Weight and Hormones
Obesity and Reproductive Hormones
Weight loss increases progesterone and leads to resumed ovulation in 87% of patients
Before and after a weight loss of at least 5% of initial body weight we analyzed LH, FSH, estrogen, prolactin, testosterone, DHEA-S, oral glucose tolerance test and progesterone, weight, BMI, waist/hip ratio and total body fat percentage. The mean weight loss was 9.5 kg, which represents a weight loss of 10.96% from initial body weight, with 26 patients (86.6%) resuming spontaneous ovulation. The women's mean plasma testosterone, LH, estradiol and DHEA-S decreased significantly and there was significantly increased on progesterone.
http://www.ncbi.nlm.nih.gov/pubmed/10544539
Being overweight lowers FSH, LH, inhibin B and estrogen
Overweight and obese fertile women have lower FSH, LH, inhibin B, and estradiol levels in the early follicular phase, with a possible direct inhibitory effect of body mass on gonadotropin and estradiol production, independently of age, insulin (concentrations and sensitivity), and other hormones.
Obesity lowers progesterone and LH
Reduced whole-cycle mean, normalized pregnanediol glucuronide (a measurement of progesterone) was observed in obese (38.2 . 2.1 .g/mg creatine) compared with normal-weight women (181.3 . 35.1 .g/mg creatine), without significant differences in LH, FSH, or estrone conjugate. Early follicular phase LH pulse frequency did not differ from normal weight women, but both amplitude and mean LH were dramatically reduced in obese women (0.8 . 0.1 and 2.0 . 0.3 IU/liter) comparedwith controls (1.6 . 0.2 and 3.4 . 0.2 IU/liter).
Higher BMI increases DHEAS and reduces SHBG
Concentrations of dehydroepiandrosterone sulfate (DHEAS) during follow-up were higher among girls with greater body mass index (BMI) at baseline. The mean for the lowest BMI quartile was 63.0 microg/dL compared with 78.8 microg/dL for the highest quartile, and each kg/m(2) increment in baseline BMI was associated with a 4.3% increase in DHEAS levels during follow-up. Concentrations of SHBG during follow-up were lower among girls with greater BMI at baseline. The mean for the lowest BMI quartile was 94.8 nmol compared with 57.5 nmol for the highest quartile, and each kg/m(2) increment in baseline BMI was associated with an 8.8% decrease in SHBG levels during follow-up. Estrogen and progesterone concentrations were similar across BMI quartiles. These findings suggest that adiposity may alter DHEAS and SHBG levels in girls.
Weight loss in infertile overweight women lowers LH, insulin, testosterone, boosts SHBG
We studied follicular phase LH and FSH secretion and glucose metabolism before and after weight reduction in 10 severely overweight infertility patients. A 6-week very low calorie diet was followed by a 4-week normocaloric period. We observed a decrease of 8% in percent body fat mass and a 5% reduction in waist to hip ratio. Mean LH decreased by 45%, whereas mean FSH remained unchanged. Insulin-stimulated glucose uptake increased by 41%, which was accounted for by a significant increase in nonoxidative glucose disposal. Serum sex hormone-binding globulin concentrations increased by 39%, and insulin-like growth factor (IGF)-binding protein-1 (IGFBP-1) levels increased by 46%. Fasting serum insulin concentrations decreased by 38%, those of leptin by 37%, those of androstenedione by 32%, those of testosterone by 20%, and those of dehydroepiandrosterone sulfate by 13%. The percent change in LH correlated negatively with glucose uptake and the increase in serum sex hormone-binding globulin and positively with the percent change in waist to hip ratio . The absolute LH levels after weight reduction correlated significantly with fasting insulin concentrations and negatively with glucose uptake. Our findings suggest that weight reduction with a very low calorie diet results in a decrease in LH concentrations, a reduction in the LH/FSH ratio, and FSH predominance favoring folliculogenesis. The decrease in LH concentrations is inversely related to the severity of insulin resistance. It is possible that the decrease in LH secretion with weight reduction is more dependent on the absolute levels of insulin sensitivity than on the degree of general adiposity.
