Time for something meaty, and I don't mean pictures of my meals.
The concept of "insulin resistance" is key to understanding why people get fat and why LCHF works. Unfortunately, there is an awful lot of nonsense written about it, mostly by people who don't understand basic physics and physiology.
UC Davis appear to be the thought leaders in this field. Various departments there crimp off regular lengths of BS about insulin resistance: their core belief is that insulin resistance is a disease state, and that it's caused by saturated fat blocking the insulin receptors, a statement so stupid that a double facepalm is probably appropriate. The first reason it's false is pretty damn obvious: if fat blocks insulin receptors, then we'd all be dead within the first few days of our life, not least because our bodies use saturated fat as a primary storage mechanism. There would therefore be no human life on earth - or, at best, natural selection would weed out those with this disastrous malfunction.
If you enjoy mocking people with PhDs, as I do, have a look at the website of UC Davis, eg., here:
ucdintegrativemedicine.com/...
Here's the more complicated reason why it's false.
We're all aware that insulin is the 'master switch' for anabolic processes and energy management. But how does that work exactly? When you eat a bowl of rice, what happens to it as it passes through your intestinal wall as glucose?
The uptake rate (which you can visualize as power) is essentially uncontrolled. It happens as fast as glucose can diffuse into your bloodstream, which in turn is related to the physical composition of whatever is in your intestine. If you have eaten starch and little else, the power flow peaks at around 3-4 times your basal metabolic rate (ie. 3-4METs). Your body must therefore reroute ~70% of that power flow, or blood sugar will rise to unhealthy levels. Your pancreas ramps up insulin output, telling everything that might be interested that glucose is available for uptake.
In fact, insulin+glucagon (a complex-valued control signal) has a wide range of meanings, but we'd best not go there. Let's stick with the glucose issue: it should be obvious that, since there is no mechanism for your pancreas to tell your liver to take this much and your fat cells to take that much, then every organ must decide for itself how energy is apportioned. And yet ... these organs can't communicate with each other to co-ordinate an optimum power split. There are two distinct but related metabolic features that solve this problem.
Glucose is transported across a cell membrane via micromachines called glucose transporters; there are 14 different types, GLUT1-GLUT14, and they're exposed through the cell membrane via molecule-sized tubular structures ('GLUT Storage Vesicles', GSVs) that can be withdrawn inside the cell, thereby preventing glucose from entering, or (in some cases) from being pumped out; for example, the bidirectional GLUT2 allows your liver to send out glucose (from glycogenolysis or gluconeogenesis) under conditions of low blood sugar.
Some receptors are more 'aggressive' in their operation than others; that is, they have various levels of affinity for glucose and various power capacities (maximum rates of glucose transport). For example, GLUT3, expressed within neurons, will scavenge all the glucose that it can, because your brain relies heavily on glucose. That's the first level of power partitioning.
The second level involves insulin resistance. Insulin resistance is not a malfunction. The idea that evolution would have gifted us with a complicated mechanism that does absolutely nothing except cause diabetes is so utterly foolish that I'm amazed that it even needs refutation. Still, here goes.
Insulin resistance is a tuning mechanism. It is analogous to the way neurons alter their connection strengths in response to firing rates, in order to achieve some desired goal state. When insulin is present, GSVs respond instantly to present glucose transporters outside the cell membrane. When the cell has taken what it needs, the GSVs are withdrawn, and the thresholds for mobilization and withdrawal are tweaked, slowly and continuously, depending on the downstream rate of energy utilisation (all energy sources - not just glucose). That is insulin resistance. Under normal circumstances, this distributed tuning process allows each organ to take an optimal fraction of available energy.
The precise mechanism of insulin resistance is still not completely characterized and it appears there may be other adaptive processes at work, but this one is fairly well-understood.
Each cell in any given organ will have a range of different thresholds for GSV presentation and withdrawal. The net result is that the organ as a whole has a 'soft' threshold for glucose, even though individual cells have a 'hard' (on/off) threshold.
As long as the peak power-handling capacity of all cells, in aggregate, is higher than the peak power entering your bloodstream from your intestine, it should be obvious that all will be well. Nothing will "overflow", and glucose can be maintained in the bloodstream at an appropriate level by the 'master switch', insulin.
What happens if more glucose continues to flood into your bloodstream, long after your fat cells, muscle, and liver have stopped accepting it? Well, your pancreas will not be happy, because its setpoint for blood glucose has not been reached. It therefore performs its own tuning process, pumping out more insulin in response to incoming glucose, forcing your body's organs to up their game. And up to a point, they can respond by enhancing their power-handling capacity. Your fat cells, for example, can get larger. New fat cells can be created (although unfortunately they tend to get stuffed into places where they really shouldn't exist). If you become more active, your muscles will be capable of absorbing a higher peak power than they otherwise would.
The key phrase here is "up to a point". When there is no mathematical solution to the problem - when it is physically impossible for your body's organs to match the rate of incoming power, even after performing some adaptations, the whole thing starts to fall to pieces. Insulin resistance and insulin output are cranked up and up and up in a pointless war of attrition, eventually pinning both in a dysfunctional state: diabetes.
Fortunately, this doesn't mean your body is broken. It just means it's horribly out of calibration. Those adaptive mechanisms are still working: they're just locked up. When someone is overweight and prediabetic, LCHF works by releasing the pressure to adapt in the wrong direction.
I was several pounds lighter in the first half of last year but have let it drift. I'd like to get back there again
