Dr. Eric Westman has been a vocal proponent of carbohydrate restriction to gain control over diabetes, as have Drs. Richard Bernstein, Mary Vernon, Richard Feinman, and Jeff Volek.
Several studies over the years have demonstrated that reductions in carbohydrate content of the diet yield reductions in weight and HbA1c (glycated hemoglobin, a reflection of average blood glucose over the preceding 60-90 days).
Among the more important recent clinical studies is a small experience from Duke University’s Dr. Eric Westman. In this study, obese type 2 diabetics reduced carbohydrate intake to 20 grams per day or less: no wheat, oats, cornstarch, or sugars. Participants ate nuts, cheese, meats, eggs, and non-starchy vegetables.
After 6 months, average weight loss was 24.4 lbs, BMI was reduced from 37.8 to 34.4. At the end of the study, 95% of participants on this severe carbohydrate restriction reduced or eliminated their diabetes medications.
That was only after 6 months. Note that the ending BMI was still quite well into the obese range. Imagine what another 6-12 months would do, or achieving BMI somewhere closer to ideal.
Curiously, this idea of severe low-carbohydrate restriction to cure or minimize diabetes is not new. Sir William Osler, one of the founders of Johns Hopkins Hospital and author of the longstanding authoritative text, Principles and Practice of Medicine, advocated an diet identical to Dr. Westman’s diet. So did Dr. Frederick Banting, discoverer of the pancreatic extract, insulin, to treat childhood diabetics. Before insulin, Banting and his colleagues at the University of Toronto used carbohydrate elimination (less than 10 g per day) to prolong the lives of children with diabetes.
This lesson was also learned many times during war time, when staples like bread were unavailable. The Siege of Paris in 1870 yielded cures for diabetes in many (or at least they stopped passing urine that tasted–yes, tasted–sweet and attracted flies), only to have it recur after the siege was over.
These are lessons we will have to relearn. As long as the American Diabetes Association and most physicians continue to advocate a diet of reduced fat, increased carbohydrate that includes plenty of “healthy whole grains,” diabetics will continue to be diabetics, taking their insulin and multiple medications while developing neuropathy (nervous system degeneration), nephropathy (kidney disease and failure), atherosclerosis and heart attack, cataracts, and die 8 to 10 years earlier than non-diabetics.
All the while, we’ve had the combined wisdom from antiquity onwards: Carbohydrates cause diabetes; elimination of carbohydrates cures diabetes.
(This applies, of course, only to adult overweight type 2 diabetics, not type 1 or some of the other variants.)
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I tend to agree with what Stargazey is getting at here and Dr. Davis has since rephrased: VLC is not a cure for diabetes. VLC is clearly one way of managing one of the major symptoms implicated in health risks associated with diabetes (e.g. hyperglycemia -> glycation).
However, eating VLC does not cure diabetes, which at its core is pancreatic beta cell dysfunction. Indeed it seems it can exacerbate the dysfunction as illustrated by the anecdotal evidence (don't like it but we have no real studies on this that I am aware of) that long term low carbers become more and more sensitive to any carb in the diet = worsening glycemic control.
A normal person can handle quite the glucose excursion and mounts an appropriate insulin response to handle it. A diabetic cannot handle this, and neither can VLC'ers or the advice to carb up with 150g/day for several days in advance of an OGTT would not be circulating around the web.
Can diabetes be cured? Well, apparently yes. I'm not suggesting gastric bypass surgery, but the remission rate – as in cessation of meds and "passing" an OGTT – is remarkable in morbidly obese diabetics undergoing the procedure. In the 80-85% range in a matter of days/weeks prior to significant weight loss.
This tells me that our beta cells are remarkably more resilient than we give them credit for – we're talking some of the most deranged metabolisms snapping back to "normal" relatively quickly.
In the short run, especially in IR obese and with weight loss, low carb generally seems to be a more successful approach. But long term, more moderate approaches with higher carb and lower fat intake seem to be better, especially once compliance is taken to account.
(In Westman, after randomized assignments of 97 participants, 10 of those who drew the LCKD diet didn't show up to do the study, while only 3 of the LGID did. So they started with 38 and 46 respectively. Of these 5 KD's dropped out for refusal/dissatisfa41%ction with the diet while only 2 dropped out of GI diet. 17 total dropped from each group. So from assignment to completion, 27/48 = 56% of screened recruits effectively dropped the LCKD while only 20/49 = 41% dropped out of LGID. This can definitely impact results. And the post-6 month rebound is common in longer term studies.)
