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

In the search for possible causes for the enormous increase in testicular cancer incidence in Denmark, we tested the hypothesis that a high fat or calorie intake in adolescence and consequently relative obesity is a promotional factor for testicular cancer. A total of 438 cases and three controls for each case were included in the study. Data originated from health examination of men liable for military service. Data were analysed by logistic regression analysis. No systematic statistically significant differences in body measurements [height, weight and body-mass index (weight/height2)] could be shown. Rather than being obese a slight trend was observed towards the future victims of testicular cancer being lighter, smaller and thinner than unaffected controls.
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PMID:Body size and cancer of the testis. 236 39

The relationship of risk of testis cancer, and subdivisions of the tumour by histology, to variables which may be related to hormonal status, sexual behaviour and fertility was investigated in data from a case-control study with 259 cases and 2 sets of controls. No consistent association was found between testis cancer risk and age at puberty, need to shave, obesity, alcohol intake, animal fat intake, and sexual behaviour. There was a significant excess of seminomas in very tall men. Testis cancer cases showed lower fertility than controls according to various measures, but this reflected the greater frequency of cryptorchidism among cases compared to controls. Among non-cryptorchid subjects there was no clear evidence that infertility was associated with risk of testis cancer.
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PMID:Testis cancer: post-natal hormonal factors, sexual behaviour and fertility. 253 27

Although a rare tumor, testicular cancer shows substantial international variation in incidence. In whites, the peak incidence occurs at 25-30 years of age, with a second increase in old age. Blacks have much lower rates than do whites. The rate of increase in the incidence and mortality of this cancer has been consistent but low during the past 40 years. Risk factors identified in epidemiology studies of testicular cancer include cryptorchidism (best documented), inguinal hernia, testicular injury, wearing of tight-fitting underclothing, obesity, maternal use of exogenous estrogens during pregnancy, higher social class, and professional occupations. Epidemiological evidence provides two etiologic hypotheses: a relative hormone imbalance, particularly an excess of estrogen, and a failure of normal thermal regulation of the testis. In the Pacific Basin region, notable variation in incidence rates is also seen. High-risk populations include whites, Polynesians (in Hawaii and New Zealand), and Native Alaskans. Low-risk groups include Filipinos (in Hawaii and Manila), Japanese (in Hawaii and Japan), Indians, and Malays. Most of this variation occurs in the younger ages (0-54 yr). Several areas for potentially fruitful research on this cancer in the Pacific region are given.
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PMID:Epidemiology of testicular cancer in the Pacific Basin. 716 80

In spite of the improvement on chemotherapy results in treating testicular cancer and the introduction of adjuvant chemotherapy to node negative (as well as node positive) breast cancer patients, there is still present a wide spectrum of early and late toxic manifestations. The combination of cisplatin, vinblastine and bleomycin given to testicular cancer might result in cariovascular, neurological, gastrointestinal and renal problems. Late effects of cyclophosphamide, methotrexate and 5-fluorouracil given to breast cancer patients might cause obesity, amenorrhea and infertility. We report a persistent asymptomatic indirect hyperbilirubinemia which was observed in two cancer patients (breast; testis) 3 and 14 months following the cessation of chemotherapy. Metastatic liver disease and involvement of other sites, as well as other causes of hyperbilirubinemia, were excluded. The exact cause of the indirect hyperbilirubinemia remained obscure.
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PMID:Chemotherapy-related persistent indirect hyperbilirubinemia. 788 4

