When I decided to write about the concept of “safe starches” as espoused by Paul Jaminet in his book The Perfect Health Diet a few weeks back, I had no idea there would be such a vitriolic response from so many people thinking I was attacking Paul personally. But I should know better by now after being in the blogosphere for so many years that if you bring up things you’re not supposed to talk about, then the boo-birds will come out in force against you. I really don’t mind dissension when it’s done in a civilized manner with the focus on the issues at hand rather than the personalities involved–just as Jaminet did so beautifully and respectfully in his reply to my original blog post. Unfortunately, some enthusiastic readers took to examining my supposed ulterior motives for writing about this.
Most of my long-time readers will tell you I’ve always been about learning as much as I can about various aspects of nutritional health. I do that by asking questions, digging deeper on topics that are being discussed in the blogosphere, and attempting to find answers so my readers can make an informed decision about what to do for their health. There’s no “hidden agenda” with what I do–I’m just an average Joe living my life the best way I know who is always attempting to learn and apply the latest information about living as optimally healthy as possible. What you see is what you get.
Because so many of my readers were asking about these “safe starches” that are being promoted as such by Jaminet and others, I felt it was important to get it out in the open, share the major concerns with using such verbiage in describing foods that would never be consumed on typical high-fat, low-carb nutritional plan, and begin a discussion between those who are both for and against including these in the diet. I’d say mission accomplished! Here’s just a small sampling of the rumblings out there in the Paleo/low-carb/health blogosphere that began after I wrote about this in early October:
WEIGHT MAVEN: “Why I don’t eat low-carb”
MIDWEST PRS: “DR. JAMINET’S RESPONSE ON JIMMY MOORE’S LIVIN’ LA VIDA LOW-CARB SHOW BLOG”
THAT PALEO GUY: “A week of it…”
LATEST IN PALEO: “Latest in Paleo 36: Insanely Great”
EXCEPTIONALLY BRASH: “Pillar Envy”
LOW-CARB WISDOM: “Silence Explained”
EVOLVIFY: “Rice, Potatoes, Wheat, and Other Plants Interfere with Human Gene Expression”
SUZAN’S SPOT: “Relax. Eat Real Food”
THE PRIMAL PARENT: “Are Low Carb Diets Really Necessary?”
FREE THE ANIMAL: “White Rice: Agent of Disease, a Sensible Choice, or Healthsaver?”
CROSSFIT FIRE OF THE GODS: “Jaminet’s on LLVC”
I’m happy to see this conversation continue because it is an important issue worth debating regardless of whether you are for or against the inclusion of “safe starches” into your diet. Talking about it at least helps lead people to a greater understanding of whether this is a concept that they should consider trying for themselves. In fact, I had shared in my previous writings that I would possibly be willing to put these “safe starches” to the test utilizing Paul’s principles under his guidance. But after talking with some medical doctors I was advised it probably wouldn’t be a good idea for me right now considering some issues with fat metabolism/insulin resistance that I’m working through (I’ll have more on this in another post coming soon–suffice it to say I have suspended my n=1 experiments until further notice).
I spoke at great length with Paul Jaminet on the telephone last week explaining my concerns about trying his plan in light of what is possibly some non-nutrition-related concerns and he understood–although he was disappointed. He fully believes low-carbers who add back in these “safe starches” he discusses will find relief from insulin resistance and find Perfect Health as the title of his book so clearly and boldly states. In fact, one of my readers shared her testimony about how “safe starches” have helped her in an e-mail:
Hi Jimmy –
Just wanted to take the time to share some experience of mine in reply to your post about the Jaminet’s “safe starch” ideas.
First off, thanks for that great post with input from so many wonderful bloggers/researchers. So helpful! My favorite answers so far is Dr. Cate Shanahan’s. I really believe she nailed it with her two questions: 1) Are some carb/sugar sources better for us than others, and 2) do we need to eat any glucose or can we truly make all we need from conversion from proteins.
Here’s my experience. For the second time in my life, just about six months ago, I started a low-carb eating plan following Mark Sisson’s Primal Blueprint. About 10 years previously, I tried a low carb eating plan following The Carbohydrate Addicts’ book (remember that one?).
My experience both times has been remarkably similar. Initially, I felt great, had increased energy, lost weight. But, about six months into the diet, I started to have some issues. I started to have some real problems with anxiety, up to the point of having some panic attacks. Intuitively, I knew it had something to do with what I was eating. Ten years ago, I didn’t have anywhere near the knowledge or experience with nutrition I have now. I freaked out! I completely threw the baby out with the bathwater and completely dumped the whole low-carb approach. The panic attacks stopped shortly after starting to eat more carbs, but, all the weight all came back. Boo.
Fast forward to 2011. I’m eating much healthier than 10 years previously…..organic, local, grassfed meat, coconut oil, raw milk, yada yada. Initially felt great on the Primal Blueprint plan….increased energy, lost weight, etc. Also, I have had some AMAZING results from giving up gluten. My seasonal allergies are tremendously improved, morning fog gone, achy joints gone. Yay!!!
But, about five months in, started having some issues…..episodes of anxiety again. This time, I didn’t overreact. I totally believe in this eating plan, so I thought, how can I modify things to deal with this that is obviously something to do with my unique metabolic/digestive issues?
I saw a holistic nutritionist. I had tests run in which he could tell how my digestion was doing (urine and saliva testing). Low and behold, I was digesting fats and carbs well, but my protein digestion was not good. I talked to him about my anxiety problems resurfacing on low carb. When I told him that I was waking up most nights around 3 or 4 in the morning with racing heart, he said he believed that I was waking up because my liver was trying to do its thing at this time, but was running out of glucose, giving me low blood sugar. In response to low blood sugar, the adrenals release adrenaline, which was causing the rapid heart beat and eventually woke me from sleep. Bingo!
He had given me an eating plan that recommended I needed around 600 gm of glucose from my diet daily. He also recommended that I eat 1 to 2 servings of STARCH daily (3 oz portions) from POTATOES or rice. Jimmy, I kicked and screamed at that because I was doing low carb! What??? But, my symptoms were really bothering me, so I gave in and tried it.
Within a couple days, my episodes of anxiety/panic feelings had decreased amazingly. Within a week or so, I stopped waking up at night with my heart racing. What a relief!
