Maternal Obesity: Understanding Its Impact and Consequences

Abstract

The goal of this review is to thoroughly examine the effects of maternal obesity on the course of pregnancy and the ensuing long-term health implications for both the mother and the unborn child. This review attempts to shed light on the complex impacts of obesity during pregnancy, including increased risks of gestational diabetes, hypertension, and other problems, by synthesizing the information that has already been published. This study, which makes use of a literature review methodology, looks at data from several research papers to explain the possible effects of maternal obesity on the health of her offspring, including the higher risk of obesity and metabolic diseases later in life. The results highlight the vital significance of preemptive measures and strong support networks for pregnant moms in mitigating the detrimental impacts of obesity on the health of mothers and their offspring. In the end, this analysis recommends focused initiatives to address the intricate interactions between maternal obesity and its effects on future generations. These initiatives should include implementing preventive measures, increasing public awareness, and offering complete healthcare assistance.

1. Introduction

Globally, obesity is now the main concern. An unhealthy sedentary lifestyle or inadequate balanced food intake, as well as an aberrant metabolism in utero, are the causes of this epidemic affecting children and adolescents [1]. Numerous studies and experiments conducted all around the world have demonstrated that a person’s predisposition to obesity can start as early as postnatal development because of nutritional exposure and early-life experiences [2].

The potential connection between factors in early life and adult cardiovascular and metabolic diseases is first mentioned by Hales and Barker [3]. It is yet unknown what exact mechanisms underlie the embryonic programming of obesity. However, disparate outcomes in terms of early-life calorie, protein, or fat intake may be producing adult-life repercussions that are comparable, pointing to a shared mechanism underpinning the developmental programming of adult disease. This connection between the fetal nutritional pattern and postnatal growth and adult obesity has been demonstrated by several epidemiological studies as well as experimental investigations [4].

The purpose of this study is to evaluate and summarize the existing data about the contribution of early-life nutritional exposures to the development of obesity, with an emphasis on finding recurring themes in both epidemiological and experimental studies. We want to elucidate the mechanisms by which early-life factors impact obesity risk by utilizing a thorough review methodology. This will provide a strong basis for the development of focused interventions. In the end, we want to help shape early preventive and intervention measures so that the worldwide obesity epidemic may be managed more skillfully (Figure 1) [5].

Figure 1.

Maternal obesity programming.

Due to an imbalance of energy consumption with energy expenditure, obesity cases in the population are increasing day by day. This condition also contributed significantly to pre-pregnancy body mass index (BMI). Overnutrition during pregnancy and early development may influence or “program” appetite, affect metabolic regulation, and increase the risk of other metabolic diseases in adulthood. Figure modified from Velkoska and Morris [5].

2. Materials and methods

2.1 Search strategy

Based on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) previously described, a search for potentially relevant papers was conducted for this study. We determined the keywords for article searches using Boolean operators. The following keywords were chosen: (1) obesity in mothers OR (2) obesity in children OR (3) hypothalamic influence. The period covered by the literature search was January 2000 to December 2023.

2.2 Inclusion criteria

This review only included animal research (in vivo). Every English-language article that was published and had full-text accessibility was chosen for additional screening. All of the following details must be included in the selected articles: (1) the use of an animal model; (2) the specifics of the intervention, such as the type, dosage, and duration; (3) the use of a behavioral test; and (4) the results that center on the hypothalamic/neuro research.

2.3 Exclusion criteria

No additional reviews were conducted for any secondary papers, thesis dissertations, proceedings, patents, or case reports. Articles written in languages other than English and those without sufficient details as specified by the inclusion criteria were immediately disqualified from further examination. Excluded from consideration were any articles that addressed human trials (retrospective or prospective), in vitro, or ex vivo.

