Early satiety in EDs
One of the side effects of eating disorders is a rapid sense of satiety; that is, you feel more full when eating less food. Some of this is strictly physical, as the stomach shrinks during starvation, and food empties into the digestive tract slower. The formal medical name for this is delayed gastric emptying or gastroparesis. It almost always reverses upon normalization of eating patterns, but it can take a while. Some of this satiety may be anxiety-based (that stomach-churning feeling really isn't condusive to eating lasagna, let alone with gusto), and sometimes, it was a matter of my believing my own BS. If I just ate X, I damn well better be full!
Then, of course, we have to add neurochemicals to the mix. I've blogged several times on leptin in eating disorders (What's Leptin Got to Do With It?, Leptin and You, and Food and Sex and Leptin- Oh My!), and the protein, which signals satiety, has been much researched in relation to both anorexia and obesity. Gina Kolata's book Rethinking Thin has a great chapter on the discovery of leptin and some of the interesting research going on about the protein.
Ghrelin is kind of the ugly stepsister to leptin--it has the opposite function (ghrelin signals hunger as opposed to satiety), and it's gotten the shorter end of the stick in terms of research (at least recently). Unlike leptin, which is primarily synthesized by adipose tissue, ghrelin is synthesized in the stomach upon eating. A drop in ghrelin levels typically happens after eating and is thought to be linked to the release of insulin, which tells the body's cells to absorb the glucose from the meal.
Considering that people with anorexia are objectively starving, they generally have high levels of ghrelin as their bodies signal them to go get some food, levels that return to normal upon refeeding. However, a new study suggests that the excessive release of insulin by people with AN (known as hyperinsulinemia) also blunts the hunger-signaling effects of ghrelin. That is, the sudden drop in ghrelin upon eating even small amounts of food tells the brain that the person is full and the meal is finished.
The increased insulin sensitivity makes sense from a biological standpoint: the body will want to make the most use out of limited energy intake, so cells would do well to become more sensitive to insulin to slurp up more glucose. Whether the drop in ghrelin is an abnormality completely separate from the insulin sensitivity, or just a really ironic side effect, has yet to be seen. However, it adds another piece to the puzzle of why people with AN find it so difficult to eat more: they really do feel full.
4 comments:
Thanks for highlighting this Carrie :) It's something many people don't understand about EDs (anorexia nervosa especially).
A 25+ year history of very low weight restricting anorexia nervosa has left me with symptoms of gastroparesis. This was confirmed recently when I needed an MRI scan of the GI tract. The process took twice as long as it should do because the litre of 'gross stuff' (gastrografin) I needed to drink pre-scan just sat in my stomach.
Many of the endocrine changes of anorexia nervosa do reverse with re-feeding. Indeed, leptin levels shoot up with inpatient re-feeding, even before there is significant weight gain.
For me, personally, eating is getting easier but it's taken me 4 years to reach a near healthy weight and to maintain that weight. Initially, eating was just too damn difficult and unpleasant.
It is often said that the term 'anorexia' is a paradox in anorexia nervosa because appetite is not really lacking. That may be true in the earlier stages of the illness, but after many years of restricting anorexia nervosa eating can be really unpleasant. My relationship with food nowadays is an essential one. It keeps me alive but I don't enjoy it. The only food/drink I actually enjoy is frothy, whole milk cappuccino.... Thanks goodness for Starbucks!
I would be really interested to see some research on how these factors change during the refeeding process. When I was first starting weight restoration, I could consume a large meal (even by non-ED standards, I swear!) that made me uncomfortably full, but then would still have true hunger (not just appetite) only an hour later, it frustrated me to no end that I actually spent more time hungry than I had when I was restricting! I know there are metabolic and biochemical reasons for this, but it would be interesting to see what ghrelin and leptin are doing in cases like that.
It's interesting- I still tend to get full quickly after eating, even after being weight restored for a month or two. If I just paid attention to hunger cues, I would eat half my dinner, be really full, and then be absolutely famished an hour later. Which I now realize is probably (at least in part) due to the ghrelin signaling. I'd be curious to see if they did time tests in people to get a natural curve and see how it differed in people with EDs.
Here I am, more than a decade later and yet this is still accurate- I've been trying to recover since 2017- my ED starting in my mid teens in 2015, one of my first symptoms when I started recovery was struggling through meal times due to early satiety. Although as Ed's go, my recovery has been on and off yet this is an ongoing symptom with periods of extreme hunger.
My theripast stated these were normal in the recovery process, and in my best times of extended recovery, my stomach was able to maintain the slightest more of an appetite. Albeit with practice. That's why my theripast recommended doing the 3 meals, and 3 snacks method to maintain an appetite and proper nutrition.
To anyone reading this, recovery is worth it:)
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