Dataset Information

Dietary and Physical Activity Habits in Adolescent Girls with Polycystic Ovary Syndrome (PCOS)-HAstudy.

ABSTRACT: The role of inappropriate lifestyle in the etiology of polycystic ovary syndrome (PCOS) and its metabolic and reproductive complications has attracted much attention in recent years; however, most studies involve adult patients. Thus, the study aimed to compare dietary patterns, physical activity, metabolic, anthropometric and inflammatory markers of 14-18-year-old girls with and without PCOS (n = 61 and n = 35, respectively) as well as to assess correlations between concentrations of metabolic and inflammatory markers and macronutrient intake and to identify the independent predictors of PCOS, related to diet and physical activity (PA). Compared to the control group, PCOS girls consumed significantly more total fat (p = 0.0005), including both saturated (SFA) (p = 0.03), monounsaturated (MUFA) (p = 0.0003) and polyunsaturated fatty acids (PUFA) (p = 0.01). A significantly higher percentage of PCOS patients consumed high and medium glycemic index (GI) foods (p = 0.03) and represented a low level of PA, both during school and in leisure time (41.67 vs. 6.06%; p = 0.0001 and 32.79 vs. 5.71%; p = 0.003, respectively). The PCOS group had also significantly higher waist circumference (WC), C-reactive protein (CRP) (p = 0.01), LDL cholesterol (p = 0.01), fasting insulin (p = 0.002) and HOMA-IR (p = 0.006) levels. There was an inverse correlation between fiber intake and fasting insulin, (p = 0.0002, r = -0.37), HOMA-IR (p = 0.0004, r = -0.35), WC (p = 0.029; r = -0.222) and a positive relationship between high and medium GI diet and insulin concentration (p = 0.003; r = 0.3). An increase of 10 g/day in total fat intake per day increases the probability of PCOS by 1.4 times. If the SFA or MUFA intakes increase by 10 g, the probability of PCOS increase 1.7-fold and 2.5-fold, respectively. The consumption of foods with a medium GI raises the probability of PCOS by more than 3 times, after adjusting for age. The odds ratio decreased for the moderate and high PA at school/work and in leisure time. Further research in girls with PCOS is needed to test whether low GI and dietary fatty acid reduction combined with increased PA is effective in the nonpharmacological treatment and prevention of PCOS complications. ClinicalTrial.gov Identifier: NCT04738409.

SUBMITTER: Mizgier M

PROVIDER: S-EPMC8396824 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:PCOS is a complex genetic disease reflecting the interplay of susceptibility genes and environmental factors. The cardinal reproductive feature of the syndrome, hyperandrogenemia, appears to play a direct role in the pathogenesis of the associated metabolic abnormalities. Male as well as female first-degree relatives have reproductive and metabolic phenotypes including increased prevalence rates of type 2 diabetes (T2D), metabolic syndrome (MBS) and other risk factors for cardiovascular disease (CVD). Northwestern University (NU) investigators lead a team that has extensive experience in phenotyping PCOS and in the genetic analysis of complex diseases including genome-wide association study (GWAS). Together with an expert group of collaborators from the Hershey Medical Center, and The University of Chicago, we have conducted a GWAS to identify PCOS susceptibility alleles using a large cohort of extensively and consistently phenotyped PCOS cases. Population controls for this study come from the NUgene project described below. NUgene project: In 2002, Northwestern committed to the development of a DNA repository to serve as a platform for the identification and validation of genotype-phenotype associations that will impact healthcare. The NUgene Project is a repository with longitudinal medical information from participating patients at affiliated hospitals and outpatient clinics from the Northwestern University Medical Center. Participants' DNA samples are coupled with data from a questionnaire (2 versions were used, 1 before and 1 after February 2006, both are included) and continuously updated data from our Electronic Medical Record (EMR) representing actual clinical care events. Northwestern has a state-of-the art, comprehensive inpatient and outpatient EMR system of over 2 million patients. NUgene has broad access to participant data for all outpatient visits as well as inpatient data via a consolidated data warehouse. NUgene participants consent to distribution and use of their coded DNA samples and data for a broad range of genetic research by third-party investigators.

Project description:Polycystic ovary syndrome (PCOS) was hypothesized to result from functional ovarian hyperandrogenism (FOH) due to dysregulation of androgen secretion in 1989-1995. Subsequent studies have supported and amplified this hypothesis. When defined as otherwise unexplained hyperandrogenic oligoanovulation, two-thirds of PCOS cases have functionally typical FOH, characterized by 17-hydroxyprogesterone hyperresponsiveness to gonadotropin stimulation. Two-thirds of the remaining PCOS have FOH detectable by testosterone elevation after suppression of adrenal androgen production. About 3% of PCOS have a related isolated functional adrenal hyperandrogenism. The remaining PCOS cases are mild and lack evidence of steroid secretory abnormalities; most of these are obese, which we postulate to account for their atypical PCOS. Approximately half of normal women with polycystic ovarian morphology (PCOM) have subclinical FOH-related steroidogenic defects. Theca cells from polycystic ovaries of classic PCOS patients in long-term culture have an intrinsic steroidogenic dysregulation that can account for the steroidogenic abnormalities typical of FOH. These cells overexpress most steroidogenic enzymes, particularly cytochrome P450c17. Overexpression of a protein identified by genome-wide association screening, differentially expressed in normal and neoplastic development 1A.V2, in normal theca cells has reproduced this PCOS phenotype in vitro. A metabolic syndrome of obesity-related and/or intrinsic insulin resistance occurs in about half of PCOS patients, and the compensatory hyperinsulinism has tissue-selective effects, which include aggravation of hyperandrogenism. PCOS seems to arise as a complex trait that results from the interaction of diverse genetic and environmental factors. Heritable factors include PCOM, hyperandrogenemia, insulin resistance, and insulin secretory defects. Environmental factors include prenatal androgen exposure and poor fetal growth, whereas acquired obesity is a major postnatal factor. The variety of pathways involved and lack of a common thread attests to the multifactorial nature and heterogeneity of the syndrome. Further research into the fundamental basis of the disorder will be necessary to optimally correct androgen levels, ovulation, and metabolic homeostasis.

Dataset Information

Dietary and Physical Activity Habits in Adolescent Girls with Polycystic Ovary Syndrome (PCOS)-HAstudy.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets