Differential effects of obesity and hypertension on brain structure and cognitive ability: A subgroup analysis from nested study

Abstract

BACKGROUND:

Obesity and hypertension are widespread health issues associated with changes in brain structure and cognitive function, especially in individuals who lead sedentary lifestyles. This research examines the connections between obesity, high blood pressure, brain structure, and cognitive abilities in people who lead a sedentary lifestyle.

MATERIALS AND METHODS:

The study involved 90 individuals aged between 18 and 35 years, who were categorized into three groups: control (n = 30), obese (n = 30), and hypertensive (n = 30). The researchers used magnetic resonance imaging (MRI) scans to examine the brain’s structure, specifically analyzing the volume of different regions. The researchers assessed cognitive function using the flanker task to measure selective attention and the n-back task to evaluate working memory. Statistical analysis involved the use of one-way analysis of variance (ANOVA) and Games-Howell post-hoc tests.

RESULTS:

The findings revealed notable variations in the volume of the left parahippocampal gyrus (lPHG) among the different groups, with the control group exhibiting the highest volume, followed by the obese group, and finally the hypertensive group. The cognitive performance varied greatly among the groups in both the flanker and n-back tasks, with a significant difference observed in all measures (P and lt;.001). The group with high blood pressure showed the lowest performance, followed by the group with obesity, with the control group performing the best.

CONCLUSION:

Our findings reveal a gradient of cognitive impairment and reduced lPHG volume in sedentary individuals, with hypertension showing more pronounced effects than obesity alone. These findings underscore the importance of considering the cognitive effects of obesity and hypertension in individuals who lead sedentary lifestyles, underscoring the necessity for comprehensive care strategies that address both physical and cognitive dimensions of these conditions.

Introduction

The rising rates of obesity and hypertension have become major health issues[1,2] with research showing a strong connection to changes in brain structure and cognitive abilities, especially in individuals who lead sedentary lifestyles. As physical inactivity frequently occurs alongside these conditions, comprehending their combined impact on neurological health has become a crucial study area. Research has indicated that obesity is linked to smaller brain volumes and decreased cognitive abilities.[3] Kim et al. (2020)[4] found that hypertension can lead to similar structural brain changes and cognitive impairments as Alateeq et al. (2021)[5] and Shang et al. (2021).[6]

The inactive lifestyle, marked by extended periods of inactivity, may worsen the detrimental effects of obesity and hypertension on brain health. Studies have shown that spending more time being inactive is linked to lower cognitive abilities, regardless of how much physical activity one engages in[7] This implies that the absence of physical activity might exacerbate the cognitive impairments seen in individuals who are obese and have high blood pressure.[8]

Recent research has utilized particular cognitive tasks to investigate the connections between obesity, hypertension, and cognitive function. The flanker task, which measures attention and inhibitory control, shows reduced performance in individuals who are obese and have high blood pressure.[9] Similarly, the n-back task, which assesses working memory, has shown deficits in obese individuals[10] and those with hypertension.[11]

The connection between physical activity, brain size, and cognitive abilities has been extensively studied and documented in various research papers. Raja and his colleagues discovered a positive correlation between the total amount of physical activity and the size of the left hippocampus, suggesting that exercise may have neuroprotective benefits.[12] However, obesity has been associated with structural brain abnormalities, such as reduced total brain volume and gray matter (GM) volume.[3]

Hypertension, which often coexists with obesity, has also been linked to changes in brain structure and function. Gonzalez and his colleagues published a study showing that hypertensive individuals experienced decreases in prefrontal, temporal, and hippocampal volumes, suggesting a possible link between high blood pressure and brain shrinkage.[13] Additionally, hypertension has been associated with cognitive decline, specifically in memory, executive functions, and information processing speed.[14,15]

Surprisingly, certain studies have indicated that engaging in physical activity can help preserve cognitive function, even if a person is overweight or has high blood pressure. Boidin et al.[16] discovered that individuals who were obese and had good aerobic fitness performed better in tasks related to executive function and short-term memory.[16] In a similar vein, Lv et al.[17] found a negative correlation between the intensity of physical activity and cognitive impairment in hypertensive patients.[17]

The current research seeks to fill the existing knowledge gap by examining the connections between obesity, hypertension, brain structure, and cognitive function using the flanker and n-back tasks in sedentary individuals. By concentrating on this group, we can more accurately determine the impact of obesity and hypertension, without the interference of differing levels of physical activity. We predict that in individuals who are not physically active, the group without obesity or high blood pressure would have larger brain volumes and better cognitive abilities compared to those who are obese or have high blood pressure.

