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Annals of Allergy, Asthma & Immunology... Aug 2022Maternal obesity may affect offspring asthma and atopic disease risk by altering fetal immune system development. However, few studies evaluate gestational weight gain...
BACKGROUND
Maternal obesity may affect offspring asthma and atopic disease risk by altering fetal immune system development. However, few studies evaluate gestational weight gain (GWG).
OBJECTIVE
To evaluate relationships between maternal body mass index (BMI), GWG, and persistent wheeze, eczema, allergy, and asthma risk in offspring through middle childhood.
METHODS
A total of 5939 children from Upstate KIDS, a population-based longitudinal cohort of children born in upstate New York (2008-2019) were included in the analysis. Persistent wheeze or asthma, eczema, and allergy were maternally reported at multiple study time points throughout early and middle childhood. Poisson regression models with robust SEs were used to estimate adjusted risk ratios (aRRs) and 95% confidence intervals (CIs) for offspring atopic outcomes by maternal prepregnancy BMI and GWG.
RESULTS
Prepregnancy BMI was associated with increased risk of persistent wheeze by 3 years of age even after adjustments for maternal atopy (class I obesity: aRR, 1.58; 95% CI, 1.13-2.20; class II or III obesity: aRR, 1.69; 95% CI, 1.22-2.35). Associations with reported asthma in middle childhood did not reach statistical significance. Furthermore, no associations were found between prepregnancy BMI and atopic outcomes in either early or middle childhood. GWG was not associated with higher risk of early childhood persistent wheeze or middle childhood asthma.
CONCLUSION
Maternal prepregnancy BMI was associated with increased risk of offspring wheeze, whereas excessive GWG was generally not associated with childhood asthma or atopy.
Topics: Asthma; Body Mass Index; Child; Child, Preschool; Eczema; Female; Gestational Weight Gain; Humans; Hypersensitivity; Obesity; Obesity, Maternal; Pregnancy; Respiratory Sounds; Risk Factors; Weight Gain
PubMed: 35552010
DOI: 10.1016/j.anai.2022.04.032 -
Journal of Public Health (Oxford,... Sep 2016Maternal obesity is emerging as a public health problem, recently highlighted together with maternal under-nutrition as a 'double burden', especially in African... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Maternal obesity is emerging as a public health problem, recently highlighted together with maternal under-nutrition as a 'double burden', especially in African countries undergoing social and economic transition. This systematic review was conducted to investigate the current evidence on maternal obesity in Africa.
METHODS
MEDLINE, EMBASE, Scopus, CINAHL and PsycINFO were searched (up to August 2014) and identified 29 studies. Prevalence, associations with socio-demographic factors, labour, child and maternal consequences of maternal obesity were assessed. Pooled risk ratios comparing obese and non-obese groups were calculated.
RESULTS
Prevalence of maternal obesity across Africa ranged from 6.5 to 50.7%, with older and multiparous mothers more likely to be obese. Obese mothers had increased risks of adverse labour, child and maternal outcomes. However, non-obese mothers were more likely to have low-birthweight babies. The differences in measurement and timing of assessment of maternal obesity were found across studies. No studies were identified either on the knowledge or attitudes of pregnant women towards maternal obesity; or on interventions for obese pregnant women.
CONCLUSIONS
These results show that Africa's levels of maternal obesity are already having significant adverse effects. Culturally adaptable/sensitive interventions should be developed while monitoring to avoid undesired side effects.
Topics: Africa; Age Factors; Female; Humans; Mothers; Obesity; Parity; Prevalence; Risk Factors
PubMed: 26487702
DOI: 10.1093/pubmed/fdv138 -
Nutrition Reviews Dec 2020In the United States and Mexico, the obesity epidemic represents a significant public health problem. Although obesity is often attributed to a Western-style, high-fat... (Review)
Review
In the United States and Mexico, the obesity epidemic represents a significant public health problem. Although obesity is often attributed to a Western-style, high-fat diet and decreased activity, there is now compelling evidence that this, in part, occurs because of the developmental programming effects resulting from exposure to maternal overnutrition. Human and animal studies demonstrate that maternal obesity and high-fat diet result in an increased risk for childhood and adult obesity. The potential programming effects of obesity have been partly attributed to hyperphagia, which occurs as a result of increased appetite with reduced satiety neuropeptides or neurons. However, depending on maternal nutritional status during the nursing period, the programmed hyperphagia and obesity can be exacerbated or prevented in offspring born to obese mothers. The underlying mechanism of this phenomenon likely involves the plasticity of the appetite regulatory center and thus presents an opportunity to modulate feeding and satiety regulation and break the obesity cycle.
