Many of you may recall a kerfuffle raised by a controversial article claiming that we’ve got it all wrong about insulin. Far from being a driver of weight gain, according to the article, insulin is actually an acute appetite suppressant. It makes us less hungry, by gosh, not more.
That article seems to show up on diet-related social media sites on a regular basis. A few weeks ago, some born-to-be-lean jock who joined the Fat Head Facebook group for the sole purpose of being an annoying jackass posted a link to it. I responded, which started a back-and-forth debate.
If insulin is such a fabulous appetite suppressant, I asked, then explain this: type 2 diabetics produce high levels of insulin. They’re also far more likely than other people to be overweight or obese. So why isn’t the acute appetite suppressant causing them to eat less and lose weight?
The response (I’m paraphrasing here): Well, ya see, ya big dummy, type 2 diabetics are insulin resistant by definition. So they don’t experience the effects of the acute appetite suppressant.
Hmmm. Okay, then, explain this one: People will start eating foods that provoke a high insulin response — a big tub of popcorn, or a big bag of chips — swearing to high heaven they’re only going to eat, say, half. Then they eat the whole thing. Then after cursing at themselves for not having any discipline, they go get more. Why isn’t the acute appetite suppressant kicking in and stopping them from eating way more than they intended?
The response (I’m paraphrasing again here): Well, ya see, ya big dummy, the food-reward properties of the popcorn or chips override the appetite-suppressant effect of the insulin.
Ahh, I see. So there’s really no need to adopt a diet that reduces your insulin levels, because insulin is actually an acute appetite suppressant … unless 1) you’re insulin resistant (like so many obese people), or 2) when you reach for high-carb foods, you choose the ones that taste good.
Well, that is fabulous news indeed for all the obese people out there who aren’t insulin resistant and prefer carbohydrate foods with little or no flavor.
I chose not to engage in an endless online debate because I had more important things to do, like write software code for work, take the girls to their piano lessons, and rearrange my shoes by size, color and length of service.
But while digging up some research for the book project, I stumbled across a study abstract that caught my attention because it mentioned something about using insulin to induce weight gain. So I called upon one of my super-secret, deeply embedded, password-protected double-agents in academia to get a copy of the full paper.
The paper, published in 1966, is titled WEIGHT REGULATION IN NORMAL AND HYPOTHALAMIC HYPERPHAGIC RATS.
It’s the normal rats I’m interested in. Here are some quotes from the paper:
To induce overeating and weight gain in normal rats without brain damage, we used periodic injections of long acting insulin. Measurements of body weight and ad-lib food (powdered Purina chow) and water intake were taken on 23 Sherman female rats, housed at 80 ± 2° F. during a 2-wk. control period, 2 wk. of insulin treatment, and a 2-wk. recovery period. The insulin dose was 8 units per injection for the first 3 days, then 12 units thereafter.
Boy, those researchers must have been disappointed. Here they were, hoping to induce overeating and weight gain, and yet they injected the rats with an acute appetite suppressant. Big mistake, obviously.
All rats given protamine zinc insulin increased their food intake, presumably in response to hypoglycemia. In the short term experiment, 11 of the 23 rats survived by consuming nearly twice their normal daily food intake.
The rats who didn’t survive apparently died because they couldn’t eat enough to keep their little bodies fueled while the insulin drove down their blood sugar and locked up their fat cells. They were eating like crazy, but starving at the cellular level.
That reminds me of the conclusion from another paper in my files: appetite is largely a function of how much fuel is available at the cellular level, not how much fuel is consumed.
Their average weight gain was 58 gm. during the 2 wk. of insulin treatment, as compared to 13 gm. during the previous 2 wk.
This confirms the original observations of Mackay et al. (1940) and extends their results to indicate that marked obesity as well as overeating can be produced with insulin.
So marked obesity and overeating can be produced with injections of the acute appetite suppressant. Got it. Well, perhaps the rats injected with insulin just happened to find that powdered Purina chow waaaay more rewarding all of a sudden. Maybe the researchers added salt.
Every rat taken off the insulin regime after 2 wk. ate subnormal amounts of food and lost weight precipitously. On the average they were anorectic for 4 days, and lost 46 gm., which was 79% of the weight previously gained under the influence of insulin.
Researchers stopped injecting the rats with the acute appetite suppressant, and the rats responded by eating less and losing weight.
Boy, that almost sounds like what happened when I jettisoned a lot of insulin-producing foods from my diet. Reduce circulating levels of that acute appetite suppressant, and I’m just not as hungry.
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