Your Skeleton Would Like a Word
It’s the season of skeletons – dangling from porches, lounging on lawns, grinning at you from the drugstore aisle next to the overpriced fun-size candy. Meanwhile, the skeleton you actually live in has been trying to get your attention for years -- and not just at Halloween.
Bone doesn’t communicate real well as it thins. There’s no pain, no warning light, no concerning lab value on your annual bloodwork that, on its own, sends up red flags. For most women, the first sign of osteoporosis is a scary result from a DEXA scan (if you’re “lucky”), or a fracture (if you’re not). And statistically, 1 in 2 women over the age of 50 in North America will experience an osteoporosis fracture.
There’s a real timing conundrum in all this: Routine DEXA screening starts at age 65, but the fastest rate of bone loss most women will ever experience starts more than a decade earlier. By the time many women get an initial DEXA, the most impactful “How-to” chapter in our bone health story has already been written.
So let’s dig into this grave subject (see what I did there?) and discuss what’s happening with your skeleton, why the perimenopause years matter so much, and what you can do about it at any age.
The Call Is Coming From Inside the House
Bone seems so … permanent. It’s what physically remains when everything else is gone. But living bone is active tissue, constantly being broken down and rebuilt in a process called remodeling. Did you know that most of the adult skeleton is replaced about every 10 years?
There are two main types of cells running this remodeling job:
Osteoclasts – cells that dissolve old bone (a process called resorption)
Osteoblasts – cells that form and build new bone
When these two work well together, the demo and construction stay balanced – so your skeleton renovation stays on schedule (so to speak).
BUT – estrogen is one of the main influences on the balance between bone resorption and bone remodeling. It keeps the brakes on osteoclast formation and activity. Remove that brake – which is what happens as we lose estrogen in the menopause transition – and bone resorption starts outpacing bone formation. In other words, the body starts breaking down bone faster than it rebuilds it.
There’s also your personal bone health situation. We build most of our bone in childhood and adolescence, and bone mass peaks somewhere in our mid-to-late 20’s. After that, we need to be in preservation mode: the bone you bring into mid-life is the bone you have to protect throughout the rest of it.
And I can’t stress this enough: bone density is not the whole story! Bone quality and structure matter at least as much as its mass for strength. A standard DEXA (dual-energy X-ray absorptiometry) scan measures mineral density, while trabecular bone score (TBS) software analyzes the DEXA image to estimate the internal architecture. TBS analysis is not generally included with a standard DEXA scan. Just so you know, TBS also declines during the menopause transition.
Let’s do a quick review, so we’re all on the same page:
Osteoporosis literally means ‘porous bone’, and the official verdict comes from a number on your DEXA report called a T-score. It compares your bone density with that of an average healthy young adult – so in a way, your skeleton is graded against its own peak. However, the standard reference group behind the hip score is white women in their 20s (worth remembering the next time someone says bone density is “objective”).
-1.0 or higher: considered normal
-1.0 to -2.5: low bone mass, widely considered osteopenia
-2.5 or lower: osteoporosis
While osteopenia isn’t a disease, it’s not a diagnosis to shrug off (more and more clinicians prefer the term ‘low bone mass’). Think of it as a yellow light, because a score above the osteoporosis cutoff doesn’t mean you’re in the clear. Diagnosed osteoporosis raises fracture risk, but not having the diagnosis doesn’t eliminate that risk. Because, in other scary reminders, fracture risk isn’t only about how strong your bones are. It’s bone strength + bone quality + the odds of your skeleton meeting the floor (which is why we’ll also be talking about muscle strength and balance a little later).
Ghosted: What Happens to Bone When Estrogen Declines
The steepest bone loss most women will experience starts about a year before their final menstrual period (FMP) – and there’s really no reliable way to predict that from your cycles alone. Your FMP only becomes “official” 12 months later, so we can only identify the start of rapid bone loss in hindsight!