3. Maternal obesity and fetal development

This subsection’s goal is to investigate how maternal obesity affects fetal development, with a particular emphasis on the processes by which a mother’s obesity may put her offspring at risk for metabolic diseases, obesity, and abnormal developmental patterns. Examining how prenatal and postnatal factors influence the long-term health of children born to obese moms is one aspect of this investigation.

Researchers have found that women are more likely than men to be obese, according to several of their investigations. Studies have indicated that women often gain the most weight between the ages of 25 and 44. Furthermore, Goodrich et al. [6] state that one of the variables contributing to the development of obesity in women is the retention of prenatal weight gain throughout pregnancy.

According to the World Health Organization’s (WHO) BMI criteria for obesity, the Ministry of Health Malaysia reported in 1997 that, in comparison to men, 17.9% of women were overweight and 5.7% were obese. In this study, 2.9% of people were obese, and 15.1% were overweight. This demonstrates that the distribution of adipose tissue, inflammation, and the likelihood of acquiring a chronic illness vary by sex, especially in women [7]. Males have less total body fat, and their adipose tissue is primarily localized viscerally; females have a larger body fat content, with the fat localized or collected in the subcutaneous region [8].

There are a growing number of overweight women because of the current obesity epidemic [9]. The offspring of these obese mothers will likely grow up with disrupted developmental patterns, such as an increased risk of preterm conception too little for gestational age and an inclined toward higher nativity weight, including macrosomia (birth weight > 95%) and higher neonatal fat mass during childbirth [10]. Lastly, Poston [10] found that maternal weight has long-term effects on metabolic disorders, adolescence, and neonates. The developing fetus may be impacted by maternal obesity through a variety of genetic, environmental, and inter-relationship routes.

Numerous equivocal studies revealed that maternal obesity produces chronic inflammation and oxidative stress, even if it is unclear how this may program obesity and related metabolic diseases during pregnancy and after delivery [11]. These disorders may impair placentation, the basis for a sufficient blood supply, and perhaps alter fetal digestion [12]. The development and formation of the fetus alters the body in ways that increase the risk of insulin blockage early in pregnancy and improve gestational diabetes. Many people, meanwhile, continue to have doubts about these unpleasant metabolic effects [13]. While overweight women are more at risk, there is growing evidence that approximately 16% of all pregnant women may show signs of troubling metabolic effects, especially in glucose homeostasis, regardless of body weight [1]. Raising glucose levels alone can raise the risk of developing heftiness, which makes this worrying [14].

According to research done in 2009 by Hui Chen et al. [15], offspring of obese dams gain much more weight than offspring of lean dams. During the two-week weaning phase, the offspring’s bodyweight increased dramatically for obese dams as opposed to lean group dams. Additionally, it demonstrates a strong correlation between postnatal high-fat diet (HFD) and maternal obesity in terms of increasing calorie intake. A fasting blood glucose test was used to demonstrate it, and the results indicate that the groups fed an HFD had greater levels of glucose (p < 0.001) than the groups fed regular chow. The study also demonstrated that rats bred in small litters had reduced levels of mRNA expression in arcuate nucleus neuropeptide Y (NPY).

In contrast, mice fed a high-fat diet (HFD) had higher levels of the paraventricular nucleus (PVN) Y1 receptor mRNA. Additionally, the Y1 receptor mRNA expression and calorie intake are positively correlated, according to this research. Arcuate nucleus proopiomelanocortin (POMC) mRNA is upregulated in HFD-fed groups as well, although it is downregulated in rats from fat dams [15].

When a mother is obese and consumes a high-fat diet, her offspring may experience hyperphagia and become more susceptible to fat deposition. In comparison to lean groups, HFD also resulted in higher plasma concentrations of insulin and leptin in children whose mothers were obese. Because of the potential implications for the delayed development of hepatic impairment, the kids of obese mothers also exhibit substantially higher levels of plasma and hepatic triglycerides. Hasnah Bahari et al. [16] found that post-weaning HFD caused a notable obese phenotype in female children of obese mothers, including increased adiposity and plasma insulin and leptin concentration levels.

