Obesity has emerged as a pervasive public health concern worldwide, with its prevalence increasing rapidly across diverse populations. Globally, an estimated 890 million adults are classified as obese, reflecting a substantial burden of excess adiposity in both developed and developing regions [1]. Concurrently, hypertension affects more than 1.2 billion adults and is a leading contributor to cardiovascular morbidity and mortality [1]. The coexistence of obesity and elevated blood pressure has been consistently demonstrated in epidemiological studies, indicating that greater adiposity significantly increases the risk of developing hypertension [1,2].

A growing body of evidence from large-scale population surveys supports a positive association between measures of obesity and blood pressure levels. Analyses incorporating data from national health surveys in China and the United States have shown that increasing waist circumference and body mass index (BMI) are associated with higher risk of hypertension, independent of other risk factors [2,3]. Similarly, cross-sectional analyses from heterogeneous cohorts have established that individuals with obesity exhibit elevated mean systolic and diastolic blood pressure compared with normal-weight counterparts, highlighting the graded relationship between adiposity and hemodynamic parameters [3,4].

The pathophysiological mechanisms linking obesity to hypertension are multifactorial, involving complex interactions between increased sympathetic nervous system activity, altered renal sodium handling, activation of the renin–angiotensin–aldosterone system, and adipose tissue–mediated inflammation [2]. These processes contribute to vascular dysfunction and increased peripheral resistance, both of which are central to the development and maintenance of high blood pressure in obese individuals.

Understanding the relationship between obesity and blood pressure in specific populations is crucial for informing targeted preventive strategies and mitigating the rising burden of cardiovascular disease. Despite substantial global data, region-specific studies—especially in South Asian populations—remain limited, underscoring the need for focused investigations into how obesity influences blood pressure in diverse demographic groups.

Study design and setting: This study was designed as a cross-sectional, observational investigation conducted at a tertiary care teaching hospital. All procedures were performed in accordance with institutional research standards and ethical principles. Study population: The study population consisted of adult individuals classified as obese according to standard anthropometric criteria. Participants were recruited from outpatient departments and routine health check-up clinics of the hospital using a consecutive sampling approach. Inclusion criteria • Adults aged 18–60 years • Body mass index (BMI) ≥ 30 kg/m² • Individuals willing to participate and provide informed consent Exclusion criteria • Known cases of secondary hypertension • History of cardiovascular disease, chronic kidney disease, or endocrine disorders affecting blood pressure • Pregnant or lactating women • Individuals on long-term antihypertensive, steroidal, or weight-altering medications Sample size estimation: The sample size was determined based on the expected prevalence of elevated blood pressure among obese individuals. Assuming a prevalence of 50% to achieve maximum sample size, with a confidence level of 95% and an absolute precision of 10%, the minimum required sample size was calculated using the formula: n=Z2×p×q/d2 Where: • n = required sample size • Z = standard normal variate at 95% confidence (1.96) • p = anticipated prevalence (0.5) • q = 1 − p • d = allowable error (0.1) The calculated minimum sample size was 96. To account for possible non-response or incomplete data, a total of 100 participants were included in the study. Data collection procedure: After obtaining written informed consent, demographic details including age and sex were recorded. Anthropometric measurements were obtained using standardized techniques. Body weight was measured to the nearest 0.1 kg using a calibrated digital weighing scale, with participants wearing light clothing and no footwear. Height was measured to the nearest 0.1 cm using a stadiometer. BMI was calculated as weight in kilograms divided by height in meters squared (kg/m²). Blood pressure was measured using a calibrated mercury sphygmomanometer following standard guidelines. Participants were advised to rest in a seated position for at least five minutes before measurement. Blood pressure was recorded in the right arm, supported at heart level, using an appropriately sized cuff. Two readings were taken at an interval of five minutes, and the average of the two readings was considered for analysis. Systolic blood pressure was identified by the appearance of Korotkoff phase I sounds, and diastolic blood pressure by the disappearance of Korotkoff phase V sounds. Outcome measures: The primary outcome variables were systolic and diastolic blood pressure levels. Blood pressure status was categorized according to standard classification criteria into normotensive, prehypertensive, and hypertensive ranges for analytical purposes. Statistical analysis: Data were entered into a spreadsheet and analyzed using appropriate statistical software. Continuous variables were expressed as mean ± standard deviation, while categorical variables were presented as frequencies and percentages. The association between obesity-related parameters and blood pressure levels was assessed using appropriate statistical tests. A p-value of less than 0.05 was considered statistically significant.

