The ketogenic diet (for the control/reversal of diabetes) is based on the notion that excessive consumption of carbs leads to Insulin Resistance which is the basis of diabetes. Thus, reducing carbohydrates results in a reversal of diabetes because it improves Insulin Sensitivity (ie, it decreases Insulin Resistance).
The author of the Zone Diet agrees that Insulin Resistance is the core issue in weight loss but disagrees with the cause of Insulin Resistance. From (Insulin Resistance and Weight Loss. Dr. Sears. Apr 6, 2018):
It is constantly elevated insulin levels that makes you gain weight, and keep the weight on. The reason is that if the muscle cells are not taking in enough glucose from the blood, the increased insulin levels drive that glucose into the fat cells instead and that accelerates the storage of dietary excess calories as stored fat. This makes you gain weight. Furthermore, these increased insulin levels prevent your fat cells from releasing stored fat to be used as energy for the body. This keeps the weight on.
Agreed. And, that is the premise of the ketogenic diet as well.
Insulin is a hormone that helps regulate the amount of glucose, a breakdown product of carbohydrates, in our blood required for optimal brain function as well controlling enzyme activities, gene expression and the distribution and storage of energy.
Here Dr Sears shows a common but fundamental misconception about the role of dietary carbohydrates. Carbohydrates are not required to produce glucose. The liver can produce more than enough glucose in the liver though Gluconeogenesis (GNG) from other substrates such as body fat. If dietary carbohydrates were required then the blood sugar during fasting would not level out – which it does.
To be fair, I assume Dr Sears knows better.
So What’s the Difference of Keto vs Zone?
The Zone Diet has a different diagnosis to the cause of Insulin Resistance. With the Zone Diet, it’s not carb intolerance that is postulated to be the core issue, it’s inflammation that causes Insulin Resistance. From Dr Sears:
insulin resistance … is caused by increased cellular inflammation.
There are several factors that play a role in insulin resistance, but cellular inflammation is the biggest culprit.
Dr Sears explains his view of cellular inflammation in this article (What is Cellular Inflammation? Dr. Barry Sears. Jan 10, 2012). In the article he cites quite a few papers but many of these are his own papers.
Back to the original article:
Cellular inflammation results from an imbalance of two key fatty acids in our blood, Arachidonic Acid (AA) and Eicosapentaenoic Acid (EPA). When the levels of arachidonic acid are in excess it leads to the generation of hormones known to be pro-inflammatory. This inflammation makes it difficult for insulin to communicate with our cells in the liver, muscle, and adipose tissue.
Let’s check out Dr. Sears assertions. From (Essential fatty acids in health and chronic disease. Artemis P Simopoulos. The American Journal of Clinical Nutrition, Volume 70, Issue 3, 1 September 1999, Pages 560s–569s):
Human beings evolved consuming a diet that contained about equal amounts of n−3 and n−6 essential fatty acids. Over the past 100–150 y there has been an enormous increase in the consumption of n−6 fatty acids due to the increased intake of vegetable oils from corn, sunflower seeds, safflower seeds, cottonseed, and soybeans.
n−3 Fatty acids, however, have antiinflammatory, antithrombotic, antiarrhythmic, hypolipidemic, and vasodilatory properties. These beneficial effects of n−3 fatty acids have been shown in the secondary prevention of coronary heart disease, hypertension, type 2 diabetes, and, in some patients with renal disease, rheumatoid arthritis, ulcerative colitis, Crohn disease, and chronic obstructive pulmonary disease.
Most of the studies were carried out with fish oils [eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)]. However, α-linolenic acid, found in green leafy vegetables, flaxseed, rapeseed, and walnuts, desaturates and elongates in the human body to EPA and DHA and by itself may have beneficial effects in health and in the control of chronic diseases.
This particular paper, at least, supports Dr Sears’ position on dietary causes other than high carbohydrates being the source of hyperinsulinemia and Type 2 Diabetes. However, one of the referenced papers sheds light on this as a diabetic therapy.
In a randomized, double-blind, placebo-controlled, crossover trial, patients with type 2 diabetes consumed 6 g n−3 fatty acids (EPA and DHA)/d for 6 mo in addition to their usual oral therapy (14). Fasting serum glucose concentrations increased by 11% during the n−3 fatty acid phase and by 8% during the placebo phase (olive oil), showing a nonsignificant net increase of 3%.
Similarly, there was no significant change in glycated hemoglobin concentrations.
However, fasting triacylglycerol concentrations decreased by 43%, which is a highly significant change. This study is the largest and longest reported placebo-controlled trial of the effect of n−3 fatty acids on type 2 diabetes. It showed convincingly that n−3 fatty acid intake, along with oral therapy for diabetes, can lower triacylglycerol concentrations with no adverse effects on glycemic control.
This was more than enough time for an improvement in HbA1C values, but there was no improvement on blood sugar control. There was an improvement in triaglycerol concentrations (Connor WE, Prince MJ, Ullmann D, et al. The hypotriglyceridemic effect of fish oil in adult-onset diabetes without adverse glucose control. Ann N Y Acad Sci 1993;683:337–40.)
Diabetic control as judged by five criteria did not deteriorate after 6 months of fish oil compared to 6 months of olive oil supplementation in 16 patients with NIDDM who were eating a low fat, high complex carbohydrate diet.
Plasma total and VLDL triglyceride and cholesterol decreased significantly after fish oil supplementation; plasma total and HDL cholesterol concentrations did not change.
The LDL cholesterol level was significantly increased with fish oil supplementation, suggesting that patients with NIDDM who are given a fish oil supplement to decrease the plasma total and VLDL triglyceride levels may also need further dietary and/or pharmaceutical therapy to maintain an LDL cholesterol level compatible with a low risk of coronary disease. The study emphasizes the safe use of fish oil over a 6-month period in diabetic patients.
Here’s a metastudy that looked at 26 studies on the subject (Fish Oil and Glycemic Control in Diabetes. DIABETES CARE, VOLUME 21, NUMBER 4, APRIL 1998. Frieberg, et.al.):
The use of fish oil has no adverse affects on HbA1 c in diabetic subjects and lowers triglyceride levels effectively by almost 30%. However, this may be accompanied by a slight increase in LDL cholesterol concentration. Fish oil may be useful in treating dyslipidemia in diabetes.
Fish oil administration resulted in a tendency for fasting blood glucose levels to be higher in NIDDM subjects (0.43 mmol/l [95% CI, 0.00–0.87], P = 0.06) and to be significantly lower in IDDM patients (-1 . 86 mmol/l [95% CI, -3.1 to -0.61], P = 0.05). This difference in fasting blood glucose responses to fish oil between NIDDM and IDDM subjects was significant (P = 0.01).
Fish oil consumption lowered serum triglycerides significantly by 25–30% in both types of subjects and resulted in a slight but significant increase in LDL cholesterol levels in NIDDM subjects only.
So it sounds to me like fish oil has no real/consistent effect on blood sugars and they raise LDL levels a bit. They do lower serum triglycerides which is a good thing. Makes me glad I take them.
So Dr Sears’ argument that Diabetes is ultimately caused by incorrect amounts of Omega-3 to Omega-6 ratios is demonstrably refuted by the actual evidence that supplementation doesn’t improve HbA1C. This may also be the reason that people on the Zone diet don’t get cured from Diabetes – except to the extent that their weight drops.