INTRODUCTION: Children who have a familial predisposition to metabolic or cardiovascular disorders are more likely to develop these conditions later in life. Detecting early signs—such as disturbances in lipid levels or irregular BMI—can support timely preventive measures and early management. AIMS AND OBJECTIVES: To study the lipid profile and BMI in children aged between 5-15 years, born to parents having ischemic heart disease (IHD) and/or diabetes mellitus (DM) and/or hypertension (HTN). METHODS: This is a case control study conducted with total of 130 children with parental history of ischemic heart disease (IHD) and/or diabetes mellitus (DM) and/or hypertension (HTN) (Cases group; n=65). Children having no parental history of IHD and/or DM and/or HTN were grouped in Control group (n=65). BMI was calculated according to standard methods, and lipid profiles were measured by enzymatic colorimetric method in the blood sample of study subjects. RESULTS: There was no statistically significant difference in distribution of patients between groups with regards to age (p = 0.600) and gender (p = 0.720). However, consumption of junk food ≥3 times/week by patients in cases group was relative higher proportion than those in control group (84.6% vs. 23.1%; p<0.0001). Among the case group, majority of the study subjects i.e., 46.1% were born to hypertensive father followed by diabetic father (27.7%), diabetic mother (13.8%), and hypertensive mother (12.3%). The lipid profile such as total cholesterol (p<0.0001), triglycerides (p<0.0001), LDL-C (p = 0.001), and VLDL-C (p<0.0001) were significantly at higher levels in cases group compared to control group. The HDL-C levels were significantly (p = 0.036) at lower levels in cases group compared to control group. The was slight increase in ratio of TG/HDL in cases group than in control group (4.09 vs. 3.68; p = 0.241). The mean BMI in the cases and control groups was non-significant (18.33 kg/m2 vs.18.09 kg/m2; p = 0.198). CONCLUSION: Among the lipid profile, the triglycerides, VLDL, and LDL were higher, and HDL values were lower in the children with a family history of HTN and/or DM, and/or IHD without significant difference in BMI among cases and controls. The derangement of lipid profile in children with a parental history of HTN and/or DM and/or IHD could be suggestive of genetic predisposition. This study findings highlight the importance of early interventions to address modification of lifestyle factors in children at risk of developing metabolic disorders due to genetic predispositions.
Ischemic heart disease (IHD) in the Indian population tends to present earlier, progress more rapidly, and behave more aggressively. In India, 52.2% of cardiovascular deaths occur before the age of 70, whereas in developed countries the proportion is only 22.8% [1]. Additionally, individuals from South India exhibit a higher susceptibility to IHD, largely due to lifestyle patterns and high carbohydrate intake [2]. The current burden of morbidity and mortality reflects long-standing exposure to behavioral risk factors such as unhealthy diet, low levels of physical activity, and increased tobacco use, as well as biological risk factors like obesity, hypertension (HTN), dyslipidemia, and diabetes mellitus (DM) [1].
HTN is a major contributor to severe health complications in adults and is well recognized as a predictor of cardiovascular morbidity and mortality [3,4]. Numerous studies over the past decades have highlighted the genetic influence on HTN and demonstrated familial clustering of blood pressure across various populations [5,6]. Research also indicates a rising trend in elevated blood pressure and HTN among children and adolescents [7], and those with higher blood pressure early in life are more likely to develop HTN and cardiovascular disease as adults [8]. Consequently, early detection and preventive measures in children with elevated blood pressure are essential. Understanding familial patterns of HTN between parents and offspring can help assess the risk of elevated blood pressure in younger populations, facilitating early prevention and management of cardiovascular conditions [9].
Children may have one or both parents affected by HTN and IHD, and conditions like DM, HTN, and IHD often coexist because HTN increases the likelihood of IHD, while DM predisposes individuals to both HTN and IHD. At any given time, one condition may be evident while another remains undetected [10]. Moreover, children with parental history of IHD have been shown to exhibit elevated levels of several lipid components, with total cholesterol being the most prominent [11].
