Before I say another word, my conscience tells me to add a BIG trigger caution here. If you are a size acceptance proponent and are feeling the least bit susceptible to the call of the weight-loss diet fairy, skip today’s post. If you’re feeling brave, however, I’d love your response as well as that of my maintainer friends.
In my last post I explained Katarina Borer’s methodology for comparing the effects of food intake and exercise on appetite and on certain endocrine secretions. Dr. Barry Braun describes it as “a multicondition crossover design to cleverly disentangle the relationships between energy imbalance, exercise, energy intake, putatative energy-regulating hormones and perceived appetite.” Yup. That’s what it was. Now, let’s see whether I can explain in plain English what happened and what was correlated and what was not.
In her first study, Appetite Responds to Changes in Meal Content, Whereas Ghrelin, Leptin and Insulin Track changes in energy Availability, Dr. Borer found:
- Human appetite is influenced by the passage of food through the mouth and gastrointestinal tract. When food went through the mouth, it triggered GIP, a gut peptide that is activated and serves as a marker for GI activity but seemingly has no affecting qualities of its own. This peptide rose and fell in concert with participants’ reported appetites.
- Participants’ appetites responded to the size of meals that came in through the mouth, but were insensitive to calorie replacements (or saline placebos) that came through an IV. Moreover, exercise did not increase appetite, but marginally suppressed it. This led her to state that “between-meal increases in circulating nutrient load and exercise energy expenditure are not under homeostatic feedback control.”
- Ghrelin, leptin and insulin respond in slightly different ways to changes in energy availability, but had no influence on participants’ appetites. Whoa. Interesting, yes? Dr. Borer thought so too.
The graph array that interested me most, as a maintainer, however, was Figure 2 (in the second study it was reposted as Figure 4). I was surprised, in fact, that it was not included as a “finding” in the Discussion section.
It looks fuzzy in my preview, but I was able to click on it to get a blown-up view that was very clear. Column 4 describes the trial day that participants were given a small breakfast and no replacement nutrients in their IV, then compelled to exercise, and, hence, went to lunch with an energy deficit. Interestingly, they ate less than the other days, though, presumably, they ate to satisfaction – ad libitum. It looked to me as though they were satisfied with less food and a smaller energy balance after exercise. The narrative of the study seemed to indicate this too, even though it wasn’t a “finding” of its own. Could that be true?
In the caption to the Figure it reads: “Midday meal did not compensate for the significantly lower energy balance in SED-R and EX trials (Fdf4,45 = 77.13; P < 0.0001), which remained uncorrected after the meal (Fdf4,45 = 10.17; P < 0.0001).”
Huh? Uncorrected why?
I emailed Dr. Borer. I asked whether that meant that the meal did not, in total, contain enough calories to compensate or whether the participants chose to eat less. She clarified that they were allowed to eat to satisfaction and had plenty of food. Then she said, “It looks like the exercisers (without extra calories infused into their veins) ate a bit less, but it was not statistically significant.” (Italics mine.) She went on to say, after some commentary . . . “They just lost or did not eat 400 to 500 Kcal.” My jaw dropped reading that. Unconsciously foregoing 400 to 500 kcal may be statistically insignificant, but my God! AND, I’ll grant you, that over the course of a week or so, a standard-issue person will likely compensate for 400 to 500 kcal. However, we as radical weight-loss maintainers are, ourselves, as I’ve said before, statistical outliers. If 97 percent of people who lose weight regain it, then our results, and the behaviors we employ to produce those results, are so out-of-the-norm as to qualify us as statistically insignificant. Nothing about us is standard issue, whether we choose to be “inspirational” or cynical. So, my statistically insignificant maintainer buddies, how does this graph read to you? To me it says exercise is not merely for energy balance, but suppresses the endocrine (which, according to these studies, is not necessarily leptin and insulin, since their rise and fall does not track consistently with appetite) that triggers our “eat impulses.”
Dr. Borer attached two articles to her email that she thought I might find meaningful. They are by MacLean, et. al. You may note in the et. al. is Holly Wyatt, who we know here as the scientist who looks like Farrah, and is now associated with the National Weight Control Registry. Also in the et. al. is James O. Hill, co-founder of the NWCR, which gives me pause. I know he comes with the bias that behavior can and should be duplicated in service to radical weight-loss maintenance. I’m on heightened alert for the presences of this bias, and haven’t read the studies yet, but they look interesting, nevertheless. Here are their titles, and links:
Now, back to Dr. Borer and her work. The concept of homeostasis has apparently haunted her. She was troubled enough by it, in fact, to look at her own data with fresh eyes.
We have struggled here at this blog with the idea of homeostasis. Among its problems, it only works one way: it will increase our appetites and slow down our movement to protect a higher weight. On the other hand, when we all-too-easily gain weight (the Freshman 15, for example) it doesn’t blunt our appetites and speed us up to return us to our lower weight. (Or at least not all of us. It is exasperatingly inconsistent.) Dr. Borer notes that some human and rat studies show increases in activity in subjects when weight loss is imposed on them (I wonder if that is their ancient “hunt and gather” wiring telling them to get busy and go find food) and decreases in activity when obesity is imposed (the body saying, “you may relax now; you’ve got stores”).
For Dr. Borer: “The inconsistencies between the contemporary homeostatic concept of energy regulation and evidence implicating nonhomeostatic controls prompted us examine the role of leptin and insulin in the control of human meal-to-meal eating and appetite.”
Her original study did not find a tidy correlation between the rises and falls in leptin and insulin that would track with participants’ perceived appetites. And instead of writing off the perceptions of her participants, she has proposed that insulin and leptin may function differently in our bodies than often supposed. She discussed findings on circadian rhythms and hedonic circuitry that also influence our desire to eat (or not), in addition to homeostatic forces. Her assertion:
“Substantial evidence suggests that involvement of insulin and leptin in nonhomeostatic control of meal eating and physical activity is mediated through their actions on the brain substrates of reward.”
In other words, surges in insulin and leptin don’t communicate with us about our physical satiety; they may just shut down the mental reward party. Specifically (Borerese): “Low insulin and leptin levels enhance, whereas high insulin and leptin levels dampen, the rewarding value of stimulation of this circuit by suppressing the release of dopamine and related neurotransmitters.”
This theory regarding insulin and leptin suggests to me one reason for the diverse adiposity of humans. At Big Fat Blog we have discussed, from time to time, that some fat people do fit the stereotype – they eat to excess by many people’s sensibilities. Often, they’re “fat and jolly,” or could be but suppress that impulse, lest they get labeled as “bad” fatties, v. the “good” fatties who exercise ferociously and eat in moderation but still get fat. This does seem unfair. Maybe some people’s mental food reward parties are just better and last longer than others’. Maybe they take enormous pleasure in food, for long periods of time; while other people simply don’t. It is sad that our society, because of the “war on obesity,” has lost the ability to celebrate fat people who enjoy food, or simply accept them and treat them with basic dignity.
But I digress. Borer’s study seems to reinforce the nonhomeostatic role for leptin and insulin on a meal-to-meal basis. This doesn’t mean that homeostasis doesn’t exist (if defined as our bodies’ long-range compulsion to protect or return to our highest established weight) nor does it mean that leptin and insulin don’t trigger homeostatic forces, but they do so through a relationship with the brain’s reward system, not by regulating physical satiety, meal by meal over the course of a day.
I have talked an awful lot today, and am just going to force myself to stop, even though I’d like to talk about exercise more. Again, go up and look at Figure 2 and tell me what you think. Or the findings. Those are interesting fodder for discussion too. The floor is open.