Part 3: Insulin and Diabetes
Well, we could keep dancing around the subject, but we’re going to have to talk about insulin sooner or later. But we’ll need a good segue. We can’t just rush into it cold.
“Speaking of metabolic disorders…”, there’s the metabolic disorder, Syndome X, the Metabolic Syndrome. What about that?
Well, two chief symptoms of the Metabolic Syndrome are overweight and insulin resistance. Hey, we’ve already been talking about overweight, that’s interesting! So, what does this insulin do, when it’s working properly?
All right, most people know that insulin lowers blood sugar, and that diabetics have some sort of problem with high blood sugar. We’re going to have to know a little more, though.
Let’s start with this: insulin is how your body signals its cells that you’re well-fed, particularly with sugars and other carbohydrates. “There’s plenty of food available, everybody dig in!” In response, muscle cells and liver cells take up glucose and store fuel as glycogen. Fat cells take up glucose and free fatty acids and store fuel as triglycerides. Protein degradation is suppressed. It’s a free feed.
When insulin levels drop, the liver tears down glycogen and releases it as glucose into the bloodstream, fat cells tear down triglycerides and release them as free fatty acids into the bloodstream, and the muscle cells…just hang on to their glycogen, if they can. It’s theirs. But if push comes to shove, and no food shows up, muscle protein will be torn down to make fuel for everyone else.
This is a simplification, of course, but the effect of insulin is enormous, and the simplification is useful. In particular, this point can’t be over-emphasized: if you want your fat cells to get smaller, you’ve got to lower your insulin levels, so that energy flows out of the fat cells, rather than into them.
Okay. Next up — diabetes! There are (at least) two types:
Type 1 (’juvenile’ diabetes): Type 1 diabetics basically don’t make enough insulin, due to an auto-immune destruction of the insulin-producing beta cells in their pancreas. If untreated, they’re hungry (and especially thirsty) all the time, and no matter what they eat, they don’t put on weight.
Type 2 (’adult-onset’ diabetes): Type 2 diabetics are typically overweight, at least, at first. Their pancreas still makes enough insulin, or what would be enough insulin in a normal person. But their body cells have become resistant to the insulin signal, and the blood sugar level remains stubbornly high. The pancreas responds with even more insulin. Ultimately, if untreated, their body cells become so resistant to insulin, and their pancreatic beta cells so exhausted, that they can’t put on weight, and end up as emaciated as untreated Type 1 diabetics. Also, like Type 1 diabetics, Type 2 diabetics are characteristically hungry, and thirsty, as their blood sugar spills over into their kidneys and is excreted in urine.
Okay, well, that’s really, uh, fascinating, but what does that have to do with me and my weight problem?
Ah! Step with me into the Wayback Machine, Sherman. We’re going all the way back to 1905 (”Wow, that’s over 100 years ago, Mr. Peabody!” “Quiet, you.”), when Carl von Noorden fomulated the third of his speculative hypotheses of obesity:
…what he called diabetogenous obesity. His ideas were remarkably prescient. They received little attention because insulin had not yet been discovered, let alone the technology to measure it.
Von Noorden suggested that obesity and diabetes are different consequences of the same underlying defects in the mechanisms that regulate carbohydrate and fat metabolism. In severe diabetes (Type 1), he noted, the patients are unable either to utilize blood sugar as a source of energy or to convert it to fat and store it. This is why the body allows the blood sugar to overflow into the urine, which is a last resort since it wastes potentially valuable fuel. The result is glycosuria, the primary symptom of diabetes. The diabetics must be incapable of storing or maintaining fat, von Noorden noted, because they eventually become emaciated and waste away. In obese patients, on the other hand, the ability to utilize blood sugar is impaired, but not the ability of the body to convert blood sugar into the fat and store it. “Obese individuals of this type have already an altered metabolisms for sugar,” von Noorden wrote, “but instead of excreting the sugar in the urine, they transfer it to the fat-producing parts of the body, whose tissues are still well prepared to receive it.” As the ability to burn blood sugar for energy further deteriorates and “the storage of the carbohydrates in the fat masses [also suffers] a moderate and gradually progressing impairment,” sugar appears in the urine, and the patient becomes noticeably diabetic. Using the modern terminology, this is the route from obesity to Type 2 diabetes. “The connection between diabetes and obesity,” as von Noorden put it, “ceases in the light of my theory to be any longer an enigmatical relation, and becomes a necessary consequence of the relationship discovered in the last few years between carbohydrate transformation and formation of fat.”
…from Good Calories, Bad Calories (Knopf, 2007), by Gary Taubes, p. 377
Now, this theory fits insulin resistance and the metabolic syndrome rather nicely, and no one has ever disproven it: suppose that the body’s non-fat cells become relatively more resistant to insulin than its fat cells (which have been described, by the way, as being exquisitely sensitive to insulin)? You’d have the very scenario described in part 1, with the top hats. The fat cells, fattening. The other body cells, basically starving, in the middle of an ocean of fat.
Okay, that sounds bad, but what do to? We’re going to have to deal with this problem head-on.
Continued in Part Four…