Paternal Body Mass Index Research Articles

Healthy Lifestyle in the First 1000 Days and Overweight and Obesity Throughout Childhood.

Investigate associations of different family healthy lifestyle scores (HLS) during the first 1000 days with childhood overweight and obesity (OWOB). Cohort-specific analyses were conducted on participants (n = 25 006) from 4 European birth cohorts (The study on the pre- and early postnatal determinants of child health and development [EDEN], Elfe, France; Generation R, the Netherlands; and Lifeways, Ireland). Three composite HLSs were calculated: a maternal pregnancy HLS based on prepregnancy body mass index (BMI) and diet quality, physical activity, smoking status, and alcohol consumption during pregnancy; a parental pregnancy HLS additionally considering paternal BMI and smoking status; and an infancy HLS based on breastfeeding duration, age of solid food introduction, and exposure to passive smoking. Associations with child BMI (primary outcome) and waist-to-height ratio (WHtR, available in 2 cohorts) in early (5-5.5years), middle (7-8years), and late childhood (9-12years) were assessed using linear (BMI and WHtR z-scores) and robust Poisson (International Obesity Task Force [IOTF] categories) regression analyses adjusted for sociodemographic confounders. Only a small proportion of families had favorable lifestyle factors during pregnancy and early infancy, with 3.4% to 10.0%, 1.9% to 3.7%, and 12.2% to 23.6% scoring maximum for maternal, parental, and infancy HLS, respectively. Associations between higher HLSs and a lower risk of OWOB when measured by BMI z-scores or IOTF categories were found for maternal HLS and early (3/4 cohorts with available data), middle (1/2), and late childhood (2/4); parental HLS and early (3/4), middle (2/2), and late childhood (4/4). Associations between infancy HLS and childhood OWOB were less consistent and did not remain significant after additional adjustment for parental HLS. Associations with WHtR were solely significant in EDEN at 5.5years. Greater maternal and parental adherence to healthy lifestyle behaviors during pregnancy was associated with a lower risk of offspring OWOB throughout childhood, illustrating the importance of promoting healthy lifestyle behaviors at the family level during pregnancy.

Maternal Prepregnancy Obesity and Offspring Intelligence Quotient at 5 Years: A Multicohort Analysis.

The relationship between maternal obesity and childhood cognitive development remains unclear. Prior studies did not adjust for important confounders, and preterm infants are a developmentally distinct group that remains scarcely examined. To determine whether maternal prepregnancy body mass index (BMI) is associated with offspring intelligence quotient (IQ) up to 5 years and whether this relationship varies with gestational age. Data from two French birth cohorts, EDEN (all gestational ages) and EPIPAGE-2 (preterm children born between 24 and 34 weeks of gestation), were used for this study. Maternal prepregnancy weight and height were used to calculate prepregnancy BMI. The Wechsler Preschool and Primary Scale of Intelligence was used to assess child IQ around 5 years. Multivariable models were adjusted for confounders, including socioeconomic status and paternal BMI. Analytical cohorts included 1100 children from EDEN and 2629 from EPIPAGE-2. Lower intellectual functioning (full-scale IQ < 85) was observed in 8.1% of children in EDEN and 19.6% in EPIPAGE-2. The prevalence of maternal obesity was 13.6% (EDEN) and 21.3% (EPIPAGE-2) among children with lower intellectual functioning compared to 8.9% (EDEN) and 12.9% (EPIPAGE-2) among children with normal intellectual functioning. Maternal prepregnancy obesity was associated with an approximately 3-point decrease in full-scale IQ scores in fully adjusted models (adjusted β -2.8, 95% confidence interval [CI] -5.6, -0.1 and -2.6, 95% CI -4.7, -0.6 in EDEN and EPIPAGE-2, respectively). In EDEN, maternal obesity was associated with lower scores in the verbal IQ domain. Among infants born preterm (EPIPAGE-2), maternal obesity was associated with lower scores in the processing, reasoning, and verbal IQ domains. Adjustment for paternal BMI did not change the magnitude of the relationship with maternal obesity. High maternal prepregnancy BMI is associated with child cognitive development around 5 years of age.

