May 2019 Health Bulletin
New findings from the Grollo Ruzzene Foundation Young Women’s Health Study
Mrs Marina Skiba has presented our latest findings from the Grollo Ruzzene Foundation Young Women’s Health Study at the US Endocrine Society Annual Meeting in New Orleans, in the President’s Award Poster Session. The Study involves 6,986 women aged 18–39 years recruited from across Victoria, NSW and Queensland. 761 women who were not pregnant, breast feeding or taking any medication that would affect their menstrual cycles or hormone levels provided a blood sample. Sex steroids (oestrogens and androgens) were measured by Professor David Handelsman at the ANZAC Institute in Sydney. The sex steroids measured included what are considered classical androgens (testosterone, DHEA and androstenedione) and non-classical androgens (11-ketotestosterone and 11-ketoandrostenedione). The non-classical androgen 11-ketoandrostenedione has been reported to act like testosterone in cell studies.
This is the first study to report on levels of the non-classical androgens in detail in healthy premenopausal women.
The non-classical androgens did not change during the menstrual cycle whereas testosterone and androstenedione levels varied during the cycle and were lowest during the early part of the cycle (when women are menstruating). Blood levels of the nonclassical androgens were approximately 4-fold greater than testosterone and androstenedione.
Levels of all of classical and non-classical androgens declined between the aged of 18 and 39 years- testosterone declined by approximately 25% and 11-ketotestosterone by approximately 14%. This study shows that in premenopausal women a large proportion of circulating androgens is made up of nonclassical androgens. Whether these sex steroids have significant biological actions in healthy women remains to be determined.
Preventing osteoporosis, are we focusing on the correct risk factors?
It has been clearly established that having a low bone mineral density (BMD) measured by a DEXA scan is associated with a greater likelihood of a person having a low trauma fracture. However, bone density declines with age. Therefore, an important question is how much of the fracture risk in older people is a consequence of low bone density and how much is a result of ageing? Mai and colleagues have investigated this in the Dubbo Osteoporosis Study which included 2,320 women and 1,380 men, all aged 50 years and above at the time of study enrolment (average age 69 years)1. Over the 20-year follow-up 37% of women and 20% of men experienced a fragility fracture. In the first year of follow up approximately 20% of the risk of low trauma fracture could be attributed to low bone density, but by the 15th follow up year this attributable risk fell to 11%. However, when low bone density and advancing age were combined, these two factors explained 34% and 35% of the attributable risk in women and men respectively. Further analysis revealed the greatest component of the risk was advancing age. However, 2/3rds of the risk of fragility fracture was not explained by either osteoporosis or advancing aged in women and men over the age of 50 years. It is noteworthy in this study that approximately 73% of women and 94% of men who had had a fracture during follow-up were not osteoporotic at baseline according to the standard definition of a BMD T-score below -2.5.
The authors concluded that a significant health care burden of low trauma fracture is in people younger than 70 years and people without osteoporosis, such that “treatment of men and women with osteoporotic BMD is unlikely to reduce a large number of fractures in the general population”. They suggest fracture prevention needs to focus on people with other risk factors such as risk of falling and physical frailty.
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