Vegetable stall in a Market, Beijing
Creative Commons License photo credit: DPerstin

In response to Diabetes, Fructose and Natural Appetite Regulation Akemi asked me some good questions. In the process of replying I found myself essentially writing another article so I thought I’d post it up so everyone gets a chance to read it. Akemi’s comment is below and my response follows.

Thank you for the explanation. So I guess you don’t think bananas and other tropical foods are not necessarily worse than apples and berries in terms of fructose intake and effects on diabetes?

People say different things on nutrition, and I’m still a bit confused. For instance, here is an article (in fact, it’s two articles) with lots of medical citations that says high protein, high fat diet worsens diabetes or even causes diabetes. I’m sure you have something interesting to say about her view: Victoria Boutenko on Curing Diabetes Naturally

Akemi

On Tropical Fruit
I love your comments because you’re helping me fill in the gaps in my article. It can be really hard to cover everything in regards to subjects like this in one go. Almost impossible actually.

Nope, I have no problems with tropical fruits. If you feel good an hour after eating them then keep on eating them. Their glycemic load (different from glycemic index) are generally quite low because of all the fiber they contain.

The problem exists in a situation where, for example you had someone eating junk that is high in fructose and then thinking eating a bunch of fruit at the same time is going to make up for all the junk. Much worse would be thinking that drinking some “natural” juice is going to make up for the soda and other junk while also eating processed foods labeled low-fat (high in sugar) from the supermarket.

My point is that while fruit in a balanced healthy diet is great adding more sugar from fruit to an already massive amount of sugar is not likely to be a good thing. Despite the fact that fruit in the right context is very much a good thing. I hope that clears up my position?

Type 1 Diabetes is Different from Type 2 Diabetes
Now for your second question. There are a lot of different things being said on nutrition isn’t there. Sometimes I wonder whether I’m just contributing to the confusion. I try my best not to by not simply making statements. Instead I try where possible to explain the mechanism behind things.

The article you linked to appears to be in regards to type 1 diabetes, as this is the type of diabetes the son was diagnosed with. All the articles on my site that mention diabetes thus far are in regards to type 2 diabetes. The vast majority of cases of diabetes are type 2. Type 1 diabetes has a very different cause to type 2 diabetes and I’ve got to wonder whether the author of that article originally knew this or not or even fully understands this fact and its implications now.

From Robb Wolf’s website (a former research biochemist specializing in lipid metabolism) – Type 1 Diabetes is a failure of the beta cells of the pancreas to produce insulin. This is generally acknowledged to be the result of an autoimmune response, usually attributed to a viral infection or some kind of trauma. What is less known is the role of grain lectins in this process.

In humans, exposure to gluten before 3 months of age increases the risk for Type 1 Diabetes (1). Multiple studies also implicate bovine milk in Type 1 Diabetes (2). A higher intake of Omega 3 fatty acids (3) and vitamin D (4) may reduce the risk for type 1 diabetes.

If you read Robb Wolf’s website you’ll see many comments by people (including a mother of a young child) who have type 1 diabetes who are following his advice to eat a Paleolithic type diet (high protein, low carb, moderate fat) and who are seeing amazing results from doing so.

Clearly the cause of type 1 diabetes is very different to type 2 diabetes. Type 2 diabetes used to be known as adult onset diabetes and is usually the result of long-term insulin resistance.

The Importance of Understanding Physiology
Looking at the article and the research presented in the article you linked to there is no explanation of the actual physiological mechanisms at play in the type 1 diabetes condition as it relates to increasing carbohydrate and reducing fat so its difficult to comment on what was actually going on. I notice that everyone in her household were found to have high blood sugar readings. Something was either wrong from the very beginning or perhaps when she changed her son to a high carbohydrate diet the whole family changed to that diet and high blood sugar readings were the result for them.

I did notice that in the 1976 study the doctor gave the subject three times more fiber while increasing the carbohydrates consumed by only 32 percent. This suggests a shift to carbohydrate foods that also contained far more fiber than those previously consumed, i.e. fibrous vegetables vs. bread or pasta made from grains which irritate the type 1 diabetes condition.

I can’t imagine a case where increasing fiber while reducing irritants wouldn’t be a good thing. However, if these subjects reduced carbohydrate intake from grains (irritants of the type 1 diabetes condition) and increased carbohydrate intake from vegetables the reduction in irritation from grains and increase in fiber could explain the results much more clearly than simply increasing carbohydrate consumption.

Again I emphasize that a calorie is not a calorie because different compounds have very different effects on the body. Note also that the author’s son only really got a lot better when put on a raw food diet not simply a high carbohydrate diet. A raw food diet excludes most grains and gain products as they are typically cooked and processed.

I also noticed that the original diet used in the 1920’s and 1930’s to help diabetics was a low carbohydrate, high fat diet. Interesting that the recommendations now are the opposite as high carbohydrate and low fat. And the prevalence of diabetes? Far higher than it has ever been. Personally I eat a low (ish) carbohydrate diet (fibrous vegetables, some fruit) and high fat and I certainly do not have diabetes of any type.

Obviously there is more to what was going on inside those patients that were given a high carbohydrate and low fat diet. I personally have not investigated type 1 diabetes to the point where I can provide an in depth look at type 1 diabetes at this time. I probably will in the future and will certainly write about what I find.

I must say I agree with the final conclusions of the author in regards to the possibility of resolving diabetes through a diet and lifestyle. I go further though and suggest that such diet and lifestyle must be founded on an understanding of the underlying physiological mechanisms at play. Not just results of experiments carried out by other people that don’t explain why what happened, happened.

I do feel that personal experimentation is very important. The problem though for people with chronic illness is that personal experimentation not based on an understanding of human physiology can be dangerous. I feel sad that some of the very people she has recorded her experience to help seem to have attacked her. I give her much credit for being so proactive in helping her son overcome his heath problems and for now trying to help others.


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References
1.Ziegler A-G, Schmid S, Huber D, Hummel M, Bonifacio E. Early infant feeding and risk of developing type 1 diabetes-associated autoantibodies. JAMA 2003;290:1721–8.

2. Knip M, Veijola R, Virtanen SM, Hyöty H, Vaarala O, Akerblom HK. Environmental triggers and determinants of type 1 diabetes. Diabetes. 2005 Dec;54 Suppl 2:S125-36.

3. Norris JM, Yin X, Lamb MM, Barriga K, Seifert J, Hoffman M, Orton HD, Barón AE, Clare-Salzler M, Chase HP, Szabo NJ, Erlich H, Eisenbarth GS, Rewers M. Omega-3 polyunsaturated fatty acid intake and islet autoimmunity in children at increased risk for type 1 diabetes. JAMA. 2007 Sep 26;298(12):1420-8.

4. Hyppönen E, Läärä E, Reunanen A, Järvelin MR, Virtanen SM. Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study. Lancet. 2001 Nov 3;358(9292):1500-3