Abstract
Many studies have shown that drinking coffee and tea may be associated with the risk of hypertension and dementia. Limited research exists on their impact on dementia risk in hypertensive patients. This study aimed to determine the association between coffee and tea consumption and the risk of dementia development in hypertensive population by utilizing Cox proportional risk modeling with 453,913 participants from a UK biobank. Our findings reveal a J-shaped and U-shaped association between the risk of all-cause dementia and the consumption of coffee and tea respectively in hypertensive people. The hypertensive patients who drink 0.5–1 cup of coffee or 4–5 cups of tea per day have the lowest risk of dementia. A U-shaped relationship was observed between daily caffeine consumption and the risk of developing all-cause dementia and vascular dementia in the hypertensive population. Furthermore, the significant association between the amount of coffee and tea consumed and the risk of all-cause and vascular dementia were more likely to be found in hypertensive patients than in the non-hypertensive population.
Keywords: Hypertension, Dementia, Coffee consumption, Tea consumption, Caffeine
Subject terms: Diseases, Medical research, Risk factors
Introduction
Hypertension and related complications are major public health issues with high morbidity and mortality, affecting a third of adults worldwide: In 2019, 1.3 billion people worldwide suffered from hypertension, with prevalence rates as high as 33 percent among people aged 30–79 years1. Reducing systolic blood pressure to 110–115 mm Hg would prevent 11.8 million deaths in 20191. However, this goal has not yet been achieved, resulting in a huge health and economic burden on society. Therefore, preventing hypertension and related complications is paramount. Dementia commonly occurs in individuals with hypertension, with around 11 to 20 percent of dementia cases linked to abnormal blood pressure2. Hypertension accelerates cognitive aging and increases the risk of Alzheimer's and other dementias3,4. Preventing hypertension not only reduces the burden of hypertension but also has the potential to significantly decrease the occurrence of dementia in the medium to long term. For example, the incidence of dementia could be reduced by 40 percent through managing and controlling 12 risk factors such as hypertension4. It is therefore of great public health benefit to investigate measures to delay or prevent the onset and development of dementia in people with hypertension. Caffeine, the active ingredient in coffee, tea, and other beverages, is currently the most widely used stimulant in the world and plays a neuroprotective role in the fight against neurodegenerative diseases5. Therefore, high caffeine beverages such as coffee and tea are currently attracting significant interest in the field of dementia prevention. Longitudinal studies have shown that the type and amount of coffee and tea consumed are significantly associated with the risk of developing dementia in the future6,7. Although the mechanism has not been fully elucidated, experts agree coffee and tea components such as caffeine may reduce dementia risk by decreasing neuroinflammation or providing neuroprotective benefits8–10. Research in animal models demonstrates that drinking caffeinated beverages can not only lower the risk of hypertension, but also inhibit Aβ peptide production in the mice brain11–13, reduce pro-inflammatory cytokine production14, and maintain blood–brain barrier function15. These benefits may slow down the progression of vascular inflammation, blood–brain barrier leakage, and β-amyloid microvascular deposition in hypertensive patients16, potentially delaying the onset of Alzheimer's disease. In addition, chlorogenic acid and caffeic acid in coffee and tea not only may improve symptoms of hypertension and reduce blood pressure17,18, but also inhibit acetylcholinesterase (a key enzyme in the pathogenesis of Alzheimer's disease), reduce lipid peroxidation, prevent neuronal damage, and delay neurodegenerative disease19. While most experimental results are derived from animal studies and observational human experiments, these positive effects may also benefit humans in preventing or delaying dementia progression in hypertension patients. In addition, the association between coffee and the risk of developing dementia varies according to the type of coffee20. Caffeinated coffee lowers dementia risk more than decaf coffee6.
To date, there have been limited studies on the relationship between coffee and tea consumption and the risk of dementia in people with hypertension, and it is unclear whether the benefits of these two drinks on dementia also apply to people with hypertension. To addressthese gaps, we employed information from a large and representative source of data, the UK Biobank (UKB), and performed a comprehensive analysis of the association between coffee and tea consumption and the risk of dementia among individuals with hypertension and compared these with the population without hypertension (Fig. 1).
Fig. 1.
Flowchart of participants included in the analysis.
