How to Protect Your Bones in Perimenopause: Tests, Nutrition, Exercise and HRT

If you haven't read the first post in this series, I'd encourage you to start there. Understanding why bone loss accelerates in perimenopause, and the role inflammation and hormones play, makes everything in this post land differently.

But if you're here for the practical side, let's get into it.

First: Know Where You Stand

Osteoporosis is a silent disease. There are no symptoms until a fracture happens. This is why getting a baseline scan matters, especially once you're heading into the perimenopause window.

DEXA scan is the gold standard. It measures bone mineral density at the lumbar spine and femoral neck (hip) and expresses the result as a T-score compared to a healthy 30-year-old of the same sex. A score between -1 and -2.5 is classified as osteopenia; below -2.5 is osteoporosis. For premenopausal women and those under 50, a Z-score is used instead, which compares to age-matched peers.

A word of caution: DEXA measures density in 2D, not 3D, and positioning matters enormously. Hip positioning needs to be precise, with the iliac crest visible on both sides. A large lumbar curve can affect the reading significantly. If you feel your result doesn't match your clinical picture, it's worth asking about this.

You can ask your GP for a DEXA scan. Framing it around family history of fractures tends to get results.

REMS is a newer option that uses ultrasound rather than radiation and tells us about trabecular architecture as well as density. It's particularly useful for tracking how interventions are working over time, since it captures bone quality (the honeycomb structure) rather than just mineral density.

The FRAX tool is an algorithm that calculates your 10-year risk of major fracture. It incorporates clinical risk factors including smoking, alcohol use, steroid use, and prior fractures, and can be done with or without a DEXA scan.

If you want to go further, bone turnover markers can be measured through blood and urine tests. CTX and NTX tell you how much resorption is happening; osteocalcin and bone-specific alkaline phosphatase tell you how much formation is occurring. These aren't routinely available on the NHS outside specialist clinics, but they're worth asking about if you're working with an osteoporosis practitioner.

Nutrients That Actually Move the Needle

Calcium: 1000 to 1200mg per day from food. Good sources include dairy (hard cheeses like Gouda and Edam are particularly concentrated and tolerated even by many lactose-intolerant people), dark leafy greens, tinned fish with bones, tahini, tofu, oats, chia seeds, and baked beans. If you're supplementing, use algae-based calcium. Regular calcium carbonate or citrate supplements can deposit calcium in arteries rather than bone, particularly in menopausal women. Algae-form calcium also tends to naturally contain vitamin K2, which helps direct calcium to where it's needed.

Vitamin D: target serum levels of 75 to 100 nmol/L. Diet and sun exposure are not sufficient for most people in the UK. A maintenance supplement of 1000 to 2000 IU daily is a reasonable starting point; you'll need more if you're correcting a deficiency. Vitamin D is essential for calcium absorption in the duodenum and jejunum, and is also activated by PTH in response to low calcium, making deficiency a compounding problem.

Vitamin K2: 90 to 180mcg daily. K2 activates osteocalcin, the protein that binds calcium and directs it into bone. Without adequate K2, you can have plenty of calcium circulating and still not be building bone effectively. Fermented foods contain K2, but supplementation is often needed to reach therapeutic levels.

Protein: 1 to 1.2g per kilogram of body weight per day. Type 1 collagen is the structural scaffold of bone, and you need protein, particularly glycine and lysine, to synthesise it. Spread protein across meals rather than loading it all into one sitting. Bone broth is an excellent glycine source.

Magnesium: 300 to 400mg per day. Even mild magnesium deficiency can increase PTH secretion, which accelerates bone turnover. Nuts, seeds, whole grains, and dark leafy greens are your best food sources.

Supporting nutrients: boron, silicon, zinc, and vitamin C all contribute to collagen synthesis and bone mineralisation. Don't overlook them.

A note on acid-alkaline balance: chronic mild metabolic acidosis, the result of a diet heavy in processed foods and light on vegetables, shifts the body toward using bone minerals as a pH buffer. If you drink sparkling water, choose a natural mineral water rich in bicarbonate, like Gerolsteiner, rather than plain carbonated water.

Phytoestrogens and Bone: The Underrated Category

Phytoestrogens bind weakly to oestrogen receptors and can have a meaningful effect on bone mineral density, particularly in the context of declining endogenous oestrogen.

The most research-backed source is red clover, which contains isoflavones including daidzein, biochanin A, and formononetin. The most active forms for bone are genistein, daidzein, and equol (the most potent of all), but biochanin A and formononetin need to be converted by gut bacteria to become active. For this reason, a pre-fermented red clover product is preferable to a raw supplement. Regobone by Herrens Mark is a good product. It tastes quite something, but the evidence behind it is solid.

Soya isoflavones (from fermented soy sources rather than processed soy products) also support bone density, as do legumes generally.

Equol and resveratrol are also worth considering as standalone supplements for bone-specific support.

