The typical onset of TS occurs at 6–7 years of age and is characterized by the appearance of simple, recurrent motor tics, followed by the manifestation of phonic tics after several months [12]. In most children, TS symptoms undergo a progressive exacerbation, which reaches its zenith at the beginning of puberty (11–12 years of age), and is then followed by a gradual remission in the majority of patients
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The implication of neuroactive steroids in Tourette syndrome pathogenesis: a ... - 0 views
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Multiple neurotransmitters have been implicated in TS, including dopamine (DA), serotonin, norepinephrine, acetylcholine, glutamate and γ-amino-butyric acid (GABA)
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the typical age of onset coincides with adrenarche (6–7 years old); symptoms increase in severity until the beginning of puberty (12 years old) and then undergo a spontaneous amelioration, which becomes apparent with the end of puberty (at 18–19 years of age)
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a number of clinical observations showed that tics in TS patients could be exacerbated by anabolic androgens
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steroidogenic enzymes and androgen receptors may serve as putative therapeutic targets for this disorder
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26% of females were found to experience exacerbation of tics in the estrogenic phase of the menstrual cycle, and this phenomenon was found to be correlated with increased tic severity at menarche
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biochemical hallmark of adrenarche is the acquisition of 17,20 lyase activity by cytochrome P450 C17 (CYP17A1)
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increased synthesis of dehydroepiandrosterone (DHEA) and androstenedione, which leads to the growth of axillary and pubic hair as well as enhancement in the oiliness of the skin
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interesting read on hormones and tourette's.. Proposed that 5 alpha reductase activity is involved in worsening of tics. This makes sense as Testosterone in men with low T is known to increase dopamine and dopaminergic dysfunction is known to play a role in tourette's; the clinical presentation of girls vs boys is very different. The authors of this article propose that 5 alpha reductase activity controls a back door method where by progesterone is converted to androgens.
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International Journal of Obesity - Abstract of article: Pubertal timing and adult obesi... - 0 views
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Association between Lead and Cadmium and Reproductive Hormones in Peripubertal U.S. Girls - 0 views
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The Effect of Fluoride on the Physiology of the Pineal Gland - 0 views
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Testosterone Concentrations In Young P... [Clin Endocrinol (Oxf). 2012] - PubMed - NCBI - 0 views
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obesity overweight men males boys low T low Testosterone low T testosterone estradiol hormone hormones insulin resistance
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Dihydrotestosterone Treatment in Adolescents with Delayed Puberty: Does it Explain Insu... - 0 views
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http://www.researchgate.net/profile/Costanzo_Moretti/publication/12777565_Leptin_and_an... - 0 views
www.researchgate.net/...02bfe50e5334207a93000000.pdf
leptin low T low Testosterone obese men male hormone hormones obesity
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Normal leptin levels are critical to puberty; but in obese men, increased leptin is associated with gonadal decrease in Testosterone. It appears to occur through a decrease in 17-OH progesterone to Testosterone: suggesting an inhibitory activity in the conversion of 17-OH progesterone to Testosterone in obese men.
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http://www.nature.com/ijo/journal/v24/n2s/pdf/0801281a.pdf?origin=publication_detail - 0 views
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SHBG IR insulin resistance insulin Estrogen Estradiol obesity hormone hormones
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Elevated insulin levels in men is associated with decreased liver production of SHBG and thus reduced SHBG levels. Obesity is associated with decreased urinary cortisol in this study. The authors found the low cortisol also contributed to the low SHBG as well. Low SHBG is associated with puberty, obesity, IR, hypothyroidism, and during androgen therapy. SHBG is increased as a result of aging, short-term fasting, Estrogen, hyperthyroid, and liver disease.
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Testosterone and glucose metabolism in men: current concepts and controversies - 0 views
joe.endocrinology-journals.org/...R37.full
Low T Testosterone metabolic syndrome MetS Diabetes men male glucose hormone hormones g
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Around 50% of ageing, obese men presenting to the diabetes clinic have lowered testosterone levels relative to reference ranges based on healthy young men
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The absence of high-level evidence in this area is illustrated by the Endocrine Society testosterone therapy in men with androgen deficiency clinical practice guidelines (Bhasin et al. 2010), which are appropriate for, but not specific to men with metabolic disorders. All 32 recommendations made in these guidelines are based on either very low or low quality evidence.
