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Background: Previous research has shown that people who have been diagnosed autistic are more likely to die prematurely than the general population. However, statistics on premature mortality in autistic people have often been misinterpreted. In this study we aimed to estimate the life expectancy and years of life lost experienced by autistic people living in the UK. Methods: We studied people in the IQVIA Medical Research Database with an autism diagnosis between January 1, 1989 and January 16, 2019. For each participant diagnosed autistic, we included ten comparison participants without an autism diagnosis, matched by age, sex, and primary care practice. We calculated age- and sex-standardised mortality ratios comparing people diagnosed autistic to the reference group. We used Poisson regression to estimate age-specific mortality rates, and life tables to estimate life expectancy at age 18 and years of life lost. We analysed the data separately by sex, and for people with and without a record of intellectual disability. We discuss the findings in the light of the prevalence of recorded diagnosis of autism in primary care compared to community estimates. Findings: From a cohort of nearly 10 million people, we identified 17,130 participants diagnosed autistic without an intellectual disability (matched with 171,300 comparison participants), and 6450 participants diagnosed autistic with an intellectual disability (matched with 64,500 comparison participants). The apparent estimates indicated that people diagnosed with autism but not intellectual disability had 1.71 (95% CI: 1.39-2.11) times the mortality rate of people without these diagnoses. People diagnosed with autism and intellectual disability had 2.83 (95% CI: 2.33-3.43) times the mortality rate of people without these diagnoses. Likewise, the apparent reduction in life expectancy for people diagnosed with autism but not intellectual disability was 6.14 years (95% CI: 2.84-9.07) for men and 6.45 years (95% CI: 1.37-11.58 years) for women. The apparent reduction in life expectancy for people diagnosed with autism and intellectual disability was 7.28 years (95% CI: 3.78-10.27) for men and 14.59 years (95% CI: 9.45-19.02 years) for women. However, these findings are likely to be subject to exposure misclassification biases: very few autistic adults and older-adults have been diagnosed, meaning that we could only study a fraction of the total autistic population. Those who have been diagnosed may well be those with greater support needs and more co-occurring health conditions than autistic people on average. Interpretation: The findings indicate that there is a group of autistic people who experience premature mortality, which is of significant concern. There is an urgent need for investigation into the reasons behind this. However, our estimates suggest that the widely reported statistic that autistic people live 16-years less on average is likely incorrect. Nine out of 10 autistic people may have been undiagnosed across the time-period studied. Hence, the results of our study do not generalise to all autistic people. Diagnosed autistic adults, and particularly older adults, are likely those with greater-than-average support needs. Therefore, we may have over-estimated the reduction in life expectancy experienced by autistic people on average. The larger reduction in life expectancy for women diagnosed with autism and intellectual disability vs. men may in part reflect disproportionate underdiagnosis of autism and/or intellectual disability in women. Funding: Dunhill Medical Trust, Medical Research Council, National Institute for Health and Care Research, and the Royal College of Psychiatrists.
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Background: Autism has long been viewed as a paediatric condition, meaning that many autistic adults missed out on a diagnosis as children when autism was little known. We estimated numbers of diagnosed and undiagnosed autistic people in England, and examined how diagnostic rates differed by socio-demographic factors. Methods: This population-based cohort study of prospectively collected primary care data from IQVIA Medical Research Data (IMRD) compared the prevalence of diagnosed autism to community prevalence to estimate underdiagnosis. 602,433 individuals registered at an English primary care practice in 2018 and 5,586,100 individuals registered between 2000 and 2018 were included. Findings: Rates of diagnosed autism in children/young people were much higher than in adults/older adults. As of 2018, 2.94% of 10- to 14-year-olds had a diagnosis (1 in 34), vs. 0.02% aged 70+ (1 in 6000). Exploratory projections based on these data suggest that, as of 2018, 463,500 people (0.82% of the English population) may have been diagnosed autistic, and between 435,700 and 1,197,300 may be autistic and undiagnosed (59-72% of autistic people, 0.77%-2.12% of the English population). Age-related inequalities were also evident in new diagnoses (incidence): c.1 in 250 5- to 9-year-olds had a newly-recorded autism diagnosis in 2018, vs. c.1 in 4000 20- to 49-year-olds, and c.1 in 18,000 people aged 50+. Interpretation: Substantial age-related differences in the proportions of people diagnosed suggest an urgent need to improve access to adult autism diagnostic services. Funding: Dunhill Medical Trust, Economic and Social Research Council, Medical Research Council, National Institute for Health Research, the Wellcome Trust, and the Royal College of Psychiatrists.