Impact of maternal hormone profile and paternal sperm DNA fragmentation on clinical outcomes following assisted reproduction

Success of assisted reproductive techniques depends on multiple factors including maternal endocrine status, hormonal balance, and paternal sperm quality. A comprehensive pre-treatment evaluation allows better prediction of outcomes and avoidance of unnecessary procedures and expenses. To examine the impact of female hormonal profiles and sperm DNA damage on the success of assisted reproduction, medical data were extracted from the clinical records of infertile couples including couples' age and levels of maternal anti-Mullerian hormone (AMH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), and prolactin (PRL), as well as the DNA fragmentation index (DFI) in men. Any correlation between these parameters and clinical outcomes was investigated. DFI and FSH independently influenced the rate of high-quality embryos. A decrease in maternal age and PRL levels increased the rate of these embryos. On the other hand, an increase in maternal body mass index (BMI) or AMH levels was associated with a reduced chance of achieving high quality embryos. In addition, any reduction in PRL levels could be associated with a higher fertilization rate. FSH levels above the normal range contribute to a reduced rate of high-quality embryos. Overall, our findings demonstrate the complex interplay between different factors and their influence on fertilization success and emphasize the importance of optimizing these variables to achieve the best possible outcome. Several factors can influence the outcome of infertility treatment. These factors include paternal DFI, maternal age, BMI, AMH, FSH, and PRL levels.

Effect of Paternal Body Mass Index on Cumulative Live Birth Rates: Retrospective Analysis of 3048 Embryo Transfers in Couples Using Autologous Gametes.

Obesity is a multifactorial disease present worldwide and correlated with hormonal alterations that may cause a decrease in reproductive outcomes and seminal quality. However, the specific mechanisms involved are unknown. This led us to examine the relationship between paternal body mass index (BMI) and clinical reproductive outcomes by evaluating the cumulative live birth rates (CLBRs) per number of embryo transfers (ETs), embryos replaced (EmbRs), and oocytes used (OUs) in consecutive treatments until achieving the first newborn. A retrospective study was performed, and Kaplan-Meier survival curves were created to observe CLBRs with regard to the paternal BMI, adjusted by relevant confounders through Cox regression models. The participants were couples undergoing intracytoplasmic sperm injection (ICSI) and ET in Spanish IVIRMA clinics using autologous gametes. The cohort was subdivided based on paternal BMI: normal (18.5-24.99 kg/m2) (N), overweight (25-29.99 kg/m2) (OV), or obese (≥30 kg/m2) (OB) patients. A total of 4750 ICSI cycles were included, encompassing 49,485 mature oocytes, 23,963 blastocysts, and 3048 ETs. When calculating CLBRs based on the number of ETs carried out until live birth was achieved, no statistically significant differences were found (p = 0.72). After adjusting for maternal age and BMI, female infertility diagnosis, the use of preimplantation genetic testing, and the number of ETs, Cox regression showed that there were no statistically significant differences between the BMI groups (HR: 0.94 [95% CI: 0.7-1.2]; p = 0.59). When calculating CLBRs considering EmbRs, there was a similarity between the BMI groups (p = 0.57). However, there were no statistically significant differences in the adjusted Cox regression (HR: 0.93 [95% CI: 0.7-1.2]; p = 0.51). Finally, when calculating CLBRs considering OUs, the results were comparable among BMI subgroups (p = 0.75), and there were no statistically significant differences with adjusted Cox regression (HR: 0.95 [95% CI: 0.8-1.2]; p = 0.66). In conclusion, paternal BMI was not associated with clinical reproductive outcomes when considering the ETs, EmbRs, or OUs needed to reach the first liveborn (LB).

Relationship between paternal excessive weight and neonatal anthropometry in a clinical trial of nutritional counseling for pregnant women with overweight.

Human studies suggest that fathers with obesity influence infant growth and development. This study aimed to evaluate the relationship between paternal body mass index (BMI) and waist circumference (WC) with neonatal anthropometry and adiposity. This study is a cohort nested in a randomized controlled clinical trial of nutritional counseling for pregnant women with overweight. In total, 89 partner-pregnant woman-neonate triads were included. Paternal anthropometric measurements were taken at the time of the interview. Secondary data related to birth were obtained through access to the health information systems. Neonatal skinfold thickness was assessed and the adiposity was estimated using a predictive anthropometric model. Pearson's correlation and adjusted multivariate linear regression models were employed to evaluate the relationship between paternal BMI and WC with neonatal anthropometric measurements and adiposity. In total, 57.0% of the fathers presented a BMI ≥ 25 kg/m² and 14.6% a waist circumference ≥102 cm. The mean ± SD birth weight of the newborns (g) was 3357 ± 538. Paternal BMI and WC were inversely correlated with head circumference at birth [r = -0.31 (p = 0.004), r = -0.23 (p = 0.03), respectively]. Paternal BMI was also inversely correlated with the birth weight standardized by gestational age (z-score) [r = -0.23 (p = 0.03)]. In adjusted multivariate linear regression models, the paternal BMI (kg/m²) was inversely associated with the head circumference at birth (cm) [β = -0.07 (95% CI -0.15; -0.001) p = 0.04]. The data suggest that paternal excessive weight have a negative effect on fetal development, as assessed by anthropometric measurements. The inverse association between paternal BMI and the head circumference at birth was independent of confounders. Future studies with larger sample sizes are necessary to confirm or refute such hypotheses.

