European Journal of Cardiovascular Medicine

Tobacco smoking remains a leading modifiable risk factor for cardiovascular morbidity and mortality worldwide. While its deleterious effects on the respiratory and vascular systems have been extensively documented, the biochemical alterations in lipid metabolism due to smoking are garnering increasing attention, especially in younger individuals [1]. Lipid profile abnormalities are strongly associated with atherosclerosis and are frequently observed among smokers due to oxidative stress and altered lipid handling pathways [2].

Cigarette smoke contains numerous free radicals and reactive oxygen species (ROS) which interfere with lipid homeostasis, accelerating lipid peroxidation and altering serum lipid levels such as increased low-density lipoprotein (LDL), total cholesterol (TC), and triglycerides (TG), along with reduced high-density lipoprotein (HDL) levels [3]. These changes are closely linked to the dose and duration of smoking, making it essential to assess lipid profile in correlation with the severity of smoking exposure, particularly in younger age groups who may not yet manifest overt cardiovascular symptoms [4].

Recent studies have shown that even low-to-moderate smoking intensity in younger populations can significantly elevate atherogenic lipid fractions, contributing to early endothelial dysfunction and subclinical atherosclerosis [5]. The underlying mechanisms include increased hepatic lipase activity, insulin resistance, and nicotine-induced catecholamine surge, all of which stimulate lipolysis and modify plasma lipid composition [6]. Moreover, smoking affects lipoprotein oxidation and impairs reverse cholesterol transport, further enhancing cardiovascular risk [7].

Epidemiological data from South-East Asia suggests a growing trend of smoking among the youth, particularly among males aged 20–40 years, making early screening of lipid profiles a crucial preventive strategy [8]. Identifying lipid alterations at this stage can help in implementing early lifestyle modifications or pharmacological interventions. Several cross-sectional and cohort studies have also reinforced the strong association between smoking and dyslipidemia, with significantly higher atherogenic index and LDL/HDL ratios in smokers compared to non-smokers [9].

Therefore, this study seeks to evaluate the lipid profile variations in young smokers versus non-smokers, with a specific focus on the severity of smoking exposure. Such an approach is not only timely but critical in reinforcing tobacco cessation strategies and targeted lipid monitoring in the younger demographic [10].

This prospective, observational, comparative study was conducted in the Department of General Medicine at a tertiary care teaching hospital over a period of 12 months. A total of 200 male participants aged between 20 to 40 years were included in the study and categorized into two equal groups: 100 smokers and 100 non-smokers. The participants were selected using purposive sampling, ensuring that the smokers had a consistent smoking history of at least one year, while the non-smokers had no history of tobacco use in any form. All participants provided informed consent before enrollment.

Detailed histories were recorded, and a thorough clinical examination was carried out for each participant. Smokers were further categorized based on the severity of their smoking habits using the smoking index (number of cigarettes smoked per day multiplied by the number of years smoked). Participants with chronic illnesses such as diabetes mellitus, hypertension, renal or hepatic dysfunction, or those on lipid-lowering medications were excluded from the study to eliminate confounding factors.

After a 12-hour overnight fast, 5 ml of venous blood was collected aseptically from each participant. The serum was separated and analyzed for lipid parameters including total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and very low-density lipoprotein cholesterol (VLDL-C) using an automated biochemical analyzer. The atherogenic index (AIP) was also calculated using the formula: log (TG/HDL-C).

All data were recorded in Microsoft Excel and subjected to statistical analysis using SPSS version 26. Descriptive statistics such as mean and standard deviation were used to summarize continuous variables. The independent t-test was employed to compare the lipid profile parameters between smokers and non-smokers, while the Chi-square test was used for categorical variables. A p-value of less than 0.05 was considered statistically significant.

