Introduction Medical education in sexual health in the United States and Canada is lacking. Medical students and practicing physicians report being underprepared to adequately address their patients' sexual health needs. Recent studies have shown little instruction on sexual health in medical schools and little consensus around the type of material medical students should learn. To address and manage sexual health issues, medical students need improved education and training. Aim This meeting report aims to present findings from a summit on the current state of medical school education in sexual health and provides recommended strategies to better train physicians to address sexual health. Methods To catalyze improvements in sexual health education in medical schools, the summit brought together key U.S. and Canadian medical school educators, sexual health educators, and other experts. Attendees reviewed and discussed relevant data and potential recommendations in plenary sessions and then developed key recommendations in smaller breakout groups. Results Findings presented at the summit demonstrate that the United States and Canada have high rates of poor sexual health outcomes and that sexual health education in medical schools is variable and in some settings diminished. To address these issues, government, professional, and student organizations are working on efforts to promote sexual health. Several universities already have sexual health curricula in place. Evaluation mechanisms will be essential for developing and refining sexual health education. Conclusions To be effective, sexual health curricula need to be integrated longitudinally throughout medical training. Identifying faculty champions and supporting student efforts are strategies to increase sexual health education. Sexual health requires a multidisciplinary approach, and cross-sector interaction between various public and private entities can help facilitate change. Areas important to address include: core content and placement in the curriculum; interprofessional education and training for integrated care; evaluation mechanisms; faculty development and cooperative strategies. Initial recommendations were drafted for each.

We have studied a 2-year-old girl with acanthosis nigricans, glucose intolerance, marked hyperinsulinemia, and somatic features characteristic of the leprechaunism syndrome. Circulating plasma insulin levels were increased up to 50-fold and the patient showed a blunted hypoglycemic response to an injection of exogenous insulin (0.2 units/kg), indicating the presence of severe insulin resistance. Insulin purified from the patient's plasma was normal on the basis of chromatographic, electrophoretic, and immunologic criteria. Furthermore, the purified insulin competed effectively with 125I-labeled insulin for binding to insulin receptors on cultured IM-9 lymphocytes and rat fat cells and also exhibited normal biological potency when tested on rat fat cells. Anti-insulin receptor and anti-insulin antibodies were not detected in the patient's plasma, and plasma levels of glucagon, growth hormone, and cortisol were normal. Insulin binding to the patient's circulating mononuclear leukocytes was only slightly depressed into the low normal range and could not account for the severe insulin resistance. Studies on the patient's fibroblasts revealed normal levels of insulin receptors but a total absence of insulin's ability to accelerate glucose transport. Because rates of glucose transport and metabolism were normal in the basal state in the absence of insulin, we conclude that this patient's insulin resistance is due to an inherited cellular defect in the coupling mechanism between occupied insulin receptors and the plasma membrane glucose transport system. Leprechaunism is a rare, inherited disease characterized by an unusual facial appearance, hirsutism, cliteromegaly, and sparse subcutaneous fat stores (1-3). We have performed detailed metabolic studies on a 2-year-old girl with this syndrome who also presented with acanthosis nigricans and severe insulin resistance. Theoretically, insulin resistance can be due to abnormal beta cell secretory products, circulating insulin antagonists, or a cellular defect in insulin action (4). To elucidate the etiology of this patient's insulin resistance, each of these possibilities was examined in detail. Thus, we studied the integrity of her circulating insulin, assayed for potential insulin antagonists, measured cellular insulin receptors, and studied the insulin responsiveness of the patient's cultured fibroblasts in vitro. The results indicate that this patient's insulin resistance is due to a defect in insulin action distal to the insulin receptor. CASE REPORTThe patient, an 18-month-old white girl, had been born after a full-term (41-week gestation) uncomplicated pregnancy and delivery to a gravida I para 1 28-year-old mother who had takenThe costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U. S. C. §1734 solely to indicate this fact. 3469 no medications during her pregnancy; birth weight was 2600 g. At birth she was noted to have bilateral ingui...

Introduction This article discusses a blueprint for a sexual health communication curriculum to facilitate undergraduate medical student acquisition of sexual history taking skills and includes recommendations for important elements of a thorough sexual history script for undergraduate medical students. Aim To outline the fundamentals, objectives, content, timing, and teaching methods of a gold standard curriculum in sexual health communication. Methods Consensus expert opinion was documented at the 2012, 2014, and 2016 Summits in Medical Education in Sexual Health. Additionally, the existing literature was reviewed regarding undergraduate medical education in sexual health. Main Outcome Measures This article reports expert opinion and a review of the literature on the development of a sexual history taking curriculum. Results First-year curricula should be focused on acquiring satisfactory basic sexual history taking skills, including both assessment of sexual risk via the 5 Ps (partners, practices, protection from sexually transmitted infections, past history of sexually transmitted infections, and prevention of pregnancy) as well as assessment of sexual wellness—described here as a sixth P (plus), which encompasses the assessment of trauma, violence, sexual satisfaction, sexual health concerns/problems, and support for gender identity and sexual orientation. Second-year curricula should be focused on incorporating improved clinical reasoning, emphasizing sexual history taking for diverse populations and practices, and including the impact of illness on sexual health. Teaching methods must include varied formats. Evaluation may be best as a formative objective structured clinical examination in the first year and summative in the second year. Barriers for curriculum development may be reduced by identifying faculty champions of sexual health/medicine. Clinical Implications Medical students will improve their skills in sexual history taking, which will ultimately impact patient satisfaction and clinical outcomes. Future research is needed to validate this proposed curriculum and assess the impact on clinical skills. Strengths & Limitations This article assimilates expert consensus and existing clinical guidelines to provide a novel structured approach to curriculum development in sexual health interviewing in the pre-clinical years. Conclusion The blueprint for developing sexual history taking skills includes a spiral curriculum with varied teaching formats, incorporation of a sexual history script that incorporates inquiry about sexual wellness, and longitudinal assessment across the pre-clinical years. Ideally, sexual health communication content should be incorporated into existing clinical interviewing and physical examination courses.

