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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent international agreement on the definitions of polycystic ovary syndrome (PCOS) has helped to clarify the clinical approach to diagnosis of PCOS. However, in the precise assessment of an individual patient it is still necessary for a detailed history of menstrual disorder (especially oligo- and amenorrhoea and anovulatory dysfunctional uterine bleeding), infertility or miscarriage, hyperandrogenism (mainly acne, hirsutism and scalp hair loss, distinguished from virilization) and obesity supplemented by the demonstration of polycystic ovaries on transvaginal ultrasound scanning. Assessment of endocrine changes in serum levels of luteinizing hormone, follicle stimulating hormone, oestradiol and prolactin, plus appropriate measures of circulating androgens (especially total and free testosterone, sex hormone binding globulin, 17 hydroxy-progesterone, dehydro-epiandrosterone sulphate and sometimes a 24-hour urinary free control) might help in further defining the abnormalities. Assessment of ovulatory status, obesity (body mass index and waist-hip ratio) and insulin resistance (oral glucose tolerance test with serum insulin levels) are also important in most cases. PCOS is a highly variable condition and investigation and management needs to be individualized. Long-term follow-up is also to a great extent dictated by the constellation of symptoms and clinical features of individual patients, but potential long-term hazards should be defined and patients warned of these.
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PMID:Current recommendations for the diagnostic evaluation and follow-up of patients presenting with symptomatic polycystic ovary syndrome. 1538 Jan 49

Oral exogenous estrogen raises C-reactive protein (CRP) concentrations, but the impact of endogenous hormones is unknown. We examined the cross-sectional relation of several serum hormones with CRP, fibrinogen, and white blood cell count - three inflammatory markers linked prospectively to coronary artery disease. Serum hormones were measured on a sample (n = 317) of postmenopausal female participants, with or without carotid intima-media thickening, in the Atherosclerosis Risk in Communities (ARIC) Study. Fibrinogen and white blood cell count were available on all and CRP in a subset (n = 57). Adjusted for age, race, and case-control status, mean CRP was 2-fold greater in the highest vs. lowest quartiles of estrone and androstenedione, and CRP was 2-fold less across quartiles of sex hormone binding globulin. These associations were not all statistically significant with this sample size. Fibrinogen and white blood cell count also were associated positively with estrone, androstenedione, and testosterone (and fibrinogen also with dehydroepiandrosterone sulfate). Adjustment for other risk factors and especially body mass index, a known determinant of endogenous hormone levels, attenuated most associations. In conclusion, several endogenous sex hormones may influence basal levels of inflammatory markers. Obesity appears to play a modulating role.
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PMID:Association of endogenous hormones with C-reactive protein, fibrinogen, and white blood count in post-menopausal women. 1633 33

Excessive visceral adiposity is associated with metabolic and reproductive abnormalities. Adipose tissue is an active endocrine gland and participates in multiple mechanisms in the reproductive function of women. The nature of the complex interaction of obesity with the female reproductive function remains a challenge. Several links have been implicated in the gonadal dysfunction of obese women, like insulin resistance and hyperinsulinemia, via which ovarian androgen production is stimulated resulting in hyperandrogenemia, increased peripheral aromatization of androgens to estrogens, altered gonadotrophin secretion, decreased sex hormone binding globulin, decreased GH and IGFBPs, increased leptin levels and altered neuroregulation of the hypothalamic-pituitary-gonadal axis. The impact of obesity in these mechanisms and their influence on female reproductive function are discussed in this article.
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PMID:Obesity and gonadal function of women. 1644 76

Nutrition is an important regulator of the tempo of growth and obesity is usually associated with tall childhood stature and earlier pubertal development. Several longitudinal studies have demonstrated that timing of puberty is most closely linked to infancy weight gain: suggesting an early window for programming of growth and development. Earlier puberty in the UK MRC 1946 birth cohort was related to smaller size at birth and rapid growth between 0 and 2 years. Rapid early weight gain leads to taller childhood stature and higher insulin-like growth factor I (IGF-I) levels, possibly through early induction of growth hormone (GH) receptor numbers, and such children are also at risk of childhood obesity. In the Avon Longitudinal Study of Parents and Children, rapid infancy weight gain was associated with increased risk of obesity at 5 and 8 years, with evidence of insulin resistance, exaggerated adrenarche and reduced levels of sex hormone binding globulin (SHBG). Potentially the elevated IGF-I and adrenal androgen levels, increased aromatase activity and increased 'free' sex steroid levels consequent to lower SHBG levels could all promote activity of the GnRH pulse generator. In addition obese children have higher leptin levels, a proven permissive factor in initiating LH pulsatility. Obesity could also affect the rate of progression through puberty as nutrition and SHBG may act respectively as an accelerator and brake on peripheral sex steroid action. Early weight gain and early pubertal development might also be associated with loss of the pubertal growth spurt perhaps through obesity-related suppression of GH secretion. Trans-generational recurrence of low birth weight, early catch-up weight gain, earlier menarche, and shorter adult stature have been observed in women, and could contribute to the strong heritability in age at menarche.
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PMID:Early and late weight gain and the timing of puberty. 1682 79

