No bones about it
There were a couple interesting papers this week that looked at hormones and bone formation in the context of eating disorders.
The first one, Relationships of hormones of adipose tissue and ghrelin to bone metabolism, looks at how one of my favorite compounds--leptin--affects bone mass. Besides regulating hunger and fullness, and, as a consequence, eating behaviors, leptin also helps lay down bone mass during puberty. Adequate fat stores is required for leptin production, which helps explain why people with AN during puberty can have both low bone mass and stunted growth. Lowered body fat means lower leptin levels, and lower leptin leads to less-than-optimal bone formation.*
The study concluded that adipose tissue, far from being inert globules of stored Crisco, has a profound impact on bone formation.
A different study, Hormone Predictors of Abnormal Bone Microarchitecture In Women with Anorexia Nervosa, tried to tease out the importance of either hormonal and nutritional deficiencies in the development of osteopenia/osteoporosis in people with AN. The researchers found that women with AN had more tiny, microscopic spaces within bone itself and a reduced bone volume compared to control women. The researchers also measured the hormone levels in the two groups of women and found three major hormones that could predict reduced bone microarchitecture: leptin, androgens, and insulin-like growth factor 1. What's interesting is that these hormone levels were predictive regardless of the person's BMI. Part of this could be due to the fact that the hormone levels are related to BMI, ergo the effect will still be there even if you don't know BMI. The other aspect could be due to the fact that weight is a pretty individual thing, and so what is an abnormally low BMI in one person could be perfectly healthy in another.
Still, both studies agree on this: EDs can have dramatic, negative effects on bone structure that can last for a lifetime.
*I'm also wondering if this is why "small body frame" is a risk factor for osteoporosis- could a smaller frame mean lower circulating leptin levels? Interesting...
5 comments:
There are few things I know about my future, but taking Boniva with Sally Field is most assuredly going to be one of them.
I've read many studies that talk about the development of AN in adolescence causing poor bone development. I developed anorexia after adolescence. I've only had two bone scans -- one before treatment, one after. It showed that I did build back bone, which I guess is contrary to some studies. I'm afraid to check it out now. I hadn't heard of leptin before reading your blog, so that's been an eye-opener for me.
My bone density has been improving as well, but I'm due for another scan this fall. I'm more than a little chicken to find out what the damage of the past year was.
And Amy? We can synchronize our Boniva days and Skype while we sit or stand for half an hour before we put our teeth in and have our first cup of coffee...
There's a lot of work out there on the idea that architecture is way more important [for AN/young ppl w/bone loss] than bone density, so DXA scans may not be the best measure of true bone loss/fragility.
For example, I had several severe vertebral & femoral frx's w/ Z/T scores only -1.5 below the mean. So yeah, not stellar bone density for a 23 y/o, but not awful, you know? Not so severe you'd think I'd get frxs just from ambulating on crutches [got one side frx'd from running, was on crutches, frx'd the other side].
What my endorcine doc said was that the architecture was awful. On 3T MRI's you could see all of these moth eaten areas of missing bone. The trabeculae were shot. It's been speculated that this was due to the frequent weight loss/refeedings-- bone is constantly broken down & then tentatively rebuilt.
I'm not on my school network right now, so I don't have access to the paper but look up Anne Loucks if you're interested in learning more about bone metabolism & energy turnover. I think this is the abstract for the article I liked: http://www.jbmronline.org/doi/abs/10.1359/JBMR.040410
Really cool because she demonstrated the immediate nature of the bone/energy imbalance changes. That was super helpful for me mentally to understand that even though it took me months to regain all the weight, my body was doing *something* with the food I was taking in. Has also been useful in a relapse prevention sorta mindset, the knowledge that even a little restricting even for a little while can increase my bone breakdown [even without dramatic weight loss, massive hormonal shifts, etc]
My position-- based on science/seeing some of the top docs in the endocrine field & optimism-- is that it is absolutely possible to restore NORMAL bone density & bone architecture. And the application of osteoporosis information derived from the study of normal weight post-menopausal women to anorexics isn't useful. And the use of bis-phosphonates in EDd people (and patients with less severe OI) shouldn't happen.
Even though I don't think DXA's measure what's right to measure for my type of bone problems, mine did go up in a statistically significant way 6 months after I'd hit my normal weight (about 18 months after I'd begun refeeding).
More significantly, my MRI's show much better bone quality too, and I have a lot less bone pain. [When a doc I didn't particularly like remarked on this change I shrugged & smugly said-- See, I TOLD you I was eating!]
Calcitonin has been really, really helpful for me with the pain. It's not usually used for anorexic type bone pain (mostly for cancer) but it's been instrumental in getting me back to walking pain free. And even running again!! My next marathon is in 9 weeks, and I'm pain free, it's kinda miraculous, really.
Despite the debate about the utility of bis-phosphonates to treat osteoporosis in a.n., I was put on Fosamax from age 19-21 and significantly improved bone density. I have been told since then by doctors that the only way to improve bone density in patients with a.n. is to restore weight.
But I can attest that bone density can improve long after adolescence. (I am now in my late 20s and, after a relapse, am once again improving my bone density.)
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