Abstract
The aims of our study were to examine whether initial or subsequent adiposity status had a greater effect on hypertension. We collected data in 1992 and again in 2007 from the same group of 597 individuals in the middle age. The subjects were classified into four groups: individuals with a normal body mass index (BMI) in 1992 and 2007 were in Group I; those with a normal BMI in 1992, but became overweight or obese in 2007 were in Group II; those who were overweight or obese in 1992, but had a normal BMI in 2007 were in Group III; and those who were overweight or obese in 1992 and 2007 were in Group IV. Their demographic data were recorded. The relationship between adiposity status and hypertension was analyzed using logistic regression model. The cumulative incidence of hypertension was 35.5%, 56.3%, 50.0%, and 65.1% for Group I to IV, respectively. Compared with Group I, after adjusted factors, the hazard ratio (HR) was 1.80 for Group II (P = .001), 1.40 for Group III (P = .150), and 2.31 for Group IV (P < .001). Adiposity status in 2007 could predict hypertension (OR = 2.5, P < .001), as opposed to the initial adiposity status (P = .148). Subsequently adiposity status could have major effects on hypertension. Our society is very short of public health resources, particularly in developing countries, we should pay more attention to current adiposity status and encourage middle‐aged people to lose weight.
Keywords: adiposity status, BMI, cardiovascular disease, hypertension, middle‐age
1. INTRODUCTION
Hypertension is an important predictor of premature death especially for cardiovascular diseases, such as heart failure, stroke, and coronary heart disease (CHD). Globally, the prevalence of hypertension is increasing. 1 , 2 , 3 Inevitably, hypertension and its complications will emerge as one of the major threats to future public health resources throughout the world. In adults, hypertension often rises with increasing body weight. 4 Being overweight or obese has been closely associated with the development of hypertension. 5 , 6 , 7 , 8 , 9 , 10
Recently, Hasan and colleagues 11 showed that weight gain from young adulthood through middle age, and into later life, could increase the risk of hypertension, and that reaching normal weight after being obese from young adulthood into middle age could reduce the subsequent risk of developing hypertension. Although a previous study 12 showed that weight loss could reverse the adverse effects of obesity on diabetes relative to age, it is unclear whether weight loss could reverse the adverse effects on hypertension in middle age. Few studies discuss whether initial or subsequent adiposity might have a greater effect on hypertension in middle age. Therefore, the main aims of our study were to examine whether weight loss could reverse the adverse effects of initial obesity on hypertension in middle age, and whether initial or subsequent adiposity status had a greater effect on hypertension.
2. METHODS
2.1. Study population
This study enrolled the study sample population from a Chinese Multi‐provincial Cohort Study (CMCS) over a 15‐year follow‐up period from 1992 to 2007, a nationwide, multicenter prospective cohort study. Among which, the healthy volunteers in middle age (25‐64 years) who took part in a sampling survey of cardiovascular disease (CVD) risk factors in 1992 and again in 2007 in the same group in an urban community in Chengdu, Sichuan Province, China, were included. There were 1450 subjects accepted health examination in Chengdu in 1992, and 1229 participants follow‐up in 2007, but only 711 who accepted health examination from the same group were included in this study. This study was approved by the Ministry of Health of China, and by the Ethics Committee of West China Hospital of Sichuan University. All participants provided written informed consent.
