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Fertility and Sterility Jun 2019Parental excess weight and especially pregestational maternal obesity and excessive weight gain during pregnancy have been related to an increased risk of metabolic... (Review)
Review
Parental excess weight and especially pregestational maternal obesity and excessive weight gain during pregnancy have been related to an increased risk of metabolic (obesity, type 2 diabetes, cardiovascular disease, metabolic syndrome) and nonmetabolic (cancer, osteoporosis, asthma, neurologic alterations) diseases in the offspring, probably mediated by epigenetic mechanisms of fetal programming. Maternal underweight is less common in developed societies, but the discrepancy between a poor nutritional environment in utero and a normal or excessive postnatal food supply with rapid growth catch-up appears to be the main candidate mechanism of the development of chronic diseases during the offspring's adulthood. The role of the postnatal environment in both scenarios (parental overweight or underweight) also seems to influence the offspring's health. Lifestyle interventions before and during pregnancy in both parents, but especially in the mother, as well as in children after birth, are advisable to counteract the many undesirable chronic conditions described.
Topics: Adolescent; Adolescent Behavior; Adolescent Development; Age Factors; Child; Child Behavior; Child Development; Child Health; Child of Impaired Parents; Child, Preschool; Disease Susceptibility; Female; Gestational Weight Gain; Health Status; Humans; Infant; Infant, Newborn; Male; Maternal Health; Overweight; Pregnancy; Pregnancy Outcome; Risk Assessment; Risk Factors; Thinness
PubMed: 31036339
DOI: 10.1016/j.fertnstert.2019.02.128 -
Drug and Alcohol Dependence Jan 2022Alcohol-use disorders (AUD) in parents are associated with adverse outcomes in offspring. It is less known whether other forms of parental drinking such as binge...
BACKGROUND
Alcohol-use disorders (AUD) in parents are associated with adverse outcomes in offspring. It is less known whether other forms of parental drinking such as binge drinking may also be a risk factor for offspring's outcomes -- specifically, high school non-completion.
METHODS
These questions were examined in a sample of 3101 offspring (M = 16.1 , SD = 1.68; 49.5% girls) from 2510 2-parent families who participated in the Nord-Trøndelag Health Study in Norway (HUNT3; Young-HUNT3) in 2006-08 and were followed-up through the National Education Database (NUDB) until 2014. Associations between maternal and paternal binge drinking patterns as reported in HUNT during offspring's adolescence and offspring's subsequent high school completion were examined using logistic regression models while accounting for a comprehensive set of socio-demographic, parental, and offspring characteristics as assessed at HUNT baseline. Effect modifications of these putative associations by offspring characteristics were also explored.
FINDINGS
Approximately 1 in 6 offspring (13.6% girls, 21.1% boys) failed to graduate high school within the officially designated time period, while roughly 1 in 5 mothers (20.4%) and 1 in 2 fathers (51.2%) reported any binge drinking. Weekly or more frequent binge drinking in fathers was prospectively associated with more than doubled odds of high school non-completion in offspring; OR = 2.23, 95% CI = 1.50-3.31. This effect remained substantively identical after adjustment for all covariates (aOR = 2.20, 95% CI = 1.38-3.50) and uniform across offspring characteristics such as gender, academic orientation and performance, anxiety and depression, typical alcohol consumption, and witnessing parental intoxication as assessed at HUNT baseline.
CONCLUSIONS
Weekly or more frequent binge drinking in fathers negatively affected high school graduation prospects in their offspring.
Topics: Adolescent; Alcohol Drinking; Binge Drinking; Fathers; Female; Humans; Male; Parents; Prospective Studies; Registries; Schools
PubMed: 34896931
DOI: 10.1016/j.drugalcdep.2021.109189 -
BMJ Open Jul 2022Hyperglycaemia during pregnancy is associated with cardiometabolic risks for the mother and the offspring. Mothers with gestational diabetes mellitus (GDM) have signs of...