Obviously, my body needs a bit more glucose/carb. I’m still certainly low carb compared to the SAD most folks eat, though. After reading what Dr. Shanahan posted, I’m wondering if my body just isn’t so efficient with the whole gluconeogenesis thing. My tests revealed problems with protein digestion, so if I can’t break down protein enough for my liver to use efficiently, then maybe it just could not make enough glucose to do its thing. My symptoms and the resolution to them seems to indicate that may have been the case.
So, that’s my story. For me personally, adding starch to my diet helped my body out. I don’t think that’s the case for everyone, but I can’t ignore what I’ve experienced. I believe deeply in the Paleo eating approach. I am a big supporter of the Weston A. Price Foundation approach too. But something I think not enough folks are addressing is that many of us have really screwed up metabolisms and digestion from years of eating SAD, from antibiotic use, from toxins, etc. We are not starting from the same place that the indigenous folks Price studied were, or our Paleolithic ancestors were. They did not have antibiotic use and refined sugar, grain, and processed foods to screw up the microflora in their guts. I think that it would do everyone a service to talk about the possible problems one might encounter with digestion. I love the GAPS diet approach of Dr. Campbell-McBride. Heal the gut first! No matter how great your diet, if you can’t digest it, you can’t use it.
Anway, long email but I hope this is helpful feedback. Thanks so much for all you do, Jimmy! The quality of your guests and of your own analysis is just outstanding. I’ve learned so much from your work.
Clearly there seems to be something there with these “safe starches” for my reader and I don’t deny she experienced the improvements she outlined. As you know, I’m all about people finding what works for them, following it exactly and then continuing to do it as long as you are finding benefit from doing it. Those benefits can run from weight loss/maintenance to various improvements in health and quality of life.
Hear me clearly on this: if you are able to implement the strategies of The Perfect Health Diet and not have an adverse impact on your blood sugar, insulin, lipids and other key metabolic markers, then I say GO FOR IT! I’ll be working with Paul in December on putting together a general plan for my “Livin’ La Vida Low-Carb” readers to try for themselves to see how they do with the “safe starches.” If you’re curious about this, then we’ll have full details about how you can give it a go for yourself coming soon.
In the meantime, the discussion continues about this concept of “safe starches” and what the implications are for people who try to add them back into their diet. A UK-based senior nutritionist for Hannah Sutter’s Go Lower named Emily Maguire wanted to chime in on this discussion and share her educated perspective on this:
On first inspection, I would have to say that working as a nutritionist who specialises in low carb diets and taking it from that approach, terming starch foods as “safe” is not only difficult to comprehend but could also result in very misleading information for normal individuals following a low carbohydrate programme. Taking the terminology of “safe starches” aside, what strikes me as surprising is that potatoes and white rice would be included in any form of low carb recommendation. Basic principles of metabolism and nutrition would show that these foods cause the greatest spike in blood sugar levels and for obese individuals with insulin resistance or type 2 diabetes, this is definitely a state which should be avoided at all costs.
What I also find quite surprising is their recommendation that it is important to avoid a glucose deficiency since defects in glycosylation are characteristics of the cancer phenotype. Now I am no expert in this area but from what I understand from Thomas Seyfried’s group is that actually glucose is a major fuel for most-glycolysis-dependent brain tumor cells and an elevation in glucose levels can be associated with poor prognosis. Now this may only be true for brain cancer and no other categories but one thing I feel about the book is that explanations can be often lacking and they would need to be a lot more specific, especially when recommending dietary treatments for cancer patients.
On the whole I would re-iterate that in my opinion the terminology of “safe starches” is very misleading in the world of low-carbohydrate diets and a further and more clear explanation on why he is promoting this is definitely needed so that we can try to understand his theory a little better.
And that’s been my biggest concern about “safe starches” as well–it gives people permission to consume them when clearly not everyone can or should. I understand Jaminet is not referring to the blood sugar impact but rather the toxicity. Even still, any food that unnecessarily raises blood sugar levels is “toxic” for my body and very likely most of the people who read my blog. Many of the people who have tried to add in “safe starches” are either physically fit or don’t have the metabolic challenges that so many of us have to deal with.
One of the most engaged and civilized participants from my original blog post about this was Dr. Ron Rosedale, a medical doctor who has used low-carb diets to treat his patients with obesity, diabetes and chronic diseases for over two decades. After reading Paul Jaminet’s response post on my blog, he asked if he could offer up a response of his own. This is precisely the kind and scope of discussion that needs to take place on this and any other subject brought up that is somewhat controversial in nature. I’ll warn you now–this is quite long. But it is chock full of lots of studies and information that are important to this discussion:
First of all, thank you Jimmy and Paul for the opportunity to reveal some very relevant, important, and what I think is interesting science. Exchanges such as this will hopefully advance the field of nutrition. I aim only to reveal what I feel is the correct and deeper science. Hopefully, this will not offend anyone, most especially Paul.
Some general background;
Paul mentions in his response that the debate boils down to two points which he states are;
1. On low-carb diets, is it better to eat 400 carb calories per day, as we argue, or some lower number of carb calories, say 100 calories per day?
2. Are “safe starches” the best source of carb calories?
I can answer the 1st point very simply; there is no such thing as a safe non-fiber starch such as rice or potatoes, unless perhaps they are used for an art project. Mr. Potatohead looks friendly enough.
Eating starch will raise blood sugar to some extent in all living beings that do so, and that will cause some degree of harm in everybody. Therefore, the term “safe starch” is an oxymoron. ‘Tolerably harmful’? Perhaps for some. This makes answering the second point, why are ‘safe starches’ safer, moot. Those who wish to just take my word for it can now go on with their lives and be much the wiser. Otherwise, read on…
We can go a tad deeper. Point 1 is a question that becomes a statement by Jaminet and others, for the need to eat ‘safe starches’, and is predicated on two major speculations;
Speculation 1. There is a threshold of blood glucose that going above is bad but being below is not harmful and perhaps healthy.
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. This seems to be quite clear, and would put the issue to rest.
Speculation 2. There is a healthy need for dietary glucose met by eating what he and others call “safe starch”. Jaminet is recommending an intake of 400 cal per day (approximately 100 g) of glucose to meet these ‘needs’, or one can experience what he calls “glucose deficiency symptoms”.