2.2. Variables
Under the Multinational Monitoring Trends and Determinants in Cardiovascular Disease (MONICA) protocol, 13 medical professionals did a survey of CVD risk factors in 1992 and again in 2007 of the included participants. This survey included a standardized questionnaire, physical examination, and laboratory tests. The questionnaire included sex, age, and CVD risk factors (smoking, alcohol intake, physical activity, family history of hypertension, heart disease history). The physical examination included measurement of body mass index (BMI), heart rate, blood pressure, fasting serum total cholesterol (TC), triglycerides (TG), high‐density lipoprotein cholesterol (HDL‐C), low‐density lipoprotein cholesterol (LDL‐C), and fasting plasma glucose (FPG). The blood pressure was recorded from the right arm of each participant while seated using a regular mercury sphygmomanometer after resting for ≥5 min, two consecutive blood pressure readings were obtained and the mean was calculated from these. The height and weight were measured by electronic height and weight measuring meter in the morning after a 12‐h fast. The details have been reported elsewhere. 14 , 15 , 16
2.3. Related definitions
Hypertension was defined as a systolic blood pressure (SBP) of at least 140 mm Hg and/or diastolic blood pressure (DBP) of at least 90 mm Hg, and/or currently taking antihypertensive medications. Smoking was defined as an average cigarette consumption of at least one per day. Alcohol intake was defined as an average of at least 50 g/day. Physical activity was defined as exercise one or more times per week, at least 20 min each time. BMI was calculated as weight (kilograms) divided by height (meters) squared. Overweight or obesity was defined as a BMI ≥ 25 kg/m2, and normal BMI was below this. 17
2.4. Classification of adiposity status
According to adiposity status in 1992 and 2007, the subjects were categorized into four groups. Group I: individuals with a normal BMI in 1992 and 2007 (sustained BMI < 25 kg/m2); Group II: those with a normal BMI in 1992, but overweight or obese in 2007 (BMI increased to ≥ 25 kg/m2); Group III: those who were overweight or obese in 1992, but had a normal BMI in 2007 (BMI decreased to <25 kg/m2); Group IV: those who were overweight or obese in 1992 and 2007 (sustained BMI ≥ 25 kg/m2).
2.5. Statistical analysis
For statistical analysis, the SPSS software package (version 17.0; SPSS, Chicago, IL) was used. Statistical significance was defined as P < .05. Data were presented as mean ± standard deviation (SD) for normal variables and as number (percentage) for categorical variables. Smoking, alcohol intake, physical activity, and family history of hypertension were used as dummy variables. Analyses of covariance and nonparametric tests were used where appropriate to compare continuous variables. We used the chi‐square test for trend, to estimate the cumulative incidence across different groups. The smoothed conditional mean of BMI changes (BMI in 2007−BMI in 1992) given blood pressure (BP) changes (BP in 2007−BP in 1992) was fit with an unadjusted generative additive model to visually explore the linearity of the association between BMI changes and BP changes between 1992 and 2007. The Cox proportional hazards model was used to estimate the hazard ratios (HRs) of hypertension associated with the adiposity status groups.
Odds ratios (OR) for new onset of hypertension among the baseline adiposity status groups were calculated using logistic regression models. Model 1: included the status of overweight or obesity in 1992. Model 2: included the status of overweight or obesity in 2007. Model 3: included the status of overweight or obesity in 1992 and 2007. Model 4: included age, sex, smoking, alcohol intake, physical activity, family history of hypertension, TC, TG, HDL‐C, LDL‐C, FPG and the status of overweight or obesity in 1992. Model 5: included age, sex, smoking, alcohol intake, physical activity, family history of hypertension, TC, TG, HDL‐C, LDL‐C, FPG and the status of overweight or obesity in 2007. Model 6: included age, sex, smoking, alcohol intake, physical activity, family history of hypertension, TC, TG, HDL‐C, LDL‐C, FPG and the status of overweight or obesity in 1992 and 2007. In the models, the adjusting variables are those of the 1992 visit.
3. RESULTS
3.1. Demographic data of the population in 1992 and 2007
A total 711 participants took part in the survey, 114 subjects were diagnosed with hypertension in 1992 and excluded from this analysis. Therefore, only 597 subjects with complete data (male: 58.1%) were available for analysis. Table 1 presents the characteristics of the individuals in 1992 and 2007, according to their adiposity status. The study cohort consisted of 597 participants (male: 58.1%), with a mean age of 47.7 ± 6.1 years in 1992. With respect to the adiposity status groups defined, there were 373 subjects in Group I, 70 in Group II, 48 in Group III, and 106 in Group IV. Groups III and IV tended to be characterized by higher levels of BP, when compared with Group I and II in 1992 (P < .05). After a 15‐year follow‐up, Group II and IV tended to have higher levels of BP, when compared with Group I and III in 2007 (P < .05). There was no significant difference in sex, age, smoking, alcohol intake, physical activity, family history of hypertension, heart disease history, heart rate and FPG between the four groups both in 1992 and 2007 (P > .05) (Table 1). From 1992 to 2007, the association between BP changes and BMI changes in the overall sample is positive and linear from a BMI increase of 0 to 10. With increasing BMI, both DBP and SBP increase accordingly (Figure 1A,B).
TABLE 1.
