Diane E. J. Stafford

The International Olympic Committee Consensus Statement on age determination in high-level young athletes

Most youth sports around the world are classified on the basis of chronological age to guarantee equal chances within each of the different age groups. At the elite level, international sporting federations organise competitions in various age classes ranging from as low as under-13 up to under-21, depending on the sport. In August 2010, the International Olympic Committee (IOC) is conducting the first Youth Olympic Games in Singapore for 14–18-year-old athletes. The standing of these youth competitions has increased to the stage at which there may be considerable rewards, individual fame or national prestige associated with winning, not only for the athlete but for the coach and his or her entourage. These competitions also represent important showgrounds for young athletes; in some sports, this is often where talented athletes are identified for a future professional career. Unfortunately, in a number of sports it is suspected that the chronological age of the participating players is higher than the age stated on the official documents used to determine the eligibility of the individual. Players with a greater relative age are more likely to be identified as talented because of the likely physical advantages they have over their ‘younger’ peers.1 International sporting federations have uncovered several cases of document fraud, presumably aimed at allowing over-age athletes to gain a performance advantage by competing in a lower age class. At the other end of the spectrum, there are also documented cases of under-aged athletes competing in events in which there is a lower age limit (eg, the age of 14 years in the Olympic Games); particularly in sports in which late maturers may be at an advantage, such as in gymnastics. It should be noted that the participation of over-age or under-age athletes is not always due to intentional cheating. To verify age, …

Altered Hypothalamic-Pituitary-Ovarian Axis Function in Young Female Athletes

Young women have become increasingly active in athletics during the 20th century. Those involved in sports that emphasize lean body type are at high risk for the development of menstrual dysfunction, including amenorrhea. This is mediated by an alteration in function of the hypothalamic-pituitary-ovarian (HPO) axis, with loss of normal secretion of luteinizing hormone, and subsequent lack of estrogen production. Disruption of the HPO axis appears to be dependent on the body’s recognition of an energy imbalance, which may be due to a lack of compensatory caloric intake in the face of significant energy expenditure. Other pituitary hormones, such as triiodothyronine, growth hormone, and insulin-like growth factor-1 may also be affected. These metabolic changes have an impact on bone mineralization during a critical period in the development of bone mass.Recognition by physicians of the so-called ‘female athlete triad’, consisting of disordered eating, amenorrhea, and osteoporosis, may allow therapeutic intervention. Diagnosis of eating disorders and decreased bone mineral density can have significant impact on the health of the young athlete. Treatment is aimed at restoring normal menstrual function by increasing caloric intake to balance the increased energy demands of athletic participation. Concurrent treatment of the hypoestrogenemic state using estrogen replacement is controversial, but may aid in alleviating further loss of bone mass.

Adolescent androgen abnormalities.

Purpose of review Polycystic ovary syndrome is one of the most common endocrinopathies affecting premenopausal women. This review focuses on this major cause of hyperandrogenism in adolescents and young women, highlighting new diagnostic and therapeutic strategies that are under investigation. The pathophysiologic role in the disorder are the subject of several recent reports. Recent findings Recent studies have found a 33% prevalence of abnormal glucose tolerance in a cohort of affected adolescents, higher fasting insulin levels and lower insulin sensitivity, and that glucose tolerance testing appears to be necessary for routine screening. The effects of hyperinsulinism may be counteracted by insulin sensitizing agents. In adult women with polycystic ovary syndrome, metformin treatment reduced hyperinsulinemia and hyperandrogenemia. In some obese adolescents, metformin therapy resulted in declines in body mass index, insulin, and glucose. Restoration of regular menses may also occur after metformin treatment. Thus, data is accumulating that insulin-sensitizing agents may be helpful in decreasing the pathophysiologic effects of hyperinsulinism and insulin resistance associated with polycystic ovary syndrome. Other hormonal alterations in polycystic ovary syndrome have also been the subject of recent reports. Leptin secretion was found to be markedly irregular in these women. Elevated LH secretion may be secondary to accelerated gonadotropin-releasing hormone pulse generator activity, although the etiology of the pulse alterations is unclear. Summary Although polycystic ovary syndrome is the most common endocrine disorder affecting young women, it is one of the least understood, reflected by the wealth of research in this area. One area of focus has been the pathophysiologic link between insulin resistance and this disorder, including the effects of promising new agents to counteract these effects.

