Six common beliefs addressed, Part 231

1. I am so tired of reading about insulin levels in these low carbohydrate groups.

They are pushing BS. On this blog, we focus on insulin function which deteriorates over time when insulin demand is abnormal.

What would cause abnormal insulin demand? When your post postprandial blood glucose reaches 200 mg/dL, from a slice of pizza, and then insulin has to help clear this astronomically high blood glucose. Not only does this put a high insulin demand on the body, but blood glucose continues dropping after fasting, due to this high insulin output, which not only takes time to clear in the serum but continues its expression on certain organs and tissues after it does leading to insulin resistance over time. This erratic blood glucose and abnormal insulin expression sets the stage for a metabolic adaptation that chronically under expresses leptin leading to the storage and sparing of body fat.

Insulin resistance does not always correlate with insulin serum levels as insulin can be rather erratic, especially after meals. Fasting insulin levels are a better indicator of insulin function, but that also doesn't always match up in everyone. The best way to determine how your insulin is functioning, in the context of metabolic syndrome, is whether you are overweight/obese or not.

2. If the carbohydrate insulin hypothesis (CIH) is not true, then why are carbs still being blamed for overweight/obesity?

Because CIH is not true, but the Carbohydrate Obesity Hypothesis (COH) is. Remember insulin is not an obesity hormone. It is simply an anabolic/anticatabolic hormone. That is all. Obesity is a metabolic adaptation to starvation not an "insulin disease". It takes a lot of metabolic dysfunction to create this adaptation and insulin is only one hormone in that conveyor belt of abnormality.

Carbs cause a pathology in blood glucose regulation setting the stage for this adaptation to occur. So, carbs directly impact obesity just not through insulin, but through blood glucose disparities instead, which eventually deteriorates insulin function over time. This deterioration in function takes many forms. From insulin resistance in various tissues, to varying degrees, to not enough first phase insulin output to stop catabolism to adrenal over expression. This affects many systems in the body. It's like a domino effect that becomes more complex as more glucoregulatory systems are affected.

But it all begins with postprandial blood glucose abnormalities of which carbs are the culprit. This doesn't mean that there aren't other mechanisms that can cause this metabolic adaptation towards obesity. After all, anything that affects proper blood glucose regulation will eventually drive this adaptation. There are many things, other than diet, which can dysregulate blood glucose. Diet is just the most common culprit in modern obesity.

3. Most of the low carbohydrate doctors seem to have moved away from "keto" or disappeared altogether. I hardly hear them speak on fasting anymore.

A lot of them have disappeared to desperately try and find another shtick. It's been some years since fasting and "keto" have been thrown around and the overweight/obese are still the same as when they started. Most of the ones who did see improvement, are slowly seeing their numbers revert back to diabetic status. This means that their movement has slowly lost momentum because still being fat and sick after five years of "keto" is certainly not a good business model.

A lot of these doctors are cutting their losses and moving on to the next gimmick. Many of them jumped from low carb to "keto", then fasting and then carnivore but that's basically the last straw. There's nowhere else to go from there except somewhere else.

4. Some people fast with great success and others seem to get fatter.

"Great success" is up for interpretation......

In the end, all diets and other obesity interventions like fasting only work as well as your leptin expression allows. No one yet knows the exact mechanism of how leptin expression fails, though insulin is involved, or how to regain it. For this reason, there is no known cure for overweight/obesity. What we do know is that overweight/obesity interventions work best the earlier they are applied as obesity is a time dependent condition. The longer you have it, the more intractable it becomes. So, people who were overweight/obese for a short time in their lives, tend to respond to treatments better. The longer you have been obese, especially if you had childhood obesity, the less you will respond to treatments.

Overweight/obesity is an adaptation towards starvation and one of the main hormones that drive this is leptin. So, of course, if your leptin expression is already compromised, fasting will only make it worse causing for more body fat to be accumulated.

This is why there is no one intervention for obesity because your results are completely determined by how much proper blood glucose regulation you can regain and sustain. Results are not at the discretion of the treatment but of your metabolic response.

5. If I have urine ketones, it means I'm burning body fat.

No. It means you are burning dietary fat, if you are following "keto". The type of ketosis you want is when the ketones being produced are from the burning of your own body fat. Those are the only types of ketones that will treat overweight/obesity.

If you are treating another condition with ketosis, then it wouldn't matter where the ketones are coming from as you just need the ketones.

Overweight/obesity is treated through the burning of body fat. It's not treated by the presence of ketones. That's why we don't track any of that silly stuff on this blog. The best way to know if you are burning body fat is when the mirror, scale and the measuring tape reflects it.

6. If the person eats less food than the body requires, it causes the burning of body fat.

Fat is always being burned, whether you eat the body's requirement or not. This is because fat is the primary fuel that the body uses for everything, even while sleeping. The body never "stops" burning fat, unless you're dead.

How much fat is burned and where it's coming from (glucose conversion, dietary fat, body fat) is at the discretion of your neuroendocrine system, not whether you ate "less food than the body requires". Metabolism always compensates for nutrient availability. This is why an obese person can eat the same amount of food as a lean person but remain obese, while a lean person can eat the same amount of food as an obese person and remain lean.

All body fat loss and gain is at the discretion of your neuroendocrine system. If this system is healthy and working properly, you can just use a simple metric such as the body's daily energy requirements in calories and fluctuate your weight up or down. But when you are overweight/obese, you need to use more sophisticated nutrient information for this system to respond properly and not overcompensate.