The first thing the reporter asked me in the telephone interview was “why is the American Diabetes Association (ADA) opposed to low carbohydrate diets?” I said I didn’t really know. I admitted that they had allowed themselves certain indulgences but I pointed out that they are trying to back into low carbohydrate diets however weakly. In any case, the ADA is many people and I doubted that the rank and file members of the ADA even know what the nutritional committee has to say. So, although the ADA represents, in some way, the establishment position, nobody really knows what practicing physicians and clinics actually do.
Carbohydrate restriction in the management of diabetes
Out of love and concern for the truth, and with the object of eliciting it, I have laid out the basic principles behind carbohydrate restriction as the “default diet” (the one to try first) in the treatment of diabetes. Dietary carbohydrate restriction derives from fundamental biochemistry and has been a traditional therapy for diabetes before and since the discovery of insulin. The strategy is based on the fundamental idea that diabetes is a disease of carbohydrate intolerance (inadequate or absent insulin in response to carbohydrate (type 1) or inability to respond to insulin accompanied by deteriorating pancreatic function (type 2). Control of blood glucose has positive effects on all of the downstream sequelae including lipid markers for and incidence of cardiovascular disease. No experimental or clinical data has shown any contradiction to these principles. The following 15 theses are the basis for re-evaluation of the role of carbohydrate restriction in treatment of type 2 diabetes and adjunct to treatment of type 1 diabetes.
The Fifteen Theses.
- Almost all of the increase in calories during the epidemic of diabetes is due to increased carbohydrate. Fat, if anything, went down. Consumption of most foods, including fruits and vegetables increased. The exceptions were red meat and eggs.
- Dietary carbohydrate restriction reduces insulin fluctuations and is the most effective approach to glycemic control, the primary targets of nutritional therapy.
- Adherence to low-carbohydrate diets is at least as good as other dietary interventions and frequently substantially better. Adherence is frequently comparable to that for drug recommendations. In practice, diabetes clinics and internet sites recommend carbohydrate counting and “eating to the meter.”
- No dietary intervention is better than carbohydrate-restriction for weight loss. Low-carbohydrate diets generally do better than low-fat diets for whatever period they are compared. Long term trials of low-fat diets such as the Women’s Health Initiative have a consistent record of poor performance.
- Contrary to stereotypes, low-carbohydrate dieters do not substantially increase either fat or protein consumption. Whereas per cent fat may increase, the absolute amount of fat does not change much before and after a carbohydrate-restricted diet. Low-carbohydrate diets are high in vegetables and, in practice, are not particularly iconoclastic. Such diets are relatively low in fruits but researchers emphasize that fruits and vegetables are nutritionally different: per gram, fruits have, on average, more calories, more carbohydrates, more sugar, fewer antioxidants and lower potassium.
- The best predictor of microvascular and, to a lesser extent, macrovascular complications is hemoglobin A1C which is substantially under the control of chronic dietary carbohydrate restriction.
- Although carbohydrate-restricted diets do not require the addition of saturated fat, numerous studies have shown that, contrary to popular opinion, dietary total and saturated fat are not associated with incidence of cardiovascular disease (CVD).
- Dietary carbohydrate restriction is the single most effective method (except for total starvation) of reducing triglycerides, and is as effective as any intervention, including most drugs, at increasing HDL and reducing the number of small-dense LDL particles. Beyond lipid markers, carbohydrate restriction improves all of the features of metabolic syndrome.
- Intensive glucose lowering by dietary carbohydrate restriction has no side effects comparable to intensive pharmacologic treatment as, for example, in the ACCORD trial or other agents whose safety is continually challenged.
- Beneficial effects of carbohydrate restriction do not require weight loss. Under weight maintenance conditions, dietary carbohydrate restriction dramatically improves glycemic control, hemoglobin A1c and lipid markers.
- Patients on carbohydrate-restricted diets reduce and frequently eliminate medication whereas high-carbohydrate, low-fat diets may lead to increased use.
- Diets based on carbohydrate-restriction are, in fact, widely practiced clinically, if in an unsystematic way. Contrary to recommendations of government and private health agencies, individual practitioners and clinics frequently recommend dietary carbohydrate restriction.
- Even as establishment nutrition slowly accepts low-carbohydrate diets there is a consistent failure to recognize or cite the work of researchers in this field. This contentious “two worlds” approach has added to the confusion for patient and practitioner alike.
- A variety of sources — input to government hearings, popular books and internet forums — have documented a large population of patients who are significantly dissatisfied with current medical treatment and feel that they have not been offered a valuable treatment and, in fact, have been harmed by recommendations of their physicians and health agencies. Added to the patients who feel that low-fat recommendations have misled them on obesity, we have created a population of people who distrust all health recommendations. .
- The palpable opposition to carbohydrate restriction of granting agencies has narrowed the focus of basic research. Downstream insulin signaling, for example, is more likely to be funded if it does not mention that carbohydrate stimuli for insulin signaling.
Moving forward.
The 15 theses above are my take on the problem, subject to anybody else’s input. I am not sure it would do much good to nail them to the door of the ADA, but they may be good arguing points for trying to move forward. My suggestions, as noted before, are to ask for:
- Open hearings on nutrition in which all credentialed researchers participate and, in particular, researchers in low carbohydrate diets meet with their critics (a kind of Diet of Worms).
- Funding of a comparative study in which researchers in carbohydrate restriction and experts in other diets cooperate in the design and analysis of outcomes. Possible results and their meaning are agreed upon in advance and finally,
- New oversight agencies (possibly from National Science Foundation or Office of Science and Technology Policy) where truly neutral scientists can evaluate information and make recommendations (or not if there is no evidence).
When I was Dx’d with type 2 in 1996, my first question to my doctor was, “If diabetes is a disease in which you can’t metabolize carbohydrate, why was I handed a diet that would require me to increase my carbohydrate intake over what I’m currently eating?” He thought a bit and then said, “Well, when you have diabetes, you’re at high risk of heart disease, and fats increase heart disease, so you can’t eat a lot of fat. Diabetics are also at high risk of kidney disease, and protein damages kidneys, so you can’t eat a lot of protein. The only thing left is carbohydrate.”
Now, since then, we’ve learned that fats DON’T cause heart disease and protein DOESN’T cause kidney disease, so that logic no longer applies.
However, many people in the LC world bash physicians and dieticians, suggesting that they’re too dumb to understand that it’s carbohydrates that raise blood sugar. Physicians, at least, certainly do understand this. But they, or their instructors when they were in med school, think like my physician, that the risks of high blood glucose are lower than the alleged risks of fat and protein. [This was before the DCCT results were in, so some people didn’t even believe that high BG levels caused microvascular complications.)