Topics: Animals; Appetite; Diet, High-Fat; Diet, Western; Female; Humans; Hyperphagia; Infant; Infant Nutritional Physiological Phenomena; Infant, Newborn; Maternal Nutritional Physiological Phenomena; Obesity; Obesity, Maternal; Overnutrition; Pregnancy; Satiation
PubMed: 33196091
DOI: 10.1093/nutrit/nuaa121 -
Irish Journal of Medical Science Jun 2022Maternal obesity and depression are common and both have been associated with adverse pregnancy outcomes. (Observational Study)
Observational Study
BACKGROUND
Maternal obesity and depression are common and both have been associated with adverse pregnancy outcomes.
AIMS
The aim of this observational study was to examine the relationship between maternal body mass index (BMI) category and self-reported depression at the first antenatal visit.
METHODS
Women who delivered a baby weighing ≥ 500 g over nine years 2009-2017 were included. Self-reported sociodemographic and clinical details were computerised at the first antenatal visit by a trained midwife, and maternal BMI was calculated after standardised measurement of weight and height.
RESULTS
Of 73,266 women, 12,304 (16.7%) had obesity, 1.6% (n = 1126) reported current depression and 7.5% (n = 3277) multiparas reported a history of postnatal depression. The prevalence of self-reported maternal depression was higher in women who had obesity, > 35 years old, were socially disadvantaged, smokers, had an unplanned pregnancy and used illicit drugs. After adjustment for confounding variables, obesity was associated with an increased odds ratio (aOR) for current depression in both nulliparas (aOR 1.7, 95% CI 1.3-2.3, p < 0.001) and multiparas (aOR 1.8, 95% CI 1.5-2.1, p < 0.001) and postnatal depression in multiparas (aOR 1.4, 95% CI 1.3-1.5, p < 0.001). The prevalence of current depression was higher in women with moderate/severe obesity than in women with mild obesity (both p < 0.001).
CONCLUSIONS
We found that self-reported maternal depression in early pregnancy was independently associated with obesity. The prevalence of depression increased with the severity of obesity. Our findings highlight the need for implementation of strategies and provision of services for the prevention and treatment of both obesity and depression.
Topics: Adult; Body Mass Index; Depression; Depression, Postpartum; Female; Humans; Obesity; Obesity, Maternal; Pregnancy; Pregnancy Complications; Pregnancy Outcome
PubMed: 34131811
DOI: 10.1007/s11845-021-02665-5 -
Brain, Behavior, and Immunity May 2022The obesity epidemic affects 40% of adults in the US, with approximately one-third of pregnant women classified as obese. Previous research suggests that children born...
The obesity epidemic affects 40% of adults in the US, with approximately one-third of pregnant women classified as obese. Previous research suggests that children born to obese mothers are at increased risk for a number of health conditions. The mechanisms behind this increased risk are poorly understood. Increased exposure to in-utero inflammation induced by maternal obesity is proposed as an underlying mechanism for neurodevelopmental alterations in offspring. Utilizing a non-human primate model of maternal obesity, we hypothesized that maternal consumption of an obesogenic diet will predict offspring peripheral (e.g., cytokines and chemokines) and central (microglia number) inflammatory outcomes via the diet's effects on maternal adiposity and maternal inflammatory state during the third trimester. We used structural equation modeling to simultaneously examine the complex associations among maternal diet, metabolic state, adiposity, inflammation, and offspring central and peripheral inflammation. Four latent variables were created to capture maternal chemokines and pro-inflammatory cytokines, and offspring cytokine and chemokines. Model results showed that offspring microglia counts in the basolateral amygdala were associated with maternal diet (β = -0.622, p < 0.01), adiposity (β = 0.593, p < 0.01), and length of gestation (β = 0.164, p < 0.05) but not with maternal chemokines (β = 0.135, p = 0.528) or maternal pro-inflammatory cytokines (β = 0.083, p = 0.683). Additionally, we found that juvenile offspring peripheral cytokines (β = -0.389, p < 0.01) and chemokines (β = -0.298, p < 0.05) were associated with a maternal adiposity-induced decrease in maternal circulating chemokines during the third trimester (β = -0.426, p < 0.01). In summary, these data suggest that maternal diet and adiposity appear to directly predict offspring amygdala microglial counts while maternal adiposity influences offspring peripheral inflammatory outcomes via maternal inflammatory state.