First, let’s dispel the notion that it is necessary to eat some sugar (not withstanding those who are in a hypoglycemic crisis). There is no known need to eat sugar or starches. If there were, it would be an essential nutrient, of which glucose is not. It is not listed on any list of essential (or even conditionally essential) nutrients (that we must obtain because we cannot make them sufficiently ourselves), that I am aware of.
Whether or not “glucose deficiency symptoms” exists, they would not be due to a lack of glucose. Jaminet even points out that, “blood sugar levels don’t leave the normal range during human starvation either”. So If a problem did have to do with glucose, it is not because of a lack of it. He also states, “peripheral glucose utilization is not determined by blood glucose levels, but is hormonally regulated.” This is only partially correct. It is not true for those tissues where insulin is not necessary for glucose to enter the cell, where insulin resistance cannot protect against intracellular hyperglycemia, and where much glucose toxicity as a result of glucose levels per se occurs, such as the endothelium of blood vessels.
This is quite critical, we will see later. Jaminet is on the right track in recognizing the importance of outside influences on glucose utilization as opposed to just glucose level, however he does not go far enough or in the right direction with this. Any problem or hormonal influence secondary to dietary glucose deficiency, were it to exist, is not primarily from thyroid deficiency. Any effect would have far more to do with insulin and leptin (leptin largely influencing thyroid activity), and the effect is not a detriment but instead confers great genetic expression advantage to health and longevity. I address this a bit when I comment later to some specific statements in Jaminet’s response.
He is correct to refer to so-called “glucose deficiency” as a symptom. However, it is not symptoms that we must treat. As much as possible we need to get down to the underlying disease. Even if the symptom had to do with glucose, the disease would not be due to a lack of glucose but rather to wrong instructions about what to do with it. Just consuming more of a nutrient or building block without the body properly knowing what to do with it is likely to cause more harm than good. Osteoporosis, for instance, at least in this country, is rarely due to a lack of calcium. There is a strong positive correlation between those with osteoporosis and those with coronary calcifications. The calcium is there, it’s just in the wrong places. Just taking calcium supplements or drinking lots of milk, will not build bones, (and even if it did would not build strong bones. That is much more predicated on the protein content and quality of the bone matrix than on calcium). Taking extra glucose will no more build mucus or immunity than taking calcium will build bone, or piling bricks on a lawn will miraculously erect a house. I have talked about this extensively for many years. I can quote myself, “A disease is never a disease of the individual part. Diabetes is not a disease of blood sugar, osteoporosis is not a disease of calcium and heart disease is NOT a disease of cholesterol. A disease is caused not by the breakdown of the part itself, but corruption in the instructions to that part, a disruption in the unity of the whole.”
However, I will help Paul and the other ‘safe starch’ proponents out a little bit. The first ‘point’/question can be rephrased into another better question that can be asked even if there is no need for any dietary sugar or starch intake.
Need or not, is it healthier to get glucose, any glucose, from diet or from gluconeogenesis?
I will talk about that and some other thoughts and then present some revealing studies. Afterward I will comment on a number of statements made by Jaminet in his “safe starch” reply that he and others use to support the ‘safe starch’ position, that I feel are important to correct and clarify.
First, it is important to note that we are in complete agreement that a low carbohydrate diet is far better than a high carbohydrate diet. However, it must be understood that what we’re talking about here is optimal diet that can get people the healthiest they can be for as long as possible. Can some people tolerate starches better than others? Yes. However, it must be noted that what might be apparent on the surface may be quite different when one digs deeper (for instance looking at insulin rather than blood sugar), and short-term results may not reflect long-term results. Regardless, that is not what we’re talking about. We are not talking about whether eating 400 cal. of glucose is tolerable, but whether it is safe, and in fact healthier than having not eaten it.
Second, I would like to clear up some confusion and misinformation about how much glucose is necessary in a person who is well adapted to little to no carbohydrate intake. Jaminet states, “This [3 day] fasting level of glucose production of about 600 calories per day is a key number: the body must obtain glucose at at least this level, either through diet or endogenous production, if it is to avoid a glucose deficiency.”
I don’t think anybody here is talking about benefits of a three-day diet. We are talking about results of a much longer-term dietary program, hopefully lifelong. It takes at least several weeks to fully adapt to extremely low sugar intake, such that the body can effectively burn fatty acids and ketones. Therefore, giving numbers for a three-day fast are not very relevant.
Let’s see what George Cahill has to say about glucose needs in a person well adapted to no carbohydrate intake. He is considered one of the world’s experts in the metabolism of starvation and recently wrote a paper summarizing many of his long professional career’s findings. They are the following:
FUEL METABOLISM IN STARVATION
Annu. Rev. Nutr. 2006.26:1-22.
George F. Cahill, Jr.
Department of Medicine, Harvard Medical School
“Total splanchnic glucose production [to fulfill body needs] in several weeks’ starvation amounts to approximately 80 grams daily. About 10–11 grams/day come from glucose synthesis from ketone bodies, 35–40 grams from recycled lactate and pyruvate, 20 grams from fat-derived glycerol, and the remaining 15–20 grams from protein-derived amino acids, mainly alanine.”
[Therefore, under a fully adapted, zero carbohydrate milieu, one only needs approximately 80 g (~320 cal) of glucose daily, the vast majority of which could be derived from fat and non protein sources. Only 15 to 20g need come from proteins, and likely less if one was actually eating fat that would allow for greater glycerol production and protein sparing.]
“Many studies suggest human brain cells can survive with little to no glucose [in adapted conditions].”
“Returning to fasting man, brain use of beta OHB [ketones], by displacing glucose as its major fuel, has allowed man to survive lengthy periods of starvation. But more importantly, it has permitted brain to become the most significant component in human evolution.”
“The increased glycerol from adipose lipolysis would increase hepatic glucogenesis and spare muscle nitrogen accordingly, similar to eating small amounts of carbohydrate.”
“In vitro studies using brain slices show the priority of CNS usage of beta OHB [ketones] over glucose…”
“An approximation for clinical use is that if a diet contains over 100 grams carbohydrate, there is no ketosis (<0.1 mM) [italic mine]. As one decreases dietary carbohydrate, ketogenesis begins...Glucose administration to fasting normals reverses starvation metabolism rapidly.."