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OBJECTIVE: To evaluate bone mineral density (BMD) by age in premenopausal elite long-distance runners at 2 time points, 5.02 ± 0.5 years apart. DESIGN: Follow-up study. SETTING: University Research Institute. PARTICIPANTS: Twenty-three elite-level distance runners (baseline age, 24.9 ± 3.9 years; body mass index, 18.7 ± 1.1; running distance, 89.3 ± 19.4 km/wk) participated in the study. MAIN OUTCOME MEASURES: Dual-energy x-ray absorptiometry (iDXA; GE Healthcare)-derived BMD z-scores for the total body (TB), lumbar spine (LS) (L2-L4), and proximal femur. A z-score of <-1.0 indicated low BMD by age. RESULTS: Lumbar spine BMD z-scores had increased significantly by follow-up for all runners (baseline, -1.1 ± 0.9; follow-up, -0.7 ± 0.7; P = 0.04) and for formerly amenorrheic runners with restored menstruation (n = 10; baseline, -1.5 ± 0.9; follow-up, -0.9 ± 0.6; P = 0.03). Total body, but not proximal femur z-scores, had also increased (P < 0.05). Improvements in z-scores correlated with an increased body fat (LS: R2 = 0.27; TB: R2 = 0.35; P < 0.01) and menstrual history score (LS: R2 = 0.36; TB: R2 = 0.27; P < 0.05). There were no associations with lean mass or running volume at any skeletal site (P = 0.07-0.89). CONCLUSIONS: Low BMD by age in highly-trained female runners may be at least partially reversible before the age of 30 years, even when competitive running is continued. This seems to be related to restored menstruation and an increased body fat. Further larger studies are required to clarify our findings.
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Densidade Óssea , Pré-Menopausa/fisiologia , Corrida/fisiologia , Absorciometria de Fóton , Tecido Adiposo/fisiologia , Adulto , Fatores Etários , Atletas , Composição Corporal/fisiologia , Índice de Massa Corporal , Feminino , Seguimentos , Humanos , Região Lombossacral/fisiologia , Menstruação/fisiologia , Adulto JovemRESUMO
LAY ABSTRACT: This study explores autistic women's experiences of eating disorder services. About 20%-30% of people with anorexia nervosa are also autistic, and current treatments seem not to work as well for them. We interviewed 15 autistic women with experience of anorexia nervosa, 12 parents of autistic women with anorexia nervosa, and 11 healthcare professionals working in eating disorder services. We asked autistic women and parents about their experiences of eating disorder services, and we asked healthcare professionals about their experiences treating autistic women with anorexia nervosa. Participants' views were represented by three overall themes: misunderstanding autism and autistic traits, one treatment does not fit all, and improving accessibility and engagement within services. We found that autistic women face many barriers when in treatment for anorexia nervosa, often because of a lack of autism understanding within eating disorder services. Future research should look at developing anorexia nervosa treatments that can specifically help autistic individuals.
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Transtorno do Espectro Autista , Transtorno Autístico , Transtornos da Alimentação e da Ingestão de Alimentos , Transtorno Autístico/terapia , Atenção à Saúde , Transtornos da Alimentação e da Ingestão de Alimentos/terapia , Feminino , Humanos , PaisRESUMO
Autistic women are overrepresented among people in treatment for Anorexia Nervosa (AN). The current study aimed to: (1) better understand how AN develops and persists in autistic individuals from the perspective of autistic women, parents and healthcare professionals; (2) derive a theoretical model of restrictive eating difficulties in autism. We conducted 44 semi-structured interviews and used Thematic Analysis to identify patterns of meaning across the data. Themes related to sensory sensitivities, social interaction and relationships, sense of self and identity, difficulties with emotions, thinking styles, and a need for control and predictability. We developed a model of potential autism-specific mechanisms underlying restrictive eating difficulties. This study generated novel insights, which have the potential to inform treatment adaptations following empirical testing.
