Reddit reviews The Diabetes Reset: Avoid It. Control It. Even Reverse It. A Doctor's Scientific Program

> That type 2 is specifically caused by a bad diet.

Sure, we can attack this from many different angles. We could look at it from the reverse perspective and see which diets in T2 patients have the best outcomes:

http://www.ncbi.nlm.nih.gov/pubmed/25984419
>the greatest emphasis of treatment for this patient centered on a low-carbohydrate, whole-foods diet and regular exercise that shifted the focus to the patient's role in controlling their disease.


http://www.ncbi.nlm.nih.gov/pubmed/15288740
>Diabetics treated by diet only have significant rates of complications and are less likely than those on medication to be adequately monitored.


http://www.ncbi.nlm.nih.gov/pubmed/26971990
>Of the 3 distinct diet patterns characterized, the carbohydrate-based pattern was most closely associated with cardiometabolic risk factors.

http://www.ncbi.nlm.nih.gov/pubmed/24015695
>A low-carbohydrate diet was well tolerated and achieved weight loss over 24 weeks in subjects with diabetes. Glycemic control improved with a reduction in requirements for hypoglycemic agents.

http://www.ncbi.nlm.nih.gov/pubmed/25527677
>As previously reported, among women with PCOS, the lower-carbohydrate arm showed decreased fasting insulin (-2.8 μIU/mL; P < 0.001) and fasting glucose (-4.7 mg/dL; P < 0.01) and increased insulin sensitivity (1.06 arbitrary units; P < 0.05) and "dynamic" β-cell response (96.1 · 10(9); P < 0.001). In the lower-carbohydrate arm, women lost both IAAT (-4.8 cm(2); P < 0.01) and intermuscular fat (-1.2 cm(2); P < 0.01). In the lower-fat arm, women lost lean mass (-0.6 kg; P < 0.05). Original to this report, after the lower-carbohydrate arm, the change in IAAT was positively associated with the change in tumor necrosis factor α (P < 0.05).

http://www.ncbi.nlm.nih.gov/pubmed/26224300
>The LC diet, which was high in unsaturated fat and low in saturated fat, achieved greater improvements in the lipid profile, blood glucose stability, and reductions in diabetes medication requirements, suggesting an effective strategy for the optimization of T2D management.

http://www.ncbi.nlm.nih.gov/pubmed/25071075
>These improvements and reductions in GV and antiglycemic medication requirements were greatest with the LC compared with HC. This suggests an LC diet with low saturated fat may be an effective dietary approach for T2DM management if effects are sustained beyond 24 weeks.


We could look at the progression of Type 2:

http://www.ncbi.nlm.nih.gov/pubmed/24186880
>Increased TG and low HDL levels are independently associated with increased rate of progression of diabetes.

(Guess what causes low HDL and high HDL - carbohydrates 1, 2, 3


http://www.ncbi.nlm.nih.gov/pubmed/17991135
>Impaired glucose tolerance and impaired fasting glucose represent two potentially reversible prediabetes conditions.


You could also look at populations and their development of diabetes and what caused it:

http://www.ncbi.nlm.nih.gov/pubmed/25218727
>During this period there has been an increase in the rates of obesity and a reduction in physical activity. Many of the changes in lifestyle and diet are a result of increased economic development and urbanisation. In addition to an increasingly westernised diet, the traditional Chinese diet also plays a part, with the quantity and quality of rice intake linked to the risk of type 2 diabetes.

http://www.ncbi.nlm.nih.gov/pubmed/20980490
>Elevated intake of white rice is associated with an increased risk of type 2 diabetes in Japanese women. The finding that is suggestive of a positive association of rice intake in physically inactive men deserves further investigation.

