Women and Lung Disease: the Statistics
Asthma: According to the CDC, over 60% of asthma patients in the US are female. Female asthmatics are 50% more likely to visit the physician, have more frequent hospitalizations and are 40% more likely to die from asthma than their male counterparts.
COPD: Although, the incidence of COPD is currently higher in men, it is on a steady rise for women due to an increased rate of smoking. Women, it appears, develop COPD more easily than men, with much less exposure and die more frequently from the disease. Despite a lower incidence, the number of women dying from COPD now surpasses men.
Cystic Fibrosis is a rare genetic disorder affecting both genders, but for unknown reasons life expectancy for women is shorter. Epidemiological data for lung diseases affecting women suggest the involvement of female hormones in meditating the onset of asthma, COPD, and CF.
Steroid Hormones: Background
Steroid hormones are made in the ovaries, adrenal glands, placenta (when pregnant), adipose (fat) tissue and even in the brain. Three major natural estrogens in women are estriol, estradiol, and estrone. Estriol is the predominant estrogen in pregnant women, while estradiol is the predominant form in the non-pregnant premenopausal women. Estrone is the predominant estrogen in menopausal women. For more information on hormones, click HERE.
Estradiol and progesterone concentrations fluctuate dramatically across the menstrual cycle, but also across pregnancy/postpartum and again at menopause.
Sex hormone binding globulin (SHBG) is an important steroid hormone binding protein in human plasma and regulates sex hormone delivery to tissues and cells. In healthy men and women, between 40-65% of circulating testosterone and between 20-40% of circulating estradiol is bound to SHBG. When the hormone is bound to SHBG it is considered inactive and, in that way, hormones bound to SHBG act much like reserve storage.
Why Hormones may be Linked to Lung Disease in Women
Before puberty the incidence of asthma is higher in boys than in girls, but following puberty, the pattern switches, and by adulthood, the prevalence of asthma is nearly 50% higher in women than in men. It is also well known that asthma severity fluctuates over the course of the menstrual cycle. As with asthma, menstrual cycles may also affect lung function in female patients with CF but not in the same phasic manner. Asthmatics demonstrate the best lung function in the peri-menstrual period, while female CF patients have the highest lung function during the luteal phase and the lowest lung function during the pre-ovulatory phase.
Researchers have found that fluctuating estradiol concentrations may, via some very specific mechanisms (estradiol inhibits Cl- secretion in the CF lung and up-regulates mucus production) impact lung function. Progesterone may also play a role in inflammatory airway disease by amplifying airway inflammation.
Not only do women have a higher prevalence of asthma, CF, and COPD, they appear to have worse prognoses than their male counterparts. The exact mechanism of this process is still uncertain. Emerging data suggest that female sex hormones play a role in these inflammatory airway conditions through different, but related, mechanisms. With the rise in the burden of these diseases worldwide, there is a pressing need to better understand the biological roles of sex hormones in modulating airway inflammation, mucus production and cigarette de-toxification and other processes relevant to COPD, asthma and CF.
Synthetic versus Endogenous Hormones
It is not clear from this review whether the risk for these diseases changes or is resultant from the use of synthetic hormones. Most of the studies reviewed did not account for hormonal contraceptives or hormone replacement therapies. Instead they looked receptor distribution and other variables that would fluctuate relative to cycling hormones. Additional research should be undertaken to disentangle the effects of endogenous hormones versus those associated with synthetic hormones. Particularly in the longer term, the effects at the receptor are likely to be different.
This article was originally published on Hormones Matter in May of 2012.