Results
Baseline characteristics of the participants
Table 1 displays participant characteristics. Out of 453,913 participants, 54.62% had hypertension. The average age was 72.39 ± 8.11 years, with 54.33% being female and 94.13% being white. During an average follow-up time of 15.12 years, the population with hypertension appeared to have a higher incidence of all-cause dementia (3.11% vs 1.11%), Alzheimer’s disease (1.37% vs 0.50%), and vascular dementia (0.76% vs 0.18%), along with a shorter median survival compared to those without hypertension. There were statistically significant differences in age, sex, ethnicity, education level, occupation, TDI, BMI, smoking status, dietary patterns, alcohol consumption, physical activity, social relationships, duration of sedentary behavior, family history of dementia, APOE genotype, depression, history of cancer, history of cardiovascular disease, aspirin use status, lipid-lowering medications use status, dyslipidemia, hypertriglyceridemia, and serum 25(OH)D status between population with hypertension and without hypertension (P < 0.001). After adjusting those covariates, population with hypertension appear to be at a greater risk of developing all-cause dementia (HR = 1.149, 95% CI 1.059–1.247, P = 0.001), Alzheimer’s disease (HR = 1.137, 95% CI 1.006–1.286, P = 0.040), and vascular dementia (HR = 1.281, 95% CI 1.061–1.548, P = 0.010) compared to the population without hypertension (Table 2). Additionally, a multiple-adjusted restricted cubic spline with three knots was utilized to illustrate the relationship between coffee, tea, and caffeine consumption and all-cause dementia. Findings indicated that tea and caffeine intake exhibited a non-linear association with all-cause dementia (p for nonlinearity < 0.001), whereas coffee intake demonstrated a predominantly linear connection with all-cause dementia (P for nonlinearity > 0.001) (Figs. 2 and 3).
Table 1.
Characteristics of participants with or without hypertension.
| Characteristic | Total population (N = 453,913) | Participants without hypertension (N = 205,991) | Participants with hypertension (N = 247,922) | χ2/F | P-value |
|---|---|---|---|---|---|
| Age, years, mean (SD) | 72.39 (8.11) | 69.67 (8.09) | 74.65 (7.40) | 46,683.806 | < 0.001 |
| Sex, n (%) | 8348.035 | < 0.001 | |||
| Female | 246,589 (54.33) | 127,171 (61.74) | 119,418 (48.17) | ||
| Male | 207,324 (45.67) | 78,820 (38.26) | 128,504 (51.83) | ||
| Race/ethnicity, n (%) | 310.136 | < 0.001 | |||
| White | 427,270 (94.13) | 193,394 (93.88) | 233,876 (94.33) | ||
| Asian | 10,505 (2.31) | 5087 (2.47) | 5418 (2.19) | ||
| Black | 7577 (1.67) | 3049 (1.48) | 4528 (1.83) | ||
| Other | 6965 (1.53) | 3730 (1.81) | 3235 (1.30) | ||
| Missing | 1596 (0.35) | 731 (0.35) | 865 (0.35) | ||
| Occupation status, n (%) | 19,256.755 | < 0.001 | |||
| Employed | 263,718 (58.10) | 140,752 (68.33) | 122,966 (49.60) | ||
| Unemployed | 34,760 (7.66) | 16,214 (7.87) | 18,546 (7.48) | ||
| Retired | 151,148 (33.30) | 47,005 (22.82) | 104,143 (42.01) | ||
| Missing | 4287 (0.94) | 2020 (0.98) | 2267 (0.91) | ||
| Education level, n (%) | 3653.492 | < 0.001 | |||
