Katie Wells, CTNC, MCHC, Founder and CEO of Wellness Mama, has a background in research, journalism, and nutrition. As a mom of six, she turned to research and took health into her own hands to find answers to her health problems. WellnessMama.com is the culmination of her thousands of hours of research and all posts are medically reviewed and verified by the Wellness Mama research team. Katie is also the author of the bestselling books The Wellness Mama Cookbook and The Wellness Mama 5-Step Lifestyle Detox.
Exercise– Even the mainstream medical community recognizes the advantage of exercise, as it increases the muscles ability to use insulin and over time can help fix insulin resistance. All exercise isn’t created equal though and fortunately, smaller amounts of high intensity exercise have been shown to have a better effect on insulin levels (and weight loss) than an hour of daily moderate cardio. According to the Healthy Skeptic: “A pair of studies done at McMaster University found that “6-minutes of pure, hard exercise once a week could be just as effective as an hour of daily moderate activity“, according to the June 6, 2005 CNN article reporting on the study.” I recommend high intensity exercise anyway for its various health advantages, and it is great for diabetes control. too.
A healthy balance of carbohydrates, proteins, and fats in your diet will help keep your blood glucose on target. How much of each will depend on many factors, including your weight and your personal preferences. Watching your carbohydrates -- knowing how much you need and how many you are eating -- is key to blood sugar control. If you are overweight, either a low-carbohydrate, low-fat/low calorie, or Mediterranean diet may help you get your weight to goal. No more than 7% of your diet should come from saturated fat, and you should try to avoid trans fats altogether.
Change in fasting plasma glucose (A), 2 h post-oral glucose tolerance test (B), and homeostasis model assessment (HOMA-B) insulin secretion (C) during the 16-year follow-up in the Whitehall II study. Of the 6,538 people studied, diabetes developed in 505. Time 0 was taken as the diagnosis of diabetes or as the end of follow-up for those remaining normoglycemic. Redrawn with permission from Tabák et al. (80).
The role of physical activity must be considered. Increased levels of daily activity bring about decreases in liver fat stores (43), and a single bout of exercise substantially decreases both de novo lipogenesis (39) and plasma VLDL (92). Several studies demonstrated that calorie control combined with exercise is much more successful than calorie restriction alone (93). However, exercise programs alone produce no weight loss for overweight middle-aged people (94). The necessary initial major loss of body weight demands a substantial reduction in energy intake. After weight loss, steady weight is most effectively achieved by a combination of dietary restriction and physical activity. Both aerobic and resistance exercise are effective (95). The critical factor is sustainability.

Chronic exposure of β-cells to triacylglycerol or fatty acids either in vitro or in vivo decreases β-cell capacity to respond to an acute increase in glucose levels (57,58). This concept is far from new (59,60), but the observations of what happens during reversal of diabetes provide a new perspective. β-Cells avidly import fatty acids through the CD36 transporter (24,61) and respond to increased fatty acid supply by storing the excess as triacylglycerol (62). The cellular process of insulin secretion in response to an increase in glucose supply depends on ATP generation by glucose oxidation. However, in the context of an oversupply of fatty acids, such chronic nutrient surfeit prevents further increases in ATP production. Increased fatty acid availability inhibits both pyruvate cycling, which is normally increased during an acute increase in glucose availability, and pyruvate dehydrogenase activity, the major rate-limiting enzyme of glucose oxidation (63). Fatty acids have been shown to inhibit β-cell proliferation in vitro by induction of the cell cycle inhibitors p16 and p18, and this effect is magnified by increased glucose concentration (64). This antiproliferative effect is specifically prevented by small interfering RNA knockdown of the inhibitors. In the Zucker diabetic fatty rat, a genetic model of spontaneous type 2 diabetes, the onset of hyperglycemia is preceded by a rapid increase in pancreatic fat (58). It is particularly noteworthy that the onset of diabetes in this genetic model is completely preventable by restriction of food intake (65), illustrating the interaction between genetic susceptibility and environmental factors.

Normally, blood glucose levels are tightly controlled by insulin, a hormone produced by the pancreas. Insulin lowers the blood glucose level. When the blood glucose elevates (for example, after eating food), insulin is released from the pancreas. This release of insulin promotes the uptake of glucose into body cells. In patients with diabetes, the absence of insufficient production of or lack of response to insulin causes hyperglycemia. Diabetes is a chronic medical condition, meaning that although it can be controlled, it lasts a lifetime.
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