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How to Reverse Male Bone Loss

At-a-Glance:

  • By the time men reach their fifties, 27.5% have lost bone density, increasing to almost 41% by age 65.
  • Bone loss leads to 20% of all men breaking a bone in their lifetime.
  • Discover the most significant risks, recommended tests, and how to increase bone density and maintain strong bones. 
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By Dr. John Neustadt

Most of the focus on bone loss has been on women, but men are also at risk. By the time men reach their fifties, 27.5% have lost bone density, increasing to almost 41% by age 65 and beyond.1 This affects about 2 million men in the United States, contributing to an estimated 600,000 fractures annually.2 Bone loss leads to 20% of all men breaking a bone in their lifetime, but most men don’t even know they’re at risk because only 6% get a bone density test.3,4

Fracture Risk and Mortality

Several factors influence fracture risk in men, including bone mineral density (BMD), age, comorbidities, and lifestyle choices. While men generally have larger and stronger bones than women, they experience fractures later in life, often when they have other illnesses, leading to higher post-fracture mortality rates. 

Hip fractures in men are linked to a greater risk of life-threatening events and mortality compared to women. The mortality rate following a hip fracture in men is approximately twice that of women.5 

Low T

Testosterone plays a crucial role in maintaining male bone health by stimulating bone formation and promoting muscle growth. It is also converted into estradiol, which is essential for preserving bone mass and structure. 

Testosterone levels increase during puberty and then gradually decrease around the age of 40 at a rate of approximately 1% per year. Approximately 24% of men aged 30 to 79 have low total testosterone (< 300 ng/dL), a figure that rises to 30% by age 70.6 By age 80, more than 50% of men will have low testosterone, while studies indicate that 38% of men visiting doctors have low testosterone.7,8

As men age, the natural decrease in testosterone, referred to as andropause, causes uncomfortable symptoms, decreases the quality of life, and increases the risk of heart disease, osteoporosis, diabetes, obesity, arthritis, dementia, depression, low libido, strokes, and more. However, recent research shows that many more men, and at younger ages, are at risk for low testosterone (low T). 

Testosterone levels in American men are steadily declining. Scientists first noticed this in 2007, when a study of over 1,500 men reported a decrease in testosterone levels between 1987 and 2004 that could not be attributed to age, weight, illness, or lifestyle.9 Other studies have confirmed this trend.10 This decline adds to the gradual, inevitable loss of testosterone that occurs with aging, placing more men than ever at risk.

While there is still much to learn about why men’s testosterone levels are declining at younger ages, one potential cause identified by researchers is the significant increase in toxic chemicals in our environment. Many of these chemicals are endocrine disruptors that block and interfere with hormones.11

Low testosterone (Low T) decreases bone mineral density (BMD) and increases the risk of fractures. For example, a study involving men aged 65 and older found that those with low testosterone were twice as likely to have osteoporosis compared to men with normal testosterone levels. Additionally, testosterone deficiency in older men was associated with accelerated bone loss, particularly at the hip, which further heightens the risk of fractures.12

Testosterone replacement
Studies have also demonstrated the benefits of testosterone on bone health. Testosterone directly acts on osteoblasts to promote bone formation.13 Multiple clinical trials show that replacing testosterone in testosterone-deficient men increases bone density, quality, and strength. In a clinical trial involving 211 men with low testosterone, hormone replacement for one year resulted in a 6.8% increase in bone density.14 In another study, giving testosterone for 24 months led to a 7.4% increase in the men’s spine bone density and a 3.8% increase in the hips.15

Estradiol in men

Testosterone and estradiol work together to support bone health. Estradiol is transported throughout the body by sex hormone-binding globulin (SHBG); however, when it’s connected to SHBG, your cells cannot use it. For that to happen, estradiol must be present, but in its free, unattached form. This is called bioavailable estradiol (bioEs). 