Demographic data of the population in 1992 and 2007.
| Group I (n = 373) | Group II (n = 70) | Group III (n = 48) | Group IV (n = 106) | |||||||
|---|---|---|---|---|---|---|---|---|---|---|
| Variable | 1992 | 2007 | 1992 | 2007 | 1992 | 2007 | 1992 | 2007 | P value in 1992 | P value in 2007 |
| Sex (male) | 226 (60.5) | 39 (55.7) | 24 (50.0) | 58 (54.7) | .406 | |||||
| Age (years) | 47.6 ± 6.1 | 62.1 ± 6.4 | 46.7 ± 6.3 | 63.3 ± 5.1 | 49.8 ± 6.4 | 62.7 ± 5.9 | 47.9 ± 5.9 | 64.2 ± 6.4 | .064 | .058 |
| Smoking | 153 (41.1) | 106 (28.5) | 30 (42.3) | 18 (25.4) | 15 (31.3) | 10 (20.8) | 33 (31.1) | 21 (19.8) | .173 | .262 |
| Alcohol intake | 62 (16.7) | 57 (15.3) | 10 (14.1) | 9 (12.7) | 6 (12.5) | 4 (8.3) | 16 (15.1) | 17(16.0) | .849 | .561 |
| Physical activity | 76 (20.4) | 216 (58.1) | 17 (23.9) | 41 (57.71) | 8 (16.7) | 29 (60.4) | 21 (19.8) | 62 (58.5) | .891 | .991 |
| Family history of hypertension | 98 (26.3) | 157 (42.2) | 22 (31.0) | 34 (47.9) | 12 (25.0) | 24 (50.0) | 35 (33.0) | 50 (47.2) | .501 | .569 |
| Heart disease history | 24 (6.4) | 40 (10.8) | 3 (4.2) | 8 (11.3) | 4 (8.3) | 5 (10.4) | 8 (7.5) | 11 (10.3) | .798 | .468 |
| BMI (kg/m2) | 21.6 ± 1.8II‐IV | 21.7 ± 2.1II‐IV | 23.5 ± 1.2I,III, IV | 26.4 ± 1.7I,III,IV | 26.1 ± 0.9I, II,IV | 23.6 ± 1.4I,II,IV | 27.1 ± 1.8I‐III | 27.8 ± 2.5I‐III | <.001 | <.001 |
| Heart rate | 79.8 ± 8.9 | 77.7 ± 10.3 | 80.0 ± 8.7 | 78.2 ± 9.9 | 79.8 ± 8.1 | 77.2 ± 10.0 | 81.7 ± 9.3 | 77.6 ± 9.0 | .300 | .954 |
| FPG (mmol/L) | 4.4 ± 1.3 | 4.9 ± 1.7 | 4.3 ± 0.7 | 5.0 ± 1.2 | 4.4 ± 0.8 | 5.5 ± 1.9 | 4.2 ± 0.8 | 5.3 ± 1.6 | .431 | .085 |
| SBP (mmHg) | 109.1 ± 9.9III, IV | 129.4 ± 18.1II,IV | 108.4 ± 9.9III, IV | 136.6 ± 16.3I | 111.0 ± 9.3I, II | 133.3 ± 17.7 | 113.3 ± 10.2I, II | 141.0 ± 18.2I | .011 | .007 |
| DBP (mmHg) | 70.6 ± 6.9III, IV | 77.0 ± 9.4II,IV | 70.5 ± 6.9III,IV | 82.4 ± 10.6I,III | 74.0 ± 5.7I,II | 76.8 ± 9.4II,IV | 73.4 ± 6.9I,II | 82.5 ± 9.4I,III | .020 | .019 |
| TC (mmol/L) | 4.5 ± 0.7 | 5.0 ± 0.9III | 4.5 ± 0.8 | 4.9 ± 1.0 | 4.7 ± 0.7 | 4.6 ± 0.9I | 4.4 ± 0.8 | 4.8 ± 1.0 | .082 | .023 |
| TG (mmol/L) | 1.8(1.5,2.2)III‐IV | 1.4(1.1,2.0)II,IV | 1.7(1.5,2.4)III‐IV | 1.7(1.3,2.3)I | 2.4(1.8,3.3)I‐II | 1.4(1.1,2.2) | 2.2(1.7,2.7)I‐II | 1.9(1.4,2.6)I | .016 | .011 |
| HDL (mmol/L) | 1.3(1.1,1.4)III‐IV | 1.5(1.3,1.7)II‐IV | 1.2(1.1,1.4) | 1.3(1.1,1.5)I | 1.2(1.0,1.3)I | 1.4(1.2,1.6)I | 1.2(1.0,1.3)I | 1.3(1.2,1.5)I | .006 | .025 |
| LDL (mmol/L) | 2.3 ± 0.8 | 3.0 ± 0.8 | 2.3 ± 0.8 | 3.1 ± 0.7III | 2.1 ± 1.0 | 2.8 ± 0.8II,IV | 2.2 ± 0.9 | 3.0 ± 0.9III | .166 | .041 |
| Hypertension | 132 (35.5) II‐IV | 40 (56.3) I | 24 (50.0) | 69 (65.1) I | .001 | |||||
Note: Data are presented as means ± SD, or number (percentage).
