In my post earlier this week, I promised to talk about endocrine, and how weight-reduced people are different from people who are at the natural, highest weight that their body establishes for them. Let’s start with my favorite study, Cummings et. al in the New England Journal of Medicine, May 2002. These are actually MDs mostly, rather than PhDs. So maybe this mitigates the vitriol of my post last week, and maybe, too, it is a study that MDs feel comfortable taking seriously.
Cummings and crew compared plasma Ghrelin levels in samples of nonsurgically-assisted weight losers to people who underwent gastric bypass surgery.
Ghrelin is probably the best understood of the hunger hormones. In the chemical cotillion happening in our body, it dances monogamously with its partner Leptin, who creates satiety (fullness). When they dance with Leptin moving forward, we are satisfied, when Ghrelin moves forward, we feel hunger. Simple.
I like to think of Insulin as the party slut. She dances with all the Ose brothers – Dextr, MonoDextr, Gluc, Sucr, Fruct. They’re all such sweet boys. She bounces around inside us, giggling and flirting, and when she and a partner smacks into the monogamists – Leptin and Ghrelin – she pisses them off, so they may start dancing the wrong way. In real life, you might be minding your own business and perfectly satisfied with regard to food, but Insulin starts doing her Donna Summer thing inside of you, and suddenly your eating impulses set in, and there you are walking into the kitchen again. Insulin also, from what I understand, messes with other chemicals inside us besides the Ose family. She isn’t evil, and she’s actually necessary, like the annoying aunt you have to invite to your wedding reception, but she can be exasperating. There are scientists who devote their lives to studying her moves. Other chemicals at the cotillion may also affect Ghrelin, which is the featured chemical in the Cummings et. al. study.
Now, the results of this study have their limitations – small sample size, no follow up – but I have to say, the first time I saw this study, I gasped. It was a chilling “Eureka” moment for me when I printed off Figure 1 and studied it. “That’s me!” I thought. “On paper, that’s me.” I am now always roughly 24% more hungry at any point in the day compared with how I felt before weight-loss. When I’m hungry, I’m hungrier, and when I’m satisfied, I’m less so. And what is striking to me is how the graph moves in two almost perfect parallel lines. No meeting points ever. Wow. I have to ask, fellow maintainers, does this chart resonate with you too? Does this study, weak as it is, affect you as much as it does me?
While we non-surgical losers are dealing with increased ghrelin, the other half of this study shows a 77% suppression of plasma ghrelin among gastric bypass surgery patients. Surgical maintainers, your chart is labeled Figure 2. Note that you have nearly none of the peaks and valleys of the matched obese control group, the normal weight controls or the nonsurgical weight-losers over in Figure 1.
Post-surgical weight-loss maintenance is not my primary area of interest, so I’m not as well versed in the research, but I suspect that this suppressed hunger hormone is only temporary, and possibly caused by the systemic shock of surgery itself or other causes. While I don’t have the figures (and I’m not confident that the figures out there are accurate) we know that surgery is no guarantee of permanent weight loss and many, maybe most, people regain part or all of their weight after losing from a surgical assist. So, I would ask you surgical maintainers, how long does it last? How long is ghrelin tamed? When would you advise scientists to measure plasma ghrelin, then follow up and measure again? What features of this study strike you as interesting?
While ghrelin was clearly the star of this study, I took note also of the final sentence of paragraph one in the “Results” section. I was simultaneously bemused, baffled and yet affirmed. Talking about the non-surgically assisted weight-losers, the scientists said, “Weight loss was associated with significant reductions in adipose volume, leptin levels, insulin levels, and blood pressure, as well as with increased insulin sensitivity and improved lipid profiles.” My lay translation: you take a lot of bad with the good when you intentionally reduce your weight, and the scientists won’t parse which is which, so we may need to help them. The chemical cotillion is very complex, but increased insulin sensitivity and reduced leptin levels are clearly bad things. Lower blood pressure and improved lipid profiles are good. Why would you ever put them in a sentence together?
But I don’t mean to be hard on the study du jour. Cummings et. al. gave me a thrill with that chart and is rare in how nonjudgmental it is, and so I treasure it.
I may well be living in a sick fantasy world when I play with the idea that scientists may actually, someday, take us seriously, ask our opinions. I picture a world in which scientists may stop merely observing our behavior and judging us – concluding, for example, that people regain weight because of a “failure to maintain behavior changes,” which leaves others to assume it’s the regainers’ failure to make good choices or that they just get lazy. We maintainers know there is something much more profound at play here, and we hold on to our losses by tenacity, luck and a little cleverness.
If you have a study you think we should examine, please send me the citation. I don’t guarantee I’ll address it, but I like collecting them, and yours may strike my eye.
At some point soon, too, I think we maintainers need to talk about our strategies for getting around our strong hormone impulses, post weight-loss. (That will be triggering talk for the beyond-dieting size acceptance crowd.)