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A key concept relates to making a distinction between replacement and pharmacological testosterone therapy
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Findings similar to type 2 diabetes were reported for men with the metabolic syndrome, which were associated with reductions in total testosterone of −2.2 nmol/l (95% CI −2.41 to 1.94) and in free testosterone
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Cross-sectional studies uniformly show that 30–50% of men with type 2 diabetes have lowered circulating testosterone levels, relative to references based on healthy young men
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In a recent cross-sectional study of 240 middle-aged men (mean age 54 years) with either type 2 diabetes, type 1 diabetes or without diabetes (Ng Tang Fui et al. 2013b), increasing BMI and age were dominant drivers of low total and free testosterone respectively.
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both diabetes and the metabolic syndrome are associated with a modest reduction in testosterone, in magnitude comparable with the effect of 10 years of ageing
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In a cross-sectional study of 490 men with type 2 diabetes, there was a strong independent association of low testosterone with anaemia
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In men, low testosterone is a marker of poor health, and may improve our ability to predict risk
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It remains possible that low testosterone is a consequence of insulin resistance, or simply a biomarker, co-existing because of in-common risk factors.
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In prospective studies, reviewed in detail elsewhere (Grossmann et al. 2010) the inverse association of low testosterone with metabolic syndrome or diabetes is less consistent for free testosterone compared with total testosterone
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In a study from the Framingham cohort, SHBG but not testosterone was prospectively and independently associated with incident metabolic syndrome
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low SHBG (Ding et al. 2009) but not testosterone (Haring et al. 2013) with an increased risk of future diabetes
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In cross-sectional studies of men with (Grossmann et al. 2008) and without (Bonnet et al. 2013) diabetes, SHBG but not testosterone was inversely associated with worse glycaemic control
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SHBG may have biological actions beyond serving as a carrier protein for and regulator of circulating sex steroids
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In men with diabetes, free testosterone, if measured by gold standard equilibrium dialysis (Dhindsa et al. 2004), is reduced
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Low free testosterone remains inversely associated with insulin resistance, independent of SHBG (Grossmann et al. 2008). This suggests that the low testosterone–dysglycaemia association is not solely a consequence of low SHBG.
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Experimental evidence reviewed below suggests that visceral adipose tissue is an important intermediate (rather than a confounder) in the inverse association of testosterone with insulin resistance and metabolic disorders.
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testosterone promotes the commitment of pluripotent stem cells into the myogenic lineage and inhibits their differentiation into adipocytes
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testosterone regulates the metabolic functions of mature adipocytes (Xu et al. 1991, Marin et al. 1995) and myocytes (Pitteloud et al. 2005) in ways that reduce insulin resistance.
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Pre-clinical evidence (reviewed in Rao et al. (2013)) suggests that at the cellular level, testosterone may improve glucose metabolism by modulating the expression of the glucose-transported Glut4 and the insulin receptor, as well as by regulating key enzymes involved in glycolysis.
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More recently testosterone has been shown to protect murine pancreatic β cells against glucotoxicity-induced apoptosis
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Interestingly, a reciprocal feedback also appears to exist, given that not only chronic (Cameron et al. 1990, Allan 2013) but also, as shown more recently (Iranmanesh et al. 2012, Caronia et al. 2013), acute hyperglycaemia can lower testosterone levels.
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In men with prostate cancer commencing androgen deprivation therapy, both total as well as, although not in all studies (Smith 2004), visceral fat mass increases (Hamilton et al. 2011) within 3 months
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More prolonged (>12 months) androgen deprivation therapy has been associated with increased risk of diabetes in several large observational registry studies
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Testosterone has also been shown to reduce the concentration of pro-inflammatory cytokines in some, but not all studies, reviewed recently in Kelly & Jones (2013). It is not know whether this effect is independent of testosterone-induced changes in body composition.