A total of 110 obese individuals were included in the final analysis. The mean age of the study participants was 41.8 ± 10.6 years. Males constituted 56.4% of the study population, while females accounted for 43.6%. The mean body mass index of the participants was 31.8 ± 2.4 kg/m², confirming obesity in all enrolled subjects (Table 1).

The overall mean systolic blood pressure among the participants was 134.6 ± 15.2 mmHg, and the mean diastolic blood pressure was 86.9 ± 9.8 mmHg (Table 2).

Based on blood pressure classification, 34.5% of participants were normotensive, 37.3% were prehypertensive, and 28.2% were hypertensive. Thus, a substantial proportion of obese individuals exhibited either prehypertension or hypertension (Table 3).

Gender-wise comparison showed that mean systolic blood pressure was significantly higher in males (137.2 ± 14.8 mmHg) compared to females (131.3 ± 15.3 mmHg), with a statistically significant difference (p = 0.041). Although diastolic blood pressure was higher in males than females, the difference did not reach statistical significance (p = 0.118) (Table 4).

When blood pressure status was analyzed across BMI categories, individuals with BMI ≥ 32.5 kg/m² demonstrated a higher prevalence of hypertension (39.1%) compared to those with BMI between 30.0–32.4 kg/m² (20.3%). Conversely, normotensive status was more commonly observed in the lower BMI category. The association between BMI category and blood pressure status was statistically significant (χ² test, p = 0.018), indicating a positive relationship between increasing BMI and elevated blood pressure levels (Table 5).

Table 1. Demographic and anthropometric characteristics of study participants (n = 110)

Table 2. Distribution of blood pressure parameters among obese individuals (n = 110)

Table 3. Classification of blood pressure status among study participants (n = 110)

Table 4. Comparison of blood pressure values according to gender

Table 5. Association between BMI category and blood pressure status

Chi-square test, p = 0.018

In the present study of obese adults, a high prevalence of elevated blood pressure was observed, consistent with prior epidemiological evidence linking adiposity with increased blood pressure levels. Several large-scale population studies have demonstrated a strong positive association between BMI and both systolic and diastolic blood pressure across diverse demographic cohorts, reinforcing the graded relationship observed in our cohort [5,6]. These data align with our observation that a substantial proportion of obese participants were prehypertensive or hypertensive, suggesting that progressive adiposity confers incremental hemodynamic burden.

The mechanisms underlying the obesity–blood pressure relationship are complex and multifactorial. Adipose tissue expansion promotes metabolic and neurohormonal changes including insulin resistance, increased sympathetic nervous system activation, and altered renal sodium handling, all of which contribute to heightened vascular resistance and blood pressure elevation [7,8]. Such mechanisms offer biological plausibility for the statistically significant trend toward higher hypertension prevalence with increasing BMI categories observed in this study.

Our gender-stratified findings, in which obese males exhibited higher mean systolic blood pressure than females, are in line with data from multicountry surveys indicating sex differences in the prevalence and impact of excess weight on hypertension risk, potentially attributable to differences in fat distribution, hormonal milieu, and cardiovascular regulation [9,10]. Importantly, sex-specific patterns of adiposity, particularly central obesity, may more strongly predict hypertension than BMI alone, underscoring the need for nuanced interpretation of anthropometric indices in relation to cardiovascular risk [9,10].

Regional investigations within South Asian populations have similarly reported robust associations between BMI and hypertension even at lower BMI thresholds compared with Western cohorts, consistent with a heightened cardiometabolic susceptibility in this demographic context [11,12]. This aligns with our findings in an Indian clinical sample and supports the public health imperative for early detection and management of elevated blood pressure among individuals with increased adiposity.

Collectively, these findings underscore that obesity exerts a significant influence on blood pressure regulation and hypertension risk. Strategies targeting weight reduction and lifestyle modification remain critical components of hypertension prevention and cardiovascular disease mitigation.

The present study demonstrates a high burden of elevated blood pressure among obese adults, with more than two-thirds of participants exhibiting either prehypertension or hypertension. Mean systolic and diastolic blood pressure values were within ranges indicative of increased cardiovascular risk in this population. Male participants showed significantly higher systolic blood pressure compared to females. Furthermore, a clear and statistically significant association was observed between higher BMI categories and the prevalence of hypertension, indicating a progressive rise in blood pressure with increasing severity of obesity. These findings underscore the importance of routine blood pressure screening and early preventive strategies among obese individuals to mitigate future cardiovascular morbidity.

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