What is Included in the Profile?
Estradiol (E2) at optimal physiological levels in women promotes a healthy distribution of fat in hips, thighs, breasts, and subcutaneously. However, in excess, and in the absence of progesterone, estrogen predisposes to unhealthy surplus weight gain in these tissues. Men generally have much lower levels of estradiol and higher testosterone, which is responsible for greater muscle mass and less fat distribution in areas of the body normally seen in women. In overweight men testosterone levels drop and estrogens rise leading to the same problematic weight gain in the hips, thighs, and breasts (referred to as gynecomastia) as seen in women.
Progesterone (Pg) in addition to its primary role in attenuating the effects of excess estrogen in the body by downregulating estrogen receptors, aids weight management by acting as a natural diuretic. Its natural calming effects in the brain may also reduce stress-related overeating and food cravings. As a mineralocorticoid receptor antagonist, progesterone counteracts the effects of mineralocorticoid activation, which include the stimulation of fat cell formation, increased body weight, and release of inflammatory cytokines.Excessive supplementation with progesterone to higher than normal levels can increase appetite and also slow the rate of food emptying from the stomach and moving through the digestive tract, causing slower digestion and bloating.
Testosterone (T) and DHEA-S (DS) are androgens that increase lean muscle mass and metabolic rate. As androgen levels decline, muscle mass also decreases with a corresponding increase in adiposity. Low androgens can also reduce vitality and tolerance for exercise. Weight gain itself, with its resulting hormone imbalances, can trigger a drop in testosterone as the aromatase enzyme within fat tissue converts androgens to estrogens. In men this contributes to a female-type body fat distribution, including breast tissue development. In women with polycystic ovarian syndrome (PCOS), high testosterone and DHEA are linked to insulin resistance and weight gain, particularly in the abdomen.
Cortisol (C) imbalances can create problems with blood sugar control, sleep patterns, appetite, food cravings, and tolerance exercise. Under stress, excessive cortisol production particularly in concert with insulin, promotes fat storage in abdominal adipose tissue. This visceral type of fat is closely associated with insulin resistance and metabolic syndrome and thus more hazardous to health. Chronically elevated cortisol is a known risk factor for pre-diabetes and cardiovascular disease.
Thyroid Stimulating Hormone (TSH) elevations,
even within the high-normal range, are linked with hypothyroidism, low metabolic rate and obesity. Hypothyroidism is linked to elevated cortisol and can also be a consequence of oral estrogen therapy, which increases the production of binding proteins that reduce thyroid hormone bioavailability.
Vitamin D (D2, D3) deficiency is common in obesity and particularly associated with hyperinsulinemia and visceral fat. Whether by cause or effect, identifying and correcting vitamin D3 deficiency may improve insulin sensitivity.
Fasting Insulin (In), when elevated, is a marker of insulin resistance which precedes metabolic syndrome, PCOS, and type 2 diabetes. Increased levels, particularly
in concert with cortisol lead to central obesity and increased inflammatory and other cardiovascular disease markers. Hyperinsulinemia also contributes to decreased testosterone levels in men, but increased testosterone and decreased ovulation in women.