In Table 1, the age-wise distribution of study participants across both smokers and non-smokers shows the majority were within the age groups of 28–32 and 33–37 years. Among non-smokers, the highest proportion (26%) belonged to the 33–37 years group, followed closely by the 28–32 group (24%). In smokers, the majority (41%) also belonged to the 33–37 age group, with a significantly high percentage (29%) in the 28–32 range. These findings suggest a predominant prevalence of smoking and non-smoking patterns in young adults in their late 20s and early 30s.

Table 2 presents a comparative analysis of the lipid profiles between non-smokers and smokers. Smokers showed significantly elevated levels of total cholesterol, serum triglycerides, LDL, and VLDL compared to non-smokers, with p-values <0.001 indicating strong statistical significance. In contrast, HDL levels were notably lower in smokers (44.72 ± 10.08) compared to non-smokers (49.62 ± 8.47), and this difference was also statistically significant (p = 0.002). These observations highlight the adverse impact of smoking on lipid metabolism and cardiovascular risk markers.

Table 3 stratifies lipid profile alterations by smoking severity. As the number of cigarettes or beedis consumed per day increased, so did the levels of total cholesterol, triglycerides, LDL, and VLDL. Heavy smokers showed the most elevated levels across all these parameters, with total cholesterol reaching 176.5 ± 25.62 and triglycerides at 209 ± 29.15. On the other hand, HDL levels showed a consistent decline from mild to heavy smokers, further reinforcing the dose-dependent detrimental effects of smoking on lipid parameters. Notably, even mild smokers exhibited worse lipid values than non-smokers, indicating early-onset metabolic disruption due to smoking habits.

Table 1: Age Distribution Among Non-Smokers and Smokers

Table 2: Lipid Profile in Non-Smokers and Smokers

Table 3: Lipid Profile in Relation to Number of Cigarette/Beedis Smoked Per Day

The current study underscores a compelling association between smoking and significant alterations in lipid profile parameters, particularly reflecting a pro-atherogenic pattern among smokers compared to non-smokers. These findings are consistent with emerging literature that increasingly links cigarette smoking to dyslipidemia, thereby reinforcing smoking’s role as a potent cardiovascular risk enhancer. According to Baharum et al., smoking leads to a marked elevation in total cholesterol, LDL, VLDL, and triglycerides, while reducing HDL concentrations, a profile suggestive of heightened atherogenic potential and endothelial dysfunction [11]. The oxidative stress induced by tobacco smoke results in lipid peroxidation, inflammation, and altered lipid metabolism, culminating in accelerated atherosclerotic plaque development [12].

Furthermore, Sugiura et al. observed that even mild smoking may significantly reduce HDL levels in young adults, which aligns with our subgroup analysis of mild, moderate, and heavy smokers [13]. The inverse relationship between smoking intensity and HDL levels in our results corroborates their findings and highlights how the severity of smoking may influence specific lipid fractions in a dose-dependent manner. Moreover, smokers demonstrated elevated levels of VLDL and triglycerides, as reported in a Malaysian community study, which found a direct association between VLDL elevation and number of cigarettes smoked per day [14]. The pathophysiological mechanism may involve enhanced hepatic secretion of VLDL and decreased lipoprotein lipase activity, which hampers triglyceride clearance.

Finally, the persistent dyslipidemia seen even in light smokers raises concern about the underestimated metabolic impact of occasional or recreational smoking, particularly in younger populations. A longitudinal Korean cohort study identified young smokers with marginally abnormal lipid profiles as having a significantly increased 10-year cardiovascular risk, emphasizing early lipid monitoring and intervention [15]. This highlights the need for aggressive preventive strategies targeting youth and young adults, including structured smoking cessation programs integrated with cardiovascular risk screening.

This study revealed that young smokers exhibit significantly altered lipid profiles when compared to non-smokers, including elevated levels of total cholesterol, LDL, VLDL, and triglycerides, and reduced HDL levels. These changes were more pronounced with increasing smoking intensity, highlighting a dose-dependent risk. The findings affirm the adverse cardiometabolic effects of smoking, even in youth, and call for urgent public health action focusing on early intervention, lifestyle education, and routine lipid monitoring among smokers.

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