I think bashing people makes them defensive and more apt to stick to their outdated ideas. So I think one approach would be to acknowledge that in the past physicians were doing what they could on the basis of accepted knowledge of that time, but now the evidence has changed in favor of LC. Let them squirm out of their past mistakes by saying, “New evidence shows” so they can save face. Then we could all work together to help people with diabetes, as you suggest in suggestion 2.
One issue that needs to be addressed and that I can’t find any discussion of is this:
The LC, high-fat diet was used before and even after insulin was available (one type 1 remembers his mother coming into his room as he was getting ready for bed and saying, “You haven’t had enough fat today. Eat this avocado”). A diabetes diet in a 1910 home health book I have was very similar to Atkins induction. Yet people with diabetes had cardiovascular disease at much higher rates than those without diabetes. Why?
Was it because of lack of easy blood glucose monitoring so levels were yo-yoing from very low to very high all day? (Bernstein’s were, as he discovered when he got one of the first meters sold.) Was it some yet-undiscovered aspect of diabetes that causes heart disease regardless of diet? Or was it something else?
We need answers to give when a doctor says, as one aghast Joslin Diabetes Center physician said to me when I told him I was on a LC diet, “But that’s what they used in the 1920s.”
“Now, since then, we’ve learned that fats DON’T cause heart disease and protein DOESN’T cause kidney disease, so that logic no longer applies.”
Even more, what does cause heart disease and kidney disease is persistent diabetes which can be controlled with dietary carbohydrate reduction.
“I think bashing people makes them defensive … So I think one approach would be to acknowledge that … now the evidence has changed in favor of LC. Let them squirm out of their past mistakes by saying, “New evidence shows” so they can save face. Then we could all work together to help people with diabetes, as you suggest in suggestion”
Bashing is not good but the “new evidence” is usually evidence that they have re-invented. In science, you give credit for work that others have done and you must, when it comes to recommendations, admit previous mistakes. It’s not a question of blame or face but rather getting people not to continue to follow incorrect ideas, in this case, low fat.
“A diabetes diet in a 1910 home health book I have was very similar to Atkins induction. Yet people with diabetes had cardiovascular disease at much higher rates than those without diabetes. Why?”
Before 1910, the primary form of diabetes was type 1 which could not be cured by diet alone and was only controlled after the discovery of insulin. CVD is caused by the same factors as diabetes itself, a disruption in the insulin-glucose axis.
“We need answers to give when a doctor says, as one aghast Joslin Diabetes Center physician said to me when I told him I was on a LC diet, ‘But that’s what they used in the 1920s.’”
To give answers to such a doctor, you have to determine if it is a real question or whether they are defending the party line and just jerking you around (it happens!). The LC diet did work in 1920 but, again, because the primary form was type 1, it wasn’t enough. The discovery of insulin gave rise to the idea that diabetes was a hormone deficiency disease which therefore requires insulin. It is now understood that it is a system disease, a disease of poor feedback control between glucose and insulin. Type 2, in particular, is a metabolic or system disease. But again, you have to be sure you are having a serious discussion.
“Before 1910, the primary form of diabetes was type 1″
I doubt this was true. http://www.medscape.com/viewarticle/445672_4 Look at the graph. These are rates starting in 1925, and I doubt there was a sudden surge in type 2, then called “mild diabetes,” between 1910 and 1925, although of course it is possible. Maybe all that chlorine gas on the battlefields triggered diabetes.
It *is* true that type 2 wasn’t defined until the 1930s and when it was, it wasn’t Dx’d until at a much more advanced stage, and anyone who stopped spilling glucose in urine was considered cured. So perhaps the primary form of diabetes that was treated by endos was type 1. Type 2 would have been treated by GPs.
And before it was defined, of course they assumed they were all the same disease.
Elliott Joslin wrote in 1916, “No preexistent abnormal condition has occurred more frequently among my diabetic patients than has obesity. . . ” Type 1s are generally thin.
” which could not be cured by diet alone and was only controlled after the discovery of insulin.”
Well, yes, but I was speaking about those who continued with LC diets after the availability of insulin. After the discovery of insulin, Joslin writes gleefully that children can now expect to live at least 20 more years. Of course this is an improvement on 2 years, their fate without insulin.
Of course this “new evidence” is old evidence and of course people should admit their mistakes. However, they often won’t, especially when they’re not real scientists but organizations like the ADA that have spent years telling people to eat lots of carbs. Bureaucrats spend a lot of their time defending their jobs.
I guess I was wrong about this and I suspect that if the low-carb diet was not helping that it just wasn’t being done in a systematic way.
Well done.
Only 15? Does that mean that the ADA is only 16% (m/l) as bad as the 16th century Church?
Great article! Low carb makes such supreme sense for treating diabetes, and high carb makes no sense at all. Wouldn’t it be wonderful if the ADA would devote their time and efforts into educating diabetes patients about getting on and staying on a carbohydrate restricted diet?
Hmmmm. Speaking of diets, what about that Diet of Worms? Sounds low-carb, but I dunno. . . .
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Many thanks for continuing to plug away at this common-sense approach. I am confident that inevitably, progress is being made.
Nearly spat out my drink when I read # 8 “Dietary carbohydrate restriction is the single most effective method (except for total starvation) of reducing triglycerides…” – nicely said
And I liked what you did there with the “Diet of Worms”
I look forward to “Cuius Regio, Eius Religio” followed by The Defenestration of Prague.
Which, in due course, leads to The Counter-Reformation.
Judith Wylie-Rosett has graciously agreed to a debate this Thursday on macronutrients in the treatment of diabetes at Downstate which I will report on. Although we will pull no punches we have agreed to avoid defenestration.
[...] this article: Dietary Carbohydrate Restriction in the Management of Diabetes … ← Menopause and Diabetes | Quarantine7 Blog Stopping Diabetes Before It Starts – [...]
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Gretchen asks:
The LC, high-fat diet was used before and even after insulin was available (one type 1 remembers his mother coming into his room as he was getting ready for bed and saying, “You haven’t had enough fat today. Eat this avocado”). A diabetes diet in a 1910 home health book I have was very similar to Atkins induction. Yet people with diabetes had cardiovascular disease at much higher rates than those without diabetes. Why?
As I understand it, this is because:
Insulin reduces gluconeogenesis; with type 1 diabetes there is little or no insulin, so glucose is produced by the liver at high levels, and is not taken up into cells.
I guess this is the ultimate argument against “essential carbohydrate”; that even in low-carbing type 1 diabetes, endogenous sugar levels are high enough to be toxic over time.
Also, factors such as antioxidants, omega 3s, minerals etc. were unsuspected then, green veges were not always appreciated, and some diabetes diets may have been deficient.
Or compliance was not good, some people cheated for obvious reasons, or carbs weren’t measured accurately (avocados can have significant carbs depending on variety).
