Increased SHBG and not testosterone or estradiol is associated with bone loss and fractures

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Nelson Vergel

Founder, ExcelMale.com
This makes sense since higher SHBG would result in lower free estradiol which is probably the main factor in bone density. They do not mention the relation between free testosterone and bone.


Progressive Temporal Change in Serum SHBG, but not in Serum Testosterone or Estradiol, Is Associated with Bone Loss and Incident Fractures in Older Men: The Concord Health and Ageing in Men Project


ABSTRACT


This study aimed to examine progressive temporal relationships between changes in major reproductive hormones across three waves of a cohort study of older men and (a) changes in bone mineral density (BMD) and (b) incident fractures (any, hip or non-vertebral) over an average of 6-years follow-up. The CHAMP cohort of men aged 70 years and older were assessed at baseline (2005-07, n = 1705), 2-year (n = 1367) and 5-year follow-up (n = 958). Serum testosterone (T), dihydrotestosterone (DHT), estradiol (E2), and estrone (E1) (by liquid chromatography-tandem mass spectrometry (LC-MS/MS)), and of SHBG, LH and FSH (by immunoassay) were measured at all time-points, while free testosterone (cFT) was calculated using a well validated formula. Hip BMD was measured by dual X-ray absorptiometry (DXA) at all three time-points, and fracture data were verified radiographically. Statistical modeling was done using general estimating equations (GEE). For total hip BMD, univariable analyses revealed inverse associations with temporal changes in serum SHBG, FSH and LH and positive associations for serum E1 and cFT across the three time-points. In models adjusted for multiple covariables, serum SHBG (β = -0.029), FSH (β = -0.065), LH (β = -0.049), E1 (β = 0.019) and cFT (β = 0.033) remained significantly associated with hip BMD. However for femoral neck BMD, only FSH (β = -0.048) and LH (β = -0.036) remained associated in multivariable-adjusted models. Temporal change in serum SHBG, but not T, E2 or other hormonal variables, was significantly associated with any, non-vertebral or hip fracture incidence in univariable analyses. In multivariable-adjusted models, temporal increase in serum SHBG over time remained associated with any (β = 0.060) and hip fracture (β = 0.041) but not non-vertebral fracture incidence. These data indicate that a progressive increase in circulating SHBG over time predicts bone loss and fracture risk in older men. Further studies are warranted to further characterize changes in circulating SHBG as a mechanism and/or biomarker of bone health during male ageing.

http://onlinelibrary.wiley.com/doi/10.1002/jbmr.2904/abstract
 
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DragonBits

Well-Known Member
This makes sense since higher SHBG would result in lower free estradiol which is probably the main factor in bone density. They do not mention the relation between free testosterone and bone.


Progressive Temporal Change in Serum SHBG, but not in Serum Testosterone or Estradiol, Is Associated with Bone Loss and Incident Fractures in Older Men: The Concord Health and Ageing in Men Project

ABSTRACT


This study aimed to examine progressive temporal relationships between changes in major reproductive hormones across three waves of a cohort study of older men and (a) changes in bone mineral density (BMD) and (b) incident fractures (any, hip or non-vertebral) over an average of 6-years follow-up. The CHAMP cohort of men aged 70 years and older were assessed at baseline (2005-07, n = 1705), 2-year (n = 1367) and 5-year follow-up (n = 958). Serum testosterone (T), dihydrotestosterone (DHT), estradiol (E2), and estrone (E1) (by liquid chromatography-tandem mass spectrometry (LC-MS/MS)), and of SHBG, LH and FSH (by immunoassay) were measured at all time-points, while free testosterone (cFT) was calculated using a well validated formula. Hip BMD was measured by dual X-ray absorptiometry (DXA) at all three time-points, and fracture data were verified radiographically. Statistical modeling was done using general estimating equations (GEE). For total hip BMD, univariable analyses revealed inverse associations with temporal changes in serum SHBG, FSH and LH and positive associations for serum E1 and cFT across the three time-points. In models adjusted for multiple covariables, serum SHBG (β = -0.029), FSH (β = -0.065), LH (β = -0.049), E1 (β = 0.019) and cFT (β = 0.033) remained significantly associated with hip BMD. However for femoral neck BMD, only FSH (β = -0.048) and LH (β = -0.036) remained associated in multivariable-adjusted models. Temporal change in serum SHBG, but not T, E2 or other hormonal variables, was significantly associated with any, non-vertebral or hip fracture incidence in univariable analyses. In multivariable-adjusted models, temporal increase in serum SHBG over time remained associated with any (β = 0.060) and hip fracture (β = 0.041) but not non-vertebral fracture incidence. These data indicate that a progressive increase in circulating SHBG over time predicts bone loss and fracture risk in older men. Further studies are warranted to further characterize changes in circulating SHBG as a mechanism and/or biomarker of bone health during male ageing.

http://onlinelibrary.wiley.com/doi/10.1002/jbmr.2904/abstract

I was speculating that those with a higher SHBG level would be less affected by high estradiol levels.

But then I read the following research, which suggest that there maybe different SHBG variants. The SHBG that we measure mainly binds to testosterone while there may exist a variant of SHBG that binds with estradiol, and this variant is not being measured by any standard test.

Not only that, but the way estradiol behaving in morbidly obese men changes.

http://www.eje-online.org/content/176/4/393.full

In conclusion, our data point to SHBG as a globulin mainly centered in the control of testosterone levels, with estradiol regulation taking a markedly second place, or, simply, estradiol being controlled by a different SHBG variant. These data confirm the existence of different SHBG molecular species to discriminately bind estradiol and testosterone, previously reported in cirrhotic subjects (54). The sex-related differences in the relationships of binding vs levels of hormones and SHBG could not be explained by assuming that a single dimeric protein may experience the dramatic changes in affinity for testosterone and estradiol (differently for both, in fact) observed in women and men, and the marked differential effects of obesity on the ability of the same protein to bind testosterone and estradiol (Table 3).

Thus, we postulate that SHBG protein must be present in at least two different molecular species, or isoforms, to explain its differential function for both hormones, specially affected by sex and obesity. These conclusions suggest a much needed establishment of analytical procedures to identify these physiologically distinct forms of SHBG as the sole use of antibody-based measurements could not discriminate between them.
 
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