OBJECTIVE
Hyperglycaemia during pregnancy is associated with cardiometabolic risks for the mother and the offspring. Mothers with gestational diabetes mellitus (GDM) have signs of subclinical atherosclerosis, including increased carotid intima-media thickness (CIMT). We assessed whether GDM is associated with increased CIMT in the offspring at birth.
DESIGN AND SETTING
MySweetHeart Cohort is a prospective cohort study conducted in Switzerland.
PARTICIPANTS, EXPOSURE AND OUTCOME MEASURES
This work included pregnant women with and without GDM at 24-32 weeks of gestation and their singleton live-born offspring with data on the primary outcome of CIMT. GDM was diagnosed based on the criteria of the International Association of Diabetes and Pregnancy Study Groups. Offspring's CIMT was measured by ultrasonography after birth (range 1-19 days).
RESULTS
Data on CIMT were available for 99 offspring of women without GDM and 101 offspring of women with GDM. Maternal age ranged from 18 to 47 years. Some 16% of women with GDM and 6% of women without GDM were obese. Smoking during pregnancy was more frequent among women with GDM (18%) than among those without GDM (4%). Neonatal characteristics were comparable between the two groups. The difference in CIMT between offspring of women with and without GDM was of 0.00 mm (95% CI -0.01 to 0.01; p=0.96) and remained similar on adjustment for potential confounding factors, such as maternal prepregnancy body mass index, maternal education, smoking during pregnancy, family history of diabetes, as well as offspring's sex, age, and body surface area (0.00 mm (95% CI -0.02 to 0.01; p=0.45)).
CONCLUSIONS
We found no evidence of increased CIMT in neonates exposed to GDM. A longer-term follow-up that includes additional vascular measures, such as endothelial function or arterial stiffness, may shed further light on the cardiovascular health trajectories in children born to mothers with GDM.
TRIAL REGISTRATION NUMBER
NCT02872974; Pre-results.
Topics: Adolescent; Adult; Body Mass Index; Carotid Intima-Media Thickness; Child; Cohort Studies; Diabetes, Gestational; Female; Humans; Infant, Newborn; Middle Aged; Pregnancy; Prospective Studies; Young Adult
PubMed: 35882452
DOI: 10.1136/bmjopen-2022-061649 -
Life (Basel, Switzerland) Apr 2022Maternal exposure to some dietary and environmental factors during embryonic development can affect offspring's phenotype and, furthermore, the risk of developing... (Review)
Review
Maternal exposure to some dietary and environmental factors during embryonic development can affect offspring's phenotype and, furthermore, the risk of developing diseases later in life. One potential mechanism responsible for this early programming may be the modification of the epigenome, such as DNA methylation. Methyl-group donors are essential for DNA methylation and are shown to have an important role in fetal development and later health. The main goal of the present review is to summarize the available literature data on the epigenetic effect (DNA methylation) of maternal methyl-group donor availability on reproductivity, perinatal outcome, and later health of the offspring. In our literature search, we found evidence for the association between alterations in DNA methylation patterns caused by different maternal methyl-group donor (folate, choline, methionine, betaine) intake and reproductivity, birth weight, neural tube defect, congenital heart defect, cleft lip and palate, brain development, and the development of obesity and associated non-communicable diseases in later life. We can conclude that maternal methyl-group donor availability could affect offspring's health via alterations in DNA methylation and may be a major link between early environmental exposure and the development of diseases in the offspring. However, still, further studies are necessary to confirm the associations and causal relationships.
PubMed: 35629277
DOI: 10.3390/life12050609 -
Appetite Apr 2024The internal (i.e., interoceptive) sensations that characterise hunger vary between people, and this may also be the case for thirst, although it has not been so well...
