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Maternal obesity affects about 15-20% of pregnancies posing serious risks for both mothers and children. Obese mothers are three times more likely to develop gestational diabetes, preeclampsia, and other complications during labor. Maternal obesity can also disrupt normal endocrine function, which may affect fetal development and increase the child’s long-term risk of obesity and metabolic disorders. Endocrine-disrupting chemicals in the environment further exacerbate these risks by interfering with hormone regulation in both the mother and fetus. It is important to have targeted interventions, including minimizing exposure to harmful chemicals and improving prenatal care to support healthier outcomes for both mother and child. [1]

Maternal obesity during pregnancy can program offspring to develop metabolic and cardiovascular diseases. It highlights that such programming effects are influenced by the interplay between sex chromosomes and gonadal hormones. Specific gene expressions, such as those related to the X chromosome and maternal obesity, can lead to significant long-term health issues. The study emphasizes the importance of early interventions, particularly in addressing maternal health, to mitigate these programming effects on offspring's health. Further research is needed to understand the genetic and hormonal mechanisms behind sex differences in metabolic diseases. Early nutritional interventions in maternal health could prevent or reduce these long-term health impacts on offspring.[2]

Obesity in pregnancy not only can affect the mother but the child as well. Infants born to obese mothers are at a higher risk for several health complications. These children are more likely to experience preterm birth, have congenital anomalies, and face increased chances of developing childhood obesity. Additionally, they are at risk for metabolic disorders later in life, such as type 2 diabetes. Studies indicate that maternal obesity can influence fetal development, leading to both immediate and long-term health concerns. Strategies such as maternal weight management, healthy diet, and regular exercise can help mitigate these risks. [3]

A body mass index of 25 or higher as a pregnant woman is associated with an increased risk of offspring macrosomia or weighing more than 4,000 grams at birth and being considered large for gestational age. This is further associated with moderate to severe obesity at school age, making it a predictor of offspring body composition. Each additional kilogram of gestational weight gain increases the offspring’s risk of overweight or obesity by 1-23%.[4]

Exercise therapy has also been found to help gestational diabetes mellitus by increasing insulin sensitivity and promoting glucose uptake by controlling excessive gestational weight gain. The main controllable risk factor for gestational diabetes mellitus is being a person with overweight or obesity. Offspring which were carried by a mother with the condition have 2.09 times the chance of having macrosomia than offspring born from a mother of a healthy weight. Macrosomia has been linked to obesity, hypertension and diabetes later in the offspring’s life.[5]

Maternal obesity can affect the placental cortisol metabolism and the hypothalamic-pituitary-adrenal axis of offspring in utero. Pregnant mothers with obesity tend to have higher cortisol levels, like mothers with depression or under high stress, resulting in cognitive and emotional deficits. High cortisol levels can alter the intrauterine environment which can be detrimental for fetal development and the suprarenal glands. Structurally, high cortisol can affect the fetal brain through interruption of cerebellum and biparietal growth, cortical thinning, largening of the amygdala, and reduced head circumference. Volume of adrenal glands and fetal growth reduction has been linked as well. With the adrenal gland reduction, perinatal inflammation can occur which may increase the risk of offspring developing autism spectrum disorder. Emotional deficits include an elevated stress response in female offspring, along with hyperactivity and externalizing psychological issues in male offspring. High cortisol transference has been linked to anxiety, depression, obesity and inflammation in both female and male offspring.[6]

  1. ^ academic.oup.com https://academic.oup.com/jcem/article/106/11/e4372/6311296. Retrieved 2024-11-14. {{cite web}}: Missing or empty |title= (help)
  2. ^ Shrestha, Nirajan; Ezechukwu, Henry C.; Holland, Olivia J.; Hryciw, Deanne H. (2020-11-01). "Developmental programming of peripheral diseases in offspring exposed to maternal obesity during pregnancy". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 319 (5): R507–R516. doi:10.1152/ajpregu.00214.2020. ISSN 0363-6119.
  3. ^ Stubert, Johannes; Reister, Frank; Hartmann, Steffi; Janni, Wolfgang (2018-04-20). "The Risks Associated With Obesity in Pregnancy". Deutsches Ärzteblatt International. 115 (16): 276. doi:10.3238/arztebl.2018.0276. PMC 5954173. PMID 29739495.{{cite journal}}: CS1 maint: PMC format (link)
  4. ^ Fair, Frankie J.; Soltani, Hora (2024-11-13). "Association of child weight with attendance at a healthy lifestyle service among women with obesity during pregnancy". Maternal & Child Nutrition. 20 (2). doi:10.1111/mcn.13629. ISSN 1740-8695.
  5. ^ Kuang, Jun; Sun, Suwen; Ke, Fengmei (2023-10-06). "The effects of exercise intervention on complications and pregnancy outcomes in pregnant women with overweight or obesity: A systematic review and meta-analysis". Medicine. 102 (40): e34804. doi:10.1097/MD.0000000000034804. ISSN 0025-7974. PMC 10553027. PMID 37800765.{{cite journal}}: CS1 maint: PMC format (link)
  6. ^ Volqvartz, Tabia; Andersen, Helena Hørdum Breum; Pedersen, Lars Henning; Larsen, Agnete (2023-10-20). "Obesity in pregnancy—Long‐term effects on offspring hypothalamic‐pituitary‐adrenal axis and associations with placental cortisol metabolism: A systematic review". European Journal of Neuroscience. 58 (11): 4393–4422. doi:10.1111/ejn.16184. ISSN 0953-816X.