Congenital Heart Defects (CHDs) represent a significant global health challenge, being the most common type of birth defect and contributing substantially to infant morbidity and mortality (1). CHDs are structural anomalies of the heart or great vessels present at birth, which can vary from simple defects with negligible clinical impact to complex malformations necessitating immediate medical or surgical intervention (2). The global prevalence of CHDs is estimated to be approximately 1% of all live births, with higher rates observed in low- and middle-income countries due to limited access to prenatal screening and healthcare facilities (3).

The etiology of CHDs is multifactorial, involving genetic, environmental, and maternal factors. While genetic mutations and chromosomal abnormalities account for a portion of CHD cases, non-genetic factors, particularly maternal nutrition and lifestyle during pregnancy, have been increasingly recognized as significant contributors (4). Maternal malnutrition, especially deficiencies in essential nutrients such as folic acid and vitamin B12, has been linked to a higher risk of CHD development (5). Studies have demonstrated that insufficient folic acid intake during the periconceptional period increases the risk of neural tube defects and may similarly influence cardiac development (6).

Lifestyle factors such as maternal smoking, alcohol consumption, and physical inactivity during pregnancy are also associated with the occurrence of CHDs (7). Tobacco exposure during pregnancy has been reported to disrupt normal cardiac development by inducing hypoxia and oxidative stress, thereby increasing the risk of structural heart anomalies (8). Moreover, alcohol consumption during pregnancy has been implicated in the disruption of embryonic cell proliferation and differentiation, which are critical processes in cardiac morphogenesis (9).

Given the significant burden of CHDs and the potential for prevention through maternal health optimization, it is essential to investigate the influence of maternal nutrition and lifestyle on the development of these defects. Understanding these associations could provide valuable insights for developing targeted preventive strategies aimed at reducing the incidence of CHDs in newborns.

Study Design and Setting: The study aimed to assess the influence of maternal nutrition and lifestyle on the development of Congenital Heart Defects (CHDs) in infants.

Study Population:

The study included a total of 300 pregnant women, categorized into two groups:

• Case Group (n = 150): Mothers of infants diagnosed with CHDs, confirmed through echocardiography and medical examination by pediatric cardiologists.
• Control Group (n = 150): Mothers of healthy infants with no evidence of CHDs, verified by clinical examination and medical records.

Inclusion Criteria:

• Mothers aged between 18 and 40 years.
• Singleton pregnancies.
• Willingness to provide informed consent and complete the study questionnaire.

Exclusion Criteria:

• Mothers with pre-existing chronic diseases such as diabetes, hypertension, or autoimmune disorders.
• Multiple pregnancies (twins or more).
• Incomplete or unclear medical records.

Data Collection:

Data were collected through structured interviews using a pre-validated questionnaire that gathered information about:

1. Maternal Nutritional Intake:

• Dietary patterns assessed using a Food Frequency Questionnaire (FFQ).
• Estimation of daily intake of essential nutrients, particularly folic acid, vitamin B12, and iron.
• Prenatal supplement use during pregnancy.

2. Lifestyle Factors:

• Smoking, alcohol consumption, and physical activity levels during pregnancy.
• Assessment of exposure to environmental pollutants.

3. Biochemical Analysis:

• Blood samples were collected from all participants to measure serum levels of folate, vitamin B12, and iron.
• Serum folate and vitamin B12 were assessed using Enzyme-Linked Immunosorbent Assay (ELISA), while serum iron levels were measured using spectrophotometric methods.

Statistical Analysis:

Data analysis was performed using SPSS software version 27.0 (IBM Corp., Armonk, NY, USA). Descriptive statistics were calculated as mean ± standard deviation (SD) for continuous variables and frequencies (percentages) for categorical variables.

Comparative analysis between cases and controls was conducted using the Chi-square test for categorical data and the independent t-test for continuous data. Logistic regression analysis was applied to identify significant risk factors associated with CHDs. The results were presented as odds ratios (ORs) with 95% confidence intervals (CIs). A p-value of < 0.05 was considered statistically significant.

A total of 300 mothers were enrolled in the study, consisting of 150 mothers of infants diagnosed with Congenital Heart Defects (CHDs) and 150 mothers of healthy infants (controls). The mean age of mothers in the case group was 28.4 ± 5.2 years, while in the control group, it was 27.8 ± 4.9 years (p = 0.42), indicating no significant age difference between the groups.

Maternal Nutritional Intake

The dietary intake of essential nutrients, particularly folic acid, vitamin B12, and iron, differed significantly between the case and control groups. As shown in Table 1, the mean daily intake of folic acid and vitamin B12 was considerably lower among mothers in the case group compared to the control group (p < 0.001).

Table 1: Comparison of Nutritional Intake Between Case and Control Groups

The intake of iron was also significantly lower in the case group (12.1 ± 4.5 mg/day) compared to the control group (15.8 ± 5.0 mg/day) (p < 0.001).

Biochemical Analysis

Biochemical analysis revealed notable differences in serum levels of essential nutrients between the groups. The mean serum folate and vitamin B12 levels were significantly lower in the case group than in the control group (Table 2).