| College or University | 146,710 (32.32) | 77,894 (37.81) | 68,816 (27.76) | ||
| A level/AS level or equivalent | 50,524 (11.13) | 25,160 (37.81) | 25,364 (10.23) | ||
| O level/GCSEs or equivalent | 96,903 (21.35) | 43,773 (21.25) | 53,130 (21.43) | ||
| CSEs or equivalent | 25,151 (5.54) | 12,572 (6.10) | 12,579 (5.07) | ||
| NVQ or HND or HNC or equivalent | 29,610 (6.52) | 11,361 (5.52) | 18,249 (7.36) | ||
| Other professional qualifications eg: nursing, teaching | 23,372 (5.15) | 9295 (4.51) | 14,077 (5.68) | ||
| Missing | 81,643 (17.99) | 25,936 (12.59) | 55,707 (22.47) | ||
| TDI, n (%) | 17.328 | < 0.001 | |||
| Low | 87,330 (19.24) | 39,375 (19.11) | 47,955 (19.34) | ||
| Medium | 135,265 (29.80) | 62,012 (30.10) | 73,253 (29.55) | ||
| High | 230,778 (50.84) | 104,347 (50.66) | 126,431 (51.00) | ||
| Missing | 540 (0.12) | 257 (0.12) | 283 (0.11) | ||
| BMI (kg/m2), n (%) | 28,081.082 | < 0.001 | |||
| < 18.5 | 2373 (0.52) | 1711 (0.83) | 662 (0.27) | ||
| 18.5–24.9 | 147,748 (32.55) | 89,787 (43.59) | 57,961 (23.38) | ||
| 25–29.9 | 192,247 (42.35) | 82,717 (40.16) | 109,530 (44.18) | ||
| ≥ 30 | 109,609 (24.15) | 31,054 (15.08) | 78,555 (31.69) | ||
| Missing | 1936 (0.43) | 722 (0.35) | 1214 (0.49) | ||
| Dietary patterns, n (%) | 657.363 | < 0.001 | |||
| Poor dietary pattern | 66,814 (14.72) | 27,654 (13.42) | 39,160 (15.80) | ||
| Medium dietary pattern | 234,272 (51.61) | 106,052 (51.48) | 128,220 (51.72) | ||
| Healthy dietary pattern | 152,827 (33.67) | 72,285 (35.09) | 80,542 (32.49) | ||
| Smoking status, n (%) | 2180.724 | < 0.001 | |||
| Never | 247,786 (54.59) | 117,644 (57.11) | 130,142 (52.49) | ||
| Previous | 157,209 (34.63) | 64,113 (31.12) | 93,096 (37.55) | ||
| Current | 47,248 (10.41) | 23,606 (11.46) | 23,642 (9.54) | ||
| Missing | 1670 (0.37) | 628 (0.30) | 1042 (0.42) | ||
| Alcohol consumption, n (%) | 4063.858 | < 0.001 | |||
| Quartile 1 | 113,540 (25.01) | 51,864 (25.18) | 61,676 (24.88) | ||
| Quartile 2 | 113,541 (25.01) | 56,615 (27.48) | 56,926 (22.96) | ||
| Quartile 3 | 113,354 (24.97) | 54,793 (26.60) | 58,561 (23.62) | ||
| Quartile 4 | 113,478 (25.00) | 42,719 (20.74) | 70,759 (28.54) | ||
| Physical activity, n (%) | 185.346 | < 0.001 | |||
| Low | 64,696 (14.25) | 28,971 (14.06) | 35,725 (14.41) | ||
| Medium | 178,177 (39.25) | 85,064 (41.30) | 93,113 (37.56) | ||
| High | 108,952 (24.00) | 50,311 (24.42) | 58,641 (23.65) | ||
| Missing | 102,088 (22.49) | 41,645 (20.22) | 60,443 (24.38) | ||
| Social conntact, n (%) | 153.235 | < 0.001 | |||
| Active | 309,765 (68.24) | 142,438 (69.15) | 167,327 (67.49) | ||
| Moderately | 126,510 (27.87) | 55,981 (27.18) | 70,529 (28.45) | ||
| Isolated | 17,638 (3.89) | 7572 (3.68) | 10,066 (4.06) | ||
| Duration of sedentary behaviour, n (%) | 4707.333 | < 0.001 | |||
| < 2 | 25,813 (5.69) | 14,027 (6.81) | 11,786 (4.75) | ||
| 2–3.9 | 130,518 (28.75) | 66,999 (32.53) | 63,519 (25.62) | ||
| 4–5.9 | 164,966 (36.34) | 72,658 (35.27) | 92,308 (37.23) | ||
| ≥ 6 | 132,616 (29.22) | 52,307 (25.39) | 80,309 (32.39) | ||
| Family history of dementia, n (%) | 55.955 | < 0.001 | |||
| No | 348,587 (76.80) | 154,458 (74.98) | 194,129 (78.30) | ||