Or some of the damage was done before diagnosis.
First, this post is excellent, I plan to reference it often. But, according to media reports this week, bariatric surgery is the way forward in diabetes treatment. Any solution except the simple one seems preferred. From a metabolic standpoint, the surgery seems to work by caloric restriction (I believe). So I have to wonder if over time people who have this surgery will reduce lean body mass unless they change the composition of their diet. In other words – what happens over the long term to a person who keeps eating the same proportion of carbs in their SAD diet, just less in total.
Bariatric surgery works well for a number of reasons which I don’t really know off the top of my head but, for most people, surgery is still a last resort. At some point, not recommending that a patient try a low carbohydrate diet before turning to surgery, will seem barbaric. The problem is fundamentally that medicine is currently the study of drugs and surgery. Many physicians learn nutrition only anecdotally and take the advice of highly biased physicians because they have prestige. I am one of the people who are trying to improve medical education with respect to nutrition. In any case, we are only suggesting this as the “default” diet. It is easy to do and, if it doesn’t work, you can opt for surgery or something else.
Search the diet that you must follow after bariatric surgery….its low carb high protein!! It might be the diets that folks have to follow after the surgery, not the surgery itself.
I have consulted with Dr. John Kral, a professor of surgery and an actual expert on this subject and I share some information from him.
First, saying “Bariatric surgery,” is like saying “low-carbohydrate diet.” There are many and we frequently hear it from, as Dr. Kral puts it, “haters of bariatric surgery, epidemiologists and journalists” (a list worthy of Jonathon Swift). He points out that “it is favored because it allows them to pick and choose among bad outcomes of physiologically different operations and operations different in activities-of-daily-living, with different mechanisms. The term also allows the advertisers to market the money-making procedure of their choice.” Sound familiar?
In any case, you would “have to provide data (published or even empirical) on purely gastric restrictive operations (banding only) favoring liquid and soft calories thus truly affecting macro-nutrient composition, and diversionary (“bypass”) operations with neuro-endocrine effects … with or without an intact pylorus (metering the speed of passage of nutrients and their degree of digestion when emptied).”
In general, he suggests that you have to define “parameters of the operation (and host factors, rarely, if ever analyzed sufficiently to conclude anything about ‘long-term’ [outcomes] “
You also have to distinguish between transient restrictive effects, which lead to different choices than when the restriction is gone.
“The reason I write ‘choices’ instead of recommendations because individual patients make individual choices regardless of authoritarian nutritionist, dietitian and physician recommendations, so rarely validate or followed….”
”
“The best general advice is to suggest high protein generically (in patients without compromised renal function…. It is more important, the greater the bypass, especially in the absence of a pylorus.”
“You now understand why no journalist has the space/time to publish an expert opinion…. Much better to write: “bariatric surgery requires low carbs”, Dr Atkins. 5 words, 32 characters, 4 spaces.
Bariatric surgery probably works because it alters gut hormones in some way. A type of surgery called Roux-en-Y is most successful, and it reroutes the intestine. Other less-drastic forms of bariatric surgery result in weight loss, but the effect on diabetes is not as great.
I would only consider surgery as a last resort, when everything else, including a LC diet, had failed. It affects many things and I don’t think it’s reversible. There’s a temporary product called Endobarrier that is a plastic sleeve inserted in the intestine, and it seems to have the same effect on type 2 as the surgery. I think it’s approved in England but not yet in USA. It is removed after 6 months, and can be removed if you react poorly to it, so I think it’s a better choice than Roux-en-Y, which can cause a lot of complications, some fatal.
Thanks on this.
Dr. John C. McDougall (the McDougall Diet, author of “The Starch Solution”) claims just the opposite–that a diet high in carbohydrates, especially whole grains, vegetables and fruit, NO added protein or fat (outside of what is naturally supplied by those grains, vegetables and fruits) is the best one for treatment of diabetes, heart disease, and a host of other conditions. It’s the polar opposite of Paleo/low carb. No fish, fowl, meat, dairy or oils are permitted at all.
Can both be right? What explains the improvements he claims to see in his patients (has anyone substantiated his claims)??? Looking at the diet, I see that refined carbohydrates, sucrose and chemical additives are eliminated, and PUFA’s as well, since he allows no added fats (which also means no fish or animal sources of omega 3′s either).
I live in the town where he practices, and everyone here has drunk the Koolaid and think this guy walks on water. I’ve seen my friends lose tons of weight but they look gaunt and haggard, and quickly gain it back as soon as they realize they can’t live on that food for long. (Recipe for “broccoli soup”–boil broccoli in water, mash it in the boiled water. Serve hot. I think he doesn’t allow added salt, either!). I remember when he was in his heyday in the 80′s he had a call-in radio show, and sometimes his adherents would complain of alarming increases in triglycerides. His advice would be to cut out fruit entirely.
What gives, how can his claims fit in your theory???
Maybe he is on to something. In which case, he will want to help get funding for a comparative trial so that everybody can see the benefits.
When I was Dx’d with diabetes, at first I read McDougall and company and believed the low-fat, all-natural food approach. We’ve had that message yelled at us for decades, and when you’ve heard “healthy whole grains” and “artery-clogging fat” a million times, some of it penetrates your unconscious. But my meter quickly told me it raised blood sugar too much. I did lose weight; however I was constantly ravenously hungry and decided I’d rather be dead than hungry for the rest of my life and kept reducing carbs more and more until I reached LC level. Because I reduced them gradually, I never had the large weight loss or the brain fog or fatigue people get when they go cold poultry.
If you’re not diabetic, you can lose weight with many different approaches. If you’re diabetic, you have to take blood sugar levels into account as well, and for this, the LC diet is best.
Almost *any* diet will show improvement when you compare it against the standard American diet, so be careful when you read popular press reports of diets or supplements that “improve” something. Improve compared with what? Even research scientists are careless in this aspect. I used to copy edit medical books, and I was constantly querying “compared with what?”
The trick to successful dieting is to find one you can maintain long-term. If that’s broccoli without butter or salt, go for it. I prefer my broccoli with olive oil and lemon juice.
Gretchen writes: Almost *any* diet will show improvement when you compare it against the standard American diet, so be careful when you read popular press reports of diets or supplements that “improve” something. Improve compared with what?
I think it true that in this case there is “more than one way to skin a cat”. A diet high in phytochemicals, calorie restriction, supplements, herbal medicine, can all induce some of the changes seen with carbohydrate restriction, at the gene expression level, so might be expected to have similar benefits, but wherever tested these do not seem to approach carb restriction in long-term effectiveness, except perhaps in the case of calorie restriction, which is also carbohydrate restriction, but has relatively low compliance.