A bioE2 level below 11 pg/mL (40 pmol/L) is associated with a heightened risk of male bone loss.16 Multiple studies have established this threshold as a critical level beneath which bone mineral density declines and bone turnover markers rise, leading to increased rates of bone loss and osteoporosis.17,18 Since the body converts testosterone into estradiol, measuring estradiol and ensuring it remains within a healthy range can assist doctors in determining whether to adjust the testosterone dosage. 

In rare cases, however, men might have a genetic inability to convert testosterone to estradiol—the CYP19A1 gene codes for the aromatase enzyme that facilitates this conversion. A genetic decrease in CYP19A1 causes low estradiol and bone loss. Even with testosterone replacement therapy, these men might still not be able to increase their testosterone levels high enough to build bone. In these cases, adding estradiol hormone replacement is necessary to improve bone density.19, 20 This genetic deficiency is rare, and the average age at diagnosis is 27 years. Thus, for most men, taking only testosterone replacement therapy should be enough to improve bone health.20

Men need to achieve an estradiol level greater than 20 pg/mL to increase bone density and reduce fracture risk. This was demonstrated in a man with low bone density who was genetically unable to convert testosterone to estradiol efficiently. Testosterone replacement alone did not improve his bone density, and his estradiol remained low. His bone density only improved after starting estradiol replacement therapy, at which point his bioE2 increased above 20 pg/mL.21 Notably, a study of 793 men confirmed that when a man’s serum estradiol exceeds 20 pg/mL, it is associated with a significantly lower risk of hip fractures.22

The role of Vitamin K

Multiple forms of vitamin K exist; however, the MK4 form is the predominant type that accumulates in tissues throughout the body. This includes the brain, blood vessels, bone, pancreas, and testes.23-25 MK4 has been shown to increase testosterone production in animals and significantly increase bone density in men.26,27

Other causes

Low hormone levels are not the only reason men lose bone density. Common causes include medications (e.g., prednisone, acid blockers), alcohol abuse, smoking, gastrointestinal diseases, and hyperthyroidism. Up to 60% of men with bone loss have one or more of these secondary causes.28 There is a strong gut-bone connection, and gastrointestinal dysfunction can compromise bone health. For example, bone loss occurs in up to 77% of individuals with inflammatory bowel disease (IBD). Patients with ulcerative colitis (UC) face a 41% higher risk of fractures compared to the general population, while patients with Crohn’s disease (CD) experience a 68% increased risk.29-31 If you have any other diagnosis, consult your healthcare provider to determine if it could increase your risk of osteoporosis and consider getting screened with a bone density test. 

Sarcopenia is the gradual loss of muscle, strength, and function, often occurring as people age. Skeletal muscle is essential for balance, strength, and stability, catching yourself when you stumble and preventing falls. The combination of sarcopenia and osteoporosis is known as osteosarcopenia. Muscle wasting in men predicts fractures more effectively than a bone density test, and men with osteosarcopenia face a 350% higher risk of fractures compared to those without this condition.32 Unfortunately, when a man with osteosarcopenia sustains a hip fracture, he has an 84% increased risk of dying compared to a man without osteosarcopenia.33

Fortunately, it’s never too late to build muscle. A clinical trial with volunteers 65 to older than 85 years showed that resistance exercise builds muscle. Twelve weeks of whole-body resistance exercises done three times a week significantly increased muscle mass and strength in all ages.34

To build muscle, it’s essential to get enough protein. Importantly, the amount needed increases as people age. Individuals aged 65 or older should consume about 0.60 grams of protein per pound of body weight daily, which is approximately 75% more than the US Recommended Daily Allowance (RDA) for protein.

Testing

If you are a man diagnosed with bone loss, you should have your testosterone and estradiol levels tested. Importantly, testing only total testosterone and total estradiol is not enough. You must also evaluate the levels of bioavailable hormones

Sex hormone-binding globulin (SHBG) and albumin bind testosterone and estrogen and transport them around the body. When the hormones are attached to these carrier proteins, your cells cannot use them. 