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Anorexia Nervosa/psicologia , Transtorno Autístico , Adulto , Anorexia , Emoções , Transtornos da Alimentação e da Ingestão de Alimentos , Feminino , Humanos , Resolução de ProblemasRESUMO
Over the past 20 years, there have been a growing number of reports of low bone mineral density (BMD) or premature bone loss in individuals with a high physical activity level. These skeletal problems have been documented mainly in underweight women with amenorrhea and have often been linked to a sex hormone deficiency. However, sex hormone treatment has been shown to have limited efficacy for the prevention or treatment of low BMD in such women. Studies of bone turnover in women with sustained exercise-associated amenorrhea using metabolic markers of osteoblast activities and collagen synthesis have demonstrated an apparent reduction of bone formation that is associated with a low body mass index (BMI) and with endocrine disturbances that are characteristic of energy deficit. Comparable metabolic and endocrine disturbances have been observed in anorexic women that reverse with weight gain. Furthermore, increases of BMD accompany weight gain in both groups of women, even without a return of menses. Collectively, these observations suggest an important link between energy balance and the balance of bone turnover in women with exercise and/or diet-associated amenorrhea. Although there have been few studies that have explored relations between bone turnover, BMD, and energy balance in physically active men, there is evidence for a link between reduced bone formation and an abrupt, short-term energy deficit. Interestingly, the presence of low BMD in physically active men has not been associated with a sex hormone deficiency. This review evaluates the evidence that underlies the hypothesis that an energy deficit is instrumental in the disturbance of bone turnover that has been observed in physically active individuals.
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Remodelação Óssea , Osso e Ossos/fisiologia , Metabolismo Energético , Adulto , Densidade Óssea , Exercício Físico , Feminino , Humanos , Fator de Crescimento Insulin-Like I/metabolismo , Leptina/sangue , Masculino , Fenômenos Fisiológicos da Nutrição , OsteoporoseRESUMO
PURPOSE: To link annual changes of bone mineral density (BMD) over 12 consecutive years to pharmacological intervention and to fluctuations of body mass and body composition in an amenorrheic athlete. METHODS: BMD of the lumbar spine (LS) and total proximal femur (PF) were measured using dual energy x-ray absorptiometry (DXA), every 11-13 months between ages 24.8 and 36.9 yr. Body composition was assessed every 3-4 yr from a whole body DXA scan. Body mass was recorded every 3 months. For the first 5 yr of study, the subject used oral contraceptives (OC). For the subsequent 7 yr, she used estradiol skin patches (EP) with oral norethisterone. RESULTS: The first DXA scan (age 24.8 yr) revealed a low BMD at both LS and PF, with T-scores of -1.4 and -2.8, respectively. During the next 5 yr, while adhering to OC, the BMD of her LS and PF declined by 9.8% and 12.1%, respectively. Concomitantly, her body mass fell from 45.1 to 41.4 kg, her body mass index (BMI) from 16.4 to 15.0 kg.m-2, and her percent body fat from 8.3 to <4.0%. While treated with EP and norethisterone (age 29.8-33.5 yr), her LS BMD gradually increased by 9.4%, despite a further 0.8 kg decline of body mass. From age 33.8 to 36.9 yr, voluntary weight gain (2-3 kg.yr-1; total: 8.1 kg) was accompanied by an increase of her PF BMD (16.9%), with no further increase at the LS. CONCLUSION: Changes of BMD at the total proximal femur reflected changes of body mass in this subject. At the lumbar spine, BMD declined with weight loss but increased in association with transdermal estradiol treatment in the absence of weight gain.
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Amenorreia/fisiopatologia , Densidade Óssea , Esportes , Adulto , Ciclismo/fisiologia , Anticoncepcionais Orais/uso terapêutico , Feminino , Humanos , Atividade Motora/fisiologia , Osteoporose/complicações , Corrida/fisiologia , Reino UnidoRESUMO
PURPOSE: To investigate the effects of daily oral L-leucine ingestion on strength, bone mineral-free lean tissue mass (LTM) and fat mass (FM) of free living humans during a 12-wk resistance-training program. METHODS: Twenty-six initially untrained men (n = 13 per group) ingested either 4 g/d of L-leucine (leucine group: age 28.5 ± 8.2 y, body mass index 24.9 ± 4.2 kg/m2) or a corresponding amount of lactose (placebo group: age 28.2 ± 7.3 y, body mass index 24.9 ± 4.2 kg/m2). All participants trained under supervision twice per week following a prescribed resistance training program using eight standard exercise machines. Testing took place at baseline and at the end of the supplementation period. Strength on each exercise was assessed by five repetition maximum (5-RM), and body composition was assessed by dual energy X-ray absorptiometry (DXA). RESULTS: The leucine group demonstrated significantly higher gains in total 5-RM strength (sum of 5-RM in eight exercises) and 5-RM strength in five out of the eight exercises (P < .05). The percentage total 5-RM strength gains were 40.8% (± 7.8) and 31.0% (± 4.6) for the leucine and placebo groups respectively. Significant differences did not exist between groups in either total percentage LTM gains or total percentage FM losses (LTM: 2.9% ± 2.5 vs 2.0% ± 2.1, FM: 1.6% ± 15.6 vs 1.1% ± 7.6). CONCLUSION: These results suggest that 4 g/d of L-leucine supplementation may be used as a nutritional supplement to enhance strength performance during a 12-week resistance training program of initially untrained male participants.