| Yes | 64,315 (14.17) | 29,524 (14.33) | 34,791 (14.03) | ||
| Missing | 41,011 (9.03) | 22,009 (10.68) | 19,002 (7.66) | ||
| APOE Ƹ4 genotype, n (%) | 5.490 | 0.019 | |||
| No | 336,593 (74.15) | 152,519 (74.04) | 184,074 (74.25) | ||
| Yes | 107,001 (23.57) | 48,923 (23.75) | 58,078 (23.43) | ||
| Missing | 10,319 (2.27) | 4549 (2.21) | 5770 (2.33) | ||
| Depressive status, n (%) | 2009.694 | < 0.001 | |||
| No | 345,946 (76.21) | 150,592 (73.11) | 195,354 (78.80) | ||
| Yes | 107,967 (23.79) | 55,399 (26.89) | 52,568 (21.20) | ||
| History of cancer, n (%) | 265.245 | < 0.001 | |||
| No | 412,552 (90.89) | 188,793 (91.65) | 223,759 (90.25) | ||
| Yes | 41,361 (9.11) | 17,198 (8.35) | 24,163 (9.75) | ||
| History of cardiovascular disease, n (%) | 4220.394 | < 0.001 | |||
| No | 435,404 (95.92) | 201,901 (98.01) | 233,503 (94.18) | ||
| Yes | 18,509 (4.08) | 4090 (1.99) | 14,419 (5.82) | ||
| Aspirin use status, n (%) | 11,625.82 | < 0.001 | |||
| No | 391,443 (86.24) | 190,101 (92.29) | 201,342 (81.21) | ||
| Yes | 62,470 (13.76) | 15,890 (7.71) | 46,580 (18.79) | ||
| Lipid-lowering medications use status, n (%) | 23,460.885 | < 0.001 | |||
| No | 375,165 (82.65) | 189,709 (92.10) | 185,456 (74.80) | ||
| Yes | 78,748 (17.35) | 16,282 (7.90) | 62,466 (25.20) | ||
| Hypertriglyceridemia, n (%) | 9586.886 | < 0.001 | |||
| No | 255,608 (56.31) | 131,761 (63.96) | 123,847 (49.95) | ||
| Yes | 170,386 (37.54) | 61,851 (30.03) | 108,535 (43.78) | ||
| Missing | 27,919 (6.15) | 12,379 (6.01) | 15,540 (6.27) | ||
| Dyslipidemia, n (%) | 686.504 | < 0.001 | |||
| No | 312,253 (68.79) | 144,665 (70.23) | 167,588 (67.60) | ||
| Yes | 77,924 (17.17) | 32,032 (15.55) | 45,892 (18.51) | ||
| Missing | 63,736 (14.04) | 29,294 (14.22) | 34,442 (13.89) | ||
| Serum 25(OH)D status, n (%) | 462.89 | < 0.001 | |||
| Severely deficient | 52,186 (11.50) | 22,460 (10.90) | 29,726 (11.99) | ||
| Moderately deficient | 169,510 (37.34) | 75,655 (36.73) | 93,855 (37.86) | ||
| Insufficient and above | 185,483 (40.86) | 88,062 (42.75) | 97,421 (39.30) | ||
| Missing | 46,734 (10.30) | 19,814 (9.62) | 26,920 (10.86) | ||
| Coffee intake, n (%) | 36.184 | < 0.001 | |||
| None | 100,199 (22.07) | 46,151 (22.40) | 54,048 (21.80) | ||
| 0.5–1 | 124,475 (27.42) | 56,294 (27.33) | 68,181 (27.50) | ||
| 2–3 | 140,858 (31.03) | 63,713 (30.93) | 77,145 (31.12) | ||
| 4–5 | 60,530 (13.34) | 27,046(13.13) | 33,484 (13.51) | ||
| ≥ 6 | 27,851 (6.14) | 12,787 (6.21) | 15,064 (6.08) | ||
| Coffee type, n (%) | 1337.405 | < 0.001 | |||
| Decaffeinated coffee | 68,152 (15.01) | 31,205 (15.15) | 36,947 (14.90) | ||
| Instant coffee | 195,778 (43.13) | 83,803 (40.68) | 111,975 (45.17) | ||
| Ground coffee | 80,658 (17.77) | 40,630 (19.72) | 40,028 (16.15) | ||
| Other type of coffee | 6547 (1.44) | 3030 (1.47) | 3517 (1.42) | ||
| Missing | 102,778 (22.64) | 47,323 (22.97) | 55,455 (22.37) | ||
| Tea intake, n (%) | 77.339 | < 0.001 | |||
| None | 66,366 (14.62) | 30,459 (14.79) | 35,907 (14.48) | ||
| 0.5–1 | 51,973 (11.45) | 24,345 (11.82) | 27,628 (11.14) | ||
| 2–3 | 133,057 (29.31) | 60,410 (29.33) | 72,647 (29.30) | ||
| 4–5 | 116,158 (25.39) | 52,020 (25.25) | 64,138 (25.87) | ||