The example of a healthy diet and regular exercise during pregnancy among overweight or obese women may play a crucial role in the early development of the embryo and the increased risk of obesity for the offspring. Numerous epidemiological studies have been conducted on verifiable and contemporary mother–child relationships, and research on animals has demonstrated the effects of maternal food during pregnancy and breastfeeding on the long-term health of the progeny [17]. It has been demonstrated in rodents that mothers who consume obesogenic diets prior to conception, throughout pregnancy, or during lactation cause their offspring to become overweight and acquire excess adiposity [18].

According to research by others, children of overfed mothers who gain more weight experience altered cardiovascular structure and function, higher glucose, insulin, leptin, and triglyceride concentrations, decreased adiponectin secretion, and increased fat mass and fat cell hypertrophy [19]. Even if the mothers do not gain weight, a high-fat diet (HFD) during pregnancy may cause and program offspring obesity, indicating that maternal diet may affect offspring phenotype even when parental phenotype is absent.

4. Childhood obesity

This section looks at the various variables that contribute to childhood obesity, especially in developing countries, and how they affect children’s health and well-being in the future.

In developing nations, childhood obesity has become a major public health concern due to its pandemic spread [20]. According to a study by Ward et al. [20], most kids will undoubtedly be fat by the time they are 35. According to a 2017 study, obesity declines before the age of 35 when compared to the age of 19, which can result in severe cases of obesity [21]. This finding indicates that childhood obesity is highly likely to occur. Children’s health will be impacted by this circumstance, which will also have an impact on them when they become older and may result in issues or even death [22].

Children who gain too much weight are more likely to do so due to a variety of biological, genetic, life stage, sedentary lifestyle, and environmental variables. Mommy obesity is a major contributing factor among these factors [13]. Children of obese mothers were three times more likely than children of normal mothers to experience an adverse childhood cardio-metabolic risk profile, which included low high-density lipoprotein (HDL) cholesterol, high blood pressure, elevated insulin and triglyceride levels, and high abdominal fat mass [23]. Numerous studies have observed that a child’s susceptibility to an environment that promotes obesity may be influenced by hereditary variables [24]. In rarer instances, genes such as leptin deficit cause childhood obesity [25].

Numerous studies indicate that the mechanism of childhood obesity may be influenced by hereditary factors. Excess maternal fat may cause changes in the levels of adiponectin, leptin, and insulin that are transferred from mother to kid. Consequently, the development of organs in the offspring that are involved in controlling the body’s energy balance, like the brain, pancreas, and intestines, may be impacted [25, 26]. According to a 2016 Harvard obesity prevention program article, scant data suggests obesity susceptibility is caused by mutations in several genes. Therefore, there is a greater likelihood of an obese mother passing on the altered genes associated with obesity to her offspring.

According to Mahadir Naidu et al. [27], out of the 566,787 total population, 19.9% of Malaysian primary school students (7–12 years old) are overweight. In comparison to rural areas (16.1%), the prevalence was much greater in urban areas (22.6%). She concludes by saying that the prevalence of overweight in children rose in direct proportion to the BMI status of their guardians. Children who were overweight were strongly correlated with overweight parents. This is because many parents work long hours in cities and are unable to provide their kids with home-cooked meals; as a result, the kids end up eating meals from fast-food restaurants and hawker stalls, which are higher in saturated fat and energy.

According to the National Health and Morbidity Survey (NHMS 2015), out of the total estimated population of 1,003,078 children, 11.9% of youngsters (under the age of 18) were obese. Additionally, the survey found that children in urban areas had a little greater prevalence of obesity (12.1%) than children in rural regions (11.2%). Children ages 5–9 had the highest percentage (14.8%), followed by those ages 10–14 (14.4%), according to the NHMS 2015.