Sexual health is considered to be a state of wellness with physical, emotional, mental, and social dimensions. Sexual health can contribute to our overall well-being in each of these dimensions. However, despite the intrinsic importance and positive aspects of sexuality in our lives, the United States presently faces significant challenges related to the sexual health of its citizens, including human immunodeficiency virus, other sexually transmitted infections, viral hepatitis, unintended pregnancies, sexual violence, sexual dysfunction, and cancers in reproductive tracts with serious disparities among the populations affected. In particular, high rates of poverty, income inequality, low educational attainment, stigma, racism, sexism, and homophobia can make it more difficult for some individuals and communities to protect their sexual health. Given that many pressing public health issues in the United States are related to sexual health and that sexual health has been increasingly recognized as an important national health priority, now is the time to energize and focus our efforts toward optimal sexual health of the population. In this paper, we outline the rationale for addressing sexual health as a means to better promote overall health and address sexuality related morbidities. In addition, we present a logic model outlining an approach for advancing sexual health in the United States, as well as a range of action steps for consideration by public health practitioners, researchers, and policymakers.

Postprandial and postabsorptive glucose metabolism was studied in a 3-yr-old girl with leprechaunism by substrate and hormonal measurements and by quantifying hepatic glucose output during continuous infusion of D-[6-6-2H2]-glucose. Hepatic glucogen content and the activity of glycogen synthase and phosphorylase were also measured in the post-prandial state on a separate occasion. During the 4-h postprandial state, plasma glucose, alanine, lactate, beta-hydroxybutyrate, and glycerol were normal, as were hepatic glycogen, glycogen synthase, phosphorylase, and hepatic glucose output of 7.5 mg kg-1 min-1. Intravenous injection of glucagon (30 micrograms kg-1) caused an immediate almost 3-fold rise in glucose production consistent with brisk glycogenolysis. During the 8- to 12-h postabsorptive state, however, the patient had elevated levels of glycerol (330-508 microM) and beta-hydroxybutyrate (3291-3801 microM) and decreased levels of glucose 24-29 mg/dl) and alanine (121-135 microM) consistent with a much longer period of fasting in the normal child. Furthermore, hepatic glucose output was reduced to 3.9 mg kg-1 min-1, and iv glucagon injection failed to increase this rate; both of these observations are consistent with a hepatic state generally found only later in fasting in the normal child. From these observations we conclude that the hypoglycemia reported in the leprechaunism syndrome is due to an accelerated fasting state secondary to insulin resistance. As with long-fasted, glycogen-depleted normal children, gluconeogenesis alone is often not capable of adequately meeting the child's large noninsulin-dependent cerebral glucose requirements.

Genetic forms of severe insulin resistance are often characterized by alterations in binding and/or kinase properties of the insulin receptor. To evaluate whether alterations in insulin receptor kinase of erythrocytes can be used as genetic markers, we studied patients with two apparently inherited conditions of severe insulin resistance (leprechaunism and the type A syndrome of insulin resistance) and their families. In the two propositi, [125I]insulin binding to intact erythrocytes was decreased by 64% and 45%, respectively. This was primarily due to a decrease in receptor number and was found in intact cells and solubilization of the receptors. Similar insulin binding defects were found on monocytes. Insulin-stimulated tyrosine kinase activity of the solubilized receptor from erythrocytes was also decreased and to a similar extent as binding. Parents of neither patient had clinical manifestations of leprechaunism or the type A syndrome. Furthermore, no alterations in insulin receptor binding or kinase activity were found in erythrocytes from the mothers. Insulin binding in the father of the type A patient was also normal, whereas the father of the leprechaun had decreased receptor affinity. Receptors extracted from the both fathers' cells had a 40-60% decrease in maximal insulin-stimulated phosphorylation and significant rightward shifts of the insulin dose-response curves (ED50, 141 and 42 ng/mL, respectively; control ED50, 16 ng/mL). The finding of biochemical defects in insulin receptor kinase activity in clinically unaffected parents of patients suggests that these alterations may be useful genetic markers and more sensitive than insulin binding studies for studying pattern of inheritance of these diseases.

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