The original 'oestrogen hypothesis' postulated that the apparent increase in human male reproductive developmental disorders (testis cancer, cryptorchidism, hypospadias, low sperm counts) might have occurred because of increased oestrogen exposure of the human foetus/neonate; five potential routes of exposure were considered. This review revisits this hypothesis in the light of the data to have emerged since 1993. It addresses whether there is a secular increasing trend in the listed disorders and highlights the limitations of available data and how these are being addressed. It considers whether new data has emerged to support the suggestion that increased oestrogen exposure could cause these abnormalities and reviews new data on potential routes via which such increased exposure could have occurred. Secular trends: The disorders listed above are now considered to represent a syndrome of disorders (testicular dysgenesis syndrome, TDS) with a common origin in foetal life. Testicular cancer has increased in incidence in Caucasian men worldwide and lifetime risk is 0.3-0.8%. Secular trends in cryptorchidism are unclear but it is by far the commonest (2-4% at birth) congenital abnormality in either sex. Secular trends for hypospadias are not robust, although most studies suggest a progressive increase; registry data probably under-estimates incidence, but based on this data hypospadias is the second most common (0.3-0.7% at birth) congenital malformation. Retrospective analyses of sperm count data show a global downward trend but this is inconclusive - prospective studies using standardized methodology show significant differences between countries and very low sperm counts in the youngest cohort of men. For all disorders, other then testis cancer, standardized prospective studies are the best way forward and are in progress across Europe. Oestrogen effects: Evidence that foetal exposure to oestrogens can induce the above disorders has strengthened. New pathways via which such changes could be induced have been identified, including suppression of testosterone production by the foetal testis, suppression of androgen receptor expression and suppression of insulin-like factor-3 (InsL3) production by foetal Leydig cells. Other evidence suggests that the balance between androgen and oestrogen action may be important in induction of reproductive tract abnormalities. Oestrogen exposure: Although many new environmental oestrogens have been identified, their uniformly weak oestrogenicity excludes the possibility that they could induce the above disorders. However, emerging data implicates various environmental chemicals in being able to alter endogenous levels of androgens (certain phthalates) and oestrogens (polychlorinated biphenyls, polyhalogenated hydrocarbons), and the former have been shown to induce a similar collection of disorders to TDS. Other mechanisms via which increased fetal exposure to pregnancy oestrogens might occur (increasing trend in obesity, dietary changes) are also discussed.
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PMID:The 'oestrogen hypothesis'- where do we stand now? 1253 32

Metabolic syndrome is characterized by insulin insensitivity, central obesity dyslipidemia, and hypertension. It is recognized as a risk factor for cardiovascular disease in men; by the time metabolic syndrome is diagnosed, however, most men already have entrenched cardiovascular disease. A reliable early warning sign is needed to alert physicians to those at risk for metabolic syndrome and cardiovascular disease. Low serum testosterone level has emerged as a reliable prognosticator of metabolic syndrome in men whose testosterone deficiency is genetic (Klinefelter syndrome), iatrogenic following surgery for testicular cancer, pharmacologically induced by gonadotropin-releasing hormone during prostate cancer treatment, or a natural consequence of aging. One third of men with type 2 diabetes mellitus are now recognized as testosterone deficient. Emerging evidence suggests that testosterone therapy may be able to reverse some aspects of metabolic syndrome.
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PMID:Testosterone, diabetes mellitus, and the metabolic syndrome. 1804 26

Changes in puberty timing have implications for the treatment of individual children, for the risk of later adult disease, and for chemical testing and risk assessment for the population. Children with early puberty are at a risk for accelerated skeletal maturation and short adult height, early sexual debut, potential sexual abuse, and psychosocial difficulties. Altered puberty timing is also of concern for the development of reproductive tract cancers later in life. For example, an early age of menarche is a risk factor for breast cancer. A low age at male puberty is associated with an increased risk for testicular cancer according to several, but not all, epidemiologic studies. Girls and, possibly, boys who exhibit premature adrenarche are at a higher risk for developing features of metabolic syndrome, including obesity, type 2 diabetes, and cardiovascular disease later in adulthood. Altered timing of puberty also has implications for behavioral disorders. For example, an early maturation is associated with a greater incidence of conduct and behavior disorders during adolescence. Finally, altered puberty timing is considered an adverse effect in reproductive toxicity risk assessment for chemicals. Recent US legislation has mandated improved chemical testing approaches for protecting children's health and screening for endocrine-disrupting agents, which has led to changes in the US Environmental Protection Agency's risk assessment and toxicity testing guidelines to include puberty-related assessments and to the validation of pubertal male and female rat assays for endocrine screening.
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PMID:Public health implications of altered puberty timing. 1824 14