Abbreviations: BMI, body mass index; DBP, diastolic blood pressure; FPG, fasting plasma glucose; HDL‐C, high‐density lipoprotein cholesterol; LDL‐C, low‐density lipoprotein cholesterol; SBP, systolic blood pressure; TC, serum total cholesterol; TG, triglyceride.
The adiposity groups were as follows: individuals with a normal BMI in 1992 and 2007 were in Group I (constantly BMI < 25 kg/m2); those with a normal BMI in 1992 but overweight or obese in 2007 were in Group II (turning BM I ≥ 25 kg/m2); those who were overweight or obese in 1992 but normal BMI in 2007 were in Group III (turning BMI < 25 kg/m2); and those who were kept overweight or obese in 1992 and 2007 were in Group IV (constant BMI ≥ 25 kg/m2). Superscript numbers denote groups from which the value is significantly different in pairwise comparisons.
FIGURE 1.
Scatter plots of changes in body mass index against blood pressure (BP) between 1992 and 2007. (A) Changes of body mass index and diastolic BP between 1992 and 2007. (B) Changes of body mass index and systolic BP between 1992 and 2007. Darker red denotes higher density. The black line is a smoothed condition mean, denoting the mean systolic or diastolic BP changes at a given body mass index changes.
3.2. Cumulative incidence of hypertension during a 15‐year follow‐up, according to the adiposity status
Of 597 individuals without hypertension in 1992, 265 were diagnosed with hypertension from 1992 to 2007 (incidence: 44.4%). Unadjusted total incidence of hypertension according to the adiposity status groups is shown in Table 1. The cumulative incidence of hypertension was 35.5% for Group I, 56.3% for Group II, 50.0% for Group III, and 65.1% for Group IV. The cumulative incidence of hypertension was significantly higher in Group II and IV than in Group I (all P < .05) (Table 1), however, it was no significantly different between Groups I and III (P = .057). With Group I as reference, Groups II and IV had a significantly increased hypertension risk (Figure 2).
FIGURE 2.
Adjusted cumulative incidence of hypertension in different adiposity groups. HR: hazard ratio. Group I as reference, the HR for Group II was 1.913 (95%CI: 1.421‐2.576, P = .000), Group III was 1.121 (95%: 0.777‐1.640, P = .525) and Group IV was 2.242 (95%CI: 1.508‐3.333, P = .000), respectively. The adiposity groups were as follows: individuals with a normal BMI in 1992 and 2007 were in Group I (constantly BMI < 25 kg/m2); those with a normal BMI in 1992 but overweight or obese in 2007 were in Group II (turning BM I ≥ 25 kg/m2); those who were overweight or obese in 1992 but normal BMI in 2007 were in Group III (turning BMI < 25 kg/m2); and those who were kept overweight or obese in 1992 and 2007 were in Group IV (constant BMI ≥ 25 kg/m2). Superscript numbers denote groups from which the value is significantly different in pairwise comparisons.
After adjusting for the confounders (including age, sex, smoking, alcohol intake, physical activity, family history of hypertension, TC, TG, HDL‐C, LDL‐C, and FPG), compared with Group I, Group II (HR = 1.80, P = .001) and IV (HR = 2.31, P < .001) had a significantly increased hypertension risk, Group III had no significant difference (HR = 1.40, P = .150) (Table 2).
TABLE 2.