| ≥ 6 | 86,359 (19.03) | 38,757 (18.81) | 47,602 (19.20) | ||
| Hot drink temperature, n (%) | 1136.17 | < 0.001 | |||
| Very hot | 77,034 (16.97) | 38,886 (18.88) | 38,148 (15.39) | ||
| Hot | 301,347 (66.39) | 134,819 (65.45) | 166,528 (67.17) | ||
| Warm | 70,581 (15.55) | 29,823 (14.48) | 40,758 (16.44) | ||
| Missing | 4951 (1.09) | 2463 (1.20) | 2488 (1.00) | ||
| Caffeine intake, n (%) | 133.322 | < 0.001 | |||
| Quintile1 | 93,929 (20.69) | 44,123 (21.42) | 49,806 (20.09) | ||
| Quintile2 | 95,511 (21.04) | 42,706 (20.73) | 52,805 (21.30) | ||
| Quintile3 | 89,546 (19.73) | 40,792 (19.56) | 49,254 (19.87) | ||
| Quintile4 | 87,779 (19.34) | 39,275 (19.07) | 48,504 (19.56) | ||
| Quintile5 | 87,148 (19.20) | 39,595 (19.22) | 47,553 (19.18) | ||
| Follow-up time, years, mean (P25, P75) | 15.12 (14.45, 15.72) | 15.11 (14.45, 15.71) | 15.12 (14.45, 15.73) | 12.066 | < 0.001 |
| All-cause dementia, n (CIR) | 8690 (1.91) | 2282 (1.11) | 6408 (3.11) | 1306.839 | < 0.001 |
| Alzheimer’s disease, n(CIR) | 3855 (0.85) | 1026 (0.50) | 2829 (1.37) | 552.422 | < 0.001 |
| Vascular dementia, n (CIR) | 1931 (0.43) | 374 (0.18) | 1557 (0.76) | 529.414 | < 0.001 |
| Survival time, M (P25, P75), year | |||||
| All-cause dementia | 14.50 (14.18, 15.64) | 14.71 (14.32, 15.66) | 14.32 (14.11, 15.62) | 3196.166 | < 0.001 |
| Alzheimer’s disease | 14.53 (14.20, 15.64) | 14.73 (14.33, 15.66) | 14.37 (14.13, 15.62) | 2907.032 | < 0.001 |
| Vascular dementia | 14.54 (14.20, 15.64) | 14.74 (14.33, 15.66) | 14.38 (14.14, 15.62) | 2842.196 | < 0.001 |
TDI Townsend deprivation index, BMI body mass index, APOE apolipoprotein E, CIR Crude incidence rate; M (P25, P75), median (Percentile25, Percentile75);
Table 2.
Risk of dementia in hypertensive patients compared to the general population.
| Adjusted HR (95%CI) | |||
|---|---|---|---|
| All-cause dementia | Alzheimer disease | Vascular dementia | |
| Model1 | 1.187 (1.116, 1.261) | 1.175 (1.072, 1.288) | 1.549 (1.339, 1.793) |
| P-value | < 0.001 | 0.001 | < 0.001 |
| Model2 | 1.118 (1.101, 1.266) | 1.137 (1.023, 1.264) | 1.565 (1.330, 1.841) |
| P-value | < 0.001 | 0.017 | < 0.001 |
| Model3 | 1.152 (1.070, 1.240) | 1.124 (1.006, 1.256) | 1.452 (1.225, 1.720) |
| P-value | < 0.001 | 0.039 | < 0.001 |
| Model4 | 1.149 (1.059,1.247) | 1.137 (1.006,1.286) | 1.281 (1.061,1.548) |
| P-value | 0.001 | 0.040 | 0.010 |
Model 1: adjusted for basic socio-demographic characteristics [age; sex; ethnicity; education level; occupation status; TDI; BMI].
Model 2: adjusted for Model 1 and lifestyle [smoking status; dietary patterns; alcohol consumption; physical activity; social contact; duration of sedentary behavior].
Model 3: adjusted for Model 2 and health-related issues [family history of dementia; APOE genotype; depression; history of cancer; history of cardiovascular disease].
Model 4: adjusted for Model 3 and serum markers and drug use [Aspirin use status; lipid-lowering medications use status; dyslipidemia; hypertriglyceridemia; serum 25(OH)D status].
Fig. 2.

A linear relationship between coffee consumption and incident dementia.
Fig. 3.
A non-linear relationship between tea and caffeine consumption and incident dementia.