Most of what we know here comes from SWAN data – the Study of Women’s Health Across the Nation. This was a large, multi-ethnic study that followed women through the menopause transition with annual bone scans and hormone measurements. According to those findings:
About 2 years before the FMP, ovarian function starts to decline, bone resorption rises, and bone loss follows
About 1 year before the FMP, bone loss accelerates dramatically
About 2 years after the FMP, is pace slows, but bone loss continues (at a rate of about 1% each year at both the spine and the hip)
SWAN data showed that over the 3-ish years surrounding the FMP, women lost an average of about 6% of bone density at the femoral neck/hip and 7% at the lumbar spine. Even years after the FMP, bone resorption markers were still running about 20% higher than before the menopause transition began.
Pause for a friendly reminder: These numbers are averages within a wide spread. The SWAN study found that some women lose bone rapidly during the transition -- but others lose little or none. The data can tell us about risk, but they can’t tell you where you personally land. For me, that just strengthens the argument for assessment, not assumption.
But here’s the kicker: The United States Preventative Services Task Force (USPSTF, whew!) recommends bone density screening for all women age 65 and older, and for postmenopausal women under 65 only when a clinical risk assessment shows increased fracture risk. According to the Cleveland Clinic, the average age of menopause in the US is 52. So the most dramatic bone loss has come and gone more than a decade before routine screening even begins!
What’s more, plenty of women don’t transition into menopause in their early 50’s. Roughly 1 in 10 reach menopause before 45, and 1-3% before age 40. For some, it’s not a transition at all: Removal of both ovaries ends ovarian estrogen production overnight, and small studies suggest that bone loss after surgical menopause happens faster than after a natural one. Even a hysterectomy that spares the ovaries increases the risk of earlier ovarian failure; and some cancer treatments and hormone-suppressing medications can bring on menopause and/or bone loss well ahead of schedule. That means the gap between bone loss and assessment is even wider.
Here’s where I’ll editorialize – I’d like to see every woman get a baseline bone density scan as she enters perimenopause, not at 65. That isn’t what the current guidelines recommend. But the steepest loss happens during the transition, and a baseline would give us something to measure against before that starts.
If you’re in perimenopause, or recently post-menopausal, a fair question for your doctor is whether you have risk factors that qualify you for earlier screening. Read on to learn more about what those risk factors are, including some that rarely get connected to bone health, and what can happen if we’re not asking questions.
The Real Horror Story: What a fracture costs
Osteoporosis itself doesn’t hurt anyone – it’s fractures that do the damage (and hip fractures do the most).
A 2010 meta-analysis in the Annals of Internal Medicine found that in the first three months after a hip fracture, women’s risk of death was nearly six times that of women the same age without one. A separate study found that this risk decreased after a few years – but never returned to normal, even 15 years out. Among women 65 and older, the odds of death doubled in the year after a hip fracture as compared to those without one.
The danger is often what the fracture event sets in motion. In the above study, more of the women who’d broken a hip died of pneumonia than the women who hadn’t – the downstream cost of surgery and immobility. And spinal fractures are sneakier: Many of these happen without a memorable fall or other incident (like being hit by a truck – just me?) and get filed under ‘back pain’, with the evidence showing up later as loss of height, an upper back that curves forward, or restricted mobility.
I want to point out that for decades, the face of osteoporosis has been the Brittle White Lady (I can say that, I’m one of them). The research was built mostly on women who looked like me, from the clinical trials to the risk calculator doctors use to decide who gets screened. Black women statistically do have lower rates of osteoporosis – but they’re screened less, treated less (even after a fracture), and more likely to die or end up disabled when a hip breaks. Hispanic women and white women have similar fracture rates – Asian women’s run at least as high – and for Native women, the data is so thin that nobody actually knows how common osteoporosis is.
So whoever you are, don’t wait for someone else to bring up bone health concerns. Ask whether you have risk factors that qualify you for screening before age 65, ask for your FRAX score (an assessment of fracture risk), and if you’ve broken a bone as an adult, ask whether anyone looked into why.
Skeletons in the Medicine Cabinet
Some of the biggest threats to healthy bone aren’t super obvious. I’m talking prescriptions, diagnoses, and habits that rarely get connected to your skeleton – which can leave a lot unsaid.