The best-known mechanism, with thousands of studies since the 1930s, to reverse disease and extend lifespan and youth, is through caloric restriction, with the genetic expression and physiologic mechanisms therein initiated. Eating 100g of carbohydrate will inhibit if not stop that highly beneficial process. What I have been endeavoring to do is to mimic the effects of caloric restriction (see my study http://www.jarcet.com/articles/Vol9Iss4/Kohnilias.pdf) without having to caloric restrict by using the science of the biology of aging that shows that it is carbohydrate and partial protein restriction, but not fat restriction, that is required to elicit its effects.
Is there a threshold for blood sugar that when kept below does no harm, and when above does?
All animal life, unless it is a bloodless alien, will raise their blood sugars if sugar, or sugar forming starches, are eaten. Eating rice or potatoes will, specifically and especially, raise blood sugar. The question then becomes, is the amount of elevation and accumulation of glucose in the bloodstream harmful?
The crux of the ‘safe starches’ argument is that no harm will come of this and it is, in fact, healthy. It is acknowledged that blood glucose will elevate after eating ‘safe starches’, but will generally stay below 140 mg/dl that Jaminet says is perfectly safe. Is it?? The science writing (below) is on the wall and the answer is…clearly no.
It is important to realize that this answer is no; there is no safe intake of sugar, nor a threshold level of blood sugar below which no harm will come, and I will shortly devote a fair amount of time to show this.
It is also comforting to hear Jaminet and others say that perhaps while some people cannot tolerate spikes in glucose, most people can. So he says a moderate spike in glucose is okay unless one has metabolic derangement.
Therefore, it is also important to note that the detriment of glucose applies to everyone. Some people can hold up to a greater beating than others. However, even if someone appears to tolerate something, it does not mean it is good for them. The body can compensate, tolerate, and defend itself from particular insults, but if that compensation is repeated over and over and over again the body will lose that ability to compensate and defend. The body can tolerate a windfall of glucose by spiking insulin (and leptin) to store what isn’t immediately burned for a rainy day (mostly as fat). But continuing to do this will wear the body out and will result in insulin and leptin resistance.
Let’s look at some more science:
There is no threshold for healthy blood glucose:
Is there a glycemic threshold for mortality risk?
Diabetes Care May 1999 vol. 22 no. 5 696-699
“…the lowest observed death rates were in the intervals centered on 5.5 mmol/l [99mg/dl] for fasting glucose and 5.0 mmol/l [90 mg/dl] for 2-h glucose.
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.”
“Normal” blood glucose and coronary risk
BMJ VOLUME 322 6 JANUARY 2001
“Khaw et al in this issue shows that glycosylated haemoglobin levels are positively associated with the risk of future coronary heart disease in a linear stepwise fashion, with no evidence of a threshold effect and independent of other common risk factors for coronary heart disease. These are the most convincing data available that the association between glucose and coronary heart disease occurs throughout the normal range of glucose.”
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 (2008) 51:1123–1126
“Results During follow-up of 18,406 non-diabetic men, 13,116 deaths occurred (1,189 by stroke).
Plots of stroke mortality rates versus [post challenge of 50 gms] blood glucose identified an upward inflection in risk of death from stroke at about 4.6 mmol/l [82 mg/dl]. This upward inflection in risk could be adequately described using a single linear term above this threshold. Conclusions/interpretation; An incremental elevation in stroke mortality rates occurs with increasing post-challenge blood glucose.”
How the Blood Sugar of Diabetes Affects the Body
“At present, the diagnosis of diabetes or prediabetes is based on an arbitrary cut-off point for a normal blood sugar level.”
ScienceDaily, Monash University (2008, August 22)
Killer Carbs: Scientist Finds Key To Overeating As We Age
published in ‘Nature’.
“Dr Andrews found that appetite-suppressing cells are attacked by free radicals after eating and said the degeneration is more significant following meals rich in carbohydrates and sugars. ‘The more carbs and sugars you eat, the more your appetite-control cells are damaged, and potentially you consume more,’ Dr Andrews said.”
Is There a Clear Threshold for Fasting Plasma Glucose That Differentiates
Between Those With and Without Neuropathy and Chronic Kidney Disease?
Am J Epidemiol 2009;169:1454–1462
“Recent studies suggest that no distinct glycemic threshold consistently differentiates individuals with or without retinopathy. The authors sought to determine whether the same was true [in a random sample of individuals] for other microvascular complications…Prevalence of peripheral neuropathy and chronic kidney disease gradually increased in relation to fasting plasma glucose, beginning at levels below the existing diagnostic threshold for diabetes mellitus of 7.0 mmol/L (126 mg/dL).”
One-hour postload plasma glucose and risks of fatal coronary heart disease and stroke among nondiabetic men and women: the Chicago Heart Association Detection Project in Industry (CHA) Study.
J Clin Epidemiol. 1997 Dec;50(12):1369-76
Stamler J. Northwestern University Medical School, Chicago, IL
“Plasma glucose was determined one hour after a 50-gram oral glucose load… higher glucose was significantly associated with mortality from coronary heart disease, stroke, cardiovascular diseases, and all cause mortality in men and women. This large longitudinal study provides evidence that one-hour postload plasma glucose in the absence of clinical diabetes at baseline apparently is an independent risk factor for fatal coronary heart disease and stroke in middle-aged and older nondiabetic men and women, and also for cardiovascular diseases and for all cause mortality.”
Glycated haemoglobin, diabetes, and mortality in men in Norfolk cohort of European Prospective Investigation of Cancer and Nutrition (EPIC°©Norfolk)
BMJ VOLUME 322 6 JANUARY 2001
“HbA1c was continuously related to subsequent all cause, cardiovascular, and ischaemic heart disease mortality through the whole population distribution, with lowest rates in those with HbA1c concentrations below 5%. An increase of 1% in HbA1c was associated with a 28% (P < 0.002) increase in risk of death..."
Glucose accelerates aging, oxidative stress…
Pro-Aging Effects of Glucose Signaling through a G Protein-Coupled Glucose Receptor in Fission Yeast
PLoS Genetics, March 2009 | Volume 5 | Issue 3
“…excess of glucose has been associated with several diseases, including diabetes and the less understood process of aging. On the contrary, limiting glucose (i.e., calorie restriction) slows aging and age-related diseases in most species…The pro-aging effect of glucose signaling on life span correlated with an increase in reactive oxygen species and a decrease in oxidative stress resistance and respiration rate. Likewise, the anti-aging effect of both calorie restriction and the Dgit3 mutation was accompanied by increased respiration and lower reactive oxygen species production.”