This study offers several novel contributions to our understanding of how obesity and hypertension affect brain structure and cognitive function in sedentary individuals. Firstly, by focusing specifically on a sedentary population, we provide unique insights into the neurological impacts of these conditions in the absence of regular physical activity. Our integrated analysis of both structural brain changes and cognitive performance offers a comprehensive view rarely seen in previous studies. The observed gradient of cognitive impairment, with hypertension showing more pronounced effects than obesity alone, is a novel finding in this context. Additionally, the asymmetry in parahippocampal gyrus volume changes (significant in the left but not the right hemisphere) suggests potential lateralization effects that warrant further investigation. Finally, our task-specific cognitive findings provide new insights into how obesity and hypertension differentially affect various aspects of cognitive function in sedentary individuals.

Understanding these relationships in the context of a sedentary lifestyle is crucial for informing targeted interventions, providing insights into potential additive or synergistic effects, and contributing to our broader understanding of the complex interplay between metabolic health, cardiovascular function, and cognitive performance without regular physical activity. The results of this study could have important consequences for public health efforts, medical treatments, and lifestyle advice designed to maintain cognitive abilities in populations that are becoming more sedentary.

Figure 1 illustrates the connections between a sedentary lifestyle, obesity, high blood pressure, brain structure, and cognitive function.

Figure 1.

Conceptual framework of obesity, hypertension, brain structure, and cognitive function relationships in sedentary individuals

Materials and Methods

Study design and setting

For our subgroup analysis, we utilized data from two studies conducted at the Dept of Radiodiagnosis and Imaging, Kasturba Hospital, Manipal. This was a cross-sectional study. Demographic information, including age, gender, height, and weight, was collected from all participants.

Study participants

We included participants aged 18–35 who underwent magnetic resonance imaging (MRI) brain scans as part of their clinical referral, focusing on three groups: sedentary control without comorbidities, sedentary obese, and sedentary hypertensive. The inclusion criteria are shown in Table 1. The exclusion factors were history of dementia, major psychiatric or neurologic disorders, substance abuse, head trauma, systemic diseases affecting cognitive or brain function, uncontrolled hypertension, and cardiovascular diseases.

Table 1.

Inclusion criteria

Groups	Condition
Sedentary control	METs <600 MET-min/week; BMI=18-25 kg/m2; SBP <140 mmHg; DBP <90 mmHg
Sedentary obese	METs <600 MET-min/week; BMI >25 kg/m2; SBP <140 mmHg; DBP <90 mmHg
Sedentary hypertensive	METs <600 MET-min/week; BMI=18-25 kg/m2; SBP >140 mmHg; DBP >90 mmHg

SBP (systolic blood pressure); DBP (diastolic blood pressure)

Sample size

A priori sample size calculation was performed for the primary outcome measure of the left parahippocampal gyrus (lPHG) volume. Based on pilot data and previous literature, we anticipated a medium-to-large effect size (f = 0.35, equivalent to η² ≈0.11) for the one-way analysis of variance (ANOVA) comparing the three groups (control, obese, and hypertensive). Using G*Power software (version 3.1.9.7), we calculated the required sample size with the following parameters: α =0.05, power (1-β) =0.80, number of groups = 3, and effect size f = 0.35. The analysis indicated a total required sample size of 84 participants (28 per group) to detect significant differences between groups. To account for potential dropouts and to slightly increase statistical power, we recruited 30 participants per group, resulting in a total sample size of 90. This sample size was deemed sufficient to detect meaningful differences in the primary outcome measure while also providing adequate power for secondary analyses of cognitive performance measures.

Data Collection Tools and Techniques

Physical activity assessment

The participants’ physical activity levels were assessed using the self-reported International Physical Activity Questionnaire and quantified using metabolic equivalent units. MET-min per week (METs) were calculated using Ainsworth calculations, with walking scored at 3.3 METs, moderate physical activity at 4.0 METs, and vigorous physical activity at 8.0 METs.[18]

Cognitive function assessment

Cognitive functions were assessed using computer-based tests, the n-back memory task, and the Eriksen flanker task, implemented in Inquisit Lab 6 software (version 6.6.1). Visual prompts were displayed on a laptop, and both tasks’ accuracy and reaction times were recorded and evaluated.

MRI acquisition and image processing

MRI brain scans were acquired for all the participants at the Department of Radiodiagnosis and Imaging, Kasturba Hospital, Manipal. The imaging platform employed was a United Imaging uMR 780 3-Tesla scanner equipped with a 32-channel head coil. T1-weighted 3D Spoiled Gradient Echo (SPGR) sequence was acquired for the structural analysis of the amygdala. The scan parameters for image acquisition were as follows: TR = 7.7 ms, TE = 3.1 ms, flip angle = 10°, slice thickness = 1 mm, and slice increment = 0.6 mm.

Image pre-processing and analysis were performed using MATLAB (version R2022b, MathWorks, Natick, MA, USA) with SPM12 (version 7771) and CAT12 toolboxes (version 2577). Digital Imaging and Communications in Medicine (DICOM) images were converted to NIfTi format, followed by normalization, segmentation, and homogeneity testing. Only photos with quality exceeding 70% were selected for further analysis. The CAT12 software was used to calculate volumes of GM, white matter (WM), cerebrospinal fluid (CSF), and total intracranial volume (TIV). Additionally, AAL3 atlas was used to segment and extract structural data of the amygdala. Amygdala volumes were calculated for each participant and normalized to the TIV to account for individual differences in the brain. The postprocessed report from the CAT12 Toolbox is shown in Figure 2.

Figure 2.

Comprehensive MRI analysis report from CAT12 Toolbox with detailed volumetric and quality metrics with structural visualization

Statistical analyses

All statistical analyses were performed using Jamovi software (version 2.5). Descriptive statistics for continuous variables were reported as mean and standard deviation. A one-way ANOVA was employed to compare differences in brain structure volumes and cognitive performance metrics across the three groups (control, obese, and hypertensive). For measures that showed significant differences in the ANOVA, the Games-Howell post-hoc test was used to determine specific group differences through pairwise comparisons between the control, obese, and hypertensive groups. A P value of less than 0.05 determined statistical significance.

Ethical consideration

The study received the Institutional Research Committee at Manipal College of Health Professions and the Institutional Ethics Committee at Kasturba Hospital (IEC1 320/2022 and IEC1 61/2024) and was prospectively registered in the Clinical Trial Registry of India (CTRI/2023/07/055243 and CTRI/2024/05/067086).

Results

The study was comprised of three groups—control, obese, and hypertensive—with 30 participants. Age distributions varied across groups, with mean ages of 23.4 years (SD = 3.78) for control, 24.26 years (SD = 4.45) for obese, and 27.3 years (SD = 5.67) for hypertensive participants. Heights were similar across groups, with means ranging from 160.6 cm (SD = 8.83) in the obese group to 163.5 cm (SD = 6.92) in the hypertensive group. As expected, weight differed significantly, with the obese group having the highest mean weight of 75.9 kg (SD = 10.07), compared to 57.6 kg (SD = 7.68) for control and 61.8 kg (SD = 9.99) for hypertensive groups. Physical activity levels, measured in MET-min/week, were low across all groups, classifying participants as sedentary. The hypertensive group showed slightly higher but more variable physical activity (mean = 308.36, SD = 146.35) compared to the control (mean = 260.2, SD = 118.20) and obese (mean = 267.5, SD = 120.69) groups. All groups included participants aged 18 to 35, with heights ranging from 142 to 188.4 cm, weights from 46.8 to 100 kg, and MET scores from 0 to 594 MET-min/week [Table 2].

Table 2.

Demographic characteristic details (age, height, weight) and physical activity levels (METs) for the three study groups

Group	n	Mean	SD
Age (years)
Control	30	23.4	3.78
Obese	30	24.26	4.45
Hypertensive	30	27.3	5.67
Height (cm)
Control	30	162.1	7.84
Obese	30	160.6	8.83
Hypertensive	30	163.5	6.92
Weight (kg)
Control	30	57.6	7.68
Obese	30	75.9	10.07
Hypertensive	30	61.8	9.99
METs (MET-min/week)
Control	30	260.2	118.20
Obese	30	267.5	120.69
Hypertensive	30	308.36	146.3537244

Table 3 presents the results of the one-way ANOVA test for various measurements across the groups. In structural analysis, the lPHG volume shows highly significant differences between groups (F = 121.569, P < .001) [Figure 3]. Interestingly, the right parahippocampal gyrus (rPHG) volume does not show significant differences between groups (F = 0.457, P = 0.636). Behavioral analysis measures also demonstrate considerable group differences. Both flanker task reaction time (F = 53.464, P < .001) and accuracy (F = 1046.450, P < .001) show highly significant differences. Similarly, n-back task performance differs significantly across groups in both reaction time (F = 21.625, P < .001) and accuracy (F = 11.709, P < .001). Table 3 reveals significant differences in lPHG volume (F = 121.569, P < .001) and all cognitive performance measures. Notably, the rPHG volume did not show significant differences between groups. These results suggest substantial differences between the groups in most measures, particularly in the lPHG volume and cognitive task performance. In contrast, the rPHG volume remains relatively consistent across groups.

Table 3.

One-way ANOVA (Welch’s), presenting the F-statistic, degrees of freedom (df1 and df2), and P values for each measure compared across the groups

Structural analysis	F	df1	df2	P
lHIP (mm3)	0.2781	2	54.1	0.758
rHIP (mm3)	0.0405	2	51.2	0.960
IPCC (mm3)	0.4694	2	53.7	0.628
rPCC (mm3)	0.4805	2	52.1	0.621
lAMYG (mm3)	0.2417	2	51.2	0.786
rAMYG (mm3)	0.0145	2	48.1	0.986
lSTG (mm3)	1.4968	2	57.1	0.232
rSTG (mm3)	1.7352	2	55.3	0.186
lMTG (mm3)	1.3788	2	57.3	0.260
rMTG (mm3)	1.9267	2	57.3	0.155
lITG (mm3)	0.5534	2	57.4	0.578
rITG (mm3)	1.0622	2	57.1	0.352
lPHG (mm3)	121.569	2	52.7	<0.001***
rPHG (mm3)	0.457	2	56.8	0.636
lFFG (mm3)	0.1609	2	53.1	0.852
rFFG (mm3)	0.6892	2	57.1	0.506
GMV (mm3)	0.2190	2	55.8	0.804
WMV (mm3)	0.5460	2	53.5	0.582
CSF (mm3)	2.7969	2	51.6	0.070
TIV (mm3)	0.6061	2	53.7	0.549
Behavioral analysis	F	df1	df2	P
Flanker reaction time (ms)	53.464	2	57.1	<0.001***
Flanker accuracy (%)	1046.450	2	48.3	<0.001***
N-back reaction time (ms)	21.625	2	57.7	<0.001***
N-back accuracy (%)	11.709	2	56.9	<0.001***

*P<0.05, **P<0.01, ***P<0.001. lHIP (left hippocampus volume), rHIP (right hippocampus volume), lPCC (left posterior cingulate cortex), rPCC (right posterior cingulate cortex), lAMYG (left amygdala), rAMYG (right amygdala), lSTG (left superior temporal gyrus), rSTG (right superior temporal gyrus), lMTG (left medial temporal gyrus), rMTG (right medial temporal gyrus), lITG (left inferior temporal gyrus), rITG (right inferior temporal gyrus), lPHG (left parahippocampal gyrus), rPHG (right parahippocampal gyrus), lFFG (left fusiform gyrus), rFFG (right fusiform gyrus), GMV (gray matter volume), WMV (white matter volume), CSF (cerebrospinal fluid), TIV (total intracranial volume)

Figure 3.

Comparison of left parahippocampal gyrus volume across the control, obese, and hypertensive groups

Games-Howell post-hoc tests were conducted for significant results from the ANOVA test to determine which specific groups differ from each other. The post-hoc test results for the lPHG volume reveal substantial differences among all group comparisons. The control group shows the most enormous lPHG volume, significantly exceeding both the obese group (mean difference = 0.297 mm≥, P < .001) and the hypertensive group (mean difference = 0.589 mm≥, P < .001). Additionally, the obese group’s lPHG volume is significantly larger than that of the hypertensive group (mean difference = 0.291 mm≥, P < .001). As shown in Table 4, all group comparisons for the lPHG volume were significant, with the control group showing the largest volume, followed by the obese group, and then the hypertensive group.