Perhaps one day an “ultimate diet” will be tested incorporating carbohydrate restriction, high phytochemical intake, intermittent fasting, supplements, herbs, and God knows what else. The beneficial aspects of these methods are not actually mutually exclusive.
A second reason why rates of CVD may have been high in type 1 diabetes treated with high fat diets lies in the pathogenesis of DM1:
inflammatory triggers such as gluten (and casien) digests are implicated:
http://www.rigshospitalet.dk/menu/AFDELINGER/Diagnostisk+center/The+Bartholin+Institute/Diabetes+Immunology/pathogenesis.htm
“Collectively, our data indicate that dietary gluten influences the proportion of multiple regulatory T cell subsets as well as Th17 cells in mucosal lymphoid tissue while fewer differences were observed in non-mucosal lymphoid compartments. Further, STD diet modifies the cytokine pattern of both Foxp3- T cells and Foxp3+ Tregs towards a more inflammatory cytokine profile. This mechanism may contribute to the higher T1D incidence associated with gluten intake.”
One would expect that this Th17 inflammatory pattern would also be damaging to the heart. In the infamous “China Study” there was a high association between wheat consumption and heart disease.
Wendy Pogozelski suggested that the problems in the early history of diabetes were due to the high variability in insulin preparations leading to more frequent hypoglycemic episodes than better, later preparations. Also, I think that the idea that diabetes was a hormone deficiency disease made insulin treatment more or less the definition of diabetes and diet experiments were done around a baseline of insulin-treated patients and it may have been under-appreciated that insulin had to be reduced if carbohydrate was restricted. I have not read the previous reference yet but scanning it, it seems that it was characterizing diabetes by age of onset which meant more before the difference between type 1 and type 2 was discovered.
Whether CVD was more due to glucose fluctuation, or to other inflammatory mechanisms, in high-fat pre-insulin diabetics might be determined by looking at relative incidence of microvascular complications, which might be more common than cardiovascular effects if glucose levels were still elevated.
Whether that kind of retrospective epidemiology can be reliable is another question…
I also question whether physicians were universally committed to high-fat diets in pre-insulin diabetes.
There may have been significant opposition or scepticism, or dilution of the message according to individual theories.
This is only to be expected.
Also, my understanding is that in the early days, the design of the insulins wasn’t as good. The insulin preparations took a long time to act and there was pretty much a bolus insulin only, no basal. It could be pretty dangerous. A high-carb diet guarded against these dangerous lows that could occur simply by not having the blood glucose peak correspond to the insulin peak.
Both hyperglycemia and hyperinsulinemia are causes although it is probably more the fluctuations rather than just average levels.
I am such a believer in the low-carb approach to preventing, and for most, for reversing Type II. For my brother and I, a low-carb diet has staved off the familial disease. My sister was diagnosed before we made the “discovery” of the efficacy of the low-carb approach and although she also went low-carb 12 years ago, and has avoided going on insulin (which I think is the worst thing a Type II can do), she has not achieved good blood sugar control. She recently tried eliminating dairy, nuts, and fermented foods due to a suspicion of yeast overgrowth, and seems to be doing better, but she has never lost her abdominal fat and still has some very high first morning glucose readings (they drop during the day). My question is “what is your take on this recent report about gastric by-pass?” What is the mechanism that is producing these results? I am a bit appalled that people are resorting to dangerous, expensive surgery, when for most people, a low-carb diet will reverse their “diabetes.” However, the by-pass operation seems to work immediately and almost miraculously and last long-term. What gives? Is this maybe what my poor sister should do? She is not grossly obese, maybe 40 pounds overweight. I hate seeing her struggle so much when she has made such a determined effort to control BG with diet and exercise. She really eats a strict, limited diet and is resigned to do it for life, but she is pretty miserable. Any ideas along with opinions about what is happening with the gastric by-pass?
Surgery is outside my area of expertise but there are many sources of information, some of which I will try to research for this blog. However, it is not clear what your sister is doing. You say she was on low-carb 12 years ago. Does that mean she quit. If so, why? The only opinion I have is that I would not opt for surgery without trying a low-carb diet. If she is pretty miserable because of the diet, she might seek out advise of people who are happy with such a diet which are not hard to find.
Please read that blog-post first http://diabetesupdate.blogspot.com/ about a new research concerning the effectiveness of the surgical treatments for diabetes. It doesn’t look so good.
It’s just another sign that the whole system is screwed up.
Peggy, High blood sugars in the morning, (assuming an overnight fast) tends to point to the liver’s over production of glycogen. Is she still LC? Does she test her blood glucose at bed time? What meds is she on for control? She may need a different medication for this. I had one patient whose blood sugars went up with fasting and with exercise, and I’m guessing was overmedicated, because this corrected when he stopped the medication A.M.A.
Have you had some thoughts on the “mitochondrial damage –> diabetes t2″ hypothesis?
I am mentioning this not as an alternative to your 15 theses but as an addition (the sixteenth). The reason I am interested is because of my experience with the high animal fat low carb nutrition. I noticed that not all people can increase their fat intake to about 200g per day. Diabetics and people with metabolic syndrome often don’t seem to be able to. When I started it 12 years ago I had metabolic syndrome (not diabetes) but was only able to consume 100-150g of fat max and my total caloric intake was about 1500kcal (65kg). However, before that I was able to eat much more calories. This seems to be a common experience and may be one of the difficulty for diabetics to use this method correctly. Since fat, unlike glucose, can only be metabolized in the mitochondria, there is a sharp maximum limit of calories that a person may consume or metabolize on a high fat diet or when burning own body fat. This is the problem for diabetics who are overweight and begin burning their own body fat. I noticed that some diabetic people seem to _feel_ better on a high carbohydrate diet plus insulin plus drugs because it allows them to overcome their low metabolic yield.
( see also this )
Stan
1. Thesis 5 (to which I have added a figure) emphasizes that there is no requirement to increase fat when you decrease carbohydrate and, in practice most people don’t. Low carb diets tend to be high fat compared to the DUSDAR (discredited USDA recommendation). It is said that low carb diets become hypocaloric because of the satiating effects of fat and protein although probably equally important is removing the highly reinforcing effect of high carbohydrate foods (think chocolate-chip cookies).
2. “…some diabetic people seem to _feel_ better on a high carbohydrate diet plus insulin plus drugs.” I am suggesting that low carbohydrate is the “default” approach; if you have a specific reason for something else, or it doesn’t work out, it is only one option. The fact that endocrinologists and cardiologists have limited knowledge of current nutrition research and rely on the weird recommendations of the ADA means that it is rarely even offered as an option, never mind, the best option. If you prefer drugs to carbohydrate restriction, it is your choice. It is good, however, to have all the information.
Couple of points must be clarified here, in the question as posited Gretchen is conflating TWO different groups of people.
