I summarized some articles that dispel insulin voodoo here, if you're interested: https://www.reddit.com/r/Fitness/comments/j853z/insulin_an_u...
Insulin, being necessary for healthy human life, is certainly not "bad". However, a shortage (e.g. Type 1 diabetes) or excess (e.g. Type 2 diabetes) is certainly a problem. Given the current epidemic of Type 2 diabetes, metabolic syndrome, and NAFLD, triggering excess insulin production is certainly something to be wary of.
Also of concern is impinging on the glucagon cycle, and in the linked-to post there is no mention of the important function of glucagon, which is typically considered as having effects opposite to insulin. Maintaining the insulin/glucagon cycle is important in maintenance of a healthy metabolism.
The article makes a point about how "Insulin is not needed for fat storage", but omits the fact that in reality, practically all fat storage is mediated by insulin and its effects on glucose. Insulin mediates glucose transport and promotes absorption of blood glucose into the liver, fat and muscle cells. Once the liver has filled its compliment of glycogen, it will indeed produce fat locally. Non-Alcoholic Fatty Liver Disease (NAFLD) currently afflicts about 25% of the entire human population, and the linked-to author would have the reader believe that excess insulin production isn't an issue? Very strange.
All in all, this article paints a false picture of human metabolism. People eating a typical Western diet should be concerned or at least aware of the facts of that process, and be wary of having an excess or deficit of insulin; and should know that the excess case is the more common condition. A reasonable scientifically-accurate depiction of the process can be found, for example, in Jason Fung's books, "The Diabetes Code" and "The Obesity Code".
I don't see how this is a strawman. Click through to the source article, that bullet point in particular is refuting the common belief that carbs alone are what spike insulin. Most insulin-centric discussion on fitness forums (which is where this was posted) tends to mention insulin spikes in the context of high-GI carbs.
> Also of concern is impinging on the glucagon cycle, and in the linked-to post there is no mention of the important function of glucagon, which is typically considered as having effects opposite to insulin.
Read the linked "part 1". It specifically mentions that newer research shows that glucagon does not counteract insulin as previously thought, and links some studies.
> The article makes a point about how "Insulin is not needed for fat storage", but omits the fact that in reality, practically all fat storage is mediated by insulin and its effects on glucose.
That isn't really relevant to the core point, which is debunking the idea that insulin is what makes us fat.
I just want to restate the fact that the above reddit post is a summary of articles, which themselves are a summary of studies. It is targeted at fitness people who are discussing insulin only in the context of weight loss. There is of course an oversimplification here due to omitting details the target audience might not need as well as being 2 steps removed from the source material.
> Maintaining the insulin/glucagon cycle is important in maintenance of a healthy metabolism.
No point in focusing on hormones so much. I somehow don't see people fretting over their ACTH or progesterone.
> Insulin mediates glucose transport and promotes absorption of blood glucose into the liver, fat and muscle cells.
If you look at data from humans - insulin IS NOT needed for glucose absorption. Studies on diabetic people clearly show that glucose gradient into the cell is higher, not lower, despite them being incredibly insulin resistant. 1st role of insulin in humans that's critical is shutting down liver glucogenesis and gluconeogenesis.
The problem with insulin/glucose narration is omitting the role of FFA. Intracellular FFA levels drive down the glucose absorption gradient. If the glucose absorption gradient is low and we still have glucose - that will stimulate more insulin release to drive that glucose level to normal.
Problem is that as more insulin is present cells eventually start being resistant to insulin requiring more insulin for the same job. Which makes for a problem because if insulin is there to shut down liver glucogenesis and cells are now more resistant to insulin - bad news, we need more insulin to get blood glucose to same levels with a meal that used to be no problem.
Adipose tissue is simply the number #1 a-hole here because it's usually the least resistant to insulin and the least resistant to nutrient storage since it's its primary role. It will just pack more in.
P.S. Isn't Fung a quack? E.g. https://www.myoleanfitness.com/evidence-caloric-restriction/
I respectfully disagree. When I go to USA or Mexico in particular, the frequency of obesity is astonishing. Perhaps with more understanding of the mechanisms around the phenomenon, there would be more success in dealing with the problem. As I mentioned earlier, around 25% of the entire human population has NAFLD, which is also an astonishing figure.
I'm not saying that every person must study these metabolic pathways in detail, but rather that the quick and simple rules and choices people make in daily life should take advantage of what is known, hopefully for a better outcome than what is currently observed.
> insulin IS NOT needed for glucose absorption
I'm not aware of anyone claiming insulin is needed for glucose absorption. The brain, liver, and red blood cells, for example, cannot function properly if they are sensitive to blood insulin levels; this may be because the RBC and brain rely on a steady supply of glucose, and the liver must be able to take up or release glucose on its own schedule.
On the other hand, muscle and adipose tissue DO have insulin-sensitive GLUT4 transporters. The GLUT family of transporters are passive, so glucose flows down its concentration gradient, unlike the sodium-linked transporters of the gut and kidney, which actively transport glucose against a gradient.