Mediation analysis in longitudinal study with high-dimensional methylation mediators.

Mediation analysis has been widely utilized to identify potential pathways connecting exposures and outcomes. However, there remains a lack of analytical methods for high-dimensional mediation analysis in longitudinal data. To tackle this concern, we proposed an effective and novel approach with variable selection and the indirect effect (IE) assessment based on both linear mixed-effect model and generalized estimating equation. Initially, we employ sure independence screening to reduce the dimension of candidate mediators. Subsequently, we implement the Sobel test with the Bonferroni correction for IE hypothesis testing. Through extensive simulation studies, we demonstrate the performance of our proposed procedure with a higher F$_{1}$ score (0.8056 and 0.9983 at sample sizes of 150 and 500, respectively) compared with the linear method (0.7779 and 0.9642 at the same sample sizes), along with more accurate parameter estimation and a significantly lower false discovery rate. Moreover, we apply our methodology to explore the mediation mechanisms involving over 730 000 DNA methylation sites with potential effects between the paternal body mass index (BMI) and offspring growing BMI in the Shanghai sleeping birth cohort data, leading to the identification of two previously undiscovered mediating CpG sites.

Impact of parental body mass index at diagnosis on obesity in survivors of pediatric craniopharyngioma.

It is well known that both genetic background and lifestyle influence the development of 'general' obesity. However, the role of parental body mass index (BMI) on the development of obesity in long-term survivors of childhood-onset craniopharyngioma (CP) is not well understood. This study analyzed the correlation of patients' BMI at diagnosis and last visit and parental BMI at CP diagnosis and further explored potential risk factors for obesity in CP patients. This is a registry-based retrospective cohort study. In total,291 CP patients and their parents recruited in the German KRANIOPHARYNGEOM studies were included. Correlations between patient's BMI SDS at CP diagnosis and last visit and parental BMI at CP diagnosis were analyzed. The associations between hypothalamic damage, maternal/paternal BMI and CP patients' obesity at last visit were analyzed by multivariable logistic regression. At follow-up, 52% of CP patients developed obesity (BMI > 3SDS). Patient's BMI SDS at last visit was moderately correlated with BMI-SDS at CP diagnosis (r = 0.48, 95% CI: 0.38-0.58, P < 0.001), and also with maternal BMI at diagnosis (r = 0.28, 95% CI: 0.17-0.38, P < 0.001) and paternal BMI at diagnosis (r = 0.3, 95% CI: 0.19-0.41, P < 0.001). However, the contributing role of parental BMI to the pathogenesis of obesity was small compared to the impact of hypothalamic damage. We conclude that besides hypothalamic damage, parental disposition for obesity is associated with the development of obesity in patients after CP. Our results indicate that also the family situation could have an influence on the development of obesity after CP and might be a therapeutic target. Survivors of childhood-onset craniopharyngioma are at risk of developing morbid obesity. So far, patients with posterior hypothalamic involvement and lesion were identified as a high risk group. With this study, the influence of parental body mass index on the risk of obesity was investigated. Patient's body-mass-index at last visit was correlated with maternal and paternal body mass index at diagnosis. With increasing maternal or paternal body mass index, the likelihood of obesity in individuals with CP increased. Nevertheless, the parents' weight had only a small effect on the development of patients' obesity compared to hypothalamic damage.

The apple doesn't fall far from the tree: is there a connection between the body mass indexes of adolescents and their parents?

Adolescent cases suffering from obesity tend to increase in middle-income countries. This study focused on the relationship between adolescent obesity and parents body mass index (BMI) and the variables of satisfaction, diet implementation and sports promotion. This cross-sectional study was conducted among adolescents living in the Mediterranean region (n=522, evaluated n=488). Anthropometric measurements were taken by expert researchers and data were collected using face-to-face survey technique. The average BMI of the adolescents and parents' was found to be above normal values. In adolescents, there was a positive and very good correlation with maternal BMI (r=0.711, p<0.01), a positive and moderate correlation with paternal BMI (r=0.512, p<0.01); In girl adolescents, it was positively and very well with maternal BMI (r=0.731, p<0.01), positively and moderately with father BMI (r=0.549, p<0.01); In boy adolescents, a positive and good correlation was found with maternal BMI (r=0.698, p<0.01), and a positive and moderate correlation with paternal BMI (r=0.459, p<0.01). In the analyzes comparing those who thought obesity threatened them (group 1) and those who did not think it threatened them (group 2), there was a statistically significant difference between the groups in terms of BMI distribution, satisfaction with body weight, diet program implementation, diet recommendation by the family and sports encouragement (p<0, 05). In a cross-sectional perspective paternal obesity is also significant in adolescents and the correlation with maternal obesity is relatively more effective. Also includes evidence of individual efforts and parental contribution in adolescents who see obesity as a threat.