Association between coffee consumption and dementia risk in the population with hypertension and without hypertension
After adjusting all covariates, a J-shaped relationship exists between coffee consumption and all-cause dementia risk in hypertensive patients (Fig. 4). Notably, hypertensive individuals consuming 0.5–1 cup daily had the lowest risk of all-cause dementia (HR = 0.733, 95% CI 0.613, 0.875), compared to those having 6 or more cups daily. No statistically significant connection was observed between coffee consumption and Alzheimer’s disease or vascular dementia risk in this group. Additionally, there was no correlation between coffee consumption and the risk of developing all-cause dementia, Alzheimer’s disease, and vascular dementia in the population without hypertension (Table 3).
Fig. 4.

A J-shaped relationship exists between coffee consumption and all-cause dementia risk in hypertensive patients. Model 1: adjusted for basic socio-demographic characteristics [age; sex; ethnicity; education level; occupation status; TDI; BMI]. Model 2: adjusted for Model 1 and lifestyle [smoking status; dietary patterns; alcohol consumption; physical activity; social contact; duration of sedentary behavior]. Model 3: adjusted for Model 2 and health-related issues [family history of dementia; APOE genotype; depression; history of cancer; history of cardiovascular disease]. Model 4: adjusted for Model 3 and serum markers and drug use [Aspirin use status; lipid-lowering medications use status; dyslipidemia; hypertriglyceridemia; serum 25(OH)D status].
Table 3.
Association between coffee consumption and risk of dementia in the participants.
| Coffee consumption, Cups/day | P-value | |||||||
|---|---|---|---|---|---|---|---|---|
| None | 0.5–1 | 2–3 | 4–5 | ≥ 6 | ||||
| HR (95% CI) | HR (95% CI) | HR (95% CI) | HR (95% CI) | HR (95% CI) | ||||
| All-cause dementia | ||||||||
| Participants without hypertension | Model1 | – | – | – | – | Ref. | 0.304 | |
| Model2 | – | – | – | – | Ref. | 0.650 | ||
| Model3 | – | – | – | – | Ref. | 0.608 | ||
| Model4 | – | – | – | – | Ref. | 0.945 | ||
| Participants with hypertension | Model1 | 0.784 (0.680, 0.903) | 0.688 (0.601, 0.788) | 0.718 (0.628, 0.820) | 0.753 (0.648, 0.874) | Ref. | < 0.001 | |
| Model2 | 0.785 (0.665, 0.925) | 0.729 (0.623, 0.854) | 0.762 (0.653, 0.889) | 0.788 (0.663, 0.937) | Ref. | 0.003 | ||
| Model3 | 0.797 (0.670, 0.950) | 0.749 (0.634, 0.885) | 0.771 (0.655, 0.908) | 0.782 (0.652, 0.939) | Ref. | 0.017 | ||
| Model4 | 0.768 (0.637, 0.927) | 0.733 (0.613, 0.875) | 0.746 (0.626, 0.888) | 0.763 (0.628, 0.929) | Ref. | 0.014 | ||
| Total population | Model1 | 0.817 (0.724, 0.923) | 0.725 (0.646, 0.814) | 0.762 (0.680, 0.853) | 0.807 (0.711, 0.915) | Ref. | < 0.001 | |
| Model2 | 0.838 (0.727, 0.965) | 0.777 (0.679, 0.889) | 0.822 (0.720, 0.938) | 0.858 (0.741, 0.993) | Ref. | 0.006 | ||
| Model3 | 0.863 (0.743, 1.004) | 0.801 (0.694, 0.925) | 0.836 (0.726, 0.963) | 0.866 (0.741, 1.012) | Ref. | 0.040 | ||
| Model4 | 0.825 (0.702, 0.970) | 0.784 (0.672, 0.915) | 0.804 (0.690, 0.935) | 0.829 (0.700, 0.980) | Ref. | 0.041 | ||
| Alzheimer disease | ||||||||
| Participants without hypertension | Model1 | – | – | – | – | Ref. | 0.695 | |
| Model2 | – | – | – | – | Ref. | 0.403 | ||
| Model3 | – | – | – | – | Ref. | 0.584 | ||
| Model4 | – | – | – | – | Ref. | 0.949 | ||
| Participants with hypertension | Model1 | 0.794 (0.637, 0.988) | 0.701 (0.568, 0.864) | 0.745 (0.607, 0.916) | 0.750 (0.595, 0.946) | Ref. | 0.018 | |
| Model2 | – | – | – | – | Ref. | 0.184 | ||