The internal (i.e., interoceptive) sensations that characterise hunger vary between people, and this may also be the case for thirst, although it has not been so well explored. There are probably both heritable and learning-based causes for this interoceptive variability. Consequently, it would seem plausible that parents and their offspring would have more similar patterns of hunger and thirst than pairs of strangers. We tested this idea, in addition to exploring its potential moderating variables, by studying the similarity of self-reported hunger and thirst sensations in 170 students and their primary caregivers from childhood. Both students and caregivers completed the same online-survey, covering hunger and thirst sensations, beliefs about the causes of hunger and thirst, the Three Factor Eating Questionnaire (revised) and demographic data. We find evidence of robust student-caregiver similarity in interoceptive hunger and thirst sensations (medium effect sizes), with these being moderated by caregiver beliefs about the homeostatic nature of each state (medium effect sizes). This suggests a potential role for caregivers in the development of their offspring's interoceptive cues for hunger and for thirst. In addition, thirst, like hunger, appears to be multidimensional, and varies between people. The implications of these findings are discussed.
Topics: Humans; Child; Hunger; Thirst; Sensation; Learning; Cues
PubMed: 38218415
DOI: 10.1016/j.appet.2024.107208 -
Animals : An Open Access Journal From... Oct 2021The dams of gregarious animals must develop a close bond with their newborns to provide them with maternal care, including protection against predators, immunological... (Review)
Review
The dams of gregarious animals must develop a close bond with their newborns to provide them with maternal care, including protection against predators, immunological transference, and nutrition. Even though lactation demands high energy expenditures, behaviors known as allonursing (the nursing of non-descendant infants) and allosuckling (suckling from any female other than the mother) have been reported in various species of wild or domestic, and terrestrial or aquatic animals. These behaviors seem to be elements of a multifactorial strategy, since reports suggest that they depend on the following: species, living conditions, social stability, and kinship relations, among other group factors. Despite their potential benefits, allonursing and allosuckling can place the health and welfare of both non-filial dams and alien offspring at risk, as it augments the probability of pathogen transmission. This review aims to analyze the biological and physiological foundations and bioenergetic costs of these behaviors, analyzing the individual and collective advantages and disadvantages for the dams' own offspring(s) and alien neonate(s). We also include information on the animal species in which these behaviors occur and their implications on animal welfare.
PubMed: 34827824
DOI: 10.3390/ani11113092 -
Experimental Diabetes Research 2011The adverse outcomes on the offspring from maternal diabetes in pregnancy are substantially documented. In this paper, we report main knowledge on impacts of maternal... (Review)
Review
The adverse outcomes on the offspring from maternal diabetes in pregnancy are substantially documented. In this paper, we report main knowledge on impacts of maternal diabetes on early and long-term health of the offspring, with specific comments on maternal obesity. The main adverse outcome on progenies from pregnancy complicated with maternal diabetes appears to be macrosomia, as it is commonly known that intrauterine exposure to hyperglycemia increases the risk and programs the offspring to develop diabetes and/or obesity at adulthood. This "fetal programming", due to intrauterine diabetic milieu, is termed as "metabolic memory". In gestational diabetes as well as in macrosomia, the complications include metabolic abnormalities, degraded antioxidant status, disrupted immune system and potential metabolic syndrome in adult offspring. Furthermore, there is evidence that maternal obesity may also increase the risk of obesity and diabetes in offspring. However, women with GDM possibly exhibit greater macrosomia than obese women. Obesity and diabetes in pregnancy have independent and additive effects on obstetric complications, and both require proper management. Management of gestational diabetes mellitus and maternal obesity is essential for maternal and offspring's good health. Increasing physical activity, preventing gestational weight gain, and having some qualitative nutritional habits may be beneficial during both the pregnancy and offspring's future life.