Insulin Resistance and Miscarriage
Weight loss lowers estrogen, testosterone, LH and DHEA-S and increases progesterone
The aim of the current study was to evaluate the effect of a weight loss program on the clinical and hormonal characteristics of anovulatory obese women attending our reproductive clinic. The mean weight loss was 9.5 kg. which represents a weight loss of 10.96% from initial body weight, with 26 patients (86.6%) resuming spontaneous ovulation. The women's mean plasma testosterone, LH, estradiol and DHEA-S decreased significantly and there was a significant increase in progesterone.
http://www.ncbi.nlm.nih.gov/pubmed/10544539
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High BMI associated with low SHBG
Significant inverse correlations were found between estrogen and body mass index (BMI), SHBG and BMI, DHEA-S and dietary fiber, and androstenedione (the precursor of testosterone and estrogen) and protein:carbohydrate ratio.
http://www.ncbi.nlm.nih.gov/pubmed/15213709
Losing body fat lowers free testosterone by 4.3%; exercise induced weight loss lowers it 10.4%
Concentrations of testosterone and free testosterone among exercisers who lost between 0.5% and 2% body fat declined by 4.7% and 10.4%. In controls who lost this amount of body fat, concentrations of testosterone and free testosterone declined by only 2.8% and 4.3%.
http://cebp.aacrjournals.org/content/13/7/1099.abstract
Body fat secretes estrogen and stress hormones
A growing number of cytokines have been found to be released from adipose tissue, thus acting in an endocrine manner. These adipocytokines include not only, e.g., adiponectin, apelin, resistin, and visfatin, but also inflammatory cytokines and steroid hormones such as estrogens and glucocorticoids.
Obesity leads to disrupted menstrual cycles
This study shows that more than 20% of women with simple obesity have oligomenorrhea, and suggests that central fat accumulation seems to have a possible direct role in this menstrual alteration, independently of hyperinsulinemia and/or insulin resistance.
http://www.ncbi.nlm.nih.gov/pubmed/19411803
Obesity and Birth Defects
Obesity causes neural tube defects
Mothers who are obese when they get pregnant have a higher risk of serious birth defects of the brain and spine (neural tube defects).
http://www.cdc.gov/ncbddd/bd/research.htm
Obesity and Insulin Resistance
Weight loss leads to lower insulin and less inflammation
The subjects underwent a 3-month lifestyle program, including diet education, balanced diet with caloric restriction of 1,200 kcal/day, aerobic exercise (1 hour) twice weekly and jogging for at least 10,000 steps daily. Physical examination and blood tests were performed at the beginning and at the end of the study. RESULTS: A total of 29 subjects were included in the present study. Significant reductions were observed in body weight, BMI, abdominal circumference, hip circumference, systolic blood pressure, diastolic blood pressure, fasting insulin, total cholesterol, low-density lipoprotein cholesterol, triglycerides and high-sensitivity C-reactive protein. No significant differences were observed in the levels of fasting sugar, high-density lipoprotein cholesterol or homocysteine.
Insulin Resistance and Miscarriage
Obesity and Hypercoagulation
Losing weight leads to less coagulation
Obese women had significantly higher levels of leptin, von Willebrand factor, Factor VIIa, F1+2 compared with healthy women. Factor VIIa and von Willebrand factor were independently related to leptin levels. Reduction in adipose tissue after weight loss resulted in a decrease in both circulating leptin and endothelial and coagulative activation markers.
High fat diet leads to hypercoagulability
As compared to standard feeding, high fat diet feeding significantly increased plasma levels of coagulation factor VIII, combined factor II/VII/X , and plasminogen activator inhibitor-1 in mice, causing a prothrombotic shift of the coagulation profile.
High BMI, high cholesterol lead to increased blood coagulability
In premenopausal women the important modulators of von Willebrand factor activity (plays a major role in blood coagulation) were: body mass, serum total cholesterol and sex hormone binding globulin (SHBG) levels.
http://www.ncbi.nlm.nih.gov/pubmed/11603175
Obesity and Vitamin D
Obesity lowers vitamin D
Increased body weight has a significant negative effect on 25-OH- and 1,25-(OH)2-vitamin D concentrations, but no association with PCOS was observed.
http://www.clinchem.org/cgi/content/full/51/9/1691
Obesity and Thyroid
Obesity associated with subclinical hypothyroidism
Total T4 and free T4 decreased at higher BMI levels, which is consistent with subclinical hypothyroidism.
Calorie restriction improves thyroid function
Calorie restriction has been shown to improve both immune and thyroid function
Obesity and Adiponectin
Adiponectin levels go up as body weight goes down
Adiponectin is a protein hormone that modulates a number of metabolic processes, including glucose regulation and fatty acid catabolism. Adiponectin is exclusively secreted from adipose tissue into the bloodstream and is very abundant in plasma relative to many hormones. Levels of the hormone are inversely correlated with body fat percentage in adults, while the association in infants and young children is less clear. The hormone plays a role in the suppression of the metabolic derangements that may result in type 2 diabetes, obesity, atherosclerosis, non-alchoholic fatty liver disease and an independent risk factor for metabolic syndrome.
http://en.wikipedia.org/wiki/Adiponectin