Insulin sensitivity vs insulin resistance?Published 4.17.2017
I've been thinking about diabetes a lot recently. Fortunately, I am not so afflicted, but people near and dear to me are. Several near and dear to me are on the path to diabetes, as they are losing insulin sensitivity, which is another way to say they are becoming insulin resistant.
A lot of the talk about diabetes in the low carb world centers around insulin resistance, but little is said about insulin sensitivity. I realize some will read that sentence and be perplexed. Talking about insulin resistance is talking about insulin sensitivity because the two are the inverse of the other.
And of course that’s true, but the focus is too often on controlling or reacting to insulin resistance rather than reversing it and increasing insulin sensitivity. I think that if gaining insulin sensitivity were the focus, the conversation would be different. If you have insulin sensitive, then the level of insulin in your blood after eating is less important. Instead, the whole issue becomes keeping the level of blood insulin as low as possible.
Why is being insulin sensitive so important? Insulin resistance (aka being insulin insensitive is associated with cognitive decline. This makes recovering insulin sensitivity, not just controlling insulin levels, critical. Please note: only the abstract is available at the link and I am not any sort of medical professional.
As I noted in my summary of the recent vegan-centric Mastering Diabetes Online Summit, what impressed me about a low fat approach to treating diabetes (both types) is the regain of insulin sensitivity. Low carb high fat (LCHF) diets don't do that.
In another win for the whole food plan based diet (WFPBD) folks, fresh fruit consumption is protective against type two diabetes.
This can be scored as a WFPBD “win” too. An intestinal bacteria might protect against type two diabetes, and to have this bacteria you should eat a fiber-rich diet. There is only one way to get fiber into your diet, and that is by eating plants.
Although the health benefits of diets including fresh fruit and vegetables are well established, the sugar content of fruit has led to uncertainty about associated risks of diabetes and of vascular complications of the disease. Du and colleagues studied nearly 500,000 people participating in the China Kadoorie Biobank over about 7 years of follow-up, documenting new cases of diabetes and recording the occurrence of vascular disease and death in people with pre-existing diabetes.
The researchers found that people who reported elevated consumption of fresh fruit had a lower associated risk of developing diabetes in comparison with other participants (adjusted hazard ratio [aHR] 0.88, 95% CI 0.83-0.93), which corresponds to an estimated 0.2% reduction in the absolute risk of diabetes over 5 years. In people with diabetes, higher consumption of fresh fruit was associated with a lower risk of mortality (aHR 0.83, 95% CI 0.74-0.93 per 100g fruit/d), corresponding to an absolute decrease in risk of 1.9% at 5 years, and with lower risks of microvascular and macrovascular complications.
This result is also point in favor of a low fat diet.
A high concentration of indolepropionic acid in the serum protects against type 2 diabetes, shows a new study from the University of Eastern Finland. Indolepropionic acid is a metabolite produced by intestinal bacteria, and its production is boosted by a fibre-rich diet. According to the researchers, the discovery provides additional insight into the role of intestinal bacteria in the interplay between diet, metabolism and health.
The added emphasis (bolding) is mine.
The study also identified several new lipid metabolites whose high concentrations were associated with improved insulin resistance and reduced risk of diabetes. The concentrations of these metabolites were also associated with dietary fat: the lower the amount of saturated fat in the diet, the higher the concentrations of these metabolites. Similarly to indolepropionic acid, high concentrations of these lipid metabolites also seemed to protect against low-grade inflammation.
I don't advocate any particular diet here, although I have argued against diets that require supplementation to be healthy— such as a vegan diet. I have to admit though that the LCHF diet offers very little to commend it. I've noted that my own low carb diet experiment was very short lived, I simply don't want to live that way. More recently though, objections beyond preference have become apparent. My attitude remains the same, weight loss comes down to the energy balance and adherence.
This 2006 paper was linked in the comment section of the Carb-Sane Asylum on this post. Every person out there that is fasting for days then eating a LCHF diet with the goal of reducing their insulin resistance ought to read that paper carefully. The subjects were healthy non-obese males, which is an important distinction to make. If a subject has excess adipose on his or her frame, but effect of fasting might be different.
However, I would think people using LCHF for maintenance might want to note information such as this:
Intramyocellular triglyceride or IMTG is a fancy way of saying fat stored in muscle cells, where it doesn't belong. Fasting and eating a high fat diet decrease insulin sensitivity. Exactly what you don't want to have happen.
For example, in lean, healthy individuals, short-term starvation reduces whole-body and muscle insulin sensitivity (Mansell & Macdonald, 1990; Webber et al. 1994). Starvation also elevates IMTG (Stannard et al. 2002), which is largely a function of the increased circulating free fatty acid (FFA) concentration associated with energy restriction (Cahill et al. 1966; Klein et al. 1993). Thus, a high-fat diet and starvation are similar in that they both result in IMTG accumulation and concurrent whole-body insulin resistance, despite the fact that they differ vastly in dietary fat and energy intake.
The hypothesis in the paper is that carbohydrate (CHO) restriction rather than fat content is the cause of the loss of insulin sensitivity. To test the hypothesis, they compared LCHF diet to full on fasting (short term starvation, which is what true fasting is). The control diet was not low fat, but protein was the same in the LCHF and control diets. Obviously, no food was ingested during starvation, which is why they went with an intravenous glucose tolerance test rather an oral one. Starving subject results would have been confounded by the intake of energy.
Blood glucose clearance was slower (a sign that insulin's effects are being resisted) after both the LCHF diet and starvation— suggesting that the absence of CHO rather than the presence or absence of fat is was made the difference. I've never bought the "carbs are unnecessary," line that LCHF like to spout, and these results don't convince me otherwise. Carbs are necessary for health. The goal should be insulin sensitivity, not low insulin levels.
Here is some potentially good news about type one diabetes: Artificial pancreases might be a possibility for young type ones.
In the randomized, cross-over trial, children (ages 5-8 years) with an artificial pancreas (AP) spent more time with his or her blood glucose levels in the normal range (70-180 mg/dL), compared with children with an insulin pump with continuous glucose monitoring (CGM) care at home (AP 73.1%; home 46.9%, P=0.002 after adjustment for level of activity), reported Mark DeBoer, MD, of the University of Virginia in Charlottesville, and colleagues.
Children with an artificial pancreas also experienced lower mean blood glucose (AP 152 mg/dL; home 190, P<0.001 after adjustment for activity), DeBoer said in a presentation at ENDO 2017.