Feasting, Fasting, Insulin, HGH, Fat and Livers: A Roundup

I read two marvelously detailed, researched, informative and interesting blog post today that I had somehow missed. They are both by the same reader and commenter here, Robert McLeod, who as a physicist is pretty damn good at math and plain old logic. As an example, here's a kinda fun, tongue-in-cheek look at saturated fat epidemiology.

I must warn you that these are pretty advanced. However, if you truly want to understand what's going on with fat accumulation and fat loss, I can think of no better way to spend a bit of time. The comments on both posts are good, too.

The first of these is: Feast and Fast: the dichotomy of insulin and growth hormone. In a nutshell, he explains in brief, but in excellent detail just how insulin keeps your fat locked in and accumulates more, and just how growth hormone preserves your organs and muscles and releases your fat for use by the body. Here's what most of you already know: it's the high carbohydrate that keeps insulin elevated and makes you fatter and fatter with each passing year (you know, the diet recommended by the "experts"). But, did you also know the rest?

So, to review, insulin is the hormone responsible for regulating the metabolism of glucose and most amino acids (exceptions are lysine and leucine) derived from the protein in your diet that are converted to glucose for the purpose of fuel (Gröschl et al., 2003). High levels of insulin also prevent your muscles from absorbing fatty acids in the blood: the body prefers to burn the low-energy density carbohydrates first and hold onto the superior fatty acids for lean times. A person with high levels of insulin in their blood is said to be in the feasted state.

The opposite to the feasted state is the fasted state. The hormone that characterizes the fasted state is growth hormone (review: Møller and Jørgensen, 2009). The general course of progressing from feasted to fasted goes something like this:

1. You eat a meal with carbohydrates and protein. Digestion occurs over the course of several hours and insulin levels rise in response to the absorption of these macronutrients.
2. Insulin sensitive tissues absorb glucose from the blood-stream. Glucagon, a second-tier hormone, causes the liver to break down the glycogen it stores into glucose, releasing it into the blood. This slows the rate at which insulin drops.
3. Insulin continues to drop as the liver's supply of carbohydrate is reduced. Ghrelin (which I'll discuss later) is produced, which promotes appetite and the production of growth hormone. If the increase in appetite caused by ghrelin causes you to eat, you go back to stage 1. Otherwise, you make the transition into the fasted state as GH levels rise and blood sugar levels drop (Roth et al., 1963).

Growth hormone is basically the hormone that controls when your adipose (fat) tissues release fatty acids to be metabolized by the rest of your body. No growth hormone, no significant fat loss.

I really encourage you to go and get all the details behind this and more. Bookmark it. What I like about it is that it suggested a few things I might modify or at least intensify. It's really nice to have solid knowledge backing up what you sense to be true and have actually experienced.

It also informs you as to how thoroughly messed up the world is in terms of diet and nutrition.

Now, onto Robert's next post: Synthesis of Fat in the Liver. This is quite an interesting post in which Robert ends up wondering if we ought not to eat carbohydrate and protein/fat in the same meal. It makes some sense to me.

But before that, Robert delivers quite good instruction on the liver's central role in metabolism, and how we get man boobs and wheat bellies.

...So what causes people to preferentially deposit fat around their mid-section rather than elsewhere? In researching non-alcoholic fatty liver disease, I came across the following paragraph by Postic and Girard (2008, free access), which I think is instructive:

Insulin is essential for the maintenance of carbohydrate and lipid homeostasis. Insulin is secreted by pancreatic β cells in response to increased circulating levels of glucose after a meal. A large fraction of glucose absorbed from the small intestine is immediately taken up by hepatocytes [ RM: liver cells ], which convert it into glycogen. However, when the liver is saturated with glycogen (roughly 5% of liver mass), any additional glucose taken up by hepatocytes is shunted into pathways leading to synthesis of fatty acids, which will be esterified into TG [ RM: triglycerides ] to be exported to adipose tissue as very low-density lipoproteins (VLDLs). Insulin inhibits lipolysis [ RM: fat burning ] in adipose tissue by inhibiting hormone-sensitive lipase (HSL), the enzyme regulating FFA [free-fatty acid] release from adipose tissue (10). Therefore, from a whole-body perspective, insulin has a “fat-sparing” effect by driving most cells to preferentially oxidize carbohydrates instead of fatty acids for energy. Insulin also regulates glucose homeostasis at many sites, reducing hepatic glucose production (HGP) (via decreased glucose biosynthesis [gluconeogenesis] and glycogen breakdown [glycogenolysis]) and increasing the rate of glucose uptake, primarily into skeletal muscle and adipose tissue.

As with the previous, I encourage you to go get the whole lesson.

Now, I had intended to immediately go into what I was going to tweak in my own approach, to see if it would work. But I have a better idea. How about all of you who are interested, go read Robert's two posts, and consider how that knowledge might change a thing or two in what you're doing.

Then, tomorrow, I'll give you my own thoughts.