The results in the 2 year Shai study for example: http://carbsanity.blogspot.com/2010/09/shai-and-diabetes.html
Nuttal's group has achieved some excellent results absent weight loss with their LoBAG diets – high protein (30%) with 20,30 or 40% carb splitting the 70% baby with fat. http://carbsanity.blogspot.com/2010/09/lobag-diets-for-treatment-of-type-ii.html
I think Dr. Davis is an example of what Dr. Dansinger (who treats diabetics with a relatively low carb but less extreme version than others) refers to as a "carb cripple".
I use the antioxidant R-lipoic acid as a supplement.
Daily: 3x 200mg R-Lipoic Acid
1x 1000 mg Evening Primrose Oil
1x 1000 mcg Biotin
As suggested by Richard Bernstein in his book, “Dr. Bernstein's Diabetes Solution: The Complete Guide to Achieving Normal Blood Sugars.” The Evening Primrose Oil provides gamma-linolenic acid (GLA) that is believed to increase the effectiveness of the lipoic acid effect. The biotin replaces the body’s supply consumed in the lipoic reaction.
The R-isomer is believed to be better utilized than the S-isomer.
In Germany, R-lipoic acid is used to relieve diabetic peripheral neuropathy, however, the supplement is given intravenously.
I can not say that it has improved my blood sugar control but I continue to use it more as a “universal antioxidant”, and because of Bernstein’s endorsement. R Bernstein, a type 1 diabetic, is an endocrinologist and one of the original proponents for the use of at-home meters for measuring blood sugar levels in diabetics. He is one of the very early supporters of low carbs for blood sugar control in diabetics. He is in his 70s.
I am a type 2 diabetic on metformin and low-carbs, maintaining HbA1cs at the low-end of 5%.
For supplements this is the most expensive one I take. I go back and forth between the Doctors Best and Life Extension products, whatever is cheaper on Amazon at the time.
Perhaps Jenny/Blood Sugar 101 can add a few more comments …
Very interesting to me here, thanks everyone. Beta cells, in human adults, have their individual life span; they are not replaced from stem cells.
A few at a time, of the already differentiated, Beta cells duplicate themselves. New ones form and in the absence of hyper-glycemia (high blood sugar) can become larger than their progenitors.
This might explain how Doc gets latency, CarbSane suggest a "snapping" back, and why standard carbohydrate intake does not always induce diabetes. Each Beta cell has more than one mitochondria in order to sustain it's insulin role.
Another commentator mentions that as some Type II diabetics age they (diabetics) do better off the low carbohydrate diet. Maybe the very slow time which Beta cells self-duplicate in has reached a good formation (in those individuals) and best to "use it, or lose it".
A low carb period gives fresh Beta cells enough of a break from high blood sugar then they can become large. Then that co-hort of Beta cells can follow the "normal" response; which is to get larger in response to insulin demand from blood sugar (ex: when middle age Type II diabetic does "better" off of a strict low carb diet).
What stops Beta cell self-duplication in Type I diabetes is the auto-immune T cell "attack". The immune system stymies regeneration.
In Type II diabetes the inability to prevent toxic exposure side effects can be what impedes Beta cell self-duplication. Distorted down-stream signal pathways can affect the transcription of a "fledgeling" Beta cell's replication of it's actin cyto-skeleton .
Might-o'chondri-AL, if you don't mind my asking, where do you get all your information? Are you a graduate student, perhaps?
Hi Stargzy,
I'm "semi-retired" 60 year old who hopes to avoid degeneration as I age. I've been investigating how to live well for over 40 years. Doc's blog appeals to me because he has clinical cases to draw on and good input from his readers.
When I first began looking into things maintaining health the science was much different. I am just trying to organize my thoughts on contemporary research to preserve my mental capacity.
