On 16 June 2023, I got my first DEXA scan. I was 57. Three hours later, a rogue driver plowed his car into mine and shattered my wrist in three places.
Fifty-seven is relatively young for a DEXA – or dual-energy x-ray absorptiometry – scan, which measures bone density, or the amount of calcium and minerals in your bones. The CDC recommends them for women 65 and over, but while interviewing Joanna Strober, CEO of Midi Health, a virtual care clinic for those in perimenopause and menopause, she had urged me to get one sooner. Strober had become alarmed by how many of their fiftysomething patients were finding that they had the bones of an octogenarian.
The results of my DEXA scan arrived in my inbox a week after my car crash: I had full-blown osteoporosis.
I was still recovering from multiple injuries, so the diagnosis took a back seat. I was also under the impression – because of my age, ignorance and the invisible, pain-free pathogenesis of osteoporosis – that loss of bone mass was less of an immediate threat to my health and wellbeing than my visible injuries. But, in fact, my osteoporosis had made me more susceptible to that broken wrist. Without intervention, osteoporotic bones simply deteriorate and grow increasingly more brittle with age. They also take longer to heal from fractures.
I can attest to that: fifteen months later, it still hurts to hold a pitcher of water.
Osteoporosis comes from osteo (from ostéon, Greek for bone) and poros (Greek for pore or passage). It describes just that: a hollowing out and reduction of bone mass such that the tiny holes that naturally occur in our bones widen into a gaping, irregular lattice. Osteoporosis occurs predominantly in postmenopausal women. A woman in her 50s has a 14% chance of having it. By age 80, she has a 70% chance.
It begins when the creation of new bone can no longer keep up with the loss of old bone. These hollowed-out bones are far more prone to breakage, particularly in the hip, spine, and, yes, wrist. The survival rate for women, following a hip fracture, is worse than most cancers: half will be dead in five years. Yes, men get osteoporosis, too, but the percentages are much lower. A crude estimate for men over 50 is 4.2%, and authorities don’t recommend routine bone density testing, either for men or for women my age.
But if I’ve learned anything over the course of my work reporting on women’s health, it’s that most of what we’ve been told often turns out to be wrong, and none of it has been sufficiently studied, if at all. Unsurprisingly, trying to figure out how to treat my osteoporosis has only confirmed this.
I had several risk factors for osteoporosis: small body frame (5ft 2in, thin), family history (including a great aunt who died from a broken hip), ethnicity (white; Asians are also more prone) and a prior history of fractures. So my primary care provider had agreed it couldn’t hurt to get a DEXA scan at 57 as a baseline. At my annual physical, my vitamin D levels were below normal – another red flag. My gynecologist also thought it a good idea and ordered the scan, which took three months to schedule.
The resulting diagnosis of full-blown osteoporosis shocked me. I’m an active woman in good shape for my age. I don’t smoke or drink. I eat a balanced diet. I do yoga twice weekly, ride my bike and walk 10,000 steps every day. Yet my DEXA results were similar to those of an 80-year-old woman.
DEXA scan results include T-score numbers, which indicate how many standard deviation units below the mean the subject’s bones have deteriorated in three key places for breakage: lumbar spine, femoral neck and hip. The mean is 0, for a healthy young person with strong bones. Any score between -1 and 0 is considered healthy. Scores from -1 to -2.5 point to osteopenia, which is less a clinical diagnosis and more an indication that bone mass loss has begun. Any score below -2.5 indicates osteoporosis.
My hip T-score was -2, but my lumbar spine T-score was -3.2; my left femoral neck was -2.7. “The patient has Osteoporosis lumbar spine, left femoral neck,” the radiologist wrote in my report. “Patient fracture risk is elevated.”
After recovering from the crash, I set out in search of answers. But even I, a woman who writes about women’s health, had no idea which specialist to contact. An orthopedist? A rheumatologist? An endocrinologist? A gerontologist? Some combination of all four?
The consensus among friends, family and Google was to seek out an endocrinologist. Endocrinologists treat diseases of hormonal imbalance. Osteoporosis, I was surprised to learn, is a hormone-related disease – a drop in estrogen or an overactive thyroid, parathyroid or adrenal gland can all weaken bones.
But the sole endocrinologist in network for my insurance who was taking new patients did not have an appointment for another six months.
While I waited, I scheduled a Zoom with Dr Mary O’Connor, an orthopedic surgeon I’d previously interviewed for the launch of her book, Taking Care of You: The Empowered Woman’s Guide to Better Health. At her urging, I added a daily 2000 IU Vitamin D3 supplement and upped my intake of calcium-rich foods. “If you don’t have adequate vitamin D3,” she explained, “you cannot absorb the calcium that you eat.” She also suggested lifting weights, so I bought some dumbbells and found a 30-minute online workout I actually liked.