“CVD is caused by the same factors as diabetes itself, a disruption in the insulin-glucose axis.” In 1900 virtually the entire world population was subsisting on an agrarian, or farm food type diet of fresh whole grains, eggs, meats, dairy & produce, and cancer and heart disease rates were very low, afflicting around just 3 to 5 percent of the population, and if I recall correctly Type 1 diabetes rates were even lower. They did occur, but not at anywhere close to the epidemic contraction rates we see today,
There WAS a sudden surge in Type 2 diabetes, and it started EXACTLY between 1910 and 1925, but it wasn’t “all that chlorine gas on the battlefields.” After 1910 and subsequent to the German invention of artificial trans fat vegetable oils which facilitated global production, distribution & adoption of industrial manufactured high carbohydrate processed ‘foods’, cancer, heart disease and BOTH types of diabetes have become so common that generations of people born & raised on the Standard American industrial ‘food’ diet after WWII believe or have been led to believe that these diseases are just a ‘normal’ part & fact of life, are largely unavoidable, and have never known & have little to no knowledge of any time in history when cancer & CVD contraction rates were other than they have known it to be within their lifetime. The first publication of scientific proof of a connection between the toxic industrial processed vegetable oils, UV exposure and increasing melanoma contraction rates was in 1939 when it was shown that the toxic oils oxidize & corrupt the natural reduced cholesterol in human skin and block the skin’s production of the vitamin D that skin needs for cancer protection. It really didn’t take long at all after the global adoption of industrial ‘foods’ for observant scientists around the world to notice & document the rising incidence rates of ALL diseases and the toll in human suffering and lives cut short.
Since Gretchen doesn’t give any clue as to her age other than being ‘Dx’d with type 2 in 1996′ I’m assuming that both Gretchen and the Type 1 diabetic friend she recalls were both born after WWII. The point is that in these two different groups of people, cancer, CVD & diabetes have TWO different causes, so much so that there are even two different forms of diabetes. Prior to WWII and mass adoption by the public of the industrially processed ‘food’ diet, Type 2 insulin resistant diabetes was virtually unheard of, unknown and largely unseen. Since WWII certain cancers & progressive atherosclerosis are primarily caused by the biologically dead and toxic trans fat liquid polyunsaturated vegetable oils that are used to “shelf stabilize” all industrially processed ‘foods’. The high industrially manufactured & trans fat laden carbohydrate diet is the driving force behind the rise in not only Type 2 insulin resistant diabetes, but also dietarily induced Type 1 insulin dependent diabetes in cases where chronic high intakes of manufactured trans fat laden carbohydrates cause pancreatic alpha & beta cell burn out. A little known and seldom taught but ironclad, bombproof, scientific physiological fact is that only 1 percent by weight of the human pancreas consists of JUST the beta cells devoted to the production of insulin to metabolize & drive physiologically excessive serum glucose out of the bloodstream so we don’t kill ourselves with the carbs we overeat.
The common denominator between these two eras, then and now, is the high carb diet, and so here we are back at the insulin-glucose axis and the destructive effects that both glucose & insulin inflict on the body, including heart disease. So to further clarify it’s more accurate to say that before the industrial foods diet, a high carb diet could & did induce obesity, cancers, heart disease and at least Type 1 diabetes, but since the advent of industrial oils & foods there are now at least 2, maybe even 3, 4 or even more causes; A high carb diet, industrial oils & ‘foods’, exposure to chemical and environmental toxins, some of which also didn’t exist prior to 1900, and radiation which is equally pervasively used in modern societies.
It’s no wonder that the disease rates are as high as they are, it’s a wonder that they’re not higher and that that any of us are alive at all. If humans hadn’t already crossed a reproduction threshold point before the invention of industrial ‘foods’ we’d have gone extinct.
“There WAS a sudden surge in Type 2 diabetes, and it started EXACTLY between 1910 and 1925, but it wasn’t “all that chlorine gas on the battlefields.”
Where did you find this information? I’m not suggesting it’s not true, but I haven’t been able to locate it in the past. I wasn’t entirely serious about the chlorine.
I think poor people have always been on high-carb diets because they couldn’t afford meat. I looked at an 1850 cookbook that I have, and there was a heavy emphasis on making good bread with good flour. Without good bread, the author wrote, people tend to eat more pies and cakes. However, the flour was often from the family’s own wheat, ground but not bleached. I don’t know how they kept it from going rancid without refrigeration. They wouldn’t have gone to the mill every week.
But they didn’t snack on industrial waste.
I read a long time ago that bleaching flour produces alloxan, which is the chemical they give to animals to make them diabetic. It kills beta cells.
I don’t think type 1 diabetes rates are epidemic, although they’ve doubled since pre WWW II. But because they were always rather low (I knew only one diabetic child when I was growing up and no children in my schools got cancer), the type 1 rates still aren’t enormous. Today one sees both diabetes and cancer in schools. There’s also diabetes caused by a single gene modification (MODY).
Type 2 rates are definitely up but in addition to the fact that people are fatter and are living on toxin-filled food is that the medical people lowered the bar. Doctors used to think it was normal to have high blood glucose levels when you got older and didn’t try to treat older patients. Also, people are living longer. When you drop dead at 60 you’re less likely to have had type 2 than if you live to be 98.
Lowering the bar is good because people have a chance to stop the damage before it’s too great, but it does inflate the statistics.
[...] of biochemistry at Downstate Medical Center (SUNY) in New York. A few days ago he wrote about the rationale behind carb restriction as an approach to diabetes. We’re singin’ from the same page of the [...]
[...] as a "default" approach for diabetics, see Richard Feinman's recent blog post, "Dietary Carbohydrate Restriction in the Management of Diabetes: The 15 Theses." Read the comments as well–many other folks active in the national discussion (including Gretchen [...]
Richard, I think you should add thesis #0: The primary cause of all this is the advice to reduce fat intake. This leads us to several other potential theses. For example, that dietary fat is essential for proper nourishment, therefore a reduction of dietary fat leads to malnourishment, therefore contributes to the overall pathogenesis. Or that dietary fat is essential to satiety, therefore contributes to overall caloric intake, which admittedly increased since the low fat advice.
I ignore fatty acid profile but if we have to take a stand on that, it’s easy to figure out. And I think it doesn’t make much difference in the grand scheme of things anyway.
Otherwise, that list makes much sense to me. It mirrors a whole lot I read before here and there, but puts it all neatly in the same package.
(BTW, any way you can add Google in your list of possible logins?)
I am continually modifying the theses. Not exactly following what you say, I have changed thesis 7 to:
Carbohydrate-restricted diets do not require the addition of saturated fat (SF). While plasma SF may increase insulin resistance, SF in the blood is more dependent on carbohydrate than dietary SF. In addition, numerous studies have shown that dietary total and saturated fat, again, contrary to popular opinion, are not associated with incidence of cardiovascular disease (CVD).