Table 4.

Games-Howell post-hoc test for lPHG

	Control	Obese	Hypertensive
Control
Mean difference	—	0.297***	0.589***
P	—	< .001	<0.001
Obese
Mean difference		—	0.291***
P		—	<0.001
Hypertensive
Mean difference			—
P			—

*P<0.05, **P<0.01, ***P<0.001

Interpreting the results from Table 5, we can observe significant differences in cognitive performance across the control, obese, and hypertensive groups for both the flanker and n-back tasks.

Table 5.

Games-Howell post-hoc test for flanker and n-back tasks

Flanker task
Reaction time (ms)				Accuracy (%)
	Control	Obese	Hypertensive		Control	Obese	Hypertensive
Control				Control
Mean difference	—	-44.0*	-141.6***	Mean difference	—	0.0734	7.80***
P	—	0.016	< .001	P	—	0.701	<0.001
Obese		Obese		Obese
Mean difference		—	-97.7***	Mean difference		—	7.73***
P		—	<0.001	P		—	<0.001
Hypertensive				Hypertensive
Mean difference			—	Mean difference			—
P			—	P			—
N-back task
Reaction time (ms)				Accuracy (%)
	Control	Obese	Hypertensive		Control	Obese	Hypertensive
Control				Control
Mean difference	—	-40.4	-157***	Mean difference	—	3.87	15.6***
P	—	0.304	<0.001	P	—	0.324	<0.001
Obese				Obese
Mean difference		—	-117***	Mean difference		—	11.7**
P		—	<0.001	P		—	0.002
Hypertensive				Hypertensive
Mean difference			—	Mean difference			—
P			—	P			—

*P<0.05, **P<0.01, ***P<0.001

For reaction time, all group comparisons show significant differences. The control group demonstrates the fastest reaction times, being significantly quicker than both the obese group (mean difference = -44.0 ms, P = 0.016) and the hypertensive group (mean difference = -141.6 ms, P < .001). The obese group is also significantly faster than the hypertensive group (mean difference = -97.7 ms, P < .001). Regarding accuracy, there is no significant difference between the control and obese groups (mean difference = 0.0734%, P = 0.701). However, both the control and obese groups significantly outperform the hypertensive group (control vs. hypertensive: mean difference = 7.80%, P < .001; obese vs. hypertensive: mean difference = 7.73%, P < .001). Table 5 demonstrates significant differences in cognitive performance across groups for both tasks. In the flanker task, all groups differed significantly in reaction time, with the control group being the fastest. For accuracy, the control and obese groups outperformed the hypertensive group. In the n-back task, both the control and obese groups were significantly faster and more accurate than the hypertensive group [Figure 4].

Figure 4.

Comparison of reaction time and accuracy in the flanker and n-back task across control, obese, and hypertensive groups (a) represents the Flanker's test reaction time in (ms), (b) represents the Flanker's test accuracy in %. (c) shows the N-Back test's reaction time in (ms) and (d) represents the N-Back test's accuracy results in % plotted

The Games-Howell post-hoc test results for the n-back task reveal significant differences in reaction time and accuracy across the three groups. The control group is significantly faster for reaction time than the hypertensive group (mean difference = -157 ms, P < .001). The obese group is also considerably quicker than the hypertensive group (mean difference = -117 ms, P < .001). However, there is no significant difference in reaction time between the control and obese groups (mean difference = -40.4 ms, P = 0.304). Regarding accuracy, the control group significantly outperforms the hypertensive group (mean difference = 15.6%, P < .001). The obese group also shows considerably better accuracy than the hypertensive group (mean difference = 11.7%, P = 0.002). There is no significant difference in accuracy between the control and obese groups (mean difference = 3.87%, P = 0.324) [Table 4].

Discussion

Our study aimed to investigate the relationships between obesity, hypertension, brain structure, and cognitive function among sedentary individuals. We hypothesized that the control group would have larger brain volumes and better cognitive performance compared to their obese and hypertensive counterparts. The results largely support this hypothesis, revealing significant differences in the lPHG volume and cognitive performance across control, obese, and hypertensive groups.