In the Westman study, it bears noting that the gender and racial make-up of the "completers" – which is all that counts for comparisons – varies considerably between the diet study groups:
LKCD: 67% female, 67% white, 24% African-American
LGID: 79% female, 45% white, 52% African-American
On the "carbohydrates cause diabetes" front, I remain unconvinced. When one looks at populations who are most susceptible to developing the disease, what does they tell us? The traditional Pima ate an 80% carb diet and had low diabesity. Expose to SAD – rates soar. Japanese in Japan eating traditional diet with lots of rice = low diabesity rates. Expose to SAD = rates soar. The SAD is lower in carb by % (generally comes in at 40-45% carb for "usual" diet in studies) than the traditional diets. So how can we say that carbs cause diabetes?
I tried to post this before, but it got lost.
A question for Dr. Davis: When you got diabetic blood sugars on a "healthy, whole grain" diet, were you supplementing with niacin and fish oil, which you recommend on your site? I'm curious, because both are associated with impaired glucose tolerance in type II diabetics, and I have seen the effects of fish oil on my own glucose control. There's a theory I've read that, while niacin has cardiovascular benefits, which is why you recommend it, food fortification with niacin may be in part responsible for increased rates of diabetes.
Is it possible that niacin is beneficial with low-carb, but deleterious with high-carb?
Sorry for that comment above.
Afghans (people of Afghanistan) eat a wheat based diet. In fact, wheat bread is almost the entire diet of many of them (and they suffer from iodine deficiency and other problems as a result). But they have little obesity, little diabetes, no problems with insulin-resistance:
http://maisonneuve.org/pressroom/article/2010/nov/15/the-diseases-affluence/
Things are more complicated than simply "carbs = bad".
Hi Helen,
Niacin induces vaso-dilation ("flush") from the action of prostaglandins on capillaries Prostaglandins are made from the lipids stashed in our membranes.
This is how fish oil DHA/EPA (n-3) and poly-unsaturated vegetable oil (n-6) are involved; these can form Arachidonic Acid (AA)for making prostaglandins. Aspirin (salicylic acid) works as an anti-inflammatory because it blocks the AA pathway engendering prostaglandins.
1876 salicylate was known to decrease diabetic's glucose in their urine. A modern study showed injected salicylate restored acute (ie: 1st) insulin response to glucose in
10 out of 12 Type II diabetics who were administered prostaglandin.
For the 2nd insulin phase, with a few gr. glucose challenge, 12 out of 12 Type II diabetics had a 4x increase in their 2nd insulin response (ie: with a
salicylate booster before glucose administered and having those prostaglandins they got to start the test.)Prostaglandins,
in Type II diabetics, interfere with insulin response; in the controls the prostaglandins did not blunt the 1st nor the 2nd insulin "pulse" put out.
Women (some) "flush" from effect of prostaglandins at lower concentrations (ie: less niacin)than men (some). This is believed to be related to estrogen levels; suggesting that
post-menopausal women should review their original pre-menopausal niacin dose.
Doc specificly stated no one should take more than 1,500 mg. niacin without medical supervision (ex: liver enzymes
that monitor inflammation
tests). Diabetics who see their blood sugar worsen and/or liver
tests worsen while taking niacin, might be able to find their individual dose that does not induce levels of prostaglandins interfering with insulin phases 1 and/or 2.
Aspirin, as a salicylate, could be an additional way to block AA (thus prostaglandins)and foster timely insulin secretion for glucose clearance.
Another latest study showed that carbs and fats do not mix well and results into high blood sugar. YOu need to read the full studyy, to see the whole picture. healthy subjects were given hig fat meal (only fat) in the morning and their glucose and insulin remained at the fasting level for the next 5 hours. Then they were given coffee or nothing and then did glucose challenge. Sugar shut sky high (10 mmol/l ~180sh). Coffein further increases glucose.
This study again demonstrates that fat even after many outs of eating got negative effect on glucose. If if you eat low carb diet thats ok, but like most peole eat 30-40% energy from fat that leads to disaster.
'An Oral Lipid Challenge and Acute Intake of Caffeinated Coffee Additively Decrease Glucose Tolerance in Healthy Men ' http://jn.nutrition.org/content/early/2011/02/23/jn.110.132761.abstract
THis give some explanation why low fat diet work on some ppl.
Also emaging what wouldve happen if this study was done with diabetics.
Hi L/C/Andy,
Is it more likely that caffeine's classic effect on the adrenals, causing the liver to naturally put glycogen (sugar storage molecule)into circulation, is the reason blood glucose "surged" after coffee? I admit to not having read the study, so this is speculation.