Topics: Adiposity; Animals; Chemokines; Cytokines; Diet; Diet, High-Fat; Female; Humans; Inflammation; Obesity; Obesity, Maternal; Pregnancy; Prenatal Exposure Delayed Effects; Primates
PubMed: 35217175
DOI: 10.1016/j.bbi.2022.02.024 -
Placenta Jul 2015The prevalence of maternal obesity is rising rapidly worldwide and constitutes a major obstetric problem, increasing mortality and morbidity in both mother and... (Review)
Review
BACKGROUND
The prevalence of maternal obesity is rising rapidly worldwide and constitutes a major obstetric problem, increasing mortality and morbidity in both mother and offspring. Obese women are predisposed to pregnancy complications such as gestational diabetes mellitus (GDM), and children of obese mothers are more likely to develop cardiovascular and metabolic disease in later life. Maternal obesity and GDM may be associated with a state of chronic, low-grade inflammation termed "metainflammation", as opposed to an acute inflammatory response. This inflammatory environment may be one mechanism by which offspring of obese women are programmed to develop adult disorders.
METHODS
Herein we review the evidence that maternal obesity and GDM are associated with changes in the maternal, fetal and placental inflammatory profile.
RESULTS
Maternal inflammation in obesity and GDM may not always be associated with fetal inflammation.
CONCLUSION
We propose that the placenta 'senses' and adapts to the maternal inflammatory environment, and plays a central role as both a target and producer of inflammatory mediators. In this manner, maternal obesity and GDM may indirectly program the fetus for later disease by influencing placental function.
Topics: Animals; C-Reactive Protein; Diabetes, Gestational; Female; Fetal Diseases; Humans; Immune System; Inflammation; Insulin Resistance; Interleukin-6; Obesity; Placenta; Pregnancy; Pregnancy Complications; Prenatal Exposure Delayed Effects; Tumor Necrosis Factor-alpha
PubMed: 25972077
DOI: 10.1016/j.placenta.2015.04.006 -
Romanian Journal of Morphology and... 2022Maternal obesity is associated with increased maternal and fetal morbidity and mortality, with an increased risk of gestational diabetes mellitus (GDM) and preeclampsia...
Maternal obesity is associated with increased maternal and fetal morbidity and mortality, with an increased risk of gestational diabetes mellitus (GDM) and preeclampsia (PE). This prospective study histopathologically analyzes the placentas obtained from 34 pregnant obese women studied between October 2016 and May 2020. The 10 cases of term placentas from obese pregnancies with GDM and the 12 cases with PE were examined by the Hematoxylin-Eosin (HE), Masson's trichrome (MT) and Periodic Acid-Schiff-Hematoxylin (PAS-H) classical stainings, and by the immunohistochemical evaluation and compared to placentae from uncomplicated term obese pregnancies (12 cases). We did not meet placental histopathological (HP) abnormalities that we could classify as characteristic only for the state of obese pregnancy, but we did find placental changes associated with PE and GDM, in the context of obese pregnancy. In the case of association with PE, there were common lesions, manifested by intra- and perivillous fibrinoid deposition, calcification, and placental infarction area, to which were added numerous syncytial knots. In the case of obese pregnancy associated with GDM, we found, in addition to common placental lesions of obesity, intravillositary vascular edema and in the terminal villi appearing chorangiosis. This study revealed a number of HP changes that occur in maternal obesity, even in uncomplicated obese pregnancies. A characteristic of obese pregnancies associated with PE was the presence of numerous syncytial knots, and in obese pregnancies associated with GDM, the most common HP lesion was placental chorangiosis. Certainly, we cannot conclude that these HP lesions are specific to a particular pathology, but they belong primarily to the status of maternal obesity.
Topics: Diabetes, Gestational; Female; Hematoxylin; Humans; Obesity; Obesity, Maternal; Placenta; Pre-Eclampsia; Pregnancy; Pregnancy Outcome; Prospective Studies
PubMed: 36074672
DOI: 10.47162/RJME.63.1.09 -
Cancer Reports (Hoboken, N.J.) Dec 2022About 50 000 new cases of cancer in the United States are attributed to obesity. The adverse effects of obesity on breast cancer may be most profound when affecting... (Review)
Review
BACKGROUND
About 50 000 new cases of cancer in the United States are attributed to obesity. The adverse effects of obesity on breast cancer may be most profound when affecting the early development; that is, in the womb of a pregnant obese mother. Maternal obesity has several long-lasting adverse health effects on the offspring, including increasing offspring's breast cancer risk and mortality. Gut microbiota is a player in obesity as well as may impact breast carcinogenesis. Gut microbiota is established early in life and the microbial composition of an infant's gut becomes permanently dysregulated because of maternal obesity. Metabolites from the microbiota, especially short chain fatty acids (SCFAs), play a critical role in mediating the effect of gut bacteria on multiple biological functions, such as immune system, including tumor immune responses.