The observed reduction in the lPHG volume in obese and hypertensive individuals compared to controls aligns with previous research. Han et al.[3,19] and Kim EB et al. reported that obesity is associated with structural brain abnormalities, including lower total brain volume and GM volume.[3,19] Likewise, Shang et al.[6] found that hypertension reduces brain volume, particularly in the prefrontal cortex, temporal lobe, and hippocampal regions.[6] Our study expands upon existing research by providing evidence that these structural alterations are detectable within sedentary populations, implying that lack of physical activity may not mitigate the neurological consequences associated with obesity and hypertension. Our findings contribute to the intricate landscape of brain structural changes associated with these conditions, as reported by Kim et al.[4,19] and Kim and Baek, who found volumetric differences in subcortical brain structures in obese individuals.[4,20]

Interestingly, we observed no significant differences in the volume of the rPHG between the groups. This asymmetry potentially suggests a heterogeneous susceptibility of brain regions to the combined effects of obesity and hypertension in individuals with sedentary lifestyles.

In terms of cognitive performance, our study revealed significant declines in both flanker and n-back tasks for the hypertensive and obese groups. These observations support our initial hypothesis and align with prior research, collectively suggesting a link between obesity, hypertension, and cognitive decline. We observed slower reaction times and lower accuracy in the flanker task for the hypertensive group, as well as slower reaction times in the obese group. These findings concur with Marshall et al.’s study, which demonstrated that hypertensive individuals displayed deficits in inhibitory control when performing the flanker task, particularly in stress conditions.[9] These observations may reflect the findings of Wang et al., who reported that obesity can affect cognition and motor performance by altering brain functions.[20]

The performance on the n-back task revealed significant decrements in both reaction time and accuracy for the hypertensive group compared to controls. Notably, the obese group did not exhibit statistically significant differences from controls on these measures. These results are partially supported by previous studies. Khoonsinthaweekul et al. reported that n-back task performance is associated with altered electroencephalogram (EEG) power spectra in obese patients, suggesting alterations in neural processing.[10] Our findings suggest that, within a sedentary population, hypertension may exert a more robust effect on working memory performance compared to obesity alone. Notably, Köhler et al.[14,15] and Rouch et al. have previously reported that hypertension is linked to declines in memory, executive function, and information processing speed.[15,16]

While the observed cognitive deficits in the obese group were less pronounced than those in the hypertensive group, these findings are nevertheless corroborated by a multitude of prior investigations. Tecellioʇlu et al. documented an association between obesity and a range of cognitive deficits, including attention, memory, processing speed, and executive functioning.[11] In line with prior investigations, overweight and obese individuals have been shown to exhibit lower cognitive performance, specifically in domains, such as fluid intelligence and short-term memory.[20,21,22,23]

The cognitive performance decline in obese and hypertensive groups may potentially be attributable to the structural brain alterations manifested by the reductions in the lPHG volume. Given its well-established role in memory consolidation, the observed reduction in the parahippocampal gyrus volume may underlie the documented impairments in the cognitive tasks reliant on memory and executive function.

The cognitive performance decline in obese and hypertensive groups may potentially be attributable to the structural brain alterations manifested by the reductions in the lPHG volume. Given its well-established role in memory consolidation, the observed reduction in the parahippocampal gyrus volume may underlie the documented impairments in the cognitive tasks reliant on memory and executive function.

It is important to note that the relationship between obesity, hypertension, and cognitive function is complex and likely bidirectional. While our study shows associations between these conditions and cognitive declines in sedentary individuals, causality cannot be inferred from these cross-sectional data. Longitudinal studies would be necessary to elucidate the temporal relationships between these factors.

Future research should explore the potential of lifestyle interventions, including diet and exercise, in mitigating the cognitive effects of obesity and hypertension in sedentary populations. Veronese et al. found that intentional weight loss in obese/overweight individuals is associated with improvements in various cognitive domains.[23] Investigating the mechanisms underlying the observed brain structural changes and cognitive impairments could provide valuable insights for developing targeted interventions. For instance, previous studies found that low-intensity exercise was associated with improvements in spatial memory and cognitive deficits in hypertensive rats, suggesting potential avenues for intervention even in previously sedentary populations.[24,25]

In conclusion, our study revealed significant differences in the lPHG volume and cognitive performance across control, obese, and hypertensive groups within a sedentary population. We observed a gradient of cognitive impairment, with the hypertensive group showing the most pronounced deficits, followed by the obese group, and then the control group. These findings highlight the potential cognitive impacts of obesity and hypertension, emphasizing the need for integrated care approaches that address both physical and cognitive aspects of these conditions in clinical settings. Future research should focus on longitudinal studies and intervention strategies to further elucidate and potentially mitigate these cognitive effects in sedentary individuals with obesity and hypertension.