“…we have created a population of people who distrust all health recommendations. .”
I am SO glad you said that! I’ve pointed out frequently that the absolute refusal of the Conventional Wisdom folks to regard the Carbohydrate / Insulin Hypothesis as anything other than pure quackery is going to come back to bite them eventually. Already many people I know have decided that personal anecdote is a better guide to treatment than advice from a real doctor – and gone further into the realm of conspiracy theories, positing collusion between the “medical establishment” and “Big Pharma” to keep people sick. The damage being done to the respect for science that people once had is nearly as bad as the damage that’s been done to people’s health.
I learned recently of a really nice doctor in the area who lost a leg, and not long afterward, his life to diabetes. A tragedy. I’ve wondered: Was he so thoroughly steeped in the-way-we-do-things that he never considered another way to treat his own life-threatening condition?
If there’s a collusion, I think it’s between “Big Pharma” and “Big Conventional Wisdom/Big Medical Organizations,” — a collusion that’s probably damaging to the health of many local doctors as well as to their patients.
I am not sure it is big pharma so much as big NIH-funded academics but, certainly, much damage is being done.
Actually, my father was chief of anesthesiology at a good-sized hospital and overall a pretty smart man. He was diagnosed with T2D and was insulin dependent. This was before I’d ever heard of carbohydrate restriction, but I still knew enough to suggest that maybe he shouldn’t be reaching for that second doughnut. He told me I was ignorant and that diabetes meant that he would DIE without sugar!
Meanwhile my mother nagged him constantly to avoid fat – even when he was on his deathbed, my mother didn’t want me to make him his favorite meal (broccoli rabe with sausage) because “the last thing he needs is arteries clogged with fat.” (I made it anyway.)
I met his diabetician only once or twice, but I doubt very much that my father was advised to eat more fat and restrict carbohydrates, only to check his blood sugar and take his insulin – advice that he didn’t take seriously either. He died in 2002 of kidney failure, a direct result of his diabetes.
I attribute this to 1) the tendency for doctors to be terrible patients, 2) obsession on the part of even diabeticians with telling patients to avoid fat, 3) and reluctance on the part of one specialty (anesthesia) to intrude on the domain of another (endocrinology).
Two months after he died, I read Gary Taubes’ “Big Fat Lie” piece in the NY Times, but I knew that if I’d had that knowlege earlier it just would have meant more fighting and more frustration.
“If there’s a collusion…”
“Never attribute to malice that which is adequately explained by stupidity.” Or in this case, ignorance.
We all have separate talents and separate parts of our life. There is also selective stupidity, which is sometimes difficult to distinguish from ignorance.
Our tax dollars at work. . .
I just did a little reading on the NIH, and noticed that the National Cancer Institute — “Research and training aimed to eliminate the suffering and death due to cancer” — was established in 1937 — 75 years ago. Based on what I see around me, they should just shut off the lights and go home. Within my circle of family and friends, since mid-February three have died and a fourth will die shortly of cancer. Three others are on the chemo-radiation-cut-out-another-body-part journey. An 8th was diagnosed last Christmas time. The old “oh, well, people are living longer now” excuse holds no water, since only two of these is/was over 70.
I am sorry to hear these stories and I think that is one reason we persevere in getting some science into the picture.
Hi Marilyn, my dearest friend died of Merkel Cell carcinoma at age 57 a couple months ago. Not a pleasant journey down the garden path to death. She was exactly 4 mos older than I. My father died of cancer also at age 57. When you read in Taubes’ GCBC about cancer, there was NONE of it where people at a “traditional diet” (i.e. LCHF). And I mean NONE. This is confirmed in all the reports sent home from doctors and missionaries in far-flung places, including those of Albert Schweitzer. One of these doctors’/missionaries’ biggest culture shocks was to find this lack of cancer. And other diseases comprising metabolic syndrome. I was “high” on reading GCBC and the immediate health … there’s not even a word for it … “benefits” is too weak… that occurred. I gave her a copy of the book. She just looked at me as I raved on (this was before her diagnosis) and said, “I know Atkins works. I’ve done it. But I like my bread, I like my dessert, I like my carbs. I’m not going to change.”
By the way, I wanted to add that one can find online Jerry Brunetti’s fascinating 2006 interview with Pam Killeen wherein he tells about how he developed his own protocols and cured himself of cancer.
First, to set out how he was uniquely qualified to figure this out.
“I developed a company that eventually became Agri-Dynamics. We primarily focused on soil fertility. We knew that livestock needed nutrient dense forages in order to be healthy. Then, clients began asking me to put together animal remedies that they could use as alternatives to pharmaceutical drugs. I started formulating nutraceuticals and botanicals that addressed specific issues that appeared in livestock operations (such as scours, mastitis, somatic cell count, foot rot etc). Pam: So you were using natural remedies to help balance the animals and the soil? Jerry: That’s correct. We tried to hit it from the preventative side (from the soil up) and then from the therapeutic side by using complementary formulas that could address an animal’s innate ability to heal itself. It’s just like you see today in the human alternative field with nutraceuticals, botanical medicines, homeopathic medicines and so on.”
RE HIS OWN CANCER:
“In 1999, I was diagnosed with an aggressive form of Non-Hodgkins lymphoma (follicular cell). Based upon the tumor size found in my abdominal cavity, I was advised that, if I didn’t take aggressive chemotherapy, I was looking at 6 months to 2 years of life left… I reviewed the research, I declined mainstream medical treatment. The chemotherapy treatment mainstream medicine offered was called, ‘M.O.P’ and ‘C.H.O.P.’ Their approach was destructive to bone marrow, kidney and liver. My quality of life would have been pretty dismal had I chosen their protocol. I decided that they didn’t give me much of a chance. I wasn’t very excited about taking products that were cytotoxic (creating a lot of collateral damage to my own healthy tissues). In order to solve the problem, I chose my own protocols. I began searching for answers by finding out where the cancer came from in the first place. …Sugar is one of the main things that can predispose people to cancer. If they do get cancer, sugar really increases their susceptibility from dying from cancer because cancer is a ‘sugar junkie’. We’re consuming about 170 pounds of sugar per capita per year here in the United States. In the early 1800’s, we consumed about 10 pounds and sugar consumption translates into insulin production. Insulin is associated with inflammatory processes. All of the drugs, COX-2 inhibitors like Celebrex, Vioxx, are all predicated on the fact that we have so many inflammatory conditions today. Inflammation is coming from a deficiency in the long chain fatty acids (EPA, DHA), an excessive amount of the omega- 6 fatty acids (which are proinflammatory) and a high amount of refined carbohydrates and sugar consumption. When people consume an excess amount of bad fats, a deficiency of good fats and lots of sugar, doctors write a lot of prescriptions for Vioxx.”