RECENT FINDINGS
Maternal obesity can pre-program daughter's breast cancer to be more aggressive, less responsive to treatments and consequently more likely to cause breast cancer related death. Maternal obesity may also induce poor response to immune checkpoint inhibitor (ICB) therapy through increased abundance of inflammation associated microbiome and decreased abundance of bacteria that are linked to production of SCFAs. Dietary interventions that increase the abundance of bacteria producing SCFAs potentially reverses offspring's resistance to breast cancer therapy.
CONCLUSION
Since immunotherapies have emerged as highly effective treatments for many cancers, albeit there is an urgent need to enlarge the patient population who will be responsive to these treatments. One of the factors which may cause ICB refractoriness could be maternal obesity, based on its effects on the microbiota markers of ICB therapy response among the offspring. Since about 40% of children are born to obese mothers in the Western societies, it is important to determine if maternal obesity impairs offspring's response to cancer immunotherapies.
Topics: Infant; Child; Humans; Female; Pregnancy; Obesity, Maternal; Breast Neoplasms; Dysbiosis; Obesity; Gastrointestinal Microbiome
PubMed: 36411524
DOI: 10.1002/cnr2.1752 -
Trends in Molecular Medicine Oct 2022The prevalence of maternal obesity is increasing at an alarming rate, and is providing a major challenge for obstetric practice. Adverse effects on maternal and fetal... (Review)
Review
The prevalence of maternal obesity is increasing at an alarming rate, and is providing a major challenge for obstetric practice. Adverse effects on maternal and fetal health are mediated by complex interactions between metabolic, inflammatory, and oxidative stress signaling in the placenta. Endoplasmic reticulum (ER) stress and activation of the unfolded protein response (UPR) are common downstream pathways of cell stress, and there is evidence that this conserved homeostatic response may be a key mediator in the pathogenesis of placental dysfunction. We summarize the current literature on the placental cellular and molecular changes that occur in obese women. A special focus is cast onto placental ER stress in obese pregnancy, which may provide a novel link for future investigation.
Topics: Endoplasmic Reticulum Stress; Female; Humans; Obesity; Obesity, Maternal; Placenta; Pregnancy; Unfolded Protein Response
PubMed: 35760668
DOI: 10.1016/j.molmed.2022.05.013 -
Journal of Hepatology Nov 2021Maternal obesity has been linked to the development of cardiovascular disease and diabetes in offspring, but its relationship to non-alcoholic fatty liver disease...
BACKGROUND & AIMS
Maternal obesity has been linked to the development of cardiovascular disease and diabetes in offspring, but its relationship to non-alcoholic fatty liver disease (NAFLD) is unclear.
METHODS
Through the nationwide ESPRESSO cohort study we identified all individuals ≤25 years of age in Sweden with biopsy-verified NAFLD diagnosed between 1992 and 2016 (n = 165). These were matched by age, sex, and calendar year with up to 5 controls (n = 717). Through linkage with the nationwide Swedish Medical Birth Register (MBR) we retrieved data on maternal early-pregnancy BMI, and possible confounders, in order to calculate adjusted odds ratios (aORs) for NAFLD in offspring.
RESULTS
Maternal BMI was associated with NAFLD in offspring: underweight (aOR 0.84; 95% CI 0.14-5.15), normal weight (reference, aOR 1), overweight (aOR 1.51; 0.95-2.40), and obese (aOR 3.26; 1.72-6.19) women. Severe NAFLD (biopsy-proven fibrosis or cirrhosis) was also more common in offspring of overweight (aOR 1.94; 95% CI 0.96-3.90) and obese (aOR 3.67; 95% CI 1.61-8.38) mothers. Associations were similar after adjusting for maternal pre-eclampsia and gestational diabetes. Socio-economic parameters (smoking, mother born outside the Nordic countries and less than 10 years of basic education) were also associated with NAFLD in offspring but did not materially alter the effect size of maternal BMI in a multivariable model.
CONCLUSIONS
This nationwide study found a strong association between maternal overweight/obesity and future NAFLD in offspring. Adjusting for socio-economic and metabolic parameters in the mother did not affect this finding, suggesting that maternal obesity is an independent risk factor for NAFLD in offspring.
LAY SUMMARY
In a study of all young persons in Sweden with a liver biopsy consistent with fatty liver, the authors found that compared to matched controls, the risk of fatty liver was much higher in those with obese mothers. This was independent of available confounders and suggests that the high prevalence of obesity in younger persons might lead to a higher risk of fatty liver in their offspring.
Topics: Adolescent; Adult; Body Mass Index; Case-Control Studies; Child; Child, Preschool; Cohort Studies; Female; Humans; Non-alcoholic Fatty Liver Disease; Obesity, Maternal; Pregnancy; Risk Factors; Sweden
PubMed: 34289397
DOI: 10.1016/j.jhep.2021.06.045