My previous post quoted from a study in which researchers induced rats to overeat and gain weight by injecting them with insulin – a.k.a. the “acute appetite suppressant,” according to some.
I’m not usually a big fan of rat studies because of how they’re conducted. Researchers will feed fats a high-fat (ahem) “Atkins” diet of frankenfats, casein and corn starch, then pretend the results have some bearing on how a diet of meats and eggs will affect the health of human beings. The study I cited in my last post, however, wasn’t a diet study. It was study of how a hormone affects appetite and weight. The insulin was injected directly.
Based on links in the comments, I looked for and found a handful of studies that demonstrate what insulin does to human subjects. Let’s take a look.
In this study, diabetes patients were treated either with 1-2 injections of insulin per day (called the conventional therapy by the researchers) or multiple daily injections (called intensive therapy by the researchers). Here are the results:
Intensively treated patients gained an average of 4.75 kg more than their conventionally treated counterparts (P < 0.0001). This represented excess increases in BMI of 1.5 kg/m(2) among men and 1.8 kg/m(2) among women. Growth-curve analysis showed that weight gain was most rapid during the first year of therapy. Intensive therapy patients were also more likely to become overweight (BMI >or=27.8 kg/m(2) for men, >or=27.3 kg/m(2) for women) or experience major weight gain (BMI increased >or=5 kg/m(2)). Waist-to-hip ratios, however, did not differ between treatment groups. Major weight gain was associated with higher percentages of body fat and greater fat-free mass, but among patients without major weight gain, those receiving intensive therapy had greater fat-free mass with no difference in adiposity.
So people treated more aggressively with insulin ended up gaining about 10 pounds more than those treated with less insulin. For many, the difference was more body fat. For others, it was a mix of more body fat and more lean mass. Well, no surprise there. Insulin spurs growth. That’s some why body-builders shoot the stuff. But if you have a tendency to get fat, higher insulin will make you fatter.
In this study, researchers treated diabetics with a sulphonylurea (drug that stimulates insulin internally), or with insulin directly, or with diet (which was labeled conventional therapy). The goal was to improve glucose control, not weight. But weight changes were included in the results:
Weight gain was significantly higher in the intensive group (mean 2.9 kg) than in the conventional group (p<0.001), and patients assigned insulin had a greater gain in weight (4.0 kg) than those assigned chlorpropamide (2.6 kg) or glibenclamide (1.7 kg).
Subjects who were either stimulated to produce more insulin or given insulin directly gained more weight than those treated with diet, and those given insulin directly gained the most.
In this study, researchers added three different insulin therapies to metformin:
In an open-label, controlled, multicenter trial, we randomly assigned 708 patients with a suboptimal glycated hemoglobin level (7.0 to 10.0%) who were receiving maximally tolerated doses of metformin and sulfonylurea to receive biphasic insulin aspart twice daily, prandial insulin aspart three times daily, or basal insulin detemir once daily (twice if required). Outcome measures at 1 year were the mean glycated hemoglobin level, the proportion of patients with a glycated hemoglobin level of 6.5% or less, the rate of hypoglycemia, and weight gain.
And the conclusion based on the results:
A single analogue-insulin formulation added to metformin and sulfonylurea resulted in a glycated hemoglobin level of 6.5% or less in a minority of patients at 1 year. The addition of biphasic or prandial insulin aspart reduced levels more than the addition of basal insulin detemir but was associated with greater risks of hypoglycemia and weight gain.
More insulin resulted in lower glycated hemoglobin (a.k.a, what’s measured in an A1C test as an indicator of average glucose levels over time), but also in more weight gain.
In this study, researchers put 50 subjects on a weight-loss diet after running a series of lab tests. They wanted to identify which factors predicted success or failure in losing weight and keeping it off. Here’s what they found:
On the basis of body weight trajectories, 3 subject clusters were identified. Clusters A and B lost more weight during energy restriction. During the stabilization phase, cluster A continued to lose weight, whereas cluster B remained stable. Cluster C lost less and rapidly regained weight during the stabilization period. At baseline, cluster C had the highest plasma insulin, interleukin (IL)-6, adipose tissue inflammation (HAM56+ cells), and Lactobacillus/Leuconostoc/Pediococcus numbers in fecal samples. Weight regain after energy restriction correlated positively with insulin resistance (homeostasis model assessment of insulin resistance: r = 0.5, P = 0.0002) and inflammatory markers (IL-6; r = 0.43, P = 0.002) at baseline.
The resistance to weight loss and proneness to weight regain could be predicted by the combination of high plasma insulin and inflammatory markers before dietary intervention.
Yes, there was more going on here than insulin levels – inflammation and a difference in gut bacteria. But the point is that those with high plasma insulin (the “acute appetite suppressant”) lost less weight and regained it more quickly. I don’t think their appetites were suppressed very effectively.
In this study, diabetics were treated with an “intensive program” of insulin for six months. Once again, the goal was glucose control, not weight control. But weight did change:
During treatment, mean serum insulin levels increased from 308 ± 80 to 510 ± 102 pM, while body weight increased from 93.5 ± 5.8 to 102.2 ± 6.8 kg.
After six months, the “intensive program” of insulin led to an average weight gain of just over 19 pounds.
I suppose the explanation from the “insulin is an acute appetite suppressant” crowd would be that these studies were conducted on diabetics who are by definition insulin resistant. Right. And so are a helluva lot of people out there who are overweight and looking for a way to drop the pounds. We see it over and over in these studies: higher insulin, whether produced internally or given as a treatment, leads to more weight gain. Dr. Lustig apparently speaks the truth when he says I can make anyone fat with enough insulin.
(Lustig is an endocrinologist, in case you’ve forgotten. Hormones are his specialty.)
So for the people most desperate to lose weight, the “insulin is an acute appetite suppressant” notion is clearly a load of bologna. If their appetites were acutely suppressed, they wouldn’t be obese; they’d be anorexic. As part of their weight-loss strategy, need to bring down their insulin levels. Period.
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