The FORTIBONE Collagen Question

Not all collagen supplements are equivalent for bone. The research-backed form is a specific bioactive collagen peptide called FORTIBONE. Look for this trademarked ingredient specifically, rather than generic collagen powders. Dynamic Multi Collagen Matrix by NutriDyn is one option; BoneBalance by BoneBalance is another. Generic collagen may support skin and joints but doesn't have the same evidence base for bone matrix specifically.

Exercise: Non-Negotiable, and More Specific Than You Think

This is the part that tends to get reduced to "do some walking and take the stairs." Walking is not enough. Bone responds to load, impact, and tension. Here's what actually works:

Multidirectional impact work is where a lot of people are missing out. Countermovement jumps, star jumps, stride jumps, side shuffles, and reactive landings create the kind of multidirectional mechanical stimulation that osteocytes respond to. This needs to happen in multiple planes, not just forward motion. Aim for this kind of movement regularly throughout the week.

Progressive resistance training is equally essential. When a muscle pulls on a bone through a tendon (during a deadlift, squat, overhead press, or row), both the muscle and the bone get stronger. The key word is progressive: the load needs to increase over time for continued adaptation.

Postural work matters especially for the spine. Back extensions, scapular retractions, and core bracing protect vertebral integrity and reduce the risk of the kind of compression fractures that happen silently in osteoporotic vertebrae.

Balance training reduces fall risk. Single-leg stands, done properly, are simple and effective.

All four categories, every week. This is the minimum for bone protection.

Medications: What to Know

Most conventional osteoporosis medications reduce bone breakdown rather than build new bone. Here's a brief overview:

Bisphosphonates (alendronate, risedronate, ibandronate, zoledronic acid) are first-line therapy. They incorporate into bone and poison osteoclasts when they try to resorb it. They improve mineral density but don't address trabecular architecture, so they strengthen the concrete without touching the internal steel frame. Poor bioavailability, need to be taken on an empty stomach, and commonly cause reflux. Used for up to 5 years.

Denosumab (Prolia) is a RANKL inhibitor, a synthetic version of OPG. Given as a subcutaneous injection every 6 months, it significantly reduces vertebral and hip fracture risk. The major limitation is a serious rebound effect: bone loss accelerates rapidly within 6 months of stopping treatment, returning to baseline. Women are typically transitioned onto bisphosphonates afterwards.

SERMs (selective oestrogen receptor modulators, such as raloxifene) act as oestrogen agonists in bone and antagonists in reproductive tissue. Used primarily in women with breast cancer. Effective for vertebral fracture prevention but doesn't reduce hip fracture risk, which is a significant limitation.

HRT is both a treatment and a prevention strategy. Transdermal oestradiol (patch at 0.25 micrograms twice weekly, or gel at 0.5 to 1mg daily) combined with micronised progesterone (100 to 200mg daily for continuous combined, or 200mg for 12 to 14 days cyclically) provides real, meaningful bone protection. Unlike bisphosphonates, HRT addresses both the oestradiol and progesterone pathways, supporting both OPG production and new osteoblast formation. The earlier you start, the more bone you preserve.

Anabolic agents (teriparatide, abaloparatide) are the only medications that actually build new bone rather than just slow its loss. They're PTH or PTHrP analogues, significantly increasing lumbar spine density over 18 to 24 months. Available on the NHS but only above a certain fracture-risk threshold. Maximum use is 24 months. All osteoporosis medications have a rebound effect when stopped, which is why transitions between treatments need to be carefully managed.

Romosozumab blocks sclerostin, the protein that inhibits osteoblast activity, and works via a dual mechanism: building bone and reducing resorption simultaneously.

Don't Overlook These

Before finishing, a few things that commonly get missed in clinical practice:

Medications that deplete bone: steroids, SSRIs, and PPIs all contribute to bone loss with long-term use. If any of these are part of your picture, that context matters.

Gut health and stomach acid: you cannot absorb calcium effectively without adequate stomach acid. If you're on a PPI, have Hashimoto's, a history of H. pylori, or pernicious anaemia, stomach acid is likely compromised and worth addressing.

Muscle mass: building muscle is the single most effective way to prevent falls, and preventing falls prevents fractures. Bone density matters, but muscle strength may matter even more for the outcomes we actually care about.

Perimenopause is the time to act. Not after a fracture. Not when your T-score hits -2.5. Now. The perimenopausal window, with its erratic and declining oestradiol and rapidly falling progesterone, is when bone loss accelerates most steeply. A DEXA scan, an honest conversation with a menopause-literate practitioner about HRT, a resistance training habit, and a diet that's genuinely rich in the nutrients above: that is the intervention.

If you'd like to explore bone health as part of a wider look at your hormones and perimenopause transition, that's exactly the kind of work we do at Vale of Health. You're very welcome to book a consultation.