Multivariate‐adjusted hazard ratios (HRs) of hypertension during the follow‐up.
| Group II (n = 70) | Group III (n = 48) | Group IV (n = 106) | |||||
|---|---|---|---|---|---|---|---|
| Group I (n = 373) | HR | P | HR | P | HR | P | |
| Model 1 | 1.0 | 1.800 (1.262‐2.568) | .001 | 1.471 (0.948‐2.285) | .085 | 2.292 (1.711‐3.070) | .000 |
| Model 2 | 1.0 | 1.782 (1.249‐2.543) | .001 | 1.456 (0.937‐2.262) | .095 | 2.310 (1.723‐3.097) | .000 |
| Model 3 | 1.0 | 1.804 (1.261‐2.579) | .001 | 1.404 (0.885‐2.226) | .150 | 2.305 (1.698‐3.130) | .000 |
Note: CI, confidence interval; HR, hazard ratio. All p values are calculated using the Cox proportional hazards model. Model: adjusted for confounders. Model 1: adjusted for age and sex. Model 2: adjusted for age, sex, smoking, alcohol intake, physical activity and family history of hypertension. Model 3: adjusted for age, sex, smoking, alcohol intake, physical activity, family history of hypertension, TC, TG, HDL‐C and LDL‐C. The adiposity groups as in Table 1.
3.3. The effects of initial and subsequent adiposity status on hypertension
We also constructed logistic regression multivariable models to predict the risk of hypertension from 1992 to 2007. The initial adiposity status in 1992 and the subsequent adiposity status in 2007 were included in the models. After adjustment for the initial adiposity status and other confounders (Model 6), the results showed that adiposity status in 2007 could predict hypertension (OR = 2.5, P < .001), as opposed to the initial adiposity status (P = .148) (Table 3).
TABLE 3.
Odds ratio (OR) of overweight or obesity in 1992 and 2007 in predicting hypertension.
| Overweight or obesity in 1992 OR (95%CI) | Overweight or obesity in 2007 OR (95%CI) | P * | P ** | |
|---|---|---|---|---|
| Model 1 | 2.4 (1.7‐3.5) | <.001 | ||
| Model 2 | 2.7 (1.9‐3.9) | <.001 | ||
| Model 3 | 1.6 (1.1‐2.5) | 2.2 (1.4‐3.3) | .028 | <.001 |
| Model 4 | 1.0 (0.8‐1.3) | .728 | ||
| Model 5 | 2.9 (2.0‐4.2) | <.001 | ||
| Model 6 | 1.4 (0.9‐2.2) | 2.5 (1.6‐3.8) | .148 | <.001 |
Note: CI, confidence interval; OR, odds ratio. All P values are calculated using the logistic regression models. Model 1: included the status of overweight or obesity in 1992. Model 2: included the status of overweight or obesity in 2007. Model 3: included the status of overweight or obesity in 1992 and 2007. Model 4: included age, sex, smoking, alcohol intake, physical activity, family history of hypertension, TC, TG, HDL‐C, LDL‐C, FPG and the status of overweight or obesity in 1992. Model 5: included age, sex, smoking, alcohol intake, physical activity, family history of hypertension, TC, TG, HDL‐C, LDL‐C, FPG and the status of overweight or obesity in 2007. Model 6: included age, sex, smoking, alcohol intake, physical activity, family history of hypertension, TC, TG, HDL‐C, LDL‐C, FPG and the status of overweight or obesity in 1992 and 2007.
* P values for the effect of overweight or obesity in 1992.
** P values for the effect of overweight or obesity in 2007.
4. DISCUSSION
The aims of our study were to examine whether reaching normal weight after being obese could reverse the adverse effects of initially being obesity on hypertension in the middle age, and whether initial or subsequent adiposity status had a greater effect on hypertension. Our findings suggest that subsequently BMI might be more important effect on hypertension in middle age. Being overweight or obese increases the risk of hypertension, and weight loss might reverse this adverse effect. Its presence has been demonstrated in two ways. First, compared with those who had a sustained normal BMI, being overweight or obese will increase the risk of hypertension; second, compared with individuals who remain overweight or obese, weight loss could reverse the adverse effects of being overweight or obese on hypertension.