Genetics is one of the primary causes of childhood obesity in girls. This is due to the possibility that weight-related genes, which are passed down from parents to their offspring, are the source of the child’s obesity. The offspring of an obese mother will most likely have low sensitivity to insulin genes. Conversely, genetic factors such as a lack of leptin, hypothyroidism, insufficient growth hormone, or adverse medication reactions from steroids may ultimately result in childhood obesity. Hereditary obesity is linked to an increase in a child’s body mass index (BMI), but it also modifies the child’s body composition. It affects the fetus’s size, which causes certain fetal anomalies including fetal macrosomia. Thus, the child’s physical health is impacted by this indicator. Rarely is childhood obesity caused by heredity treatable. However, because the cycle never ends, obese children have a higher chance of remaining obese as adults and may pass on their medical condition to their offspring [28].

Moreover, behavioral and social environments might contribute to childhood obesity in girls and create health and psychological issues [29]. Dairy products, increased consumption of high-fat foods, and increased calorie intake are a few examples of these causes. This is a result of fast food and other low-nutrient diets becoming commonplace, especially among children. After all, because it requires minimal preparation time, it may be purchased easily and conveniently. Furthermore, depression has been linked to additional health problems in children who are fat, including hypertension, hyperlipidemia, abnormal glucose intolerance, infertility, and heart-related illnesses. Nonetheless, this component is modifiable according to individual lifestyle decisions, even though the process of obesity development is not fully understood.

5. Hypothalamic appetite regulation and energy balance

The processes governing hypothalamic appetite regulation and its vital role in preserving energy balance are examined in this subsection. We will go over our present understanding of the effects of different hormones and neurotransmitters and the ways that external influences like nutrition and lifestyle affect these processes.

Energy consumption is greatly influenced by appetite regulation, which is mostly controlled by the hypothalamus. By combining peripheral inputs, the hypothalamus plays a critical role in regulating the feeding process. Food intake and energy expenditure are influenced by the hypothalamus [30]. An important part of energy balancing is played by the dorsomedial hypothalamus (DMH), arcuate nucleus (ARC), and paraventricular nucleus (PVN). ARC, often referred to as the feeding circuitry, is made up of orexigenic and anorexigenic neurons and is situated at the median eminence and third ventricle. The regulation of energy expenditure and calorie intake is mediated by this cell. Increased nutritional supply during pregnancy is associated with long-lasting alterations in the central nervous system responsible for controlling hunger in the offspring, leading to hyperphagia postpartum [31].

It is believed that the brain’s hypothalamus, a nerve center, serves as the primary integrator and processor of metabolic information. To link calorie admission to energy consumption, two groups of hypothalamic arcuate neurons work together. One group communicates the powerful hunger trigger, neuropeptide Y (NPY), and the other group suppresses appetite by producing proopiomelanocortin (POMC), the precursor of α-MSH. According to physiological principles, NPY concentrations are higher prior to meals and much lower following the start of eating; nevertheless, POMC-inferred α-MSH inhibits NPY to prevent overeating [32]. Together with insulin, the hormone leptin, which is derived from fat, lawfully reaches the nerve center to lower NPY and start the POMC articulation, which limits sustained energy intake and increases energy consumption by using the long form of the leptin receptor (Ob-Rb). In dietary weight, focal leptin and insulin blockage are typically observed. The last 7 days of the rodent’s incubation are when these mental pathways separate, and development continues until weaning (Figure 2) [33].

Figure 2.

Hypothalamic signaling controlling energy balance.

Agouti-related peptide (AgRP)/NPY and POMC neurons from the ARC and PVN play the main role in calorie intake and also energy balance. The signaling from this neuron can be influenced by insulin, leptin, and GCs. ARC, arcuate nucleus; AgRP, agouti-related peptide; GCs, glucocorticoids; GR, glucocorticoids receptor; IR, insulin receptor; Obr, leptin receptor; NPY, neuropeptide, POMC, proopiomelanocortin; α- MSH, α melanocyte-stimulating hormone; PVN, paraventricular nucleus; Y1/Y5. Y1 and Y5 receptor; 3V; third ventricle.