The unhealthy eating patterns and obesity among women in the U.S. are indicated by changes in biomarkers, such as insulin, lipoproteins, and estradiol, that are risk factors for breast cancer and cardiovascular diseases. This article models the inter-relations among diet, serum insulin, estradiol, and sex hormone binding globulin (SHBG) concentrations, plasma LDL and HDL cholesterol, and net triglyceride concentrations, using the data at baseline and 12 mo on 379 and 615 postmenopausal women in the Control and Intervention groups, respectively, of the Women's Health Trial: Feasibility Study in Minority Populations. Subjects in the Intervention group received detailed advice over a period of 1 y for reducing fat intakes and increasing the consumption of whole grains and fruits and vegetables. The main findings were that there were significant differences between the Control and Intervention groups in the changes from baseline to 12 mo in LDL and HDL cholesterol and SHBG concentrations. Second, using a comprehensive random effects modeling framework, the ratio of fiber to energy intake was significantly associated (P < 0.05) with lower insulin and triglyceride levels, and with a higher HDL cholesterol concentration in the Intervention group. Third, the subjects' waist-to-hip ratio and BMI were significantly associated with insulin, SHBG, LDL and HDL cholesterol, and triglyceride concentrations. Fourth, insulin levels were significantly negatively associated with SHBG and HDL cholesterol, and positively associated with LDL cholesterol, triglyceride, and estradiol concentrations. Overall, weight loss, especially around the waist, and increased fiber intakes are likely to be beneficial for lipid, cholesterol, and hormone profiles of U.S. women.
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PMID:Fiber intakes and anthropometric measures are predictors of circulating hormone, triglyceride, and cholesterol concentrations in the women's health trial. 1685 49

Prader-Willi syndrome (PWS) is a genetic disorder characterized by dysmorphic features, obesity, hypogonadism, hypotonia and mental retardation. Obesity has been linked to insulin resistance and the latter has also been associated with premature adrenarche. Since up to date a controlled study to investigate adrenarche and its hormonal regulation was lacking in PWS, our aim was to assess whether prepubertal PWS patients develop premature adrenarche and its relationship with markers of insulin sensitivity. Fourteen prepubertal children with PWS (6 M, 8 F) and 10 non-syndromal simple obese matched controls (5 M, 5 F) participated (mean age: 7.62 +/- 1.84 years). A fasting blood sample was obtained for adrenal and ovarian androgens, sex hormone binding globulin, insulin-like growth factor-I (IGF-I), insulin-like growth factor binding protein-1, leptin, adiponectin and a lipid profile. Thereafter an oral glucose tolerance test was performed. PWS patients were smaller at birth and a higher proportion displayed premature pubarche. No differences were found in testosterone, androstenedione, sex hormone binding globulin, free androgen index, homeostatic model assessment-IR, 2-hour insulin, leptin or adiponectin levels. 17-hydroxyprogesterone and DHEAS levels however, were significantly higher in PWS. IGF-I levels were significantly lower in PWS and correlated significantly with height SDS (p < 0.05). In conclusion, a higher proportion of premature adrenarche in our PW patients was observed, which was not explained by differences in insulin sensitivity or plasma levels of adipokines and IGF-I.
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PMID:Adrenarche in Prader-Willi syndrome appears not related to insulin sensitivity and serum adiponectin. 1708 44

American men have a lifetime risk of about 18% for prostate cancer diagnosis. Large international variations in prostate cancer risks and increased risks among migrants from low- to high-risk countries indicate important roles for environmental factors. Major known risk factors include age, family history, and country/ethnicity. Type 2 diabetes appears to reduce risk, while high birth weight and adult height are linked to increased risk of aggressive prostate cancer. Limited evidence supports an association with a history of sexually transmitted infections. A previous meta-analysis of eight cohort studies indicated no associations with plasma androgen, estrogen, or sex hormone binding globulin (SHBG) levels. However, there were dose-response relationships with baseline plasma testosterone levels in two studies that adjusted for other serum hormones and obesity. Finasteride (a drug that blocks testosterone activation) reduced prostate cancer risk by 25%. Low-frequency genes linked to familial prostate cancer only explain a small fraction of all cases. Sporadic cases were linked to relatively common polymorphisms of genes involved in (1) androgen synthesis, activation, inactivation and excretion, (2) hormone and vitamin D receptors, (3) carcinogen metabolism, and (4) DNA repair. Epidemiologic evidence supports protective roles for dietary selenium, vitamin E, pulses, tomatoes/lycopene, and soy foods, and high plasma 1,25-dihydroxyvitamin D levels. There is inadequate evidence that vegetables, fruit, carotenoids, and vitamins A and C reduce risk and that animal fat, alpha-linoleic acid, meat, coffee, and tea increase risk. Two major cohort studies found dose-response relationships with dietary calcium intake. Total dietary energy intake may enhance risk. Limited evidence supports a protective role for physical activity and elevated risk for farmers and other men with occupational pesticide exposure, particularly to organochlorine compounds and phenoxy herbicides. There is inadequate evidence for a relationship with alcohol or smoking. Most known or suspected external risk factors may act through hormonal mechanisms, but our review found little supporting evidence, and substantial further research is needed.
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PMID:Role of hormonal and other factors in human prostate cancer. 1836 55