Along with the growing epidemic of obesity, the risk of atherosclerosis, cardiovascular disease morbidity, and mortality are increasing markedly. Several risk factors for cardiovascular disease, such as visceral obesity, glucose intolerance, arterial hypertension, and dyslipidemia commonly cluster together as a condition currently known as metabolic syndrome. Thus far, insulin resistance, and endothelial dysfunction are the primary events of the metabolic syndrome. Several groups have recommended clinical criteria for the diagnosis of metabolic syndrome in adults. Nonetheless, in what concerns children and adolescents, there are no unified definitions, and modified adult criteria have been suggested by many authors, despite major problems. Some pediatric disease states are at risk for premature cardiovascular disease, with clinical coronary events occurring very early in adult life. Survivors of specific pediatric cancer groups, particularly acute lymphocytic leukemia, central nervous system tumors, sarcomas, lymphomas, testicular cancer, and following bone marrow transplantation, may develop metabolic syndrome traits due to: hormonal deficiencies (growth hormone deficiency, thyroid dysfunction, and gonadal failure), drug or radiotherapy damage, endothelial impairment, physical inactivity, adipose tissue dysfunction, and/or drug-induced magnesium deficiency. In conclusion, some primary and secondary prevention remarks are proposed in order to reduce premature cardiovascular disease risk in this particular group of patients.
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PMID:Detection of metabolic syndrome features among childhood cancer survivors: a target to prevent disease. 1906 99

It has been hypothesized that poor semen quality, testis cancer, undescended testis, and hypospadias are symptoms of one underlying entity--the testicular dysgenesis syndrome--leading to increasing male fertility impairment. Though testicular cancer has increased in many Western countries during the past 40 years, hypospadias rates have not changed with certainty over the same period. Also, recent studies demonstrate that sperm output may have declined in certain areas of Europe but is probably not declining across the globe as indicated by American studies. However, at the same time, there is increasing recognition of male infertility related to obesity and smoking. There is no certain evidence that the rates of undescended testes have been increasing with time during the last 50 years. In more than 95% of the cases, hypospadias is not associated with cryptorchidism, suggesting major differences in pathogenesis. Placental abnormality may occasionally cause both cryptorchidism and hypospadias, as it is also the case in many other congenital malformations. The findings of early orchidopexy lowering the risk of both infertility and testicular cancer suggest that the abnormal location exposes the cryptorchid testis to infertility and malignant transformation, rather than there being a primary abnormality. Statistically, 5% of testicular cancers only are caused by cryptorchidism. These data point to the complexity of pathogenic and epidemiologic features of each component and the difficulties in ascribing them to a single unifying process, such as testicular dysgenesis syndrome, particularly when so little is known of the actual mechanisms of disease.
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PMID:What is new in cryptorchidism and hypospadias--a critical review on the testicular dysgenesis hypothesis. 2092 Jul 35

Nutrient composition, particularly the omega-6/omega-3 polyunsaturated fatty acids ratio, may differently affect inflammatory mediators production in tissues, which could be causally related to increased cancer incidence in obesity. We evaluated prostaglandin E(2) levels in male Wistar rat prostate, kidney and testicle tissues after 15 days of either a high fat, cafeteria-style diet (5.50 Kcal/g, 30 percent calories from fat, omega-6/omega-3 ratio 2.33) or a standard laboratory chow diet (3.35 Kcal/g, 3 percent calories from fat, omega-6/omega-3 ratio 0.56). In the cafeteria diet compared to standard laboratory diet rats, we found both an increase in weight gain and increased prostaglandin E(2) (PGE(2)) levels in prostate, kidney and testicle tissues. The increased levels of PGE(2) induced by the cafeteria diet could drive an inflammatory process leading to increased incidence of prostate, kidney and testicular cancer in overweight patients.
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PMID:Cafeteria diet increases prostaglandin E2 levels in rat prostate, kidney and testis. 2124 56


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