Diets For Menopause Typically Tell Us To Eat Less And Exercise More: But Why? Does This Approach Actually Work?
Diets for menopause almost inevitably focus on calorie control. That is, post-menopausal women are told to restrict calories and/or to get more exercise in order to compensate for the weight gain associated with amenorrhea. But why? Why are we so obsessed with this notion that "calories count" and that eating less and exercising more can make us thinner?
The prevailing view is that the first law of thermodynamics compels us to believe that "calories count." This idea, the Caloric Balance Hypothesis, informs practically every public discussion that we have in the public arena about diets for menopause.
An alternative hypothesis, known as Lipophilia, posits a different explanation. It says that changes at the level of the fat tissue itself – physiological changes in the body driven by menopause - drive weight changes. The root cause of the weight gain is hormonal – it has nothing to do with "Calories In" and "Calories Out." Something about menopause changes the hormonal balance in the body, driving changes in the levels of insulin secretion and an enzyme called lipoprotein lipase (LPL), which in turn drive changes in the fat tissue, which in turn drive changes in caloric balance.
So let's look at some evidence and arguments about why diets for menopause so often fail.
1. Gary Taubes makes a fantastic case that diets for menopause must be based on hormonal regulation of our fat tissue as opposed to calorie control. In particular, on page 398 of Good Calories Bad Calories, he discusses a possible physiological mechanism that causes this weight gain. He argues that the activity of lipoprotein lipase (LPL) can account for how fat distribution changes in women with age and reproductive needs.
He notes that premenopausal women have significant LPL activity in their thighs and that menopausal women have increased LPL activity in their abdomens. He says that progesterone, in particular, drives up LPL activity in the thigh/buttocks region. Estrogen, meanwhile, slows LPL activity. Therefore, Taubes argues, menopause weight gain happens because, during menopause, estrogen secretion declines. Thus, LPL activity increases. Thus, post-menopausal women will gain fat. Calorie counting diets for menopause alone cannot change the hormonal situation.
This same hypothesis - that decreases in estrogen secretion drive increases in LPL activity - can be useful in explaining why women gain weight after a hysterectomy.
2. We can see further evidence that menopause weight gain is likely best explained by the Lipophilia Hypothesis here: "Weight gain at the time of menopause."
These authors found that:
"Weight gain was significantly associated with increases in blood pressure and levels of total cholesterol, low density lipoprotein cholesterol, triglycerides, and fasting insulin. Weight gain is thus a common occurrence for women at the time of menopause and is related to changes in coronary heart disease risk factors."
3. Here is another article about diets for menopause: "Weight gain during menopause. Is it inevitable or can it be prevented?"
These authors write that:
"The years surrounding the menopause are associated with weight gain, increase in central adiposity, and decrease in physical activity. Weight change occurs independent of menopausal status, adverse changes in body fat distribution and body composition may be due to hormonal changes occurring during the menopausal transition."
4. Here is another paper: "Weight gain in the menopause: a five year prospective study."
These authors conclude that "weight gain was not related to... any lifestyle factors measured."
They also said that "there is no association between weight change and... exercise."
5. Here's another article that has relevance for our discussion about diets for menopause: "The effects of menopause and insulin sensitivity, secretion and elimination in non obese, healthy women."
The authors conclude that:
"despite the occurrence of little or no variation in plasma glucose and insulin concentrations, the menopause is associated with significant changes in insulin and metabolism."
6. And here is another article: "The emergence of the metabolic syndrome with menopause."
The authors write that:
"The prevalence of the metabolic syndrome increases with menopause may partially explain the apparent acceleration in CVD [cardiovascular disease] after menopause."
They note that the transition to a postmenopausal state leads to
"increased intra abdominal body fat... a shift toward a more atherogenic lipid profile... [and] an increase glucose and insulin levels... these risk factors may be a... result of the metabolic consequences of central fat redistribution with estrogen deficiency."
Think about what this article is saying about diets for menopause. It's arguing exactly what the Lipophilia Hypothesis tells us. Estrogen levels drop. This creates a metabolic situation wherein insulin levels rise. As a result, we are driven to accumulate more fat. And we see the emergence of increased risk for all sorts of problems associated with metabolic syndrome, including weight gain.
In conclusion, diets for menopause that derive from the predictions of the Caloric Balance Hypothesis seemed destined to fail, since the evidence overwhelmingly appears to favor the Lipophilia Hypothesis.