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the observations discussed in this section suggest that it is the decrease in testosterone that causes insulin resistance and diabetes. One important caveat remains: the strongest evidence that low testosterone is the cause rather than consequence of insulin resistance comes from men with prostate cancer (Grossmann & Zajac 2011a) or biochemical castration, and from mice lacking the androgen receptor.
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Several large prospective studies have shown that weight gain or development of type 2 diabetes is major drivers of the age-related decline in testosterone levels
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there is increasing evidence that healthy ageing by itself is generally not associated with marked reductions in testosterone
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increased visceral fat is an important component in the association of low testosterone and insulin resistance
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The vast majority of men with metabolic disorders have functional gonadal axis suppression with modest reductions in testosterone levels
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men with Klinefelter syndrome have an increased risk of metabolic disorders. Interestingly, greater body fat mass is already present before puberty
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inhibition of the gonadal axis predominantly takes place in the hypothalamus, especially with more severe obesity
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Metabolic factors, such as leptin, insulin (via deficiency or resistance) and ghrelin are believed to act at the ventromedial and arcuate nuclei of the hypothalamus to inhibit gonadotropin-releasing hormone (GNRH) secretion from GNRH neurons situated in the preoptic area
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hypothesis that obesity-mediated inhibition of kisspeptin signalling contributes to the suppression of the HPT axis, infusion of a bioactive kisspeptin fragment has been recently shown to robustly increase LH pulsatility, LH levels and circulating testosterone in hypotestosteronaemic men with type 2 diabetes
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A smaller study with a similar experimental design found that acute testosterone withdrawal reduced insulin sensitivity independent of body weight, whereas oestradiol withdrawal had no effects
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Obesity and dysglycaemia and associated comorbidities such as obstructive sleep apnoea (Hoyos et al. 2012b) are important contributors to the suppression of the HPT axis
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Modifiable risk factors such as obesity and co-morbidities are more strongly associated with a decline in circulating testosterone levels than age alone
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55% of symptomatic androgen deficiency reverted to a normal testosterone or an asymptomatic state after 8-year follow-up, suggesting that androgen deficiency is not a stable state
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The hypothalamic–pituitary–testicular axis remains responsive to treatment with aromatase inhibitors or selective oestrogen receptor modulators in obese men
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Kisspeptin treatment increases LH secretion, pulse frequency and circulating testosterone levels in hypotestosteronaemic men with type 2 diabetes
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weight loss can lead to genuine reactivation of the gonadal axis by reversal of obesity-associated hypothalamic suppression
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There is pre-clinical and observational evidence that chronic hyperglycaemia can inhibit the HPT axis
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in men who improved their glycaemic control over time, testosterone levels increased. By contrast, in those men in whom glycaemic control worsened, testosterone decreased
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testosterone levels should be measured after successful weight loss to identify men with an insufficient rise in their testosterone levels. Such men may have HPT axis pathology unrelated to their obesity, which will require appropriate evaluation and management.
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Metabolic influences on neuroendocrine regulation of reproduction - 0 views
www.ncbi.nlm.nih.gov/...PMC3898855
metabolism metabolic regulation reproduction Leptin Ghrelin Insulin Kisspeptin GNRH
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Energy storage occurs mainly at the level of white adipose tissue, where adipocytes secrete the anorexigenic adipokine leptin
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humans and laboratory animals with leptin or insulin deficiency or resistance and/or increased ghrelin levels exhibit delayed or absent puberty and frequently display hypogonadotropic hypogonadism, which prevents fertility
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Ghrelin suppresses pulsatile gonadotropin-releasing hormone (GnRH) release [14,15], thus serving as a signal to suppress reproduction in times of famine
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Neuropeptides derived from POMC/CART neurons exert a potent anorectic action, thus decreasing food intake and body weight
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GnRH neurons have been shown to express insulin receptor mRNA and protein [27] and are activated by insulin
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Kisspeptins (encoded by KISS1) have been identified in the last decade as the most potent secretagogues of GnRH release.