While researching specialists, I noticed that many rheumatologists included osteoporosis as an area of expertise. They mostly treat connective tissue disorders, but I figured they could at least do the bloodwork I needed.
Dr Lauren Wong, a rheumatologist from NYU Langone, one of those rare physicians who treats you as an equal, ordered a ton of that bloodwork. At my follow-up, she had some answers. “You have hyperparathyroidism,” she told me: my PTH, or parathyroid hormone, levels had come back unnaturally high. Parathyroid hormone, she explained, regulates our calcium levels, and too much parathyroid hormone can contribute to osteoporosis by triggering the release of calcium from bone stores. Wong agreed I needed to see an endocrinologist and possibly a parathyroid surgeon after that.
“Hyperpara … what?” I’d never heard of this hard-to-pronounce disease.
My endocrinology appointment was still several months away – god bless America – so I sought the advice of Dr Babak Larian, a parathyroid surgeon in LA with an excellent YouTube channel about hyperparathyroidism. Over Zoom, Larian told me he thinks it’s absolutely ridiculous that women in this country are advised to get DEXA scans at 65, given that menopause begins in our late 40s or early 50s. “I think 50 should be the standard,” he said.
Larian also explained that we have extremely poor statistics on the prevalence of hyperparathyroidism in the US. “We’re so far off the mark,” he said, “that I don’t even know where to start the conversation.” Furthermore, “because this is a disease mainly of women, they are [often] not diagnosed”.
The Endocrine Society states that the incidence of primary hyperparathyroidism in the US is somewhere between 0.1% and 0.7%; women and African Americans are more prone to it. However, a recent retroactive survey in Canada found that 5% of Canada’s population have some form of hyperparathyroidism. Larian believes hyperparathyroidism can be triggered by menopause, and thus that more than 5% of menopausal women have it. But they are completely unaware of this because its symptoms – such as fatigue, muscle weakness, depression, memory problems – mimic those of menopause, and primary care doctors don’t routinely check women’s blood for high levels of PTH.
I redoubled my efforts to find an endocrinologist who could see me sooner and once again failed. But then I came down with another UTI – an annoyingly common event, thanks to genitourinary syndrome of menopause, though I have far fewer now thanks to vaginal estrogen – and my urologist just happened to know a young endocrinologist who was taking on new patients. A breakthrough!
The endocrinologist confirmed my hyperparathyroidism diagnosis. So she ordered more scans and tests and asked me to seek out a parathyroid surgeon or two to see if I had an adenoma – a non-cancerous growth on the parathyroid gland and the hallmark of primary hyperparathyroidism – which would then need to be removed.
I consulted with two surgeons, neither of whom found an adenoma on a scan, so I didn’t need surgery. Instead, they concluded that I had secondary hyperparathyroidism, brought on by a lack of vitamin D.
Getting to the bottom of my osteoporosis was quickly becoming a full-time job. Never mind all the visits themselves – even finding the right doctors, who were in-network, could take hours upon hours of research. At this point, I’d either seen in person or interviewed 10 doctors in total.
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OK, great, I thought. I know why I have osteoporosis at 57. Now what do I do about it?
Luckily, I was already on track. In 2022, I’d started taking estrogen, which the British Menopause Society calls “the treatment of choice for osteoporosis prevention”. The North American Menopause Society’s recent 2022 position paper on hormone therapy also states that estrogen prevents bone loss and reduces fracture risk.
In an ideal world, I’d have been prescribed estrogen the minute I had my uterus removed in 2012 for another medical issue. But back then, HRT was not the standard of care for any woman, with or without a uterus, as it was still being falsely demonized as causing breast cancer. Could the 10-year gap between my hysterectomy and commencement of hormone therapy have contributed to my osteoporosis? According to a number of doctors I consulted, quite possibly, yes.
Meanwhile, the pharmaceutical industry offers no shortage of drugs for people with osteoporosis – as doctors, friends and relatives readily reminded me – but the deeper I dug into each one, the less I was sure I wanted any of them. Bisphosphonates like Fosomax, often the first drug of choice following an osteoporosis diagnosis, inhibit bone resorption and increase bone mass density. But there isn’t much data on long-term use in younger patients like me. Plus, in rare instances, they have been shown to cause osteonecrosis of the jaw (ONJ) and atypical femur fractures – exactly the injury I was trying to avoid.