The metabolic syndrome, a constellation of interrelated risk factors for cardiovascular disease and type 2 diabetes mellitus, has become a major public health concern against the backdrop of increasing rates of obesity. Insulin resistance plays a pivotal role as the underlying pathophysiological linchpin of the various components of the syndrome. The metabolic syndrome is well recognized in adults, and there is convincing evidence that it starts in childhood, with progressive clustering of the various components over time and tracking through adulthood. Adult women and adolescents with polycystic ovary syndrome (PCOS) have higher prevalence rates of the metabolic syndrome compared with the general population. Several anthropometric (obesity, particularly abdominal obesity), metabolic (insulin resistance/hyperinsulinemia, dyslipidemia) and hormonal (low IGFBP1, IGFBP2 and low sex hormone binding globulin) features of adolescents with PCOS are also features of the metabolic syndrome. Insulin resistance, believed to be a key pathogenic factor in both PCOS and the metabolic syndrome, may be the thread that links the two conditions. Menstrual health in adolescents could be viewed as yet another component in the evaluation of the metabolic syndrome. Careful assessment of menstrual history and appropriate laboratory work-up could reveal the presence of PCOS in obese at-risk adolescent girls with a family history of the metabolic syndrome.
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PMID:Menstrual health and the metabolic syndrome in adolescents. 1857 12

New and more active concepts of steroid binding globulin action are emerging from recent research. As a result, examination of steroid levels in aging humans and the role of steroid binding globulins need to be re-visited. This review will discuss the possibility that sex hormone binding globulin (SHBG) plays an active role in the aging process. It will discuss the changes in blood levels of SHBG in aging humans in association with sexual activity, prostate hypertrophy and cancer, uterine leiomyoma, breast cancer, obesity and particularly the relationship between SHBG and HDL-cholesterol, Alzheimer's disease, osteoporosis, and cardiovascular disease. Starting with the idea that SHBG is an active participant in steroid action demands a re-evaluation of data demonstrating a primary change in blood SHBG levels in association with various pathologies. Here we discuss the postulate that SHBG may act at its own receptor at the plasma membrane level to influence other receptors such as scavenger receptors and HDL-cholesterol receptors. We will also suggest that SHBG is a critical marker for mating and thus may be an important physiological molecule in control of aging.
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PMID:Sex hormone binding globulin and aging. 1895 1

Convincing evidence now supports a probable preventive role for physical activity in postmenopausal breast cancer. The mechanisms by which long-term physical activity affect risk, however, remain unclear. The aims of this review were to propose a biological model whereby long-term physical activity lowers postmenopausal breast cancer risk and to highlight gaps in the epidemiologic literature. To address the second aim, we summarized epidemiologic literature on 10 proposed biomarkers, namely, body mass index (BMI), estrogens, androgens, sex hormone binding globulin, leptin, adiponectin, markers of insulin resistance, tumor necrosis factor-alpha, interleukin-6, and C-reactive protein, in relation to postmenopausal breast cancer risk and physical activity, respectively. Associations were deemed "convincing," "probable," "possible," or "hypothesized" using set criteria. Our proposed biological model illustrated the co-occurrence of overweight/obesity, insulin resistance, and chronic inflammation influencing cancer risk through interrelated mechanisms. The most convincing epidemiologic evidence supported associations between postmenopausal breast cancer risk and BMI, estrogens, and androgens, respectively. In relation to physical activity, associations were most convincing for BMI, estrone, insulin resistance, and C-reactive protein. Only BMI and estrone were convincingly (or probably) associated with both postmenopausal breast cancer risk and physical activity. There is a need for prospective cohort studies relating the proposed biomarkers to cancer risk and for long-term exercise randomized controlled trials comparing biomarker changes over time, specifically in postmenopausal women. Future etiologic studies should consider interactions among biomarkers, whereas exercise trials should explore exercise effects independently of weight loss, different exercise prescriptions, and effects on central adiposity.
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PMID:Physical activity and postmenopausal breast cancer: proposed biologic mechanisms and areas for future research. 1912 76


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