| Model3 | – | – | – | – | Ref. | 0.568 | ||
| Model4 | – | – | – | – | Ref. | 0.393 | ||
| Total population | Model1 | 0.834 (0.691, 1.008) | 0.754 (0.630, 0.902) | 0.807 (0.676, 0.963) | 0.830 (0.682, 1.010) | Ref. | 0.035 | |
| Model2 | – | – | – | – | Ref. | 0.174 | ||
| Model3 | – | – | – | – | Ref. | 0.709 | ||
| Model4 | – | – | – | – | Ref. | 0.565 | ||
| Vascular dementia | ||||||||
| Participants without hypertension | Model1 | – | – | – | – | Ref. | 0.106 | |
| Model2 | – | – | – | – | Ref. | 0.403 | ||
| Model3 | – | – | – | – | Ref. | 0.220 | ||
| Model4 | – | – | – | – | Ref. | 0.488 | ||
| Participants with hypertension | Model1 | 0.711 (0.539, 0.937) | 0.645 (0.496, 0.839) | 0.590 (0.455, 0.766) | 0.611 (0.453, 0.823) | Ref. | 0.002 | |
| Model2 | 0.720 (0.526, 0.986) | 0.695 (0.516, 0.937) | 0.603 (0.447, 0.812) | 0.656 (0.469, 0.919) | Ref. | 0.020 | ||
| Model3 | 0.712 (0.510, 0.994) | 0.673 (0.490, 0.923) | 0.615 (0.449, 0.842) | 0.641 (0.449, 0.917) | Ref. | 0.046 | ||
| Model4 | – | – | – | – | Ref. | 0.131 | ||
| Total population | Model1 | 0.737 (0.575, 0.944) | 0.654 (0.517, 0.828) | 0.609 (0.482, 0.769) | 0.693 (0.533, 0.900) | Ref. | 0.001 | |
| Model2 | 0.753 (0.569, 0.997) | 0.693 (0.530, 0.905) | 0.630 (0.483, 0.821) | 0.731 (0.545, 0.982) | Ref. | 0.014 | ||
| Model3 | 0.736 (0.547, 0.990) | 0.671 (0.506, 0.889) | 0.641 (0.485, 0.847) | 0.722 (0.529, 0.985) | Ref. | 0.032 | ||
| Model4 | – | – | – | – | Ref. | 0.164 | ||
Model 1: adjusted for basic socio-demographic characteristics [age; sex; ethnicity; education level; occupation status; TDI; BMI].
Model 2: adjusted for Model 1 and lifestyle [smoking status; dietary patterns; alcohol consumption; physical activity; social contact; duration of sedentary behavior].
Model 3: adjusted for Model 2 and health-related issues [family history of dementia; APOE genotype; depression; history of cancer; history of cardiovascular disease].
Model 4: adjusted for Model3 and serum markers and drug use [Aspirin use status; lipid-lowering medications use status; dyslipidemia; hypertriglyceridemia; serum 25(OH)D status].
Association between tea consumption and dementia risk in the population with hypertension and without hypertension
After adjusting all covariates, a U-shaped association between tea intake and the risk of all-cause dementia in the hypertensive population was shown in Fig. 5. Tea drinkers had a lower risk of all-cause dementia compared to non-tea drinkers. The risk was lowest for hypertensive patients who drank four to five cups of tea daily (HR = 0.744, 95% CI 0.675, 0.887). In contrast, there was no association between tea consumption and the risk of all-cause dementia, Alzheimer’s disease, and vascular dementia in the population without hypertension (Table 4).
Fig. 5.

A U-shaped relationship exists between tea consumption and all-cause dementia risk in hypertensive patients. Model 1: adjusted for basic socio-demographic characteristics [age; sex; ethnicity; education level; occupation status; TDI; BMI]. Model 2: adjusted for Model 1 and lifestyle [smoking status; dietary patterns; alcohol consumption; physical activity; social contact; duration of sedentary behavior]. Model 3: adjusted for Model 2 and health-related issues [family history of dementia; APOE genotype; depression; history of cancer; history of cardiovascular disease]. Model 4: adjusted for Model 3 and serum markers and drug use [Aspirin use status; lipid-lowering medications use status; dyslipidemia; hypertriglyceridemia; serum 25(OH)D status].
Table 4.