Evidence also suggests that the risk of IHD can be significantly lowered through dietary changes and lifestyle modification, emphasizing the need for early interventions to delay or prevent the development of atherosclerosis.1 Overweight or obese children are particularly prone to dyslipidemia, especially when their waist circumference or body fat is elevated.12 Their lipid profiles commonly show reduced high-density lipoprotein cholesterol (HDL-C) and increased triglyceride levels [12,13]. Although low-density lipoprotein cholesterol (LDL-C) values may fall within the normal range, the particles can undergo structural alterations, becoming smaller, denser, and more atherogenic [14]. Given this background, the present study was undertaken to evaluate the lipid profile and BMI in children aged 5 to 15 years who have parents diagnosed with IHD and/or DM and/or HTN.
Study population: This is a case control study conducted with total of 130 children attending outpatient department or admitted for other minor secondary illness with parental history of IHD and/or DM and/or HTN at Department of Paediatrics, Hassan Institute of Medical Sciences (HIMS), Hassan, Karnataka, India. A written informed consent was taken from all the patients participating in the study. Inclusion criteria: Children aged 5-15 years with parental age of 30-60 years and Children with either or both parents suffering from IHD and/or DM and/or HTN were included in this study Exclusion criteria: Children with hemodynamically unstable, congenital heart disease, chronic kidney disease, chronic liver disease, hypothyroidism, Cushing’s disease, and parenteral use of drugs were excluded from the study. Study design: Children who met inclusion criteria i.e., with a parental history of IHD and/or DM and/or HTN were grouped in Case group (n=65) and children having no parental history of IHD and/or DM and/or HTN were grouped in Control group (n=65). Data collection: The socio-demographic, clinical examination and BMI data were recorded. BMI of the eligible children was documented and assessed according to the recommendations of Indian Academy of Paediatrics. BMI indicates total body fat mass and it was calculated by formula: Weight in kg/Height in meter [15]. BMI was compared with reference values, and where ≥ 25kg/m2 was considered as abnormal value. Fasting lipid profile was estimated by enzymatic colorimetric method in blood sample of study subjects after 8 hours of fasting and after ruling out the causes of secondary hypercholesterolemia viz. nephrotic syndrome, hypothyroidism and parenteral use of drugs. Lipid profile was also estimated in the blood samples of children aged 5 to 15 years that include cholesterol, triglycerides, HDL, LDL-C, very low-density lipoprotein (VLDL) of both Cases and Control groups. The lipid profiles were compared with reference values range. Statistical analysis: Data were entered in Microsoft Excel 2021 and statistical analysis was done using IBM Statistical Software for Social Sciences (SPSS) version 21. Categorical variables were represented in the form of percentages, and frequencies. Continuous variables were presented as descriptive statistics (Mean and Standard deviation). Categorical variables were analysed using the Chi-square test. Comparison of continuous variables between the study groups was done using independent sample t-test. p≤0.05 was considered statistically significant.
The results on socio-demographic characteristics of the study subjects were represented in Table 1. Results depicted that there was no statistically significant difference in distribution of patients between groups with regards to age (p = 0.600), gender (p = 0.720), socioeconomic status (p = 0.720), and diet history (p = 0.720). However, consumption of junk food ≥3 times/week by patients in cases group was relative higher proportion than those in control group (84.6% vs. 23.1%; p<0.0001).
The results on comparison of study subjects based on family history was plotted in Table 2. Results depicted that among the case group, majority of the study subjects i.e., 46.1% were born to hypertensive father followed by diabetic father (27.7%), diabetic mother (13.8%), and hypertensive mother (12.3%). The distribution of study subjects based on familial history was statistically significant (p<0.001).
The results on comparison of lipid profile were represented in Table 3. Results implied that the lipid profile such as total cholesterol (p<0.0001), triglycerides (p<0.0001), LDL-C (p = 0.001), and VLDL-C (p<0.0001) were significantly at higher levels in cases group compared to control group. Furthermore, HDL-C levels were significantly (p = 0.036) at lower levels in cases group compared to control group. In addition, ratio of TG/HDL was slightly higher in cases group than controls (4.09 vs. 3.68; p= 0.241).