Effects of MetAP2 inhibition on hyperphagia and body weight in Prader-Willi syndrome: A randomized, double-blind, placebo-controlled trial

There are no treatments for the extreme hyperphagia and obesity in Prader–Willi syndrome (PWS). The bestPWS clinical trial assessed the efficacy, safety and tolerability of the methionine aminopeptidase 2 (MetAP2) inhibitor, beloranib.

Transcranial direct current stimulation reduces food-craving and measures of hyperphagia behavior in participants with Prader-Willi syndrome.

Prader–Willi syndrome (PWS) is a neurodevelopmental genetic disorder characterized by intellectual disabilities and insatiable appetite with compulsive eating leading to severe obesity with detrimental health consequences. Transcranial direct current stimulation (tDCS) has been shown to modulate decision‐making and cue‐induced food craving in healthy adults. We conducted a pilot double blind, sham‐controlled, multicenter study of tDCS modulation of food drive and craving in 10 adult PWS participants, 11 adult obese (OB) and 11 adult healthy‐weight control (HWC) subjects. PWS and OB subjects received five consecutive daily sessions of active or sham tDCS over the right dorsolateral prefrontal cortex (DLPFC), while HWC received a single sham and active tDCS in a crossover design. Standardized psychometric instruments assessed food craving, drive and hyperphagia by self‐report and caregiver assessment over 30 days. Robust baseline differences were observed in severity scores for the Three‐Factor Eating Questionnaire (TFEQ) and Dykens Hyperphagia Questionnaire (DHQ) for PWS compared to HWC while obese participants were more similar to HWC. Active tDCS stimulation in PWS was associated with a significant change from baseline in TFEQ Disinhibition (Factor II) (Ƶ = 1.9, P < 0.05, 30 days) and Total Scores (Ƶ = 2.3, P < 0.02, 30 days), and participant ratings of the DHQ Severity (Ƶ = 1.8, P < 0.06, 5 days) and Total Scores (Ƶ = 1.9, P < 0.05, 15 days). These findings support sustained neuromodulatory effects and efficacy of tDCS to reduce food drive and behaviors impacting hyperphagia in PWS. Transcranial direct current stimulation may represent a straight‐forward, low risk and low cost method to improve care, management and quality of life in PWS.

The High Direct Medical Costs of Prader-Willi Syndrome

Objective To assess medical resource utilization associated with Prader-Willi syndrome (PWS) in the US, hypothesized to be greater relative to a matched control group without PWS. Study design We used a retrospective case-matched control design and longitudinal US administrative claims data (MarketScan) during a 5-year enrollment period (2009–2014). Patients with PWS were identified by Classification of Diseases, Ninth Revision, Clinical Modification diagnosis code 759.81. Controls were matched on age, sex, and payer type. Outcomes included total, outpatient, inpatient and prescription costs. Results After matching and application of inclusion/exclusion criteria, we identified 2030 patients with PWS (1161 commercial, 38 Medicare supplemental, and 831 Medicaid). Commercially insured patients with PWS (median age 10 years) had 8.8-times greater total annual direct medical costs than their counterparts without PWS (median age 10 years: median costs

Delayed Puberty and Hypogonadism

14 907 vs

Sex Steroids and Growth Hormone Secretion

819; P < .0001; mean costs:

Turner Syndrome, Kallmann Syndrome and Noonan Syndrome

28 712 vs

Transcriptional Development of the Hypothalamic-Pituitary-Gonadal Axis

3246). Outpatient care comprised the largest portion of medical resource utilization for enrollees with and without PWS (median