6. Effect of maternal obesity on the hypothalamic

This subsection’s goal is to summarize and discuss what is now known about the effects of maternal obesity on the growth and functioning of the hypothalamus in offspring. Our goals are to highlight important systems involved in this process, look at the findings of current studies, and pinpoint areas that require more investigation.

6.1 The role of the hypothalamus in stimulating appetite (hunger)

Agouti-related peptide (AgRP) and neuropeptide Y (NPY) neurons promote eating habits and weight gain. NPY belongs to the family of overlapping peptides known as pancreatic polypeptide (PP-) (NPY, polypeptide YY (PYY), PP). The NPY neurons, which supply the paraventricular nucleus, hypothalamic nucleus, and other hypothalamic regions with their primary functions, are found in the medial arcuate nucleus. Leptin and insulin act as inhibitors of NPY release and synthesis, whereas glucocorticoids and ghrelin act as stimulants. According to Desai et al. [32], the main physiological response or task of NPY is to promote food intake through the NPY G-protein.

Because of its impact on melanocortin signaling, NPY is sometimes referred to as anorexigenic. Additionally, AgRP can be found in a medial arcuate nucleus, which is consistently recognized as NPY’s partner. AgRP’s signaling protein production sequence is comparable in humans and mice. The α-melanocyte stimulation hormone (α-MSH) is inhibited by the agouti protein, a paracrine signaling molecule. The mice with this hypo-express will have longer bodies, be overweight, and be less sensitive to insulin. According to Desai et al. [32], AgRP functions as an antagonist and aids in maintaining the energy balance.

Growth hormones (GH) and peptides like ghrelin also affect appetite behavior. This peptide is released in an endocrine cell, mostly in the stomach mucosa of the fundus, as well as in other tissues, including the pituitary gland, the hypothalamus, the small intestine, and the pancreas. The amount of food consumed affects the ghrelin hormone level. Ghrelin levels rise before eating and decrease following ingestion of meals. The G-protein receptor and the ghrelin receptor are expressed simultaneously, as is the case with the GH secretagogue receptor type 1a (GHS-R1a). The ghrelin receptor, which aids in controlling hunger and energy balance, is also present in the mesolimbic dopaminergic system, the dorsal vagal complex, and the hypothalamus nuclei of the central nervous system (CNS). Previous studies have demonstrated that ghrelin stimulates NPY and AgRP in arcuate nuclease, which increases food intake and causes weight gain. Additionally, it maintains equilibrium by promoting adipogenesis, preventing apoptosis, and oxidizing fat. In humans, ghrelin is generally the main hormone involved in fat storage and utilization [33].

6.2 The role of the hypothalamus in stimulating appetite (satiety)

Amphetamine- and cocaine-regulated transcript (CART) and proopiomelanocortin (POMC) are two other ways that the hypothalamus contributes to human satiety. POMC is highly expressed in the skin, immunological systems, and the arcuate nucleus of the hypothalamus. Adipose tissue secretes leptin, which activates the POMC in the hypothalamus. The arcuate nucleus then uses this signal to create α-melanocyte-stimulating hormone (α-MSH). This will bind to the paraventricular nucleus’s melanocortin-4-receptor (MC4R), stimulating the body’s energy balance and regulation of hunger. α-MSH will prevent feeding and cause a decrease in body weight or food consumption. AgRP is well recognized for its antagonistic effects on MC4R, which cause aberrant elevations in appetite and food consumption [33].