Preconceptional paternal obesity may increase the risk of congenital urogenital anomalies in offspring: A case-control study.

Congenital urogenital anomalies affect 4-60 per 10,000 births. Maternal obesity, along with other risk factors, is well documented as a contributing factor. However, the impact of paternal obesity on risk is unclear. Obesity is prevalent among men of reproductive age, highlighting the need for further research into the potential association between paternal obesity and offspring congenital urogenital anomalies. This study aims to determine the association between paternal obesity and the risk of congenital urogenital malformations in offspring. Case-control study conducted on 179 newborns (91 cases, 88 controls) selected from the Notre Dame des Secours-university hospital database. Cases were identified as newborns presenting at least one congenital urogenital abnormality, defined as developmental anomalies that can result in a variety of malformations affecting the kidneys, ureters, bladder, and urethra. Controls were identified as newborns without any congenital abnormalities. The exclusion criteria were maternal obesity, infections during pregnancy, chronic diseases, prematurity, growth retardation, assisted reproductive technologies for conception, substance abuse, down syndrome, and other malformations. Data were collected through phone interviews, medical records, and questionnaires. In this study, the exposure was the preconceptional paternal body mass index (BMI), which was calculated based on self-reported height and weight. According to guidelines from the US Centers for Disease Control and Prevention (CDC), individuals are considered to be in the healthy weight range if their BMI (kg/m2) is between 18.5 and<25. They are classified as overweight if their BMI is ≥ 25, obese class I if their BMI is between 30 and<35, obese class II if their BMI is between 35 and<40, and obese class III if their BMI is 40 or higher. Logistic regression analysis was employed to quantify the association between paternal obesity and urogenital conditions in offspring. Significant differences in median (minimum-maximum) paternal BMI values were noted between the cases and controls at the time of conception (cases: 27.7 (43-20.1), controls: 24.8 (40.7-19.6); p<0.0001). Logistic regression analysis confirmed that at the time of conception, compared to normal-weight fathers, overweight fathers displayed a heightened risk of offspring congenital malformations, with an odds ratio (OR) of 4.44 (95% CI=2.1-9.1). Similarly, fathers categorized as obese Class I at conception had approximately eight times higher odds (OR=8.62, 95% CI=2.91-25.52) of having offspring with urogenital conditions compared to normal-weight fathers. Additionally, fathers classified as obese Class II at conception exhibited 5.75 times higher odds (OR=5.75, 95% CI=0.96-34.44) of having offspring with urogenital conditions in comparison to normal-weight fathers. We found that the risk of urogenital malformations increased with paternal BMI during the preconceptional period. The findings suggest the importance of addressing paternal obesity in efforts to reduce the risk of urogenital congenital malformations in offspring.

Associations Between Paternal Obesity and Cardiometabolic Alterations in Offspring via Assisted Reproductive Technology.

Both assisted reproductive technology (ART) and obesity are associated with adverse cardiometabolic alterations in offspring. However, the combined effects of paternal obesity and ART on offspring cardiometabolic health are still unclear. To clarify cardiometabolic changes in offspring of obese fathers conceived using ART. This was a retrospective cohort study conducted between June 2014 and October 2019 at a center for reproductive medicine. A total of 2890 singleton visits aged 4-10 years were followed. Age-and sex-specific z-score of body mass index (BMI), blood pressure, insulin resistance, and lipid profile were examined. We observed a strong association between paternal BMI categories and offspring BMI, blood pressure, and insulin resistance. Compared with offspring of fathers with normal weight, multivariable-adjusted mean differences for BMI z-score were 0.53 (95% CI 0.37-0.68) for obese fathers, 0.17 (95% CI 0.05-0.30) for overweight fathers, and -0.55 (95% CI -0.95-0.15) for underweight fathers; corresponding values for systolic blood pressure z-score were 0.21(95% CI 0.07-0.35), 0.10 (95% CI -0.01-0.21), and -0.24 (95% CI -0.59-0.11), and corresponding values for homeostatic model assessment for insulin resistance z-score were 0.31 (95% CI 0.16-0.46), 0.09 (95% CI -0.02-0.21), and -0.11 (95% CI -0.48-0.28), respectively. The mediation analyses suggested that 57.48% to 94.75% of the associations among paternal obesity and offspring cardiometabolic alterations might be mediated by offspring BMI. Paternal obesity was associated with an unfavorable cardiometabolic profile in ART-conceived offspring. Mediation analyses indicated that offspring BMI was a possible mediator of the association between paternal obesity and the offspring impaired metabolic changes.