Disclaimer: I am not anti-medication! Many of these are necessary, some are lifesaving, and nothing you read here is a recommendation to stop anything on your own. The point is to make sure bone health is part of the conversation with whoever prescribes them.
Here are a few of the most commonly prescribed drugs that can affect bone:
Steroids/glucocorticoids
Prednisone and its relatives are the leading medication-related cause of secondary osteoporosis. According to the Handbook of Experimental Pharmacology, glucocorticoids both decrease bone mineral density and interfere with the unmineralized matrix, leading to an increase in fracture risk. And the impact is pretty immediate: fracture risk can rise even at low doses within the first month of treatment. This is critically important for those managing certain autoimmune conditions, where steroid courses can become a recurring part of life.
Thyroid hormone
Treating hypothyroidism isn’t the problem, but overtreating it can be. Per the American Thyroid Association, exogenous T4 (like Levothyroxine) that keeps TSH within normal range does not appear to be problematic. As the saying goes, “the dose makes the poison”. Fracture risk may increase with T4 doses that push TSH out of range. Be sure that your thyroid levels are being monitored by your medical professional.
Acid blockers/PPIs
Long-term proton pump inhibitor use is linked to modestly higher fracture risk, per observational studies. Plenty of people need a short-term PPI while they work on dietary and lifestyle modifications to address things like acid reflux. Also, plenty of people were started on a PPI years ago and nobody has revisited it since – and that’s a conversation worth having with your doctor.
SSRIs
Meta-analyses link SSRI use to about a 70% higher fracture risk. However, the cause is really hard to untangle, since depression itself is associated with low bone mass, falls, and fractures. Treating depression matters for its own sake – this is just a reminder to keep bone and fall risk on the radar.
Antiseizure medications
These drugs are increasingly prescribed for a range of conditions beyond seizure disorder – things like nerve pain, migraine prevention, even weight loss. The older, enzyme-inducing ones speed the breakdown of vitamin D and are most strongly linked to bone loss and fracture.
GLP-1 medications
Bone research on semaglutide/tirzepatide is still early, and findings are mixed. In some retrospective studies, greater weight loss tracked with greater hip bone loss – but overall, the current data is largely neutral. What is well established is that in older adults, weight loss is associated with lower bone density and higher fracture risk – so protein and resistance training matter even more on these drugs.
Let’s jaw about some nutrition considerations
Not eating enough
Bone needs fuel. When energy intake doesn’t cover what the body spends, estrogen can tank, cycles can falter, and bone remodeling suffers. Sports medicine has studied this for years as the Female Athlete Triad, now folded into a broader syndrome called Relative Energy Deficiency in Sport (RED-S). The research centers on female athletes, but the mechanism – not enough fuel for what the body needs – isn’t exclusive to them. A period that has stopped showing up is not a badge of discipline, it’s a sign of estrogen depletion.
The gut-bone connection
You can eat all the calcium-rich foods you like, but the body can only use (and distribute) what it can absorb – that’s why malabsorption, chronic malnutrition, and chronic liver disease all count as secondary causes of osteoporosis on the FRAX tool. It’s worth mentioning Celiac disease here too – it’s associated with a 30% higher risk of any fracture, and an almost 70% higher risk of hip fracture (per a 2015 meta-analysis). If you have low bone density along with a history of unresolved GI symptoms, iron-deficiency anemia, or a diagnosed autoimmune condition, celiac testing may be worth inquiring about.
Alcohol and smoking
Both are built into fracture-risk calculators. Long story short: Having smoked in the past is linked to significantly higher fracture risk than never smoking, though the risk is lower than if you’re currently smoking. This suggests smoking’s effect on fracture risk is at least partly reversible, which is good news if you’ve quit. As for alcohol consumption, hip fracture risk climbs at 3 or more drinks per day. Oddly enough, balance and coordination also take a hit when you drink – think there might be a connection??
If anything on this list applies to you, that’s a legit reason to ask about earlier screening. And it’s a good time to talk about what you can actually do going forward – starting with what’s on your plate.