The mean BMI in the cases and control groups was 18.33 kg/m2 and 18.09 kg/m2 respectively without any statistically significant difference (p = 0.198). There was no statistically significant (p = 0.357) difference in distribution of lean and normal proportion of study subjects among cases and control group (Table 4).
Table 1. Socio-demographic characteristics
|
Variables |
Cases |
Control |
p-value |
|
Age (Years) |
|||
|
5 – 10 |
35 (53.8) |
32 (49.2) |
0.600 |
|
11 – 15 |
30 (46.1) |
33 (50.8) |
|
|
Gender |
|||
|
Male |
40 (61.5) |
38 (58.5) |
0.720 |
|
Female |
25 (38.5) |
27 (41.5) |
|
|
Socioeconomic status |
|||
|
Upper Lower |
40 (61.5) |
38 (58.5) |
0.720 |
|
Upper Middle |
25 (38.5) |
27 (41.5) |
|
|
Diet history |
|||
|
Mixed |
45 (69.2) |
43(66.2) |
0.720 |
|
Vegetarian |
20 (30.8) |
22(33.8) |
|
|
Diet – Junk Food |
|||
|
<3 times/week |
10 (15.4) |
50 (76.9) |
<0.0001 |
|
≥3 times/week |
55 (84.6) |
15 (23.1) |
|
Values were expressed as n (%)
Table 2. Comparison of family history
|
Variables |
Cases |
Control |
p-value |
|
Apparently healthy |
0 (0) |
65 (100) |
<0.001 |
|
Diabetic father |
18 (27.7) |
0 (0) |
|
|
Diabetic mother |
9 (13.8) |
0 (0) |
|
|
Hypertensive father |
30 (46.1) |
0 (0) |
|
|
Hypertensive mother |
8 (12.3) |
0 (0) |
|
|
Apparently healthy |
0 (0) |
65 (100) |
Values are expressed as n (%)
Table 3. Comparison of lipid profile
|
Lipid Profile |
Cases |
Control |
p-value |
|
Total Cholesterol (mg/dL) |
164.49 ± 22.48 |
137.4 ± 33.43 |
<0.0001 |
|
Triglycerides (mg/dL) |
127.15 ± 14.25 |
104.26 ± 35.66 |
<0.0001 |
|
LDL-C (mg/dL) |
103.24 ± 5.74 |
95.6 ± 17.6 |
0.001 |
|
HDL-C (mg/dL) |
31.65 ± 13.41 |
35.61 ± 6.97 |
0.036 |
|
VLDL-C (mg/dL) |
32.58 ± 4.44 |
20.52 ± 10.48 |
<0.0001 |
|
TG/HDL-C ratio |
4.09 ± 2.64 |
3.68 ± 0.72 |
0.241 |
Values are expressed as mean ± SD;
LDL-C, Low-density lipoprotein-cholesterol; HDL-C, High-density lipoprotein-cholesterol; VLDL-C, Very low-density lipoprotein-cholesterol; TG, Triglycerides
Table 4. Comparison of body mass index
|
Variables |
Cases |
Control |
p-value |
|
Lean |
20 (30.8) |
25 (38.5) |
0.357 |
|
Normal |
45 (69.2) |
40(61.5) |
|
|
Mean ± SD |
18.33 ± 1.00 |
18.09 ± 1.08 |
0.198 |
Values are expressed as n (%) unless otherwise stated
Among the lipid profile, the triglycerides, VLDL, and LDL were higher, and HDL values were lower in the children with a family history of HTN and/or DM, and/or IHD without significant difference in BMI among cases and controls. The derangement of lipid profile in children with a parental history of HTN and/or DM and/or IHD could be suggestive of genetic predisposition. This study findings highlight the importance of early interventions to address modification of lifestyle factors in children at risk of developing metabolic disorders due to genetic predispositions.
26. Karimzadeh P, Taghdiri MM, Abasi E, Hassanvand Amouzadeh M, Naghavi Z, Ghazavi A, Nasehi MM, Alipour A. Metabolic Screening in Children with Neurodevelopmental Delay, Seizure and/or Regression. Iran J Child Neurol. 2017;11(3):42-47.