Another essential regulator in the hypothalamus is the cocaine- and amphetamine-regulated transcript (CART), which is consistently expressed with POMC in the arcuate nucleus. Like POMC, CART is likewise directly induced by leptin. Food intake will rise when CART is blocked, but food intake will decrease when CART mRNA expression is low. One of the satiety hormones produced in the gastrointestinal system that contributes to satiety is cholecystokinin (CCK). CCK is swiftly released into the bloodstream locally in response to nutrients in the stomach, particularly fat and protein. Its level gradually rises over the course of 10–30 minutes following the start of a meal and stays raised for up to 5 hours. Brain regions that are responsive to CCK include the lateral medulla, medial pons, and lateral hypothalamus. These systems are linked to anxiety, satiety, memory, and reward behavior. CCK is connected to two types of G-protein receptors: CCK-A and CCK-B. While CCK-B does not participate in satiety, CCK-A does. Vagal afferent neurons, which have a direct impact on food intake, are home to CCK-A. Obesity, type 2 diabetes mellitus, and hyperphagia are associated with CCK-A deficiency [33].

7. Factors contributing to maternal obesity

The purpose of this subsection is to investigate and clarify the different factors that lead to maternal obesity. It looks for factors that predispose women to obesity before, during, and after pregnancy, both biologically and environmentally.

A major contributing element to the development of maternal obesity is behavioral variables. Obesity in pregnant women is largely caused by poor eating habits, which are defined as consuming too many calories, a lot of processed foods, and not enough fruits and vegetables [34]. Furthermore, sedentary lifestyle practices including little exercise and extended sitting time increase the risk of weight gain and pregnancy obesity [35].

Maternal obesity prevalence is also influenced by sociodemographic variables such as race/ethnicity, education level, and socioeconomic status. Because they have less access to healthier food alternatives, fewer healthcare resources, and higher levels of stress, women from lower socioeconomic backgrounds are more likely to become obese while pregnant [36]. Additionally, there are differences in the prevalence of obesity between various racial and ethnic groups; African American and Hispanic women have greater rates than White women [37].

The environment in neighborhoods and communities has a big influence on the prevalence of maternal obesity. Pregnant women’s obesity and bad eating habits are influenced by the food environment, which is defined by the presence of fast-food restaurants, convenience stores, and restricted access to fresh produce [38]. Similarly, physical activity levels and the prevalence of obesity are influenced by the built environment, which includes elements like walkability, accessibility to recreational facilities, and transit options [39].

Maternal obesity is also influenced by psychosocial factors, including social support, sadness, and stress. Unhealthy eating habits, emotional eating, and weight gain have all been linked to high levels of stress and depression during pregnancy [40]. Furthermore, poor social networks and limited access to them can make it more difficult for expectant mothers to control their weight and adopt healthy lifestyle practices [41].

8. Interventions and management strategies

The purpose of this part is to examine and assess the many management approaches and treatments that have been used internationally to combat the childhood and teenage obesity epidemic. We analyze these tactics’ scalability, sustainability, and efficacy to pinpoint areas that need improvement in the current paradigm as well as best practices. This investigation is essential for guiding future research projects, program designs, and policy decisions meant to reduce obesity prevalence and enhance public health outcomes.

Preconception counseling, which encourages healthy lifestyle choices prior to pregnancy, is essential in managing mother obesity. Counseling on reaching a healthy weight through food, exercise, and behavioral changes should be provided to women who intend to become pregnant [42]. Preconception weight management programs can offer tailored advice on exercise, food, and weight monitoring to improve a mother’s health prior to becoming pregnant [43].

Reducing the risk of problems and managing maternal obesity during pregnancy can be achieved by effective lifestyle changes. According to Thangaratinam et al. [43], these interventions usually include behavioral support, exercise regimens, and dietary counseling specifically designed for pregnant women who are obese [44]. Healthy eating practices, frequent exercise, and self-monitoring techniques can help reduce gestational weight increase and enhance the results for both the mother and the fetus [45].