Prolia injections target a specific molecule that bone-removing cells need in order to work, but they also make one more susceptible to infections. With my recurring UTIs and concomitant antibiotic resistance, this, too, was a no go. Also, once you start with Prolia, you have to keep taking it twice a year, and the cost, depending on one’s insurance and eligibility for coupons, can be prohibitive. Forteo, an anabolic that is a synthetic form of parathyroid hormone, stimulates the formation of new bone and also boosts bone mineral density, but is contraindicated for people with hypercalcemic disorders such as hyperparathyroidism. Moreover, one of its side effects is dizziness, and I’m a lifelong fainter with low blood pressure and orthostatic hypotension – so probably not a great idea if I wanted to avoid falling and breaking more bones.
I told my endocrinologist I needed to think about all of this. In the meantime, I asked her to check my PTH levels again. Lo and behold, Dr O’Connor’s vitamin D3 regimen had worked! My PTH levels are now in the normal range, and my hyperparathyroidism is gone.
What effect did this have on my skeleton? My endocrinologist thought it would be worthwhile to repeat the DEXA scan at the same office where I got the first one. Alas, their next appointment isn’t until four months from now – a full 18 months after my first scan. In New York City, getting the healthcare I need should be easy. It is not.
“What if I don’t take anything?” I said to my endocrinologist. “What are my risks if I continue lifting weights to build strength and muscle, taking vitamin D and estrogen, eating calcium rich foods and exercising daily?”
Whether to take drugs, she said, was ultimately my choice, but my osteoporosis was serious. “Even a sneeze,” she said, “can break your spine.”
Great, I thought. I’ll try to avoid sneezing.
Utterly confused, I spoke with oncologist Dr Avrum Bluming, co-author of Estrogen Matters. He calls osteoporosis a disease of decreased bone resilience: the ability of bone to stretch without breaking. Drugs like Fosomax and Prolia treat bone density, he said, but not bone resilience.
Here, again, estrogen was key. “Bone mineral density is not a great test for osteoporosis, which is a lack of bone elasticity,” he said. Bone mineral density “does not correlate very well with risk of fracture. What we do know is estrogen does prolong the ability of bone collagen fibers to remain flexible or elastic, and it decreases the risk of serious fracture, especially hip fracture, by up to 50%.”
I still wasn’t sure what to do about treatment or where to turn to find out. Should I try to find a different endocrinologist? I called my daughter, who’s in her fourth year of med school, but she had no new insights from her studies.
Then, this summer, I read a revelatory new study in Nature co-authored by Dr Muriel Babey, an endocrinologist and researcher at UCSF. Its headline immediately caught my eye: “A maternal brain hormone that builds bone.” In the study, Babey and her colleagues finally answer the question that has been puzzling endocrinologists for over a century: how do the bones of breastfeeding women stay strong and resilient when they are losing so much calcium to milk production? In theory, a lactating mother should have severely osteoporotic bones. (In rare instances, called pregnancy and lactation-associated osteoporosis (PLO), they do.)
The answer lies in a newly discovered hormone: CCN3, the so-called Maternal Brain Hormone, which the researchers found almost by accident by studying the hormones of female mice, a rare occurrence as male mice are the norm for most animal studies.
When Babey’s team gave CCN3 to female mice who were very old or lacking in estrogen, it doubled the mice’s bone mass and, critically, their bones were more resilient and broke less easily. CCN3 has not yet been tested in humans, but if it works on women the way it works in female mice, Maternal Brain Hormone could be the missing magic bullet in terms of osteoporosis treatment.
I contacted Babey to ask if and when the hormone might come to market. “For pharmaceutical application,” she said, “the timeline is usually around five to 10 years”. Too late for me, alas, but it does give me hope that my daughter might have better options if she is diagnosed.
I gave Babey a brief history of my osteoporosis journey and the various treatments I’d considered. “What if I do nothing?” I said.
“I would definitely get another baseline first before even deciding if anabolic treatment will be necessary,” she said. She also suggested I get a mini-trampoline to build balance and strength, and to try exercise programs designed for people with osteoporosis. There is extremely limited data, she stressed, on the benefits of so-called rebound exercise, but one study did show an increase in bone mass in premenopausal women.
Reader, I bought a mini-trampoline. It can’t hurt.
Meanwhile, I’m still taking estrogen and incessantly calling my radiologist’s office to get an earlier appointment. Until then, I will hold off on drugs, and I will try not to sneeze or get in any more car accidents.
“Just don’t fall!” an older friend recently advised me with a shrug and a smile, when I asked how she manages her osteoporosis. As I made my way through the large stack of medical bills on my desk from this 15-month odyssey, wondering which to pay now and which to try to push off until later, this seemed as good as advice as any.
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Deborah Copaken, founder and editor of Ladyparts, is an award-winning journalist, photographer, screenwriter, and the New York Times bestselling author of seven books, including Shutterbabe, The Red Book, and Ladyparts.
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The headline of this article was amended on 22 October 2024 to reflect that the writer is now 58.