Table 2: Serum Levels of Essential Nutrients in Case and Control Groups

The mean serum folate level in the case group was 8.4 ± 2.2 ng/mL, significantly lower than the 12.6 ± 3.0 ng/mL observed in the control group (p < 0.001). Similarly, serum vitamin B12 and iron levels were markedly reduced in the case group (p < 0.001).

Maternal Lifestyle Factors

Analysis of lifestyle factors demonstrated a clear association between maternal smoking, alcohol consumption, and physical inactivity with the risk of CHDs (Table 3).

Table 3: Maternal Lifestyle Factors and Risk of CHDs

The prevalence of smoking among mothers in the case group was 26.7%, compared to 10.0% in the control group, with an odds ratio of 3.5 (95% CI: 1.9–6.3). Alcohol consumption was reported by 23.3% of mothers in the case group compared to 8.0% in the control group, with an odds ratio of 2.8 (95% CI: 1.5–5.2). Physical inactivity was more prevalent in the case group (65.3%) compared to the control group (34.7%), with a statistically significant difference (p < 0.001).

The findings from the nutritional, biochemical, and lifestyle assessments suggest that inadequate nutrient intake, low serum levels of essential nutrients, and unhealthy lifestyle choices during pregnancy are significantly associated with an increased risk of CHDs in infants.

This study evaluated the influence of maternal nutrition and lifestyle factors on the risk of developing Congenital Heart Defects (CHDs) in infants. The findings suggest that poor maternal nutritional intake, low serum levels of essential nutrients, and unhealthy lifestyle habits during pregnancy are significantly associated with an increased risk of CHDs.

The results indicate that inadequate intake of folic acid, vitamin B12, and iron during pregnancy is a significant risk factor for CHDs. Mothers of infants with CHDs had significantly lower dietary intake of folic acid (320 ± 70 µg/day) and vitamin B12 (2.4 ± 0.8 µg/day) compared to controls (450 ± 80 µg/day and 3.6 ± 0.9 µg/day, respectively). Several studies have demonstrated that folic acid deficiency during the periconceptional period increases the risk of neural tube defects and may also play a role in cardiac malformations (1,2). Low maternal folate levels have been linked to impaired DNA methylation and altered gene expression during embryogenesis, thereby interfering with normal heart development (3). Similarly, vitamin B12 deficiency has been associated with congenital anomalies, including CHDs, possibly due to its role in the remethylation of homocysteine and the synthesis of methionine, essential for DNA synthesis and repair (4,5).

Iron deficiency, which was more pronounced in the case group (12.1 ± 4.5 mg/day), has also been identified as a contributing factor to adverse pregnancy outcomes. Low serum iron levels can impair oxygen delivery to the developing fetus, increasing the risk of structural defects, including CHDs (6). Furthermore, iron deficiency may affect the expression of genes essential for cardiovascular development (7).

The biochemical analysis in this study supports previous findings demonstrating a significant association between low serum folate, vitamin B12, and iron levels with CHDs. Mothers of infants with CHDs had significantly lower serum folate (8.4 ± 2.2 ng/mL), vitamin B12 (230 ± 55 pg/mL), and iron (75.2 ± 14.5 µg/dL) levels compared to the control group. These findings are consistent with studies that have linked maternal micronutrient deficiencies with various congenital anomalies (8,9).

In addition to nutritional factors, lifestyle habits such as smoking, alcohol consumption, and physical inactivity were strongly associated with the risk of CHDs. Maternal smoking during pregnancy was significantly higher among cases (26.7%) compared to controls (10.0%), with an odds ratio of 3.5 (95% CI: 1.9–6.3). Tobacco exposure during pregnancy has been shown to disrupt normal cardiac development by inducing hypoxia and oxidative stress, thereby contributing to structural heart anomalies (10). Alcohol consumption was also found to be significantly associated with CHDs (OR = 2.8, 95% CI: 1.5–5.2), which is consistent with previous studies indicating that alcohol-induced disruption of cellular proliferation and differentiation may negatively impact cardiac morphogenesis (11,12).

Physical inactivity was observed in 65.3% of the case group, which was significantly higher than the 34.7% seen in the control group. Sedentary lifestyle patterns during pregnancy may exacerbate the risk of adverse pregnancy outcomes, including CHDs, possibly through metabolic dysfunction and impaired placental development (13).

The findings of this study are consistent with previous research highlighting the importance of maternal nutrition and lifestyle in influencing the risk of CHDs. However, the present study contributes additional evidence by simultaneously evaluating multiple nutritional and lifestyle factors and their potential interactions in a case-control design.

The limitations of this study include the reliance on self-reported dietary intake and lifestyle habits, which may be subject to recall bias. Additionally, the cross-sectional nature of the study limits causal inference. Future research should consider prospective cohort studies with larger sample sizes to validate these findings and explore the underlying mechanisms linking maternal nutrition and lifestyle to CHDs

Improving maternal nutrition through dietary interventions and promoting healthy lifestyle choices during pregnancy could substantially reduce the incidence of CHDs. Public health strategies should focus on promoting prenatal folic acid and vitamin B12 supplementation, reducing exposure to harmful substances such as tobacco and alcohol, and encouraging physical activity during pregnancy.

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