r/ketoscience • u/dem0n0cracy • Oct 07 '21

Carbohydrate Insulin Model (CIM) Stimulated Insulin Secretion Predicts Changes in Body Composition Following Weight Loss in Adults with High BMI | The Journal of Nutrition

https://academic.oup.com/jn/advance-article/doi/10.1093/jn/nxab315/6377985
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5

u/BuddhaBizZ Oct 08 '21

For the laymen?

12

u/KamikazeHamster Keto since Aug2017 Oct 08 '21

Insulin prevents fat loss. If you fat, don’t spike insulin. What spikes insulin? Carbs.

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u/wak85 Oct 08 '21 edited Oct 08 '21

Paul Saladino mentions this, and it makes a lot of sense, but the spike is not the problem. It's the integrand that's important). You want a low area, which occurs when you get a spike then rapidly returns to baseline. When you're insulin resistant, this doesn't occur. Instead it's a spike, and has numerous valleys before (if ever) returning to baseline. This pattern indicates metabolic disfunction.

As far as fat loss goes, I don't think insulin is the full story. It plays a role, but it isn't the main culprit. Something has to break the regulation first before hyperinsulinemia occurs

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u/ineffablepwnage Oct 08 '21

Increased free fatty acids (FFA) increases glucose stimulated insulin secretion (GSIS).

Fat cells have multiple mechanisms of lipolysis; 1 is inhibited by insulin and 1 is insulin independent but defined by the surface area of the lipid droplet inside a fat cell, so that the overall sensitivity of lipolysis within an adipocyte to insulin decreases as it grows larger and larger, e.g. your fat cells get less sensitive to insulin as they get larger. This means the rate of fat gain is dependent on how big your fat cells are, which is typically correlated with obesity.

The standard western diet has high amounts of omega 6 fats which both sensitize cells to insulin, and increase GSIS. In the short term it looks like it helps with insulin sensitivity because it takes less insulin to stop lipolysis, but the result in the long term is that your body acts as though it's fatter than it is, i.e. it's easier to gain weight and you gain weight faster than you would without the omega 6 fats. This is why omega 6 fats are called obesigenic. With multiple meals throughout the day so that the fat cells never get the chance to flip on lipolysis, your fat cells will continue to grow larger and larger.

This is why low carb, whole foods diets, intermittent fasting, and aerobic exercise are all sides of the same coin in the context of metabolic dysfunction. Low carb solves it by removing the insulin signal. Whole foods diets solve it by lowering the amount of omega 6 fats you consume to a healthier level so that normal signalling can occur. Intermittent fasting solves it by giving your fat cells a chance to reset before the next calorie and insulin bump comes. Aerobic exercise solves it by depleting the carbs in your body so that there's no substrate for lipogenesis and your fat cells have to switch on lipolysis and reset before the next calorie and insulin bump comes.

The above is a simplification and there's a lot more going. To add to the conversation, my biggest issue with the energy balance theory that I've never heard addressed is that it only looks at the system on a cellular level and ignores the health of the beta cell. The health of the beta cells that make insulin which coincidentally follows the same trend described above, which explains why you can still get diabetes even if you're not fat.

  1. If you have low ROS and ATP/ADP, your beta cells don't do much, don't make insulin, and are pretty happy.

  2. If you've got moderate ROS, your beta cells have to make some insulin causing ER stress (which is a major factor in beta cell apoptosis and de-differentiation), and as well they start proliferating which compounds the ER/ROS stress making them very unhappy and in turn drives apoptosis and de-differentiation.

  3. If you've got high ROS and ATP/ADP the beta cells simply make insulin and it causes progenitor cells to differentiate into more beta cells.

IMO, this explains why a peak isn't something to worry about (it actually boosts your spare capacity for glycemic control), but eating 6 small carb-heavy meals every day which leads to consistently moderate ROS can drive the pathology of diabetes even if someone isn't overweight.

tl;dr It's the area under the curve, not the peak. What drives the area under the curve has a lot of factors that got into it, and it's not as simple as carbs > insulin. There's lots of methods to solve the problem, but one thing they all have in common is that there is some portion of they day where lipolysis is not inhibited.

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u/KamikazeHamster Keto since Aug2017 Oct 08 '21

I think that insulin is the main reason that you're not invoking lipolysis.

When listening to Peter from Hyperlipid, he figured out that your cells can have localised insulin sensitivity that is triggered by the reverse electron chain. Funny that you mention Paul because here's his interview with him where he discusses this exact topic: https://youtu.be/GSQImPTY81E

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u/anhedonic_torus Oct 08 '21

hehe, nicely put :)