Pam: Why did you avoid chemotherapy and radiation?
Jerry: “Neither chemotherapy nor radiation can cure cancer. That’s admitted by the National Cancer Institute the National Institutes of Health. In Fortune magazine, March 29, 2004, there was an article illustrating that survivability rates with people who have had metastatic cancer (where cancer spreads from the primary tumor to distant organs) has not at all improved over the last 30 years. That means that we’ve seen no improvement with the four major killers (breast, prostate, lung, and colorectal cancer). Over 200 billion dollars have been spent on cancer research. There have been 1.56 million published papers on cancer and 64 billion dollars spent annually to treat people with cancer… The reports tell people that tumors don’t kill cancer patients; rather, metastatic illness kills cancer patients. Metastatic cancer spreads to the liver, brain, bones or other vital organs. That’s what kills people with cancer. In order to contain metastasis, you have to have immunity. A strong immune system is the only ‘drug’ that works against cancer. By the time a tumor is discovered there’s at least a billion malignancies in that tumor and they’re rapidly dividing – they’ve already ‘seeded’ the rest of the body by the time you’ve discovered you have cancer. In other words, you’ve got cancer seeds all over the body. What determines the survival rate of cancer patients has to do with whether or not the immune system is still operating effectively.” Etc.
Paula, I’m sorry to read about your father’s and your friend’s cancer deaths. Cancer is definitely not a garden path to death for most people. In many respects, life ends when they’re diagnosed and start treatment. I’m sure it’s been very hard for you to watch in these people so close to you.
I’ve read about the absence of cancer in the various far flung places, and have also read reports that after the native peoples have changed to the Western diet, they too began to get cancer. Another fact of Western life that didn’t exist in the far flung places was all the stuff generated by our way of living. I’m not going to get on a soap box here, but for example: A friend of mine grew up across the street from an auto factory. She and her siblings played in a vacant lot where the factory had earlier dumped all manner of stuff. The soil was so dead that no weeds ever grew there. She and all those siblings have had cancer. None of the younger siblings who grew up in another house have had cancer.
To what extent such carcinogens in our environment might be encouraged or discouraged by our diet is probably unknown. In the case of people who have reported curing their cancers with diet, my hunch is that a common theme in those diets would be minimal refined carbohydrates.
== sorry for the delay in posting this ==
Discusses “The effects of trans fats on cellular processes once they are built into the cell membrane. In 1984, Mary Enig published her doctoral dissertation, which indicated that trans fats interfered with enzyme systems that neutralized carcinogens and increased enzymes that potentiated carcinogens.” Kind of vague but she’s the ‘big wig’ on trans fats and fought a decades-long battle and finally won. She’s pro-animal fats, against hydrogenated oils.
Here Mike Eades has one of my favorite blogposts of his where he lays out studies (that were ignored) fingering hydrogenated oils at a time they were being (as they still are) trumpeted as “heart healthy.”
Saturated fat and heart disease: studies old and new
Jerry Brunetti is a smart guy.
http://www.pnas.org/content/93/5/1847.abstract
Expression of the fructose transporter GLUT5 in human breast cancer
The primary metabolic characteristic of malignant cells is an increased uptake of glucose and its anaerobic metabolism. We studied the expression and function of the glucose transporters in human breast cancer cell lines and analyzed their expression in normal and neoplastic primary human breast tissue. Hexose uptake assays and immunoblotting experiments revealed that the breast carcinoma cell lines MCF-7 and MDA-468 express the glucose transporters GLUT1 and GLUT2, isoforms expressed in both normal and neoplastic breast tissue. We also found that the breast cancer cell lines transport fructose and express the fructose transporter GLUT5. Immunolocalization studies revealed that GLUT5 is highly expressed in vivo in human breast cancer but is absent in normal human breast tissue. These findings indicate that human breast cancer cells have a specialized capacity to transport fructose, a metabolic substrate believed to be used by few human tissues. Identification of a high-affinity fructose transporter on human breast cancer cells opens opportunities to develop novel strategies for early diagnosis and treatment of breast cancer.
Interesting. Thanks.
Here’s another fructose paper. http://ajpendo.physiology.org/content/295/2/E227.full
There was a correction to the first, to the effect that GLUT5 has been found in healthy breast so the conclusions were premature. But this more recent paper seems to accept them, so there may be intervening corroboration (I haven’t looked yet).
This is interesting.
“Patients with type 2 diabetes exhibited dramatic increases in GLUT5 mRNA and protein abundance in skeletal muscle (143). These increases were specific, because expression of GLUT1, GLUT3, GLUT4, GLUT8, GLUT11, and GLUT12 did not change with diabetes and could be reversed if diabetic patients were treated for 8 wk with pioglitazone, a drug enhancing insulin action.”
I wonder if trans-fat, their precursers, and the new interesterated fats are more involved in the rise of cases of Diabetes since the first world war?
Why would you think that? Although downstream effects of diabetes are on lipids, these are most likely caused by disruption of the glucose-insulin axis.
I am thinking more of the obesity epidemic fuelling the rise in Type 2 diabetics and if there is a link between manufactured fats causing unusual levels of fat conversion into body fat as well as the high carbohydrate diet now eaten, thus leading to more diabetics?
Again, I don’t know that trans-fats have an unusual effect on conversion to body fat. Altogether, I don’t know the story on trans-fat except that the epidemiologic data is characteristically weak. I think it is another smoke-screen for not facing the science. Nobody wants to defend it, of course, but I think it has been blown out of proportion. In particular, I don’t know what the mechanism is. Do you?
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Is Judith Rosett going to argue against low carb and in favor of low fat? How could anyone argue this? What possible facts could she pull out of her hat? Prepare well!
She will say that the ADA is not opposed to low carb but it is between the patient and the health care provider. She will say that no studies that fit her criteria are unequivocal and this is a problem because people with diabetes have higher risk of CVD so they have to watch out for saturated fat. She will say that yes, Westman’s case is strong but we produce too much corn in this country. She will say that it is true that recent studies show that saturated fat is not a risk for CVD but the bodegas in Brooklyn do not have enough fruits and vegetables. We’ll see what she says.
Some interesting papers on inflammation, fatty acids and diabetes
http://diabetes.diabetesjournals.org/content/60/7/1872.full
CONCLUSIONS Suppression of FoxO1 activity by MEDICA analogs may partly account for their antidiabetic anti-inflammatory efficacy. FoxO1 suppression by LCFA analogs may provide a molecular rational for the beneficial efficacy of carbohydrate-restricted ketogenic diets in treating diabetes.
