The link between anthropometric measurements and breast cancer risk in different studies remains uncertain [1–7]. In addition, results are influenced by multiple factors such as ethnicity, lifestyle, and reproductive status [6]. Overall, it is well established that obesity has an impact on breast cancer occurrence. It is important to distinguish two types of obesity—android (WHR > 0.8) in which fat is mainly distributed in the upper body (shoulders, abdomen) and gynoid (WHR < 0.8) where fat accumulates in the lower part of the body (buttocks, thighs) [18]. In persons with android obesity, metabolic and hormonal abnormalities are more pronounced.
In our data, pre- and postmenopausal women are overweight (with BMI > 25 kg/m2) without statistically significant differences between groups. According to our investigations, central obesity increases the risk of developing breast cancer in premenopausal women—these data are consistent with previous studies [1–3, 7, 17]. However, conversely to previous reports [2–5, 7], in postmenopausal women, its effect is neutral. It may be due to a general tendency toward android obesity in elderly women caused by decreasing levels of estrogen. Despite these factors, bad dietary habits and a lack of physical activity after menopausal transition also lead to visceral obesity.
In postmenopausal women, peripheral adipocytes are the source of all estrogens which are synthesized from the conversion of androstenedione. It means that general obesity is directly linked to an increased level of mitogenic factors within cancer cells [8, 10, 19]. Obese premenopausal women have lower estrogen levels due to the storage of estrogen in fatty tissue, decrease in ovarian activity, and frequent anovulatory cycles [1, 2]. Thus, general obesity is considered as a protection for breast cancer in premenopausal women. In contrast to previous investigations [3–7, 20], our study did not reveal a correlation between BMI and the risk of breast cancer or any statistical differences in BMI among both pre- and postmenopausal women.
The harmful effect of central obesity remains complex. This type of obesity is correlated with insulin resistance, increased level of insulin-like growth factor (IGF)-1, and fatty acids [2, 3, 7, 8, 21]. Insulin inhibits hepatic production of sex hormone-binding globulin (SHBG), elevates leptin levels, and diminishes adiponectin levels (both with angiogenic effect) [22]. Furthermore, insulin modulates VEGF expression [3, 15]. Together, these substances promote mammary carcinogenesis by accelerating cell divisions and inducing the synthesis of transcriptional factors. Obesity also induces “smoldering” inflammation causing a permanently elevated level of cytokines (TNF alpha, IL-6, CRP) which promote tumurigenesis [18, 22, 23].
In regard to body shape, women with breast cancer present an android type of silhouette with the distribution of fat tissue in the central and upper parts of the body which is revealed by increased shoulder width, waist circumference, skinfold thickness of the triceps and scapula, and differences in body proportions. Anthropometric indicators showed that women with breast cancer have narrower hips and shorter trunks and are shorter with broader arms—features which are typical for men. In premenopausal women, such characteristics are not so evident; however, they deteriorate after menopause. This is due to the high level of androgens postmenopause caused by a stimulation of androgen synthesis by IGF-1 in ovarian theca cells and a lower level of SHBG. It has been stated that the level of free testosterone increases with BMI [8, 10, 13] especially in android obesity [18, 24]. Androgens may promote growth by directly binding to the androgen receptors or estrogen receptors in breast tissue or via conversion to estrogen in either peripheral or breast fat tissue [14].
Statistically significant differences in the thickness of the skeleton between premenopausal and postmenopausal women with breast cancer are an unusual finding which has previously not been described in the literature. Compared to healthy individuals, breast cancer women had elevated widths of the wrist, elbow, knee, arm, and ankle and a bigger thorax. The most substantial event during menopausal transition is decreasing ovarian activity resulting in deficient estrogen levels. The latter causes many menopausal symptoms such as a loss of bone mass [25]. It is highly probable that in overweight women this situation is inverted. Constant higher estrogen exposure during lifetime contributes to faster bone maturation which begins in adolescence. There is also an impact of the elevated level of IGF-1 (one of the mitogenic factors) [26]. In adults, estrogen diminishes bone resorption by inhibition of osteoclasts. In overweight women with breast cancer, this effect is amplified by elevated levels of androgens which also have beneficial effects on bone tissue [27]. Androgens act either by conversion to estrogen via p450 aromatase enzyme complex or by directly binding to androgen receptors. Interestingly, androgens are responsible for the periosteal expansion of bones which may be a direct explanation of our findings [27]. However, it is necessary to mention that central obesity leading to metabolic complications and inflammation may be also associated with poor bone health [28].
Study limitations and future research
The anthropometric measures used in the present study have some limitations. Firstly, BMI is not a homogenous parameter especially in comparison to modern techniques used in order to assess fat distribution such as the following: dual-energy X-ray absorptiometry (DXA), bioelectrical impedance analysis (BIA), or air displacement plethysmography. It may be misleading in individuals with normal BMI but a high content of body fat. Secondly, WHR may be also an inadequate index as it is under the influence of confounding factors such as age-related variation in muscle mass and tone.
Anthropometric measurements may be miscalculated due to bias during examination (problems in taking some measurements, non-cooperative patients, etc.). The present results are confounded by variables such as differences in age between groups, different stage of the disease, and the method used for selecting the control group. Nonetheless, the present results highlight significant body parameter changes which could be of great value in assessing breast cancer risk.
The present study highlighted some interesting avenues of future research. The bone strengths between overweight breast cancer women are another area which has yet to be explored in depth. Furthermore, the influence of testosterone on breast tissue is an interesting issue particularly after consideration of its estrogen-independent role which merits further investigation.