The Nutrition Debate #212: “Everything I (ch)eat turns to fat.”
“Once you develop diabetes, your metabolism is deeply committed to converting as many calories as it can into fat.”
We’ve all heard this sentiment expressed, or felt this depressing thought,numerous times, but I was especially affected recently when I read this quote on page 241 of Cate Shanahan’s Deep Nutrition. I urge you to read the book, or at least my review in #205 here and her deeply troubling observations about the medical “business” that I commented on in #206 here.
Shanahan’s book has hundreds of references, so I lament that this generalization is not sourced. I suppose it should be understood as a summation of the very well sourced material presented in her book. In any case, the quote can be read as the expression of exasperation that we, overweight and obese type 2 diabetics, feel as we continuously try to lose weight. I increasingly suspect that the undiagnosed as well as diagnosed pre-diabetics among us feel the same way. It does seem that everything we eat turns to fat, and it is damnably difficult to lose that fat.
As my readers know, I am always interested (from self-interest as well as for educational purposes) in understanding the mechanism behind our complex metabolic environment, or milieu intérieur as Claude Bernard, the 19th centuryFrench physiologist, first described homeostasis. And I think I have gained some insights into why it is that “everything I (ch)eat turns to fat” and why people with impaired glucose tolerance (IGT) and impaired fasting glucose (IFG), the medical terms for incipient type 2 diabetes, gain weight easily and lose weightwith difficulty.
In lay terms, both IGT and IFG are the equivalent of “carbohydrate intolerance,” described in The Nutrition Debate #84, “Carbohydrate Intolerance -- the new 'buzz' words.” They are the outward manifestation of a metabolic change called Insulin Resistance (IR), described in more detail in The Nutrition Debate #99, “Natural History of Type 2 Diabetes.”
The bottom line: as our bodies transition from a normal metabolism to a dysfunctional metabolism, very commonly accompanied by weight gain as an effect of this dysfunction, not a cause, our bodies undergo several physiological changes. These changes detailed in laboratory reports and can be summed up by your waist/hip ratio. The most frequently tested are fasting glucose, hemoglobinA1c (HgA1c), the lipid panel (Total Cholesterol, LDL, HDL, and TC/HDL ratio) and triglycerides. Sometimes, when these markers are “out of sync,” a diagnosis of Metabolic Syndrome is made. All too often, the doctor just prescribes a statin and tells the patient to “exercise and eat a low-fat diet to lose weight.”
What’s missing in this “prescription”? Among other things, a test for fasting insulin. I’ll get into the specifics of this test in another column, but for now I want to explain how and why I have come to this conclusion. When I have been very good – that is, when I not only talked the talk but walked the walk, every day in every way – my fasting blood sugars have consistently been in the 80s and 90s. I can point to weeks, even months, of never or very rarely having a FBG over 100. And since it is an elevated blood glucose that causes the pancreas to produce insulin, to transport glucose in the blood to destination cells, a slightlyelevated blood glucose is associated with a slightly elevated serum insulin level.
As my readers know, and as anyone who has read Taubes’ Good Calories-Bad Calories (The Diet Delusion in the UK), or his more approachable Why We Get Fat, elevated serum insulin causes fat storage and prevents fat breakdown for energy. My column #5, about GC-BC, presents Taubes’s summation (“10 Certain Conclusions”) from his Epilogue (pg 453-454). It is a very succinct and compelling explanation of the functional role of insulin in homeostasis, and a must read.
Anyway, these days my fasting blood glucose readings have been regularly in the 100 to 125 range. Obviously, while I have been talking the talk, I have not always been walking the walk. I admit it. I “cheat” a little almost every day;always just before or at any time after dinner. And I pay the price. It’s just a little “cheat,” so I don’t gain weight, but neither do I lose any weight EVEN THOUGH I AM EATING NO MORE THAN +/- 1500-1800 CALORIES ON MOST CHEAT DAYS.
What’s happening, I hypothesize, is that my serum insulin levels are slightly elevated – elevated just enough to turn everything I (ch)eat to fat and stop the breakdown of body fat in storage. My body’s autonomically functioning metabolism, the milieu intérieur, “gets the message” that as long as I have a supply of quick energy every night (the “cheats” that break down to carbs), it can conserve my body fat, and lay on more with every calorie that isn’t needed to maintain my basal metabolism while I sleep. The “signal” is: my slightly elevated serum insulin circulating my slightly elevated glucose. If this is still a little unclear to you, dear reader, read Taubes’s “10 Certain Conclusions” (linked above) through a few times.
This is very timely. I asked my doctor for a serum insulin test twice. The first time she said, "Oh, I KNOW you're producing insulin." The second time I requested it I explained that I thought I was overproducing insulin and wanted to know. She answered that I don't show any symptoms of hypoglycemia. I don't think she has a clue about glucose intolerance, when I talk to her I get a blank look. And this is the doctor I have because the previous two were even denser. Am looking for a private lab where I can pay for the tests myself. The only problem is, if your body does produce too much insulin, what do you do? I already eat very low carb.ReplyDelete
I can't get that "10 Certain Conclusions" link to work.ReplyDelete
try this oneReplyDelete