Treats (No Tricks) for Your Skeleton
Enough scary stuff! Here’s what can help – and the good news is that much of it already lives in your kitchen.
Food:
Calcium-rich foods
Women over 50 needs about 1200 mg/day (according to the NIH), and most of that can come from dairy, canned fish with bones, calcium-set tofu, leafy greens, and fortified foods. Supplements are for closing any gaps, not an “instead of”. If you do use them, calcium supplements are absorbed best in doses of 500 mg or less at a time, and they also come with a kidney stone risk and a still-debated cardiovascular question. This is very much a subject worth discussing with your physician or nutrition provider.
Protein
There used to be this idea that protein leaches calcium from your bones (talk about creepy), but that hasn’t held up to science. In older adults, higher protein intake is linked to fewer hip fractures – and protein is the macro that allows your body to build the muscle that loads your bones.
Prunes
Yes, really The least popular thing to toss into someone’s Trick-or-Treat bag has some of the best food trial data in bone health. About 5-6 prunes per day over a year preserved hip bone density in postmenopausal women.
Magnesium (from plants)
Higher magnesium intake tracks with modestly better hip bone density (though not with fewer fractures). Nuts, seeds, beans, and greens are rich in magnesium – along with a bunch of other minerals your bones like (including boron, strontium, vanadium, magnesium, manganese, zinc, copper, and silicon).
On Supplements:
This is where the internet loses its mind, so here’s the short version – always keep in mind that supplements are targeted tools, chosen with your clinician based on what your labs and dietary intake actually show.
Vitamin D: In the findings of a large trial (reported in the New England Journal of Medicine) of generally healthy adults, vitamin D didn’t reduce fractures. Now, that’s only one factor, and it doesn’t apply to people who are deficient or already have osteoporosis – which is why I say, “Test, don’t guess”.
Vitamin K2: It’s complicated. Recent meta-analyses seem to indicate that K2 supplementation can have a positive effect on bone mineral density of the lumbar spine; however, some of these results are difficult to tease out depending on whether K2 is added to vitamin D therapy or other compounds. It’s probably most accurate to say that vitamin K2 has been shown to indirectly promote bone mineralization and increase bone strength.
Collagen peptides: I get asked about these a lot. One randomized trial found improved bone density in postmenopausal women with low bone mass. Remember – one trial is a start, not a verdict.
Creatine: For now, trials have found no bone density benefit. (Muscle, yes; bone, not that we know yet).
Make it work!
Bone responds to force. The landmark LIFTMOR trial put postmenopausal women with low bone mass through supervised progressive heavy lifting and impact work twice a week, and their bone density improved — with no injuries. The words doing the heavy lifting here are supervised and progressive: find a qualified trainer or physical therapist. This is not a call to start deadlifting alone in your garage!
Just so you know, exercise programs cut the rate of falls in older adults by about 25%, especially those that focus on balance and functional movement. Strong bones and fewer falls are two separate insurance policies – and you want both.
Know your numbers
A DEXA scan – ideally with a FRAX score, tells you where your bones stand; labs help explain why. These are worth asking your doctor about, especially if your bone density is lower than expected:
A standard CBC and CMP
Phosphorus
25-OH-D3
PTH (parathyroid hormone)
Thyroid panel if you take thyroid hormone
24-hour urinary calcium
P1NP, BAP, and osteocalcin (related to osteoblast function)
CTx and NTx (related to osteoclast function)
Think of these as markers to discuss with your doctor, not orders to hand over (please and thank you).
The Last Word
There’s no perfect bone protocol, and you don’t need one. What works is enough protein and calcium most days, lifting something heavy (for you) on a regular basis, staying steady on your feet, and making sure someone is actually looking at your bones before they make a life decision for you.
About The Author
Stephanie Thompson is a New Orleans-based functional nutrition specialist who specializes in helping people alleviate frustrating (often mysterious) health symptoms with dietary guidance, targeted nutrients, and lifestyle modifications. She digs deep into the biochemical pathways and interconnected organ systems to find the root causes of her clients' issues for specific and sustainable relief!
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