So in the case of adipose tissue, it does require glucose in order to store fat. The glycerol backbone for intracellular triglyceride synthesis is provided by glucose. In a person without diabetes, insulin is released from the vesicles when the body detects the amino acids leucine and arginine, or the sugars glucose and mannose. So typically, insulin will also be present, and having its usual effect on the GLUT4 transporters.
This is all covered, to some degree, in the appendices to Fung's book on obesity, by the way.
> Adipose tissue is [...] usually the least resistant to insulin and the least resistant to nutrient storage since it's its primary role. It will just pack more in.
Yes that is my point as well.
> P.S. Isn't Fung a quack? E.g. https://www.myoleanfitness.com/evidence-caloric-restriction/
No, Fung is not a quack.
It doesn't seem fair to even compare Fung's work with the claims of Myolean, because Fung is a trained scientist and knows how to read, interpret, and communicate scientific information in the traditional manner that others can understand. Even if Fung's arguments were wrong, at a superficial level he would be more persuasive because he knows how to use the language and standards of science.
However, examining the discussion in some details will reveal that Fung is correct in all the major points covering this topic, as best as is known at present. (Of course there are major unknowns when it comes to human metabolism, but there is also a lot that is known).
From the link you provided, it seems quite apparent that Myolean does not understand what a non-linear feedback system is (e.g. human metabolism), and doesn't understand the role of motivation and willpower (for compliance) involved in maintaining a calorie-deficient or calorie-neutral diet.
At no point does Fung say the laws of thermodynamics don't apply, but rather that they aren't very relevant when you incorporate the variability of basal metabolism, and motivation/willpower, into the model. One of Fung's major points is that in reality, when people try to follow restrictive diets, doing it in a way that leaves you constantly hungry, with low willpower, and continuously high insulin production leads to failure of achieving desired results.
Here is Fung discussing FFA [1].
[1] https://www.dietdoctor.com/fasting-and-cholesterol
Lastly, it would be easier to take Myoleanfitness more seriously if I didn't get the feeling they are trying to sexually manipulate me with a hit of dopamine and testosterone with their ads such as [2] and [3].
[2] https://www.myoleanfitness.com/wp-content/uploads/2018/05/Su...
[3] https://www.myoleanfitness.com/wp-content/uploads/2018/12/On...
The point is, the substance of the Myoleanfitness argument is not even wrong, its just irrelevant. But the form in this case matches the content. Distracting and irrelevant.
I agree. I'm simply pointing out the fact that with the picture as complex as we know it is I have a knee jerk reaction to people going from "how to have normal BF%" to "ok, let's talk about insulin". It's the same thing with people talking about brain, attention span and productivity. 10 seconds into the discussions it's "dopamine, dopamine ... DOPAMINE"
> So in the case of adipose tissue, it does require glucose in order to store fat. The glycerol backbone for intracellular triglyceride synthesis is provided by glucose.
Yes. And? Glucose to some extent is always present in the blood. Drop the glucose low enough and brain will die. One could say that adipose tissue will always figure out how to store fat.
As we go on you reference Fung (and defend him) a fair bit. I'd like to take this opportunity to state the obvious. Jason Fung is a trained and certified nephrologist, book author, popular doctor and so on. He does not hold (to my knowledge) a PhD nor has he published any peer-reviewed studies.
Thus calling him a quack on my part was bad (I was pulling your leg a bit) but he cannot be considered a scientist either. He's an expert in his field but his books can't be considered textbooks on human endocrinolongy. He's allowed to have his own opinion but asking anybody to agree or disagree with his views without in-depth study of them is asking too much and he haven't (to my knowledge) presented them in the form of some kind of scientific paper it's not worth arguing whether he's right or not.
That being said - the link you provided on FFA is about cholesterol. I fail to see how that's relevant to discussion about FFA impact on insulin resistance?
Alas, to make my point. Obesity is certainly a multifaceted problem. Thermodynamics certainly matter, human psyche, inflammation, hormones - essentially all of that has its place. Looking from a systems point of view there's no reason (and probably there isn't one) to look for single causative agent though some certainly play a grater role.
In my experience both time-restricted feeding, caloric restriction and macro restriction work and have their place depending on the individual. Generally as a rule IF and low-carb are certainly good ideas, I'm not a fan of keto for everything.
> Insulin is not required for fat storage.
Insulin provokes fat storage, regardless of any other pathways that may exist. Spiking your insulin with refined carbs is going to provoke fat storage more than the equivalent caloric amount of fat.
> Insulin spikes do not create energy out of nowhere and don't suddenly make the same number of input calories multiply.
Unfortunately, this "law of thermodynamics" view of things is too simple.
> Also, insulin spikes are nearly unpredictable anyway. Carbs aren't necessarily the trigger, protein and fat can be too.
Fat has minimal impact on insulin levels. Refined carbohydrates can raise blood sugar very high, requiring a double dose of insulin to get back to baseline. Meals high in protein or more complex carbs will be somewhere in the middle.
> I summarized some articles that dispel insulin voodoo here
If there's anything that's being dispelled there, it's not something that I actually said. Seems like this is a pet peeve of yours and you're seeing someone else in me.