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Effects of maternal dietary exposure to cadmium during pregnancy on mammary cancer risk... - 0 views
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Cadmium heavy metals pregnancy endocrine disrupting chemicals endocrine disruptors hormones puberty
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New aspects of cadmium as endocrine disruptor. [Environ Sci. 2006] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...16788562
cadmium heavy metals hormones estrogen receptors androgen endocrine disrupting chemicals endocrine disruptors puberty
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A strong association between biologically active testosterone and leptin in non-obese m... - 0 views
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There is a growing bulk of evidence suggesting that testosterone may influence leptin levels. Testosterone administration reduces leptin levels in hypogonadal27,28 and eugonadal men
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testosterone suppression by GnRH agonist treatment of central precocious puberty in boys increases leptin levels
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Testosterone levels decreased with increasing central obesity in healthy men, while they increase with increasing obesity in healthy women, the latter irrespective of menstrual status
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this could be due to obesity-related hyperleptinemia that inhibits testosterone secretion at the testicular level.46,47 These changes, which are proposed to be components of the insulin resistance syndrome,48 are associated with increased risk for cardiovascular disease in both men and women
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in the more obese subjects, the higher leptin levels due to increased adiposity might reduce secretion of testosterone
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loss of regulation of leptin by testosterone in obese men and women could be an important feature of the insulin resistance syndrome
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Bаsic Skin Cаre Routine | Get Beauty Tips On - 0 views
beautybycagla.com/0%B0sic-skin-c%D0%B0re-routine
hormones hormone cancer Testosterone Men inflammation Disease obesity Male low
shared by beautybycagla on 24 Mar 19
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Nathan healthy skin Growing up is something, everybody. You go through а lot of chаnges in your selection preference in clothes, of music, аnd so on аs you get older. However, your body undergoes а rаnge of chаnges thаt require the greаtest аmount of cаre аnd аttention. This is becаuse аt the stаrt of puberty, usuаlly between sixteen
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Get rid of the Stretch Marks | Best Stretch Marks Removal Laser Treatment - Pixigenus -... - 1 views
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Stretch marks are formed deep within the dermis layer and happen due to rapid stretching, this causes damage to the skin's connecting tissues. To get rid of these stretch marks we are introducing to you our latest laser treatment i.e. PIXIGENUS. It is a unique technology to eliminate stretchmarks from various parts of the body. Watch the full video to know more. Stretch marks are caused because of rapid stretching of the skin that results into scars and discoloration of the skin. There are many reasons which can lead to stretch marks such as rapid weight reduction, quick weight gain, excessive exercise, steroids, pregnancy, hormonal changes, puberty etc. Millions of women have stretch marks, but this fact does little to lessen the embarrassment that most women feel at the appearance of these unattractive striations on their skin. Stretch marks, also known as striae, are a form of scarring on the skin with an off-color hue. Over time they may reduce, but will not disappear completely. Tearing of the dermis results into stretch marks.
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Pharma Injectable Sust 250mg of the faculty Men's Health - 1 views
nhathuocnamkhoa.com/...pharma-sust-250mg
hormones hormone Testosterone Men health healthy men's PHARMA SUST
shared by trungtamnamkhoa on 25 Jun 19
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Pharma Sust 250mg injections treat hypogonadism disorders in men, after the illness, impotence due to lack of hormones, menstrual symptoms in men such as reducing sexual pleasure and physiological activities. Side effects: The drug can cause erectile dysfunction, signs of excessive sexual stimulation, reduced sperm count, decreased volume of ejaculation, water & salt retention. In pre-puberty boys: develop sex early, increase the frequency of erectile dysfunction, enlargement of the penis, and early growth of bone heads.
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Penis enlargement due to where? Cause And Treatment - 1 views
trungtamnamkhoa.com/n-duong-vat-noi-mun-trang.html
penis pimples white acne male men health healthy cancer Testosterone hormone
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The body of the white pimples is a common feature of boys entering puberty. Understanding their nature will help you no longer worry. White pimples on the penis and pores, squeezing out with a white core. Do these acne affect fertility? This top concern in many young people will be answered right after.