Integrating multiple lines of evidence to assess the effects of maternal BMI on pregnancy and perinatal outcomes

BackgroundHigher maternal pre-pregnancy body mass index (BMI) is associated with adverse pregnancy and perinatal outcomes. However, whether these associations are causal remains unclear.MethodsWe explored the relation of maternal pre-/early-pregnancy BMI with 20 pregnancy and perinatal outcomes by integrating evidence from three different approaches (i.e. multivariable regression, Mendelian randomisation, and paternal negative control analyses), including data from over 400,000 women.ResultsAll three analytical approaches supported associations of higher maternal BMI with lower odds of maternal anaemia, delivering a small-for-gestational-age baby and initiating breastfeeding, but higher odds of hypertensive disorders of pregnancy, gestational hypertension, preeclampsia, gestational diabetes, pre-labour membrane rupture, induction of labour, caesarean section, large-for-gestational age, high birthweight, low Apgar score at 1 min, and neonatal intensive care unit admission. For example, higher maternal BMI was associated with higher risk of gestational hypertension in multivariable regression (OR = 1.67; 95% CI = 1.63, 1.70 per standard unit in BMI) and Mendelian randomisation (OR = 1.59; 95% CI = 1.38, 1.83), which was not seen for paternal BMI (OR = 1.01; 95% CI = 0.98, 1.04). Findings did not support a relation between maternal BMI and perinatal depression. For other outcomes, evidence was inconclusive due to inconsistencies across the applied approaches or substantial imprecision in effect estimates from Mendelian randomisation.ConclusionsOur findings support a causal role for maternal pre-/early-pregnancy BMI on 14 out of 20 adverse pregnancy and perinatal outcomes. Pre-conception interventions to support women maintaining a healthy BMI may reduce the burden of obstetric and neonatal complications.FundingMedical Research Council, British Heart Foundation, European Research Council, National Institutes of Health, National Institute for Health Research, Research Council of Norway, Wellcome Trust.

Effect of paternal body mass index on maternal and child-health outcomes of singletons after frozen-thawed embryo transfer cycles: a retrospective study

The objective was to analyze the effect of paternal body mass index (BMI) on maternal and child-health outcomes of singletons after frozen-thawed embryo transfer (FET) cycles. A retrospective cohort study was conducted between January 2019 and December 2021. Pregnancy, perinatal complications and neonatal outcomes were compared among different paternal BMI. Multivariate logistic regression was performed to evaluate the relationship between different paternal BMI and pregnancy, obstetric and neonatal outcomes. The paternal normal group was more likely to suffer from gestational hypertension than the paternal obesity group (3.59% vs. 2.42%), and paternal underweight group was more likely to suffer from preeclampsia than the other three groups (11.63% vs. 4.43%, 7.57%, 4.03%). Birthweight among infants in the paternal overweight categories was significantly higher than infants in the paternal normal weight categories. The rate of foetal macrosomia was higher among infants in the paternal overweight (12.36%) category, while lower among infants in the paternal underweight categories (2.33%). The incidence of macrosomia in the paternal overweight categories (aOR 1.527, 95% CI 1.078–2.163) was significantly higher than those normal controls after adjustment for known confounding factors. The rates of LGA babies were higher in the paternal overweight category (aOR 1.260, 95% CI 1.001–1.587) compared with those in the paternal normal weight category, before and after adjustment. The results suggest that parental pre-pregnancy overweight or obesity has an adverse effect on the perinatal complications and neonatal outcomes.

FTO and MC4R polymorphisms, and selected pre-, peri- and postnatal factors as determinants of body mass index and fatness in children: a thorough analysis of the associations

BackgroundOverweight and obesity among children have become significant global health concerns. Previous studies have highlighted the potential role of genetic factors, particularly polymorphisms in the FTO and MC4R genes, as well as environmental factors in the development of childhood obesity. This study aimed to investigate the relationships between genetic, socioeconomic and perinatal factors, adverse childhood events (ACEs), and lifestyle, and their impact on overweight, obesity and body composition parameters in children. Additionally, we explored potential interactions between genetic factors and ACEs.MethodsFour hundred fifty-six children aged 6–12 years participated in our study. Information on the socioeconomic status, perinatal factors, ACEs and lifestyle of the children was collected with a questionnaire completed by their parents/guardians. We examined the children’s body weight and conducted an electrical bioimpedance analysis. Overweight and obesity were diagnosed based on the International Obesity Task Force and McCarthy criteria. We genotyped two selected polymorphisms in the FTO and MC4R genes using the TaqMan SNP allelic discrimination method.ResultsHigher BMI (Body Mass Index) z scores were related to higher paternal BMI and lower maternal age at the child’s birth. Higher FMI (Fat Mass Index) z scores were associated with higher paternal BMI, increased gestational weight, lower maternal education and the presence of the FTO risk allele. Higher FatM (fat mass in kg) z scores were linked to lower maternal education, lower maternal age at the child’s birth, higher maternal body weight gain, paternal BMI and the presence of the FTO risk allele. Moreover, interaction effects were observed on BMI z scores between ACE and FTO AA, and on FMI z scores and FatM z scored between ACE and MC4R CC.ConclusionsThe contribution of environmental factors is more strongly related to changes in body composition than genetic ones. Additionally, the presence of the risk allele combined with unfavourable environmental factors like ACEs leads to visible interaction effects, resulting in increased BMI z scores and FMI z scores in children.

