Strong Bones, Strong Body, Stronger Second Half with Dr Jocelyn Wittstein - Part 2

Wittstein contrasts the rapid gains from exercise with medication timelines: an 8-month strength program can build 3% lumbar spine BMD, compared with 3 years of hormone therapy for a 5% gain. She cites LIFTMOR and the EPOS trial as evidence that periodized, supervised resistance training is profoundly effective. She personally does 'a couple of days a week of heavier strength training making sure you're doing large muscle groups.' She notes that these gains compound over time and that the return on investment in terms of time is substantial, especially when integrated with balance and impact work.

Wittstein loves jumping and explains that the EPOS trial included impact work. She references Tracy Glyold's basic science showing that jumping off an 8-inch step with a rebound produces sufficient impact. She personally does box jumps with a weightless jumper, noting that the jump up is a soft landing; the risky part is jumping down, so she steps off the box and then jumps again. She bundles agility and impact with cardio to save time. This practical approach makes the protocol accessible even for busy women.

Wittstein ties diet directly to the dietary inflammatory index, which she and the host have discussed. She explains that a less inflammatory diet correlates with lower fracture risk. This dovetails with her overall lifestyle-first message: hormone therapy and supplements only work optimally in the context of an anti-inflammatory diet. She doesn't prescribe a specific named diet but emphasizes fiber from diverse plant sources, reflecting her co-author's Galveston diet principles that also target inflammation.

Wittstein is transparent that there is not a study showing creatine directly builds bone. However, she sees it as a valuable adjunct because the secondary skeletal loading from increased muscle strength is beneficial. It's a low-risk, well-studied supplement that can help women break through strength plateaus, which is especially important during menopause when muscle anabolic resistance increases.

Wittstein underscores that while menopause specialists often treat hot flashes without measuring estradiol, bone specialists may insist on a level of 60 pg/mL. Her review of Menostar data and dose-response comparisons shows that even a 14 mcg patch yields significant bone protection, and 50 mcg is nearly as effective as 100 mcg. She cautions that HRT alone is insufficient without diet, exercise, and other nutrients. She also notes the WHI earlier data showed reduced joint pain with HT, though systematic reviews are mixed. She is personally on HRT and includes it in her bone protocol.

Wittstein notes most people struggle to get enough dietary calcium, so supplementation may be needed. She personally takes 2000 IU of vitamin D, which is above the minimal 600 IU, citing studies linking 2000 IU/day to reduced joint pain, dementia, and depression. She frames these micronutrients as non-negotiable partners to exercise and hormones for maximizing bone health.

Wittstein cites a study of ~9,000 subjects (5,000 women) that followed sex hormone levels and arthritis incidence. Lower testosterone levels in women were associated with higher risk of knee and hand arthritis, but no such link was found in men. She is now incorporating testosterone measurement into her upcoming cartilage resiliency study to see if it, along with estradiol and progesterone, protects cartilage. This could expand the conversation about hormone therapy to include testosterone.

She describes repurposing a machine-learning model developed for post-traumatic ACL arthritis. After 30 minutes of rest, a baseline MRI maps cartilage thickness. Then the subject walks 30 minutes on a treadmill to compress the cartilage, and serial MRIs over 30 minutes measure how quickly it returns to resting thickness. In healthy people rebound takes about 25 minutes; in ACL-injured knees it exceeds an hour. The new study will compare 50-something men and women with and without HT, measuring estradiol, progesterone, and testosterone. Her hypothesis: maintaining estrogen preserves that rebound capacity, potentially revealing HT's joint-protective effect. She is seeking $3M in funding.

Wittstein walks through the evidence: the marker study showed no extra benefit above 90 pg/mL (which approximates luteal phase levels). Yet the Menostar (14 mcg estradiol patch) trials proved that postmenopausal women with levels <20 pg/mL gained about 2.5% in lumbar spine density over two years, comparable to some osteoporosis drugs. Moreover, within the group under 20 pg/mL, those in the lowest quartile (lowest endogenous estrogen) had the greatest response to Menostar, indicating that the relative change matters. She compares 50 mcg vs 100 mcg patches: both yield around 5% spine density gains, so if a patient has side effects at 100, dropping to 50 is unlikely to compromise bone. This nuance is crucial for shared decision-making.

Wittstein notes that most hip fractures in older women happen at night when they get up with UTI-related urgency or delirium, leading to falls. She is studying her trauma center's last 500 hip fracture cases to see how many women had pre-op UTIs or were on vaginal estrogen. She explains that vaginal estrogen reduces UTI risk by about 50% but takes six weeks to rebalance the microbiome, so it's not a rescue post-fracture. Women diagnosed with UTI at the time of fracture have four times the rate of septic shock. She advocates educating fracture patients about vaginal estrogen to prevent contralateral fractures and is working to embed this thinking into her trauma service.