Topics: Adult; Animals; Antioxidants; Diabetes, Gestational; Female; Fetal Macrosomia; Humans; Infant, Newborn; Inflammation; Insulin Resistance; Lipid Metabolism; Models, Biological; Obesity; Pregnancy; Pregnancy Complications; Pregnancy Outcome; Pregnancy in Diabetics; Prenatal Exposure Delayed Effects
PubMed: 22144985
DOI: 10.1155/2011/218598 -
BioMed Research International 2018Obesity or maternal overnutrition during pregnancy and lactation might have long-term consequences in offspring health. Fetal programming is characterized by adaptive... (Review)
Review
Obesity or maternal overnutrition during pregnancy and lactation might have long-term consequences in offspring health. Fetal programming is characterized by adaptive responses to specific environmental conditions during early life stages. Programming alters gene expression through epigenetic modifications leading to a transgenerational effect of behavioral phenotypes in the offspring. Maternal intake of hypercaloric diets during fetal development programs aberrant behaviors resembling addiction in offspring. Programming by hypercaloric surplus sets a gene expression pattern modulating axonal pruning, synaptic signaling, and synaptic plasticity in selective regions of the reward system. Likewise, fetal programming can promote an inflammatory phenotype in peripheral and central sites through different cell types such as microglia and T and B cells, which contribute to disrupted energy sensing and behavioral pathways. The molecular mechanism that regulates the central and peripheral immune cross-talk during fetal programming and its relevance on offspring's addictive behavior susceptibility is still unclear. Here, we review the most relevant scientific reports about the impact of hypercaloric nutritional fetal programming on central and peripheral inflammation and its effects on addictive behavior of the offspring.
Topics: Animals; Behavior, Addictive; Female; Fetal Development; Inflammation; Maternal Nutritional Physiological Phenomena; Obesity; Overnutrition; Pregnancy; Prenatal Exposure Delayed Effects
PubMed: 30027100
DOI: 10.1155/2018/8061389 -
Children (Basel, Switzerland) Oct 2022The aim of the present review was to explore the effect of parental misperceptions of their offspring's weight status during childhood and early adolescence on weight... (Review)
Review
The aim of the present review was to explore the effect of parental misperceptions of their offspring's weight status during childhood and early adolescence on weight control strategies and children's eating behavior. Literature searching was limited to the PubMed database and to the English language from January 2000 to August 2022. Eligible studies had clearly associated parental misperception of offspring's weight with child eating habits or weight management and eating strategies in childhood to early adolescence. Sixteen studies (14 cross-sectional, 1 longitudinal and 1 with cross-sectional and longitudinal analyses) were included in the analysis. Weight loss attempts and child's eating behavior were the main outcomes. Sixteen studies found significant associations. Parental misperceptions of their offspring's weight status do influence their child's weight and eating behavior, especially in overweight children. Parents tend to follow potentially harmful methods when they overestimate their children's weight (food restriction) and when they underestimate their children's weight (pressure to eat). However, additional longitudinal studies are needed to better understand the impact of parental weight status perception on health behaviors and children's weight gain over time. The potential need for preventive intervention studies is warranted.
PubMed: 36291501
DOI: 10.3390/children9101565 -
Molecular and Cellular Endocrinology Nov 2016Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine disorder with both reproductive and metabolic abnormalities affecting women of reproductive age. While the... (Review)
Review
Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine disorder with both reproductive and metabolic abnormalities affecting women of reproductive age. While the exact origin of PCOS is unknown, observations from clinical and animal studies suggest that maternal hyperandrogenism may be a contributing factor. Because women with PCOS manifest hyperandrogenism during pregnancy, changes in the gestational endocrine milieu may play a role in the vertical transmission of this syndrome. This review discusses the potential developmental origins of PCOS, the impact of maternal PCOS on the offspring's health and contributions of the postnatal environment, capitalizing on findings from animal models that exhibit a PCOS-like phenotype. In addition, this review highlights the scarcity of data at early gestational stages in humans and the importance of animal experimentation to better understand the cellular and molecular mechanisms involved in the programming of adult diseases, therefore, helping identify therapeutic targets for preventive and treatment strategies.
Topics: Adult; Animals; Disease Models, Animal; Female; Humans; Hyperandrogenism; Phenotype; Polycystic Ovary Syndrome; Pregnancy; Prenatal Exposure Delayed Effects
PubMed: 26639019
DOI: 10.1016/j.mce.2015.11.030