Body mass index in parents and their adult offspring: A systematic review and meta-analysis.

Obesity may track across generations, due to genetics and shared family environmental factors, or possibly intrauterine programming. However, many studies only assess associations between maternal body mass index (BMI) and offspring BMI in childhood. To determine whether maternal and paternal associations with offspring BMI differ and whether associations persist into adulthood, a systematic review and meta-analysis was done. PubMed, Embase, Web of Science, and Google Scholar (to October 2022) were searched. Observational studies reporting associations between maternal or paternal BMI and adult offspring BMI were included. Offspring BMIs were reported as continuous or categorical measures. Forty-six studies were included in the systematic review. Meta-analyses were conducted using random-effects models. Parental BMI was positively associated with offspring BMI in adulthood. The pooled mother-offspring standardized mean difference (SMD) was 0.23 (95% confidence interval [CI]: 0.20, 0.26), and father-offspring SMD was similar: 0.22 (95% CI: 0.19, 0.25) in adjusted models. Offspring of mothers with overweight or obesity had the same risk of higher BMI as offspring of fathers with overweight or obesity. If these associations are causal, they support interventions targeting all family members, rather than focusing solely on mothers, to obtain a healthy weight development among offspring.

O-071 Paternal body mass index affects early embryo development but does not impact clinical outcomes: a timelapse study of 7,656 embryos in oocyte donation cycles

Abstract Study question Does paternal body mass index (BMI) affect preimplantation development and clinical outcomes in oocyte donation cycles? Summary answer High paternal BMI was associated with delays in early development and poorer embryo quality on day 3, but this did not adversely affect pregnancy outcomes. What is known already Maternal obesity is known to negatively affect preimplantation development and clinical outcomes. While oocyte competence plays a major role in early embryogenesis, male obesity has been linked to poorer semen parameters and epigenetic alterations in sperm. Such characteristics may inherently compromise preimplantation development and ultimately impair reproductive success. Only a few reports have assessed the effects of male BMI on the progression of cell divisions and embryo morphokinetic patterns. However, current findings remain contradictory, while the effects of male obesity on fertility continue to be understudied. Study design, size, duration This retrospective study included 7,656 embryos from 1,342 oocyte donation ICSI cycles, performed between April 2018 and December 2021 across two fertility centres. Sperm originated from the partner (n = 1087) or donor (n = 255) and was either fresh (n = 460) or frozen (n = 835). Only the first fresh (n = 1,140) or frozen (n = 202) embryo transfer (ET) was considered. Our database included 1,089 single and 238 double ETs performed at either the cleavage (n = 424) or blastocyst stage (n = 903) of development. Participants/materials, setting, methods Males were stratified according to BMI, based on WHO guidelines, defined as: normal weight (BMI&amp;lt;24.9, n = 677); pre-obese, (BMI=25.0–29.9, n = 533); and obese (BMI&amp;gt;30, n = 132). Patients with severe male factor and preimplantation genetic testing cycles were excluded. Univariate analyses and logistic regression were used to evaluate associations between BMI, embryo morphokinetics and clinical outcomes. Analyses were adjusted for various confounders pertaining to patient demographics, sperm and cycle parameters. A p-value of &amp;lt; 0.05 was considered significant. Main results and the role of chance Overall, obese men displayed poorer sperm motility and underwent more day 2-4 embryo transfers and freeze-all cycles, compared to pre-obese and normal weight men (p &amp;lt; 0,05). Fertilization rates were not affected by male BMI (77.0% ± 18.9 normal weight; 77.4% ± 18.1 pre-obese; 75.3% ± 19.9 obese; p = 0.62), also in our adjusted analysis. Several morphokinetic parameters were delayed in embryos from pre-obese and obese patients, including pronuclei fading (tPNf, p = 0.0064) and division timings from the 2 to 5-cell stage (t2-t3-t4-t5, p &amp;lt; 0,05). Successively, the number of good quality cleavage embryos decreased significantly with higher BMI (normal weight, 62%; pre-obese, 59%; obese, 50.8%; p = 0.02). In contrast, developmental events past the 5-cell stage, including time to 8-cells (t8), blastulation (tSB) and expanded blastocyst (tB) were comparable amongst the groups (p &amp;gt; 0.05). Similarly, we observed no effect of male BMI on blastocyst quality (normal weight, 70.2%; pre-obese, 73.4%; obese, 75.5%; p = 0.06). Despite early developmental delays, we observed no significant effects on biochemical pregnancy (normal weight, 64.7%; pre-obese 64.1%; obese, 58.7%; p = 0.45), ongoing pregnancy (normal weight, 60.0%; pre-obese, 58.8%; obese, 52.9%; p = 0.35) and live birth rate (normal weight, 41.9%; pre-obese, 42.0%; obese, 34.9%; p = 0.27). Our adjusted analysis corroborated these findings. Limitations, reasons for caution The main limitation of this study is its retrospective design, which may not account for all confounders. Moreover, lifestyle factors, such as smoking or alcohol consumption were not considered. As such, results cannot be generalized to all patient populations. Wider implications of the findings Obese males show lower motile sperm counts and delayed cleavage development. While these changes impaired day 3 embryo quality, they did not affect blastocyst development and quality. That translates into comparable clinical outcomes, suggesting that specific counselling is not required in obese patients. Trial registration number not applicable