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Suplementos Nutricionais , Leucina/administração & dosagem , Força Muscular/efeitos dos fármacos , Treinamento Resistido , Levantamento de Peso , Absorciometria de Fóton , Administração Oral , Adulto , Biomarcadores/sangue , Composição Corporal/efeitos dos fármacos , Índice de Massa Corporal , Método Duplo-Cego , Esquema de Medicação , Ingestão de Energia , Humanos , Masculino , Percepção , Fatores de Tempo , Adulto JovemRESUMO
Female athletes are susceptible to both disordered eating and menstrual cycle disturbances (MCDs). Disordered eating in combination with high energy expenditure from exercise can lead to energy deprivation. Current theories suggest that MCDs are caused by energy deprivation rather than by exercise alone. A number of endocrine adaptations occur with energy deprivation and MCDs, which are concomitant with imbalanced bone turnover, reduced bone density and potentially increased fracture risk. This chapter reviews current evidence concerning the disruption of bone metabolism that accompanies disordered eating and MCDs in physically active girls and young women, including high-performance athletes. Initially, an overview of the aetiology of exercise-associated MCDs and their link with disordered eating is provided. Thereafter, studies reporting changes in areal bone mineral density (aBMD) in female athletes with MCDs are considered in conjunction with change in athletes' physical activity, nutritional status and menstrual histories. A comprehensive overview of the disruption of bone metabolism that accompanies nutritionally related MCDs is also provided. Emphasis is placed upon the role of energy deprivation and its endocrine effects, which, when sustained, result in imbalanced bone turnover and low aBMD. Based on current evidence, recommendations are made for the prevention and treatment of disturbed bone metabolism and low BMD in female athletes with MCDs. Finally, consideration is given to the effects of intense training and energy deprivation on endocrine function and skeletal health in men.
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Doenças Ósseas Endócrinas/fisiopatologia , Remodelação Óssea/fisiologia , Metabolismo Energético/fisiologia , Transtornos da Alimentação e da Ingestão de Alimentos/fisiopatologia , Distúrbios Menstruais/fisiopatologia , Esportes/fisiologia , Adolescente , Adulto , Densidade Óssea/fisiologia , Ingestão de Energia/fisiologia , Feminino , Humanos , MasculinoRESUMO
The addition of carbohydrate (CHO) to an acute creatine (Cr) loading regimen has been shown to increase muscle total creatine content significantly beyond that achieved through creatine loading alone. However, the potential ergogenic effects of combined Cr and CHO loading have not been assessed. The purpose of this study was to compare swimming performance, assessed as mean swimming velocity over repeated maximal intervals, in high-performance swimmers before and after an acute loading regimen of either creatine alone (Cr) or combined creatine and carbohydrate (Cr + CHO). Ten swimmers (mean +/- SD of age and body mass: 17.8 +/- 1.8 years and 72.3 +/- 6.8 kg, respectively) of international caliber were recruited and were randomized to 1 of 2 groups. Each swimmer ingested five 5 g doses of creatine for 4 days, with the Cr + CHO group also ingesting approximately 100 g of simple CHO 30 minutes after each dose of creatine. Performance was measured on 5 separate occasions: twice at "baseline" (prior to intervention, to assess the repeatability of the performance test), within 48 hours after intervention, and then 2 and 4 weeks later. All subjects swam faster after either dietary loading regimen (p < 0.01, both regimens); however, there was no difference in the extent of improvement of performance between groups. In addition, all swimmers continued to produce faster swim times for up to 4 weeks after intervention. Our findings suggest that no performance advantage was gained from the addition of carbohydrate to a creatine-loading regimen in these high-caliber swimmers.