This study showed that current obese individuals tended to be higher level of BP, overweight or obese increases the risk of hypertension compared to maintaining a normal BMI. BMI might be the main causes of the different of BP and the incidence of hypertension between the four groups. Lorna and colleagues study 8 also showed similar results that weight gain may increase blood pressure, weight loss may reduce this. In the last part, results showed that the BMI in 2007 could predict hypertension in 2007, the similar results also can be observed in 1992 visit, subsequent BMI might be the major role in the development of hypertension in middle age. Hasan and colleagues 11 found this results from young adulthood through middle age. They found that men with a normal BMI at age 25, but being obese at age 45, were at increased risk (HR 1.57); but not with men who being obese at age 25, and a normal BMI at age 45. Adair and colleagues 18 suggested that greater weight gain at any age correlates with elevated adult BP. Ashleigh and colleagues 19 showed a dose‐response increase with weight category was observed for prehypertension/hypertension among US adolescents. Li and colleagues 20 found that high BMI and excessive BMI gain at any life stage, especially if recent, is associated with increased adult BP. Those previous researches were supported our results, recent weight was closely relative with blood pressure not only in young age but also in middle age.
Large studies have showed that weight loss could reduce the risk of hypertension and reverse the adverse effects of overweight or obesity on hypertension. 21 , 22 , 23 Tyson and colleagues 21 reported that SBP did not rise in patients with weight loss maintenance for 5 years while SBP increased in patients with weight gain or weight stable. Fogari and colleagues 22 evaluated the effects of body weight loss on BP in overweight non‐obese patients with stage 1 hypertension and found a mean weight reduction of 8.1 kg in 222 patients reduced SBP by 4.2 mmHg and DBP by 3.3 mmHg. A cross‐sectional analysis in China suggested that excess weight loss is a vital strategy for controlling hypertension among multi‐ethnic population in northwest China. 23 At present, our society is very short of public health resources, particularly in developing countries, we emphasized that we should pay more attention to current adiposity status and encourage middle‐aged people to lose weight and keep weight in the normal BMI range to reduce the incidence of hypertension.
Our study has some limitations. Firstly, we did not record dietary habits, such as sodium intake, and daily caffeine consumption. Secondly, we did not compare the association between BMI and hypertension by sex. Thirdly, we did not compare the association between waist circumference (WC) and hypertension. WC can predict the risk of hypertension, its dynamic change was associated with the incidence of hypertension, greater WC reduction was associated with a greater decrease in the risk of hypertension. 24 , 25 , 26 Finally, there was no comparison by race. Some studies showed that the association between being overweight or obese with hypertension differed by race. 27 , 28 Further research is necessary to the association between being overweight or obese with hypertension in different race, which would not only enhance the generality of our findings but also contribute significantly to the personalized medicine.
In conclusion, our findings suggest that being overweight or obese increases the risk of hypertension, but that weight loss may reverse this effect in the middle age. To prevent hypertension in adulthood, individuals with a normal BMI should maintain weight in the normal BMI range, and those who are overweight or obese should lose weight as subsequently adiposity status could have major effects on hypertension.
AUTHOR CONTRIBUTIONS
The conception and design of the research, drafting of the manuscript and final approval of the manuscript submitted are done by Pei Pan, Ying Yang, Sen He, Gang Zhao, Xiao‐ping Chen. The revising of manuscript for important intellectual content is done by Pei Pan, and Ying Yang. The analysis and interpretation of data are done by Sen He, Gang Zhao and Xiao‐ping Chen. All authors read and approved the final manuscript.
CONFLICT OF INTEREST STATEMENT
The authors declare no conflicts of interest.
CONSENT FOR PUBLICATION
Not applicable.
ACKNOWLEDGMENTS
This study is supported by the National Eighth Five‐Year Research Plan, China (grant no: 85‐915‐01‐02); Mega‐projects of Science Research for the 11th Five‐Year Plan, China (grant no: 2006BAI01A01).
Pan P, Yang Y, He S, Zhao G, Chen X. The effects of initial and subsequent overweight or obesity on hypertension in the middle age. J Clin Hypertens. 2024;26:525–531. 10.1111/jch.14804
Pei Pan and Ying Yang contributed equally to this work as co‐first authors.
DATA AVAILABILITY STATEMENT
The datasets used or analyzed during the current study are available from the corresponding author on reasonable request.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
The datasets used or analyzed during the current study are available from the corresponding author on reasonable request.