Rather than being good for white blood cells, glucose can oxidize them…
GLUCOSE CHALLENGE STIMULATES REACTIVE OXYGEN SPECIES (ROS) GENERATION BY LEUCOCYTES
The Journal of Clinical Endocrinology & Metabolism, Vol. 85, No. 8, Aug. 2000
“Blood samples were drawn from 14 normal subjects prior to, at 1, 2 and 3 h following ingestion of 75 g glucose…We conclude that glucose intake…increases oxidative load [in leukocytes] and causes a fall in a-tocopherol concentration.”
Sugar glycates. For those unaware, this is where glucose (and other sugars) combines with other essential molecules such as proteins and DNA affecting their shape and structure and preventing their proper function. This is a very bad. Glycation is one of the major molecular mechanisms that cause damage resulting in senescence that we notice as “aging”. That is why products of glycation, advanced glycated end products, are not coincidentally called AGEs.
There is no threshold for glycation…more glucose, greater risk of glycation…
Advanced glycated end products: a review
Diabetologia (2001) 44: 129-146
“Glycation is concentration-dependent”
Lipoprotein Lipase Mediates the Uptake of Glycated LDL in Fibroblasts, Endothelial Cells, and Macrophages.
Diabetes 50: 1643–1653, 2001
“Protein glycation is a nonenzymatic reaction of glucose with susceptible amino groups that occurs at a rate linearly related to the plasma glucose concentration.”
Significant amounts of highly reactive precursors to AGEs (advanced glycated end products) are formed after a single standard (with carbohydrate) meal…
a-Dicarbonyls Increase in the Postprandial Period and Reflect the Degree of Hyperglycemia.
Diabetes Care 24:726–732, 2001
“Chronic hyperglycemia is known to increase tissue glycation and diabetic
complications, but controversy exists regarding the independent role of increased postprandial glucose excursions. To address this question, we have studied the effect of postprandial glycemic excursions (PPGEs) on levels of methylglyoxal (MG) and 3-deoxyglucosone (3-DG), two highly reactive precursors of advanced glycation end products (AGEs)….PPGE was determined after a standard test meal. Conclusion: Increased production of MG and 3-DG [AGEs] occur with greater PPGE, whereas HbA1c does not reflect these differences.”
Insulin glycates contributing to insulin resistance…and its sequelae, diabetes, CV disease, obesity, cancer, and accelerated aging…
Glycation of insulin results in reduced biological activity in mice.
Acta Diabetol. 1997 Dec;34(4):265-70
“These data indicate that glycated insulin exhibits impaired biological activity which may contribute to glucose intolerance…”
Glycation of LDL in non-diabetic people: Small dense LDL is preferentially
glycated both in vivo and in vitro.
Atherosclerosis. 2009 Jan;202(1):162-8
“CONCLUSION: Small-dense LDL is more susceptible to glycation and this may contribute to the atherogenicity of smalldense LDL, even in non-diabetic people.”
Glucose directly contributes to aging and feeds cancer cells;
Glucose restriction can extend normal cell lifespan and impair precancerous cell growth through epigenetic control of hTERT and p16 expression.
FASEB, December 17, 2009
“Cancer cells metabolize glucose at elevated rates and have a higher sensitivity to glucose reduction…The altered gene expression was partly due to glucose restriction-induced DNA methylation changes…Collectively, these results provide new insights into the epigenetic mechanisms of a nutrient control strategy that may contribute to cancer therapy as well as antiaging approaches.”
Raising glucose, raises insulin, increases insulin resistance…
Beta-cell dysfunction and glucose intolerance: results from the San Antonio metabolism (SAM) study.
Diabetologia (2004) 47:31–39
“Conclusion/interpretation. When the plasma insulin response to oral glucose is related to the glycaemic stimulus and severity of insulin resistance, there is a progressive decline in beta-cell function that begins in “normal” glucose tolerant individuals.”
High insulin leads to insulin resistance–what I’ve said for 2 decades
Barbara B. Kahn and Jeffrey S. Flier, Harvard Medical School
The Journal of Clinical Investigation, August 2000 | Volume 106
“Hyperinsulinemia per se can cause insulin resistance by downregulating insulin receptors and desensitizing postreceptor pathways, as was confirmed by overexpression of insulin in livers of otherwise normal transgenic mice. This transgene resulted in an age-related reduction in insulin receptor expression, glucose intolerance, and hyperlipidemia without any primary genetic defect in insulin action or secretion.”
Alternative Approach to Treating Diabetes Tested
ScienceDaily (June 10, 2011)
From; Deletion of Insulin-Degrading Enzyme Elicits Antipodal, Age-Dependent Effects on Glucose and Insulin Tolerance.
Plos One June 2011 | Volume 6 | Issue 6
“It’s an example of too much of a good thing [insulin] becoming bad for you…chronic hyperinsulinemia seemed to actually cause diabetes. As they aged, the mice appeared to adapt to the chronically high insulin levels, for example, by reducing the number of receptors for insulin in their tissues. These adaptations make the mice less sensitive to insulin, which is the exact cause of type 2 diabetes.”
Insulin: In need of some restraint? Salk Institute
Proceedings of the National Academy of Sciences,March 07, 2007
“the study reveals the “dark side” of high insulin production, the kind that results from over eating and obesity. “Insulin is very effective at lowering blood sugar, and promotes fat storage, preparing the animal for times when food may not be available,” he says. “But when the hormone [insulin] is produced at too high a level for too long, the body becomes insulin resistant and blood sugar and certain blood lipids gradually creep up, which can cause progressive damage to multiple organ.”
I also know from treating hundreds of diabetic patients that reducing insulin and leptin via my diet that prevents insulin and leptin from spiking and keeps them low, rapidly improves insulin and leptin resistance, and greatly improves, if not altogether reverses, T2 diabetes and other chronic diseases of aging. The reduction in leptin and insulin happens first and appears to be a requisite. Others are now treating with a similar diet including Eric Westman and Mary Vernon who have published several papers.
