Menopause usually results from loss of ovarian follicular function due to ageing, but can also occur because of surgery, chemotherapy or radiation therapy. The number, type and intensity of symptoms of menopause may vary depending on factors, such as individual perception, obesity and other associated medical conditions.
It is suggested that the onset of menopause may be associated with decreased energy expenditure and fat oxidation, which together with an increase in total body fat and visceral abdominal fat, may predispose women to obesity, if lifestyle modifications are not made.
Obesity in the UK
A 2006 report showed that 24 per cent of adults in England were classified as obese and women are more likely to be morbidly obese than men (3 per cent compared with 1 per cent).
Using both BMI and waist circumference to assess risk of health problems, particularly cardiovascular disease and diabetes, 14, 16 and 23 per cent of women are at increased risk, at high risk and at very high risk respectively.1
In the past, it was thought that overweight women flushed less because androgen is converted to estrogen in adipose tissue.
However, findings from large epidemiological studies suggest that overweight women have 1.5 to two times increased odds of hot flushes and this risk increases with severity of obesity.2
Some studies have found that subcutaneous adiposity (the fat between skin and the abdominal muscle wall) rather than visceral abdominal adiposity (the fat behind the muscle wall and in the peritoneal space around the organs) is most related to hot flushes.
Modifiable factors, such as high BMI, may predispose a woman to more severe or frequent hot flushes.
This information may be valuable for identifying women at risk of hot flushes and for developing appropriate prevention strategies.
It is known that obesity significantly increases the risk of cardiovascular disease by impacting on several risk factors, such as diabetes, inflammatory mediators, such as CRP and lipid profiles.
Estrone, a weaker estrogen produced by the aromatisation of androstenedione, is the most abundant estrogen in postmenopausal women. In a study of 251 postmenopausal women aged 50 to 90 years, who were not using estrogen therapy, researchers analysed the correlation of BMI and blood levels of estrone with coronary artery disease.
Women with low estrone were older, slimmer, had less hypertension and diabetes and lower triglyceride and glucose levels. BMI was positively correlated with estrone levels, hypertension, and diabetes and inversely associated with HDL cholesterol.3
Metabolic syndrome is increasingly recognised as an important cardiovascular risk factor in women with hypertension. Women with metabolic syndrome have higher waist circumference, BMI, and levels of glucose, triglycerides and HDL cholesterol.
Hypertension, in the presence of a metabolic syndrome, in postmenopausal women, appears to confer a less favourable cardiovascular risk profile, characterised by significantly higher inflammatory markers, a more compromised endothelial function, and a significantly higher left ventricular mass, than hypertension alone.4
Interestingly, the metabolic diseases show a gender disparity with a 'female advantage' in the pre-menopausal women compared with men. However, women usually lose this 'protection' following menopause. They increase total body fat content, favouring the central body fat distribution, which is associated with increased cardiovascular risk.
Elevated BMI and oral treatment with estrogen both increase the risk of venous thromboembolism (VTE). Evidence suggests that transdermal estrogen appears safer with respect to VTE risk than oral estrogen (OR=1.1 (95 per cent CI: 0.7-1.7) and 4.5 (95 per cent CI: 2.6-7.7) respectively) and this risk is affected by BMI.
Among postmenopausal women the OR for VTE was 2.5 (CI: 1.7-3.7) for overweight women and 3.9 (CI: 2.2-6.9) for obesity. Compared with non-users with normal BMI, the combination of oral estrogen use and high BMI further enhanced VTE risk (OR=10.2 (CI: 3.5-30.2); and 20.6 (CI: 4.8-88.1) respectively).
However, transdermal estrogen users with increased BMI had similar risk as non-users with increased BMI.5
Pelvic organ prolapse
Pelvic floor disorders are associated with obesity, due to chronically increased abdominal pressure and neurogenic disease. They are also associated with urinary incontinence, which is increased by obesity.
Obese postmenopausal women suffer more from cystocele, rectocele and uterine prolapse than non-obese women. In the Women's Health Initiative study, most women gained weight and the rate of prolapse increased from 40.9 per cent at baseline to 43.8 per cent at year five.
Being overweight or obese at baseline was associated with progression in cystocele, rectocele, and uterine prolapse.6 Weight loss is not significantly correlated with regression of pelvic organ prolapse, suggesting that damage to the pelvic floor related to weight gain is irreversible.
Body fat mass is one of the most vital indices of obesity.
Evidence shows that fat mass may have beneficial effects on bone although protection against osteoporosis has not been demonstrated.
Obesity increases bone mass and maintaining higher levels of estrogen in obese postmenopausal women leads to an increase in bone density of the lumbar spine without changes in bone density of the proximal femur. However, this was not reflected by changes in the prevalence of vertebral, hip and non-vertebral fractures.
Studies have demonstrated a positive influence of obesity on bone density in the lumbar spine, femoral neck and trochanter, although this may be overtaken by the impact of age and estradiol deficiency. Therefore, these studies suggest that even obese postmenopausal women should be screened for osteoporosis.
Data from the Women's Healthy Lifestyle Project provide clear evidence that weight gain and increased waist circumference, along with elevations in lipid levels and other CHD risk factors, are preventable through the use of lifestyle intervention in healthy menopausal-aged women.
Given the prevalence and chronic course of obesity, weight gain prevention should be recognised as an important health goal for women before they approach menopause.
- Professor Lumsden is a professor of medical education and gynaecology, University of Glasgow, and an honorary consultant obstetrician and gynaecologist, NHS Greater Glasgow and Clyde. Dr Sassarini is a clinical research fellow, University of Glasgow
1. The Information Centre. Statistics on obesity, physical activity and diet. 2008.
2. Thurston RC. Menopausal Medicine. 2009; 17(1): s1-s6.
3. Silva TC, Barrett-Connor E, Ramires JA, et al. Maturitas 2008; 59(3): 242-8.
4. Rossi R, Nuzzo A, Origliani G,et al. Hypertension 2008; 52(5): 865-72.
5. Canonico M, Oger E, Conard J, et al. J Thromb Haemost 2006; 4(6): 1259-65.
6. Archer DF, Dupont CM, Constantine GD, et al. Am J Obstet Gynecol 2009; 200(3): 238e1-e10.