As men age, SHBG levels rise, resulting in lower bioavailable testosterone and estradiol levels.35 Therefore, even if the total levels of sex hormones are within a healthy range, you may still experience functional deficiency.

Instead, here is what should be ordered: 

      • Total testosterone
      • Free testosterone
      • Total estradiol
      • Bioavailable estradiol
      • SHBG

Additionally, if you’re a man 50 years or older who breaks a bone, the Bone Health and Osteoporosis Foundation (BHOF) recommends getting a bone density test. If you have low testosterone and/or estradiol or if you are taking a medication that damages bone and increases fracture risk, I also recommend getting a bone density test. 

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References
1 United States, 2017–2018, (2021). https://stacks.cdc.gov/view/cdc/103477

2 Finkelstein JS, Lee H, Leder BZ, et al. 2016;126(3):1114-25. 

3 Curtis JR, Carbone L, Cheng H, et al. 2008;23(7):1061-7. 

4 Compston J, Cooper A, Cooper C, et al. 2017;12(1):43. 

5 Sattui SE, Saag KG. 2014;10(10):592-602. 

6 Rohrmann S, Platz EA, Selvin E, et al. 2011;75(2):232-9. 

7 Seftel AD. 2014;191(3):751. 

8 Araujo AB, O’Donnell AB, Brambilla DJ, et al.  2004;89(12):5920-6. 

9 Bhasin S. 2007;92(1):44-5. 

10 Mazur A, Westerman R, Mueller U. 2013;8(10):e76178. 

11 Jeng HA. 2014;2:55. 

12 Fink HA, Ewing SK, Ensrud KE, et al. 2006;91(10):3908-15. 

13 Mohamad NV, Soelaiman IN, Chin KY. 2016;11:1317-1324. 

14 Katznelson L, Finkelstein JS, Schoenfeld DA, et al. 1996;81(12):4358-65. 

15 Benito M, Vasilic B, Wehrli FW, et al. 2005;20(10):1785-91. 

16 Rochira V, Kara E, Carani C. 2015:165215. 

17 Khosla S, Melton LJ, 2001;86(8):3555-61. 

18 Szulc P, Munoz F, Claustrat B, et al. 2001;86(1):192-9. 

19 Lanfranco F, Zirilli L, Baldi M, et al. 008;43(3):628-35. 

20 Rochira V, Carani C. 2009/10/01 2009;5(10):559-568. 

21 Jamall IS, Ullery MC, Rocchietti, et al. 2023;2023(2).

22 Amin S, Zhang Y, Felson DT, et al. 2006;119(5):426-33. 

23 Shearer MJ, Newman P. 2014 2014;55(3):345-362. 

24 Shearer MJ, Okano T. 2018;38:127-151. 

25 Konishi T, Baba S, Sone H. 1973;21(1):220-4. 

26 Ito A, Shirakawa H, Takumi N, et al. 2011;10:158. 

27 Sato Y, Honda Y, Kuno H, 1998;23(3):291-6. 

28 Björnsdottir S, Clarke BL, Mannstadt M, et al. 2022;36(3):101766. 

29 Bjarnason I, Macpherson A, Mackintosh C, et al. 997;40(2):228-33. 

30 Card T, West J, Hubbard R, 2004;53(2):251-5. 

31 Pollak RD, Karmeli F, Eliakim R, 1998;93(9):1483-90. 

32 Yu R, Leung J, Woo J. 2014;15(8):551-8. 

33 Yoo JI, Kim H, Ha YC, 2018;33(4):e27. 

34 Marzuca-Nassr GN, Alegría-Molina A, SanMartín-Calísto Y, et al. 2024 2024;34(1):11-19. 

35 Aribas E, Kavousi M, Laven JSE, 2021;106(10):2890-2900. 

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