The effect of a high-protein, low glycemic-load diet versus a conventional, high glycemic-load diet on biochemical parameters associated with acne vulgaris: A randomized, investigator-masked, controlled trial

BACKGROUND - No previous study has sought to examine the influence of dietary composition on acne vulgaris. OBJECTIVE - We sought to compare the effect of an experimental low glycemic-load diet with a conventional high glycemic-load diet on clinical and endocrine aspects of acne vulgaris. METHODS - A total of 43 male patients with acne completed a 12-week, parallel, dietary intervention study with investigator-masked dermatology assessments. Primary outcomes measures were changes in lesion counts, sex hormone binding globulin, free androgen index, insulin-like growth factor-I, and insulin-like growth factor binding proteins. RESULTS - At 12 weeks, total lesion Counts had decreased more in the experimental group (-21.9 [95% confidence interval -26.8 to -19.0]) compared with the control group (-13.8 [-19.1 to -8-5], P = .01). The experimental diet also reduced weight (P = .001), reduced the free androgen index (P = .04), and increased, insulin-like growth factor binding protein-1 (P = .001) when compared with a high glycemic-load diet. LIMITATIONS - We Could not preclude the role of weight loss in the overall treatment effect. CONCLUSION - This suggests nutrition-related lifestyle factors play a role in acne pathogenesis. However, these preliminary findings should be confirmed by similar studies

A low-glycemic-load diet improves symptoms in acne vulgaris patients: a randomized controlled trial

BACKGROUND: Although the pathogenesis of acne is currently unknown, recent epidemiologic studies of non-Westernized populations suggest that dietary factors, including the glycemic load, may be involved. OBJECTIVE: The objective was to determine whether a low-glycemic-load diet improves acne lesion counts in young males. DESIGN: Forty-three male acne patients aged 15-25 y were recruited for a 12-wk, parallel design, dietary intervention incorporating investigator-blinded dermatology assessments. The experimental treatment was a low-glycemic-load diet composed of 25% energy from protein and 45% from low-glycemic-index carbohydrates. In contrast, the control situation emphasized carbohydrate-dense foods without reference to the glycemic index. Acne lesion counts and severity were assessed during monthly visits, and insulin sensitivity (using the homeostasis model assessment) was measured at baseline and 12 wk. RESULTS: At 12 wk, mean (±SEM) total lesion counts had decreased more (P = 0.03) in the low-glycemic-load group (-23.5 ± 3.9) than in the control group (-12.0 ± 3.5). The experimental diet also resulted in a greater reduction in weight (-2.9 ± 0.8 compared with 0.5 ± 0.3 kg; P < 0.001) and body mass index (in kg/m(2); -0.92 ± 0.25 compared with 0.01 ± 0.11; P = 0.001) and a greater improvement in insulin sensitivity (-0.22 ± 0.12 compared with 0.47 ± 0.31; P = 0.026) than did the control diet. CONCLUSION: The improvement in acne and insulin sensitivity after a low-glycemic-load diet suggests that nutrition-related lifestyle factors may play a role in the pathogenesis of acne. However, further studies are needed to isolate the independent effects of weight loss and dietary intervention and to further elucidate the underlying pathophysiologic mechanisms

A pilot study to determine the short-term effects of a low glycemic load diet on hormonal markers of acne: A nonrandomized, parallel, controlled feeding trial

Observational evidence suggests that dietary glycemic load may be one environmental factor contributing to the variation in acne prevalence worldwide. To investigate the effect of a low glycemic load (LGL) diet on endocrine aspects of acne vulgaris, 12 male acne sufferers (17.0 ± 0.4 years) completed a parallel, controlled feeding trial involving a 7-day admission to a housing facility. Subjects consumed either an LGL diet (n = 7; 25% energy from protein and 45% from carbohydrates) or a high glycemic load (HGL) diet (n = 5; 15% energy from protein, 55% energy from carbohydrate). Study outcomes included changes in the homeostasis model assessment of insulin resistance (HOMA-IR), sex hormone binding globulin (SHBG), free androgen index (FAI), insulin-like growth factor-I (IGF-I), and its binding proteins (IGFBP-I and IGFBP-3). Changes in HOMA-IR were significantly different between groups at day 7 (-0.57 for LGL vs. 0.14 for HGL, p = 0.03). SHBG levels decreased significantly from baseline in the HGL group (p = 0.03), while IGFBP-I and IGFBP-3 significantly increased (p = 0.03 and 0.03, respectively) in the LGL group. These results suggest that increases in dietary glycemic load may augment the biological activity of sex hormones and IGF-I, suggesting that these diets may aggravate potential factors involved in acne development

Radão nas residências e risco de cancro do pulmão: Análise de dados individuais referentes a 13 estudos casos-controlo europeus

Resumo: O objectivo desta análise foi determinar o risco de neoplasia do pulmão associado à exposição em casa à radioactividade produzida pelo radão, gás que ocorre naturalmente na natureza.Envolveu 13 estudos europeus realizados em 9 países (Portugal não incluído), contabilizando-se 7148 casos de cancro do pulmão e 14 208 controlos.A concentração média de radão nas casas do grupo de controlo foi de 97 Bq/m3 (becquerels), enquanto nas do grupo dos casos a concentração média do gás foi de 104 Bq/m3.Após estratificação por estudo, idade, sexo, região de residência e tabagismo, o risco de cancro do pulmão aumentou 8,4% por cada 100 Bq/m3 de aumento da concentração do radão.Esta relação dose-resposta parece ser linear, sem limiar inferior de exposição para aparecimento do risco. Assim, a relação linear mantém-se significativa mesmo para concentrações inferiores a 200 Bq/m3, considerado o valor limite de exposição aceite (nível de acção).O risco absoluto cumulativo de cancro do pulmão aos 75 anos de idade e para níveis habituais de exposição ao radão de 0, 100, 400 e 800 Bq/m3 é respectivamente de 0,41%, 0,47%, 0,67%, e 0,93%, para indivíduos não fumadores e de 10,1%, 11,6%, 16,0% e 21,6% para fumadores â um aumento de cerca de 25 vezes.A análise colectiva dos diferentes estudos caso-controlo permitiu aos autores concluírem que o radão nas habitações contribui para cerca de 9% das mortes por cancro do pulmão e é responsável por cerca de 2% de todas as mortes por cancro na Europa. Palavra-chave: Radão, cancro do pulmã