Risk factors of persistent adolescent thinness: findings from the UK Millennium Cohort Study

BackgroundThinness during adolescence can increase the risk of adverse health outcomes across the life-course and impede development. There is limited research examining the prevalence and determinants of persistent adolescent thinness in the United Kingdom (UK). We used longitudinal cohort data to investigate determinants of persistent adolescent thinness.MethodsWe analyzed data from 7,740 participants in the UK Millennium Cohort Study at ages 9 months, 7, 11, 14 and 17 years. Persistent thinness was defined as thinness at ages 11, 14 and 17; thinness was defined as an age- and sex-adjusted Body Mass Index (BMI) of less than 18.5 kg/m2. In total, 4,036 participants, classified either as persistently thin or at a persistent healthy weight, were included in the analyses. Logistic regression analyses were conducted to examine associations between 16 risk factors and persistent adolescent thinness by sex.ResultsThe prevalence of persistent thinness among adolescents was 3.1% (n = 231). Among males (n = 115), persistent adolescent thinness was significantly associated with non-white ethnicity, low parental BMI, low birthweight, low breastfeeding duration, unintended pregnancy, and low maternal education. Among females (n = 116), persistent adolescent thinness was significantly associated with non-white ethnicity, low birthweight, low self-esteem, and low physical activity. However, after adjusting for all risk factors, only low maternal BMI (OR: 3.44; 95% CI:1.13, 10.5), low paternal BMI (OR: 22.2; 95% CI: 2.35, 209.6), unintended pregnancy (OR: 2.49; 95% CI: 1.11, 5.57) and low self-esteem (OR: 6.57; 95% CI: 1.46,29.7) remained significantly associated with persistent adolescent thinness among males. After adjustment for all risk factors, not reaching the recommended physical activity levels (OR: 4.22; 95% CI: 1.82, 9.75) remained significantly associated with persistent adolescent thinness among females. No appreciable associations were found between persistent adolescent thinness and sex, premature birth, smoking during pregnancy, income, maternal postnatal depression, mother-infant attachment or socio-emotional difficulties (p > 0.05).ConclusionPersistent adolescent thinness is not rare and appears to be associated with both physical and mental health factors, with some sex specific differences. Healthy weight initiatives should consider the full weight spectrum. Further research is required to understand thinness at a population level, including among those whose BMI changes during child and adolescent development.

Birth weight moderates the association between obesity and mortality rate

PurposeThe strength of the association between obesity and mortality rate (MR) varies by body mass index (BMI) and sociodemographic groups. We test the hypothesis that the association between obesity and MR varies, in part, due to the moderating effect of parental BMI and birth weight. MethodsData come from the 1958 National Child Development Study, an ongoing longitudinal dataset initiated in 1958 with baseline measures of birth weight from 18,059 infants born in Great Britain over 1 week. We tested whether the association between BMI and MR was moderated by parental BMI and birth weight using generalized additive proportional hazards models. ResultsThe association between adult BMI and MR was moderated by birth weight and maternal BMI, such that the association between BMI and MR was weaker among individuals with a higher birth weight (P = .0148) and stronger among individuals born to mothers with a higher BMI (P = .032). At any given level of BMI approximately greater than 25, individuals with low birth weight or born to mothers with a higher BMI, had a higher MR. Paternal BMI did not significantly modify the relationship between BMI and MR (P = .5168). ConclusionsResults suggest that the relationship between obesity and MR is modified by birth weight and maternal BMI.

Effects of paternal obesity on maternal-neonatal outcomes and long-term prognosis in adolescents.