I could go on all day with studies such as this…and that’s mostly focusing on blood glucose (BG). But the main culprits in the chronic diseases of aging are hormones that glucose both powerfully affects and is affected by…such as insulin. Raising BG raises insulin.
If BG is staying “normal” and not going above 140 (as Jaminet’s falsely theoretical safe limit), but it is taking lots of insulin to keep the BG down, that is not an advantage, nor is it ‘safe’. It is trading one evil for an even worse one. A glucose load may only be less harmful (not safe) if both insulin and glucose are staying low (i.e. one is very insulin sensitive). If one is obtaining a glucose tolerance test (that I do not advise secondary to the damage it causes), one must test insulin concurrently to get meaningful data.
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. 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.
But wait, there’s more…You’ll get two for the price of one. Raise blood glucose and you raise leptin and if you keep raising leptin you’ll get leptin resistance along with your insulin resistance…resulting in centrally mediated (by hypothalamic signals to liver) increased gluconeogenesis, high glucose, fatty liver, elevated insulin, islet burnout…diabetes…The effect on leptin, and the leptin story is, I feel, the most important, but that will be a story for another day. Those interested can refer to my book, website, and writings on the internet.
So how about the last question that I brought up? 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, these will cause a far lesser glucose excursion than the proposed ‘safe starches’ such as rice and potatoes (unfortunately for my many Asian and Irish friends).
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 rapidly spiking blood glucose…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 great and has not evolved for a long, post reproductive and healthy lifespan. The immediate physiological consequences of raising insulin are well known. They are now in every medical physiology textbook, and was the topic of a talk that I gave almost 13 years ago, “Insulin and its Metabolic Effects“ that is easily found all over the internet, that helped to kick off interest in the powerful relationship between insulin and disease. Elevated insulin 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. It increases coronary plaque formation. It stimulates cellular reproduction increasing risk of cancer, etc., etc.
#3. Repeated elevations in 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 premature 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 a glucose, insulin and leptin elevation if glucose is made via gluconeogenesis than if taken in a lump 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 requirements far better than ‘thinking’ we do, and will only make the glucose that it feels is necessary at the time. 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 upon the body 400 cal. glucose to daily.
Now I hope to shed more light by commenting on a number of Paul’s statements from his response that I feel are in need of correction and clarification.
“We do not consider glucose to be a toxin, though it may become toxic in hyperglycemia.”
However, glucose is a toxin in the same manner that oxygen can be. Glucose can non-enzymatically glycate, oxidize and cause damage just like oxygen can cause oxidation and free radical damage. Though it would be unwise to reduce oxidation by not breathing, it is not unwise to reduce glycation and free radicals by not eating glucose.
“Our “regular” diet is not specifically directed at diabetic or metabolically damaged persons.”
We are all metabolically damaged to some extent. None of us has perfect insulin and leptin sensitivity. Furthermore, there is no absolute demarcation between diabetes, impaired glucose tolerance, and so-called “normal, nondiabetic”. The classification of diabetes as a fasting sugar of 126 or above is arbitrary, as is the classification of impaired fasting glucose being a fasting sugar of 100 to 125. We all suffer from non-enzymatic (non-controlled) glycation and the same damage and diseases, for the same reasons, that occur in so-called diabetics. Furthermore, the diagnosis of diabetes as a disease of blood glucose is extremely archaic. It is not a disease of blood glucose, but a disease of what is directing it, namely hormones and namely insulin and leptin. And, as I stated above, none of us have perfect insulin and leptin signaling. It is for that reason that I say that we all have diabetes, some more than others, and should all be treated as such.
“We agree that diseases of metabolic derangement may benefit from lower carb consumption…In this case, replacing protein rather than providing
dietary carbs may be a more helpful strategy.”
See above; we all have some degree of metabolic derangement.
It is far better to replace the carbs with beneficial fats and oils than extra protein that can turn to glucose and raise mTOR.
“We agree that there is no single prescription that is optimal for every
person…’every diseased person is unhealthy in his own way.’”
However, we must attempt to seek out the common roots of these so-called “diseases”. Fortunately, I think we can. When we do, we find that many of the so-called diseases such as obesity, (T2) diabetes, vascular disease, and virtually all of the chronic diseases of aging have common roots, and it is those roots we must treat, or otherwise we are treating symptoms. Not only will we not then help, we will likely worsen the condition…as in virtually all non acute care standard medical practice, that lives off of treating symptoms rather than diseases. See the ACCORD study and so many others.
“it seems to me the debate boils down to two primary questions:
1.On low-carb diets, is it better to eat 400 carb calories per day, as we argue, or some lower number of carb calories, say 100 calories per day?
2. Are “safe starches” the best source of carb calories?
Actually, the debate boils down to one question. Is there such a thing as ‘safe starches’ or is that term an oxymoron? If the answer to #1 is oxymoron, and the less the sugar forming carbohydrate intake the better, then #2 must be rephrased to, ‘If one were to eat some carbohydrate, what kind would do the least damage’.
“Brain and nerves typically consume about 480 calories per day of glucose. Ketones can displace up to perhaps 60% of this.”
Actually, much more under adapted conditions.
“the brain always requires some glucose.”
But very little if any under adapted conditions. See Cahill above.
“After 3 days of fasting…the body’s rate of glucose manufacture in liver and kidneys is about 600 calories per day.”
I do not think that any of us are just talking about a three day diet, and 3 days is not near enough to adapt to a VLC diet to determine long term glucose needs. Under adapted conditions the rate of glucose production falls to almost half of that. See Cahill above.
“The fasting level of glucose utilization is likely to be suboptimal for health: fasting invokes glucose-and-protein-conservation measures which evolved to make us more likely to survive famine, but almost certainly have a cost in long-term health.”
This is an assumption that is likely very wrong; in fact, quite the opposite. Those adaptations evolved as strategy to improve longevity and health so as to be able to survive the famine and reproduce at a future more opportune time. And those strategies, as shown by hundreds if not thousands of CR studies, enable lifespan, (and youth) to be considerably stretched, and this should hardly be called unhealthy.
The adaptive changes to starvation are to keep the organism alive. Our endeavor is to try to connect into those same biological mechanisms without starving, and in fact try to make it easy to do that…and this is done by restricting glucose intake to keep insulin and leptin low (and protein intake moderate to keep mTOR low).
