to make babies, and apply those secrets to post reproductive years, so that we can also live a younger and longer post reproductive life, whether nature cares about that or not.

We have no footsteps to follow in that quest, but must use the best science currently available related to a long and healthy life.

That gets us to the main issue and most important question that I had asked earlier;

Is there a diet (Rosedale’s or Paul’s) or glucose (starch) intake that can better maximize the repair/damage ratio that life, health, and youthful longevity depends on? Has this been answered here yet?

A little bit, as it pertains to thyroid. Paul has said that his diet would not have the effects on thyroid as my diet, namely lowering T3, and he is likely right; see below. However, though Paul thinks lowering thyroid is disadvantageous, it is far from; in fact quite the opposite. The purposeful lowering of thyroid likely helps to mediate metabolic advantages that help confer longevity in centenarians and in calorie restriction. Note that calorie restriction has been shown to greatly improve health and increase maximal lifespan in almost every species studied since the 1930s. The holy grail of aging research (including the giant pharmaceutical corporations) has been to find a way (drug) to mimic the effects of calorie restriction without having to do so. Read on.

In the study cited previously,

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

…as my diet has been shown to do.

And the effect of calorie restriction on thyroid;

Effect of Caloric Restriction and Dietary Composition on Serum T3 and Reverse T3 in Man

The Journal of Clinical Endocrinology & Metabolism jan1, 1976 vol. 42 no.1197-200

“Subjects receiving the no-carbohydrate hypocaloric diets for two weeks demonstrated a similar 47% decline in serum T3 [as caloric restriction] … In contrast, the same subjects receiving isocaloric diets containing at least 50 g of carbohydrate showed no significant changes in either T3 or rT3 concentration.”

Very low carbohydrates such as mine has similar effects on thyroid as caloric restriction. Keep in mind that I do not calorie restrict. People are told to eat whenever they are hungry, except for 3 hrs before bedtime.

O