This study evaluated whether paternal body mass index (BMI) before pregnancy was a risk factor for maternal-neonatal outcomes and long-term prognosis in offspring. This study included 29,518 participants from eight cities in Fujian, China using a stratified cluster random sampling method from May to September 2019. They were divided into four groups based on paternal BMI. Univariate and multivariate logistic regression were used to explore the relationship between paternal BMI groups, maternal-neonatal outcomes, and long-term prognosis in offspring. Further subgroup analysis was conducted to examine the stability of the risk. The incidences of hypertensive disorder complicating pregnancy (HDCP), cesarean delivery, gestational weight gain (GWG) over guideline, and macrosomia were significantly higher in the paternal overweight and obesity group. Importantly, this study demonstrated that the incidence of asthma, hand-foot-and-mouth disease (HFMD), anemia, dental caries, and obesity of adolescents in paternal obesity increased. Furthermore, logistic regression and subgroup analysis confirm paternal obesity is a risk factor for HDCP, cesarean delivery, and macrosomia. It caused poor long-term prognosis in adolescents, including asthma, dental caries, and HFMD. Paternal obesity is a risk factor for adverse maternal-neonatal outcomes and poor long-term prognosis in adolescents. In addition to focusing on maternal weight, expectant fathers should pay more attention to weight management since BMI is a modifiable risk factor. Preventing paternal obesity can lead to better maternal and child outcomes. It would provide new opportunities for chronic diseases.

Ten-Year Differences in Nutritional Status and Obesity-Related Risk Factors in Polish Preschool Children.

The aim of this study was to assess ten-year differences in nutritional statuses and obesity prevalences between populations of preschool children from Katowice, Poland, examined in 2007 and 2017, and to determine factors associated with overweight and obesity in preschool children. A cross-sectional questionnaire was conducted among parents and legal guardians of 276 preschool children in 2007 and 259 preschool children in 2017. Basic anthropometric measurements were performed. Overall, the prevalence of overweight and obesity among our sample of Polish preschool children (median age 5.25 year) was 16.82%, whereas 4.49% of children were obese. No significant differences in the number of overweight and obese children were observed when comparing the years 2017 to 2007. Overall body mass index (BMI) z-score was significantly lower in this group of children from 2017. However, median values of the BMI z-score were higher in two of the weight categories (overweight and obesity) in 2017. The child's BMI z-score was positively correlated with birth weight (r = 0.1, p < 0.05). The BMI z-score was positively correlated with maternal BMI, paternal BMI, and maternal pregnancy weight gain, r = 0.24 p < 0.01; r = 0.16 p < 0.01; r = 0.12 p < 0.05, respectively. A decrease in overweight and obesity prevalence over the past decade and higher median values of BMI z-scores in the group of children with excessive weight in 2017 were observed. Birth weight, maternal BMI, paternal BMI, and maternal pregnancy weight gain all correlate positively with a child's BMI z-score.

Effect of Paternal Body Mass Index on In Vitro Fertilization and Neonatal Outcomes among Oligozoospermia and Asthenospermia Patients.

Male overweight and obesity could affect sperm quality and reproductive health. However, the impact of body mass index (BMI) on assisted reproductive technology (ART) outcomes in oligospermia and/or asthenospermia patients is yet lacking. This study aims to assess the impact of paternal BMI on ART and neonatal outcomes among oligozoospermia and/or asthenospermia patients undergoing in vitro fertilization (IVF)/intracytoplasmic sperm injection (ICSI). In this study, 2,075 couples undergoing their first fresh embryo transfer between January 2015 and June 2022 were recruited. Following the World Health Organization's (WHO's) categories, couples were stratified into three cohorts based on paternal BMI: normal weight (18.5-24.9 kg/m²), overweight (25.0-29.9 kg/m²), and obese (≥30.0 kg/m²). Modified Poisson regression models were used to assess the associations of paternal BMI with fertilization, in vitro embryonic development, and pregnancy outcomes. Logistic regression models were performed to investigate the associations of paternal BMI with pregnancy loss and neonatal outcomes. Furthermore, stratified analyses were performed based on fertilization methods, male infertility cause, and maternal BMI. Higher paternal BMI is associated with a lower likelihood of achieving normal fertilized (p-trend=0.002), Day 3 transferable (p-trend=0.007), and high-quality embryos (p-trend=0.046) in IVF cycles, rather than in ICSI cycles. Paternal BMI of oligospermia or asthenospermia was negatively correlated with day 3 transferable (p-trend=0.013 and 0.030) and high-quality embryos (p-trend=0.024 and 0.027). Moreover, for neonatal outcomes, paternal BMI was positively associated with macrosomia (p-trend=0.019), large for gestational age (LGA) (p-trend=0.031), and very LGA (p-trend=0.045). Our data suggested that higher paternal BMI was associated with fetal overgrowth, reduced fertilization, and embryonic development potential. Among males with oligospermia and/or asthenospermia, the impact of overweight and obesity on the choice of fertilization method and the long-term effects on their offspring need to be further investigated.