For fat soluble molecules, perhaps, although the concept of adipose tissue cacheing anything other than sugar and TAGs I’m not that familiar with.
I would think the pancreas would have a mechanism of disassembling the insulin molecule to reuse its parts.
The adipocytes have a differing relationship to insulin compared to muscle or liver for example. But I’d be surprised if they store insulin. I’m under the impression that insulin binds to membrane receptors and doesn’t enter cells.
This is an incomplete understanding of the situation. Yes, protein raises insulin but it also raises glucagon. Maintaining a favorable insulin:glucagon balance is actually the important thing when considering lipolysis.
By contrast eating carbs ONLY raises insulin.
Protein definitely does not stop fat oxidation.
Here’s a good explanation of the protein question on low carb.
What Dr. Marchegiani is talking about seems to be some really esoteric stuff, the only research I see about this, is this: Adipose tissue as an endocrine organ
So let’s say fat, protein and carbohydrates = hormones rather than thinking of them as just food substances?
Fat = X Hormones (human growth hormone, IGF-1, estrogen, testosterone, …)
Protein = X Hormones (Glucagon…)
Carbohydrates = X Hormones (Insulin…)
Oh ok I see what you’re saying. Definitely having visceral fat, especially in a male, does derange the estrogen levels. Be sure to qualify the type of fat though. I think most docs, including Fung have said subcutaneous fat isn’t endocrine disrupting.
I’ll have to give Dr Marchegiani a listen to later.
It’s not.
It’s truish. Broadly, insulin impairs the ability to access fat. It doesn’t actually shut it off completely. Aside from anything else, you are literally never without insulin in your bloodstream unless you’re a type one diabetic. If ‘can’t burn fat with insulin’ were true, no one would lose fat ever.
From an anecdotal standpoint, I’ve lost fat while taking enormous doses of exogenous insulin, in addition to the fairly huge amount my body produces all by itself.
And generally, a lot of the accepted knowledge is like that - biochemistry is ridiculously complex, and any simplified guideline should be taken as a rule of thumb, not a law of the universe. Protein spikes insulin less than carbs, but not all protein has the same effect on insulin release. And so on.
It’s possible to die from malnutrition while obese, probably, but you’d need some kind of really rare metabolic disorder to actually starve to death (which is to say, death coming from cannibalizing vital tissues).
Not at all. You need to be eating in way that keeps insulin secretion to a minimum, so that the fat in your adipose tissue can be metabolized, and so the leptin secreted by your adipose tissue can be “heard” by your hypothalamus and your appetite can go down. Then, if you eat to satiety, you will naturally be eating at an energy deficit. The energy deficit is driven by the hormones, not the other way round. It’s counter-intuitive, I know, but it works.
As I understand it, the causality is the reverse of the way you put it, or so I understand Dr. Fung to be saying: we will end up eating fewer calories if we eat right—that is, by keeping carbohydrate very low and eating to satiety—but if we restrict our calories to some arbitrary level, the body will cut the metabolic rate in response. So by listening to our body, we may eat at 1200 calories (or whatever) if we have extra fat to get rid of, but by restricting caloires to 1200 arbitrarily, we run the risk of causing the body to cut energy expenditure to compensate.
It depends on whether the drug or hormone is excitatory or not. Excitatory hormones, such as dopamine, cause cells to down-regulate their receptors in self-defense, so they don’t die. With calming hormones, such as serotonin, for example, there is no need for down-regulation.
Yes I agree with your point about restricting calories to any number but more importantly what causes the energy loss is if the person restricting fat calories has their insulin levels too high, what I mean is if they are high enough to block access to body fat. That’s when we get into trouble. Its all about keeping that access to body fat “unlocked” and not shut off due to high insulin levels caused by carbs/sugars.
Just to clarify: If our total daily calorie requirement is 2000kcal and we restrict calories to 1200kcal a day, provided insulin levels are low enough to enable access to our fat stores, we can make up the 800kcal difference by burning our fat stores. We’ve got to eat our protein requirements, that’s a given and keep carbs low, so that leaves fat as the only calories we can safely reduce. If you are insulin resistant that is harder to achieve but Fung believes fasting can bring insulin levels down.
Yes satiety signaling is important but if you are eating whole foods, our satiety receptors work perfectly. We’ve got a host of satiety signaling mechanisms, that tell us not only how much fat to eat but also how much protein, and even carbs. That’s the thing about satiety I didn’t understand, Fung explains it in a less complicated way. Processed carbs have most of the important ingredients stripped out of them and that is why we don’t feel full even though we’ve just eaten a ton of the stuff.
Thanks @PaulL. So much to learn!!!
eta: All I know is what I thought was true for years DIDN’T WORK!
I question this strictly from personal experience as of the last few months.Beginning in September (start of vacation) I stopped monitoring my daily caloric intake but maintained a whole food keto diet menu. In the last 10 weeks I have noticed my portions increasing and don’t feel satiated until it is to late and the over full feeling sets in. I have also gained 10 lbs. During this time I have reduced my fat % the caused a higher protein intake. Satiety signals seem to allude me so relating to this statement also alludes me. I am however rethinking my take on calorie levels and effects.
The satiety thing has never meaningfully worked for me. Not with whole foods or months of near zero carb. I did have a meal last week where I didn’t want to eat despite the food tasting good AND me not being full, but it seems to have been a one off.
But I don’t find keeping an eye on what I eat, portionwise, to be onerous, so it’s not a big deal. The flipside of it is that my hunger is pretty blunted too.
Exactly, before Keto I could demolish a 500-700g T Bone steak without much effort, now its a struggle for me to eat a 200g steak because I’ve been eating meals where I don’t eat much more that 110g steak or chops. So is that satiety or just an eating habit? If I tried to eat a 700g steak now I’d feel quite nauseous.
The statement should read “too much insulin switches off fat burning” and over time, it can becomes impossible to reverse the damage of “too much insulin”. However, the key for someone who has become insulin resistant is to keep insulin as low as possible.
I had to go figure out what that would be for me. I don’t eat a lot of steak but I do love hamburgers. I usually make them as 1/3 pound patties and 32oz of beef gets me 6 patties. A typical supper might include two of them when I’m pretty hungry. I’ve gone as high as three but that was too much. 700g would be eating all of but not quite the last bit of five of them. That’s a lot to me, and though I could probably do it, I wouldn’t, and I know I wouldn’t feel good afterward.
Ya got me. You win!