When it comes to managing pregnancy-related issues caused by obesity, clinical management techniques are crucial. Maternally obese women need to be closely monitored and treated medically since they have a higher chance of developing gestational diabetes, hypertension, and preeclampsia [46]. Optimizing maternal and fetal well-being and minimizing unfavorable outcomes depend on the prompt detection, diagnosis, and treatment of these problems [47].

Obese pregnant women can develop and maintain healthy living habits with the assistance of behavioral counseling and support services. Women are empowered to achieve long-lasting changes in their eating and exercise habits through counseling sessions that emphasize goal setting, self-monitoring, and problem-solving strategies [48]. Additional resources for social support and encouragement throughout pregnancy include peer support groups, internet forums, and community-based initiatives [49].

9. Challenges and future directions

This section aims to address the difficulties involved in implementing programs to prevent and treat childhood obesity, with a particular emphasis on implementation hurdles and strategies.

There are several obstacles associated with maternal obesity that make it difficult to treat the illness during pregnancy. Among these difficulties is the lack of access to healthcare. Pregnant women’s access to prenatal care and obesity management services varies depending on their socioeconomic status and the availability of healthcare resources [50]. According to Phelan et al. [42], stigma around maternal obesity frequently results in unfavorable attitudes and discriminatory actions in healthcare settings, which may discourage women from seeking assistance and care. The intricate interaction of genetic, environmental, and psychosocial factors that contribute to maternal obesity makes it difficult to address individual-level interventions alone [51].

Subsequent investigations ought to concentrate on tackling the fundamental factors that contribute to maternal obesity and devising inventive approaches for both prevention and intervention. Examining the epigenetic processes that underlie the generational transfer of characteristics linked to obesity can provide new areas of focus for intervention and prevention [52]. Maternal obesity trajectories and their long-term effects on maternal and child health outcomes can be better understood through longitudinal studies that track women from preconception through pregnancy and beyond [53]. Evidence-based practices and policies can be influenced by using implementation science concepts to assess the efficacy and scalability of obesity prevention and management treatments in practical contexts [54].

Policy initiatives are essential for creating supportive environments that facilitate healthy lifestyle behaviors and improve maternal and child health outcomes. Expanding access to prenatal care and obesity management services, particularly for underserved populations, can help address disparities in maternal obesity prevalence and outcomes [54]. Implementing anti-stigma campaigns within healthcare settings and the broader community can help combat negative attitudes toward maternal obesity and promote respectful and supportive care for pregnant women [55]. Implementing policies to improve the food environment, increase opportunities for physical activity, and reduce exposure to obesogenic factors can create environments that support healthy lifestyle behaviors during pregnancy [54].

Enacting policies is crucial to fostering circumstances that encourage healthy lifestyle choices and enhance the health of mothers and their offspring. Disparities in the prevalence and consequences of maternal obesity can be addressed by increasing access to prenatal care and obesity treatment services, especially for marginalized communities [51]. By putting anti-stigma campaigns into action, healthcare facilities and the public can counteract the stigma associated with maternal obesity and encourage considerate and helpful treatment for expectant mothers [55]. Environments that encourage healthy lifestyle behaviors during pregnancy can be created by putting policies into place to enhance the food environment, boost opportunities for physical exercise, and decrease exposure to obesogenic variables [54].

10. Conclusions

To sum up, maternal obesity is a complex issue that has a big impact on the health of both moms and their children. Combating maternal obesity calls for an all-encompassing strategy that includes healthcare interventions, support services, and education to encourage healthy lifestyles prior to, during, and following pregnancy. Preventive strategies can help lessen the negative impacts of maternal obesity and ultimately lead to healthier outcomes for mothers and their children if they are prioritized together with the provision of sufficient support networks. However, to completely comprehend the nuances of this problem and put into practice practical countermeasures against its prevalence and related health hazards, more investigation and coordinated efforts are required.

Acknowledgments

We want to thank Management and Science University and Universiti Putra Malaysia for supporting this work.

Conflict of interest

The authors declare no conflict of interest.