“This fasting level of glucose production of about 600 calories per day is a key number: the body must obtain glucose at at least this level…if it is to avoid a glucose deficiency.”
That number is incorrect when well adapted to not eating glucose. According to Cahill, 80g ~320 calories/day.
“We are a slightly or moderately low-carb diet.”
Then it is a slightly or moderately good diet. The amount of glucose forming carbohydrate that you suggest is enough to greatly diminish if not eliminate ketone production. In other words, one’s evolutionary biology would not be tricked into believing that there is a famine and that genetic compensatory mechanisms to outlive that famine, to remain healthy and reduce the rate of aging, will not be expressed.
“the biggest reason for glucose utilization is the construction and maintenance of the human glycome [for immune, mucous etc.]”
Again, no one is disputing the fact that glucose is a necessary nutrient. We’re just disputing the necessity of eating it.
“Why, if cells can run on glucose and blood glucose remains normal, do starving people die?”
Because maybe most of the cells are not meant to run on glucose, but rather ketones, and a person will die when fat stores and precursors to ketones are insufficient.
“A clue [about glucose deficiency] is the fact that starving people develop a hacking cough in their final weeks of life. Despite blood glucose levels in the normal range, they cease producing mucus…”
Starving people are protein deficient much more than glucose deficient, and mucin is a glycoprotein…and a protein deficiency affects much more than the mucous per se. including the membranes themselves, including innervation to those membranes, blood circulation to those mucous membranes that shuts down secondary to vascular dysfunction and intravascular volume depletion secondary to reduced albumin/osmolarity, and heart failure…and so many other functions that only time would limit talking about. At that point, giving a gallon of glucose probably wouldn’t help. That person needs protein and fat.
Also, you are equating a person starving and near-death, and running out of all energy substrates to stay alive, to one on a high fat, very low carbohydrate diet that evidence reveals may extend lifespan–Not quite appropriate.
Incidentally, the body preferentially maintaining blood glucose until the end reveals the vital importance of having an anaerobic fuel supply available for fight and flight emergencies. That is main reason we keep glucose around.
“The reality is this: peripheral glucose utilization is not determined by blood glucose levels, but is hormonally regulated.”
Correct, except for those tissues in which glucose entry is not regulated by hormones and where most of the damage occurs from that glucose, the endothelium to name an example. Furthermore, the hormones that do determine glucose utilization are in turn strongly influenced by glucose levels.
“What are the hormones that regulate glucose utilization? During glucose deficiency, T3 thyroid hormone levels decrease and reverse-T3 levels increase.”
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. Intracellular antioxidant systems, heat shock proteins, DNA repair, autophagy, all tricks that nature has, are up-regulated to allow the organism to increase repair and maintain itself to remain healthy and alive. 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. TSH is not elevated. 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. It is not always a sign of malfunctioning thyroid as is frequently taught, but is instead one of the redundant ways that thyroid action is controlled. Reduced thyroid level in this regard is analogous to reduced fasting insulin that generally indicates improved insulin sensitivity, which also occurs in fasting and caloric restricted animals, and is also part and parcel of the benefits seen. Sometimes our complexity is indeed paradoxical.
“Decreased production of molecules like hyaluronan and mucin and reduced levels of T3 thyroid hormone, then, are outcome of dietary glucose deficiency.”
Reduced levels of T3 occur secondary to leptin reduction that occurs secondary to reduction in glucose. This is not a detriment and is not hypothyroidism, but part and parcel of genetic expression of increased maintenance and repair. See above. As far as ‘glucose deficiency’ impairing mucin and hyaluronan production; I respect your theory but cannot agree with it as it lacks evidence, nor do I agree with the concept of glucose deficiency while on a VLC diet such as mine (moderate protein, relatively high fat).
“Do Glucose Deficiency Symptoms Actually Occur in Low-Carb Dieters?
No. There is no such thing as a glucose deficiency until one is dead or nearly so…There can be a glycosylation deficiency secondary to improper instructions about what to do with glucose often secondary to glycation and improper insulin and leptin signaling at least partially contributed to also by excess glucose. Glucose deficiency is not the same as glycosylation defects or deficiencies. Again, it is not a lack of glucose but signals that tell us what to do with it that are most critical.
“…many cases of glucose deficiency symptoms that developed on very low-carb Paleo or GAPS diets…”
It is a big jump to assume that problems were due to ‘glucose deficiency’. Were these people substituting high protein or beneficial fats for carbs…big difference?… Did they supplement with magnesium and potassium and other nutrients that are necessary when instituting a very low carbohydrate diet secondary to a fall in insulin and the diuresis of retained fluid. There are so many variables that are not accounted for here, that jumping to the conclusion that it is a glucose deficiency is not warranted.
Also, testimonies will be forthcoming from any diet, healthy or otherwise…just look at any infomercial. After using my very low-carbohydrate moderate protein and sufficient fat to satisfy hunger and energy needs diet, and after having reversed countless numbers of diabetics, including several T1s, heart failure patients, hypertensives, and even a few severe metastatic cancer patients, I could furnish a few testimonies of my own that time, space, inclination, and relevance precludes from printing here…and I have never heard of a mucus deficiency problem on my diet.
“Low-carb diets, alas, impair immunity to fungal and protozoal infections.”
Quite debatable. Fungi in particular feed on sugar and many books have been written attributing considerable success in treating fungal infections to glucose restriction.
“The Possibility of Slow-Developing Problems Cannot Be Ruled Out”
Certainty does not exist. However, the possibility, even probability of slowly developing problems can be likely ruled in secondary to dietary intake of glucose forming starches such as rice and potatoes i.e. glycation, serum elevations in insulin and leptin, etc.
“Biomedical researchers are gradually realizing the importance of glycosylation defects in leading diseases. I report these papers, not because I think they tell us how many carbohydrates we should eat – they don’t – but to remind everyone of the complexity of biology.”
Yes, these papers are not very relevant to our discussion, but yes, it is good to point out the complexity of biology, however that complexity is more complex than indicated Just eating more carbs will not fix that GnT4a deficiency.. It would need to be genetically expressed, and non-enzymatic glycation resulting from increasing BG secondary to potato and rice consumption will, if anything, hinder that.