And in mice, FOX01 suppression causes gut neuroendocrine cells to produce insulin, relieving their diabetes:
Generation of functional insulin-producing cells in the gut by Foxo1 ablation
Chutima Talchai1–3, Shouhong Xuan4, Tadahiro Kitamura5, Ronald A DePinho6 & Domenico Accili1,2
VOLUME 44 | NUMBER 4 | APRIL 2012 Nature Genetics
Restoration of regulated insulin secretion is the ultimate goal of therapy for type 1 diabetes. Here, we show that, unexpectedly, somatic ablation of Foxo1 in Neurog3+ enteroendocrine progenitor cells gives rise to gut insulin-positive (Ins+) cells that express markers of mature b cells and secrete bioactive insulin as well as C-peptide in response to glucose and sulfonylureas. Lineage tracing experiments showed that gut Ins+ cells arise cell autonomously from Foxo1-deficient cells. Inducible Foxo1 ablation in adult mice also resulted in the generation of gut Ins+ cells. Following ablation by the b-cell toxin streptozotocin, gut Ins+ cells regenerate and produce insulin, reversing hyperglycemia in mice. The data indicate that Neurog3+ enteroendocrine progenitors require active Foxo1 to prevent differentiation into Ins+ cells. Foxo1 ablation in gut epithelium may provide an approach to restore insulin production in type 1 diabetes.
Gut insulin from Foxo1 loss
Seung K Kim
Neuroendocrine cells, including those in the gut, have a vast array of functions. A new study shows that conditional inactivation of the gene encoding Foxo1 in mouse intestinal endocrine cells converts them into cells synthesizing and secreting insulin. Ectopic gut insulin production was sufficient to ameliorate glucose control in mice with conditional pancreatic b-cell loss and diabetes mellitus.
nature genetics | volume 44 | number 4 | april 2012
Can I have the laymans (or womans) version of this please?
Fox01 seems to provide a link between gut inflammation, diabetes. turn off Fox01 and gut neuroendocrine cells can produce insulin. Fructose can disregulate Fox01. Ketogenic diets can turn off its inflammatory effects and may be able to elicit insulin production.
Fox01 seems able to resolve various competing theories re. Diabetes, gut health, carbohydrate, fructose.
I am afraid that this is just the tip of the iceberg: http://www.sabiosciences.com/pathway.php?sn=Insulin_Receptor_Pathway
Yet manipulating Fox01 alone has made these gut cells produce enough insulin to save a diabetic mouse. I’m not usually impressed by this stuff, but that is a remarkable result, and it’s been replicated through more than one method of Fox01 inhibition (GLP-1 being another).
With PPAR-alpha mediated inhibition of Fox01 by ketogenic diets perhaps being the original example of these.
The $64 question now is, what can this experimental cure for insulin-dependent diabetes tell us about the causes and prevention of DM2?
Did you have some particular study in mind?
Here’s GLP-1 stimulating insulin in beta-cells; http://journals.lww.com/pancreasjournal/Abstract/2002/07000/Effect_of_Stimulators_such_as_GLP_1,_PACAP,_and.19.aspx
then the report of the GLP-1 transgenic E. Coli inducing insulin production in neuroendocrine cells:
http://www.technologyreview.com/news/415024/biotech-bacteria-could-help-diabetics/
http://www.nature.com/gt/journal/v14/n2/full/3302836a.html
The research involving ablation of Fox01 at least supports the idea that this approach is feasible, though ablation is probably not a suitable therapeutic option.
Then we have PPAR-alpha as a Fox01 inhibitor
http://www.ncbi.nlm.nih.gov/pubmed/16985262
(and fructose as a Fox01 activator, which is something Lustig incorporates in his hypothesis)
And the upregulation or activation of PPAR-alpha as an important consequence of ketogenic dieting (which I don’t remember seeing in the Lustig hypothesis)
This at least gives us a mechanism for ketogenic diets improving glycaemic control in DM2, and it explains how ketogenic diets may have benefitted some type-1 diabetics, back in the day.
So the claims about type 1 diabetes made by Dr. Jan Kwasniewski for his Optimal Diet (<50g carbohydrate) might not seem so far-fetched. http://homodiet.netfirms.com/forum/frm_homodiet5.htm
now that the mechanism for this kind of result has been shown to work experimentally.
Here are a couple of FOX01 review articles from Bone Science journals that highlight its role as a “crossroads” of metabolic regulation.
FoxO1, the transcriptional chief of staff of energy metabolism.
http://www.ncbi.nlm.nih.gov/pubmed/21816244
FoxO1: a molecule for all seasons.
http://www.ncbi.nlm.nih.gov/pubmed/21541992
It looks to be an ancient piece of machinery with multiple uses.
Thanks for these references.
Dear Dr. Feinman,
In college, one of my TA’s was the daughter of Dr. Abram Hoffer of Victoria. She told us about her father’s success with schizophrenia and that he was turning some attention to diabetes. Apparently, his experiments were successful and have found some support in the scientific community.
Here is a website that describes his work and some of the results that have been obtained:
http://www.freeobesitysolutions.com/?p=65
Very encouraging…
AL
T2 diabetic here. I absolutely applaud the analysis and intentions expressed, but . . . finding a “truly neutral” scientist is going to be infinitely more easily said than done. Not sure there is such a thing. Disagree? Take a look at the global warming debate . . .
I disagree. People outside the field are largely neutral and many who hold to the party line do so because it is not their field and will go with conventional wisdom until the problem becomes important to them. These people may be open-minded. The field is neither so sophisticated or complex that a geologist or computer scientist couldn’t be brought up to speed if they were on a government panel. But, in fact, many endocrinologists are simply not trained in or aware of nutritional interventions and have no opinion either way. It is simply not part of their practice which involves, at best, pro forma recommendations on diet and drug interventions. To understand how this is possible, look in an endocrinology journal or textbook and you see the unbelievable amount of things that they do have to know about and be able to treat. It is not surprising that they do not know about nutrition. That it is not in the medical curriculum is the problem but it is not their fault and they may well be completely open-minded. In fact, this has been my experience in talking to endocrinologists, some of whom immediately grasp the importance of carb restriction and recommend it to their patients.
As for global warming, I am open-minded because it is no my field. The recommendations of people who think we have global-warming would be useful if for no other reason than making the world less gross but that is different than saying I am able to evaluate the science.
First sensible comment about climate change I have read by a “low-carb blogger”; kudos to you, professor.
Climatologists aren’t busy posting half-baked opinions on endocrinology. At least I haven’t seen any. Maybe a few half-baked notions about meat killing the planet from some down-stream hangers on who would be saying that anyway.
I think the difference between diet change and climate change is you can run self experiments and clinical trials of dietary change.
Try doing this with climate change; if you have any luck, let me know.
Thanks. Overall, science is not as widely practiced as we’d hoped.
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