Limitations and Future Directions

It is important to note that the relationship between obesity, hypertension, and cognitive function is complex and likely bidirectional. While our study shows associations between these conditions and cognitive declines in sedentary individuals, causality cannot be inferred from these cross-sectional data. Longitudinal studies would be necessary to elucidate the temporal relationships between these factors.

Future research should explore the potential of lifestyle interventions, including diet and exercise, in mitigating the cognitive effects of obesity and hypertension in sedentary populations. Veronese et al.[23] found that intentional weight loss in obese/overweight individuals is associated with improvements in various cognitive domains.[23] Investigating the mechanisms underlying the observed brain structural changes and cognitive impairments could provide valuable insights for developing targeted interventions. For instance, previous studies found that low-intensity exercise was associated with improvements in spatial memory and cognitive deficits in hypertensive rats, suggesting potential avenues for intervention even in previously sedentary populations.[24,25,26,27,28]

Figure 5 illustrates the effects of a sedentary lifestyle on three distinct groups (control, obese, and hypertensive) and highlights differences in the IPHG volume and cognitive performance, measured through reaction time and accuracy in the flanker and n-back tasks.

Figure 5.

Impact of sedentary lifestyle on cognitive performance and brain volume

Conclusion

Our study revealed significant differences in the lPHG volume and cognitive performance across control, obese, and hypertensive groups. We found reduced lPHG volume in obese and hypertensive individuals compared to controls and impaired cognitive performance, particularly in the hypertensive group, across both flanker and n-back tasks. A gradient of cognitive impairment was observed, with the hypertensive group showing the most pronounced deficits, followed by the obese group, and then the control group. These findings highlight the potential cognitive impacts of obesity and hypertension, emphasizing the need for integrated care approaches that address both physical and cognitive aspects of these conditions in clinical settings.

Our findings align with crucial health policy benchmarks, including the World Health Organization (WHO)’s Global Action Plan for Noncommunicable Diseases, Healthy People 2030 Objectives, and AHA’s 2017 hypertension guidelines. They support the National Institute for Health and Care Excellence (NICE) guidelines for integrated obesity and hypertension management and the European Guidelines on Cardiovascular Disease Prevention. Based on these alignments, we recommend expanding public health campaigns to include the cognitive impacts of obesity and hypertension, incorporating cognitive assessments in screening programs for these conditions, developing integrated care pathways addressing both physical and cognitive aspects, and allocating resources for research on interventions targeting cardiovascular and cognitive health simultaneously. These recommendations aim to improve cardiovascular and cognitive health outcomes through evidence-based policies and guidelines.

Abbreviations

MRI: magnetic resonance imaging; lPHG: left parahippocampal gyrus; ANOVA: analysis of variance; rPHG: right parahippocampal gyrus; BMI: body mass index SBP: systolic blood pressure; DBP: diastolic blood pressure; METs: metabolic equivalent units; GM: gray matter; WM: white matter; CSF: cerebrospinal fluid; TIV: total intracranial volume; lHIP: left hippocampus; rHIP: right hippocampus; lPCC: left posterior cingulate cortex; rPCC: right posterior cingulate cortex; lAMYG: left amygdala; rAMYG: right amygdala; lSTG: left superior temporal gyrus; rSTG: right superior temporal gyrus; lMTG: left medial temporal gyrus.

rMTG: right medial temporal gyrus; lITG: left inferior temporal gyrus; rITG: right inferior temporal gyrus; lFFG: left fusiform gyrus; rFFG: right fusiform gyrus; GMV: gray matter volume; WMV: white matter volume; EEG: electroencephalogram; WHO: World Health Organization; AHA: American Heart Association; NICE: National Institute for Health and Care Excellence.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.