Believing that a glucose deficiency is behind mucus, immune, cancer and diabetes problems, is a huge leap, and is analogous to believing that most cases of osteoporosis is secondary to calcium deficiency in Western society. It is not a problem with the pieces. In nearly all of these cases we have enough of those. The problem lies in how we are putting them together, and this is hormonally controlled, and the most influential of these hormones are nutrient sensors controlled by diet that glucose consumption corrupts. It is far, far more likely for glycosylation defects to occur secondary to (non-enzymatic) glycation, than from lack of glucose.
“We cannot be sure that there may not be negative health effects from severe carb restriction that will show up only after decades.”
Well, so far they have not been found. That is why carbohydrates are a nonessential nutrient.
“I think everyone should acknowledge that very low-carb diets may have unexplored risks.”
We can say that about any diet, and in fact any event. One can only use the best science available and make the best guess available. We do know one thing for sure, a high carbohydrate diet is a major cause of all chronic disease. I see nothing wrong in running the other way.
“Fructose is treated by our evolved physiology as a toxin…”
Not necessarily true. It is very possible that animals evolved to make fat out of the fructose of autumn fruits and berries to prepare for long, hard, cold and food sparse winters.
“…it [fructose] is shunted to the liver where it is rapidly disposed of.”
…as is most of the glucose we eat also shunted to our liver, and fat, and muscle to be rapidly disposed of as fat and glycogen.
“In general, the more fructose people consume, the worse their health. Dr. Robert Lustig spoke at the Ancestral Health Symposium on this topic.”
And I agree. I spoke of this numerous times for the last 15 years; fructosylation, liver metabolism. This is far from new. But there were bigger fish to fry…such as glucose, insulin and leptin…and just because fructose can be unhealthy, does not mean that glucose is healthy.
the figure: “Marginal Benefit Curve for Nutrients”
This seems highly speculative and not based on current evidence. See studies above. A more accurate graph would just show toxicity increasing as glucose does.
“On a low carb diet, a safe starch is likely to be nourishing, regardless of its glycemic index.”
I disagree. All glucose forming starches will raise glucose, cause glycation, raise insulin, raise leptin, contribute to insulin and leptin resistance, and be far from safe.
“In diabetics, there seems to be no detectable health risk from glucose levels up to 140 mg/dl..”
Not true. See multiple studies above…and these studies are comparing to so-called normal people. I think we all want to be much healthier than what is considered normal.
“I offer as Exhibit A the experience of Haggus Lividus on Jimmy’s thread. Haggus measured blood glucose levels after consuming ~100 calories of rice and found that blood glucose levels peaked at 7.7 mmol/l = 139 mg/dl. These are safe levels of blood glucose – below 140 mg/dl at all times. Yet Haggus Lividus took these as levels to be unsafe!”
She was very right. See multiple studies above.
“Tom Naughton reports that a potato raises his blood glucose level to 175 mg/dl. But he eats a very low-carb diet, and very low-carb diets induce hormonal changes that lead to glucose conservation. One result of these changes is insulin resistance and impaired glucose tolerance.”
NOT TRUE. Quite the opposite. I have shown for almost two decades that a very low carbohydrate, moderate protein, higher fat diet greatly improves insulin resistance and glucose tolerance, often reversing diabetes, and others more recently are showing this also.
The adaptive changes to starvation are to keep the organism alive and healthy. Jaminet even admits in this post that he might recommend a lower than ‘safe carb’ carb diet for diabetics…and he should, as it will greatly improve insulin resistance and glucose tolerance, not worsen it.
Is there any difference between the damage done by fasting glucose and that from postprandial glucose? I think not. So a blood sugar of 139 mg/dl is in the fasting diabetic range whether fasted or not, and if one eats ‘safe starches’ 3-4 x/day, ones BG is in the diabetic range for half the day or longer…and this is in a so-called healthy person.
And what about insulin? It is going high to keep the glucose down. And leptin? As I have pointed out many times, if one lowers sugar at the expense of raising insulin, that is trading one evil for an even worse evil. Therefore, if one is going to do an OGTT (that I never recommend, as the testing itself then becomes harmful) then to get any meaningful information, one would have to also do an insulin level with each glucose test.
Additionally, if one consumes glucose and it is not reflected in the blood glucose, where has it gone? It didn’t just disappear. It raised insulin, and a small portion might have gone towards the manufacture of glycogen, or glycosylation (and unwanted glycation), however the remainder was turned into fat, and if that person is a bit leptin resistant (partly from having repeatedly raised leptin), then that fat will store in the viscera, i.e. fatty liver.
When there are testimonies adverse to Jaminet’s theories, he dismisses them, but gives several far less objective anecdotal reports more credence. This is not science and seems like an all too convenient way to explain away the high blood glucose after eating “safe starches”, especially since most Paleo people are on a low-carb diet.
“Tom Naughton…blood glucose rises to 175 mg/dl after consuming a potato..he must never again eat a whole potato in isolation from other foods, or he is insulin resistant in order to conserve glucose and he should eat carbohydrates more often to improve his insulin sensitivity…”
See above. Also, everyone eating a potato will raise their BG. Isn’t one of the main reasons to change diet, to improve health. It is very different saying that some can tolerate glucose foods more than others, from saying that these foods are healthy. Doesn’t it make more sense that a diet that is especially good for those who are ill, might also be good for those that, at least on the surface, do not appear to be?
“Dr. Fred Pescatore should read our book. It is not true that 200 calories of starch will necessarily take a person out of ketosis. Consumption of medium chain triglycerides or coconut oil in conjunction with starches will trigger a mild ketosis.”
It isn’t necessarily ketosis that we want…it is the burning of those ketones that is beneficial, and the two are often opposite. Ketosis is what is left over from not having burned them. Eating carbs can inhibit the burning of ketones that the MCTs may be making, thus resulting in ketosis, but not necessarily ketone utilization.
He/she who thinks he/she is totally healthy, who is totally without unwanted glycation/oxidation, insulin resistance, leptin resistance…cast the first stone…All others, avoid sugars and starch as much as possible…except perhaps to now and then appreciate the yeast that took hits of glycation from rice, while enjoying a nice small shot of hot sake.
As always, I welcome your feedback and input in the discussion of ideas. My only request is that you stick to the issues at hand and refrain from personal name calling or attacks against any individuals. THANK YOU!
11-1-11 UPDATE: Paul Jaminet responds to Dr. Rosedale.