We could talk about high carbohydrate diets causing hepatic insulin resistance:
http://www.ncbi.nlm.nih.gov/pubmed/23022226


We could talk about insulin resistance being independently associated with development of type 2, despite various levels of beta cell abnormalities in different patients:
http://www.ncbi.nlm.nih.gov/pubmed/11225637
>Theoretically one may postulate three other situations originating with a genetic beta-cell defect: some people may start off life with normal beta-cell function but experience a genetically determined accelerated deterioration; some people may start off life with reduced beta-cell function (e.g. less beta-cell s); still others may start off with reduced beta-cell function and have an accelerated rate of deterioration. In each of the above situations, at any given level of beta-cell function, the degree of insulin resistance present would alter the threshold for developing impaired glucose tolerance and ultimately type 2 diabetes; in other words, the greater the insulin resistance, the lower the threshold, the earlier the onset and the more severe the diabetes will be. It follows therefore that efforts to diminish insulin resistance and to preserve beta-cell function should both be beneficial.

We could look at a high-carb diet's effect on insulin receptors and hyperinsulinemia:

http://www.ncbi.nlm.nih.gov/pubmed/446930
>Ingestion of the high carbohydrate diet led to daylong hyperinsulinemia in both short- and long-term groups. Insulin binding to isolated adipocytes was decreased in both groups.... sustained and chronic hyperinsulinemia can lead to a decrease in the number of cellular insulin receptors.

We could talk about energy restriction and how hypercaloric diets are an even better predictor than carbohydrate content:
http://www.ncbi.nlm.nih.gov/pubmed/19079907



Let me be clear though, it's not simply the presence of carbohydrates that causes type 2 diabetes. We can see by examining the traditional Japanese diet that a high-carb, very-low fat diet actually can prevent T2D as well. In fact it's the interplay between carbohydrates raising glucose and fat decreasing insulin sensitivity and promoting inflammation (1, 2 ). I could easily make an argument for 1) A high fat, very low carb, low/moderate protein diet or 2) a high complex-carb, low-starch, low-sugar, very low fat diet for prevention of T2D.

http://www.ncbi.nlm.nih.gov/pubmed/18083355
>The short-term TG-raising effect of a very low-fat diet is dependent upon the nature of the carbohydrate, with a greater effect of a sugar-rich than a complex-carbohydrate-rich diet.


http://www.ncbi.nlm.nih.gov/pubmed/15616799
>In routine practice a reduced-carbohydrate, higher protein diet may be the most appropriate overall approach to reducing the risk of cardiovascular disease and type 2 diabetes. To achieve similar benefits on a HC diet, it may be necessary to increase fibre-rich wholegrains, legumes, vegetables and fruits, and to reduce saturated fatty acids to a greater extent than appears to be achieved by implementing current guidelines.


http://www.ncbi.nlm.nih.gov/pubmed/14984449
>Natural food-based high-CHO and high-MUFA diets have similar effects on LDL oxidative resistance and metabolic control in subjects with Type 2 diabetes. A MUFA diet is a good alternative to high-CHO diets for nutrition therapy of diabetes

There is even a whole book written on this very topic.

After reading all of these (which I'm sure you will), at the absolute very least you can see how much of a role diet influences progression of T2D and how the disease progresses with a combination of insulin resistance, obesity, hyperinsulinemia and hyperglycemia, and inflammation. There are several different types of diets that can be used to treat T2D and improve glucose tolerance in insulin sensitivity. There are also plenty of diets that destroy glucose tolerance and insulin sensitivity, regardless of beta cell dysfunction or the genetic deck you were dealt at birth. I'm not even going to bother getting into the biology of insulin resistance and the mechanisms in the body because that is stuff you should already know if you are serious about treating your condition.

For the other part of my argument, that people are walking around with developing insulin resistance without even realizing it, I will refer you to my other comment with the statistics that show the massive amount of people who already have "pre-diabetes" - 1/3 of the population of the USA.

Honestly I could go on and on and on at this point, but considering there's only a 3% chance you even made it this far, I'm going to stop listing sources now for someone who is unwilling to help themselves.


>You made the claims; I made none at all.


Exactly, you have nothing to contribute to this conversation. I make statements based on peer-reviewed studies and a basic understanding of biology and glucose metabolism and then back them up, and you sit there doing nothing except perpetuating victimization and helplessness. All of this a defensive reaction to your own struggles, undoubtedly. Here's an idea, learn about how your body works and I won't need to spoon feed you this information next time like you're a child incapable of using your brain.

Forgot one more...