Association between tea consumption and risk of dementia in the participants.
| Tea consumption, cups/day | P-value | ||||||
|---|---|---|---|---|---|---|---|
| none | 0.5–1 | 2–3 | 4–5 | ≥ 6 | |||
| HR (95% CI) | HR (95% CI) | HR (95% CI) | HR (95% CI) | HR (95% CI) | |||
| All-cause dementia | |||||||
| Participants without hypertension | Model1 | Ref. | 0.862 (0.713, 1.042) | 0.778 (0.666, 0.908) | 0.734 (0.624, 0.862) | 0.844 (0.712, 0.999) | 0.003 |
| Model2 | Ref. | – | – | – | – | 0.105 | |
| Model3 | Ref. | – | – | – | – | 0.091 | |
| Model4 | Ref. | – | – | – | – | 0.061 | |
| Participants with hypertension | Model1 | Ref. | 0.846 (0.748, 0.957) | 0.784 (0.710, 0.867) | 0.762 (0.687, 0.845) | 0.843 (0.756, 0.941) | < 0.001 |
| Model2 | Ref. | 0.871 (0.758, 1.000) | 0.768 (0.685, 0.862) | 0.763 (0.678, 0.859) | 0.772 (0.679, 0.877) | < 0.001 | |
| Model3 | Ref. | 0.866 (0.747, 1.004) | 0.793 (0.703, 0.895) | 0.768 (0.677, 0.870) | 0.798 (0.698, 0.914) | < 0.001 | |
| Model4 | Ref. | 0.826 (0.701, 0.972) | 0.788 (0.691, 0.900) | 0.774 (0.675, 0.887) | 0.820 (0.709, 0.949) | 0.003 | |
| Total population | Model1 | Ref. | 0.852 (0.768, 0.944) | 0.784 (0.721, 0.853) | 0.755 (0.692,0.824) | 0.845 (0.771, 0.927) | < 0.001 |
| Model2 | Ref. | 0.878 (0.781, 0.986) | 0.787 (0.715, 0.867) | 0.769 (0.696, 0.849) | 0.790 (0.710, 0.880) | < 0.001 | |
| Model3 | Ref. | 0.862 (0.762, 0.976) | 0.804 (0.726, 0.889) | 0.765 (0.689, 0.850) | 0.809 (0.722, 0.905) | < 0.001 | |
| Model4 | Ref. | 0.819 (0.714, 0.940) | 0.809 (0.724, 0.905) | 0.762 (0.679, 0.855) | 0.832 (0.736, 0.940) | < 0.001 | |
| Alzheimer disease | |||||||
| Participants without hypertension | Model1 | Ref. | – | – | – | – | 0.110 |
| Model2 | Ref. | – | – | – | – | 0.221 | |
| Model3 | Ref. | – | – | – | – | 0.386 | |
| Model4 | Ref. | – | – | – | – | 0.526 | |
| Participants with hypertension | Model1 | Ref. | 0.797 (0.657, 0.966) | 0.839 (0.721, 0.976) | 0.755 (0.644, 0.886) | 0.867 (0.733, 1.026) | 0.012 |
| Model2 | Ref. | 0.793 (0.635, 0.990) | 0.831 (0.696, 0.990) | 0.737 (0.613, 0.887) | 0.788 (0.646, 0.960) | 0.026 | |
| Model3 | Ref. | – | – | – | – | 0.144 | |
| Model4 | Ref. | – | – | – | – | 0.080 | |
| Total population | Model1 | Ref. | 0.799 (0.681, 0.938) | 0.824 (0.726, 0.936) | 0.752 (0.659, 0.859) | 0.822 (0.713, 0.947) | 0.001 |
| Model2 | Ref. | 0.791 (0.658, 0.951) | 0.827 (0.714, 0.957) | 0.769 (0.660, 0.896) | 0.762 (0.645, 0.900) | 0.007 | |
| Model3 | Ref. | – | – | – | – | 0.061 | |
| Model4 | Ref. | 0.722 (0.578, 0.902) | 0.870 (0.733, 1.031) | 0.800 (0.670, 0.955) | 0.831 (0.687, 1.004) | 0.038 | |
| Vascular dementia | |||||||
| Participants without hypertension | Model1 | Ref. | – | – | – | – | 0.429 |
| Model2 | Ref. | – | – | – | – | 0.796 | |
| Model3 | Ref. | – | – | – | – | 0.485 | |
| Model4 | Ref. | – | – | – | – | 0.261 | |
| Participants with hypertension | Model1 | Ref. | 0.796 (0.620, 1.023) | 0.683 (0.556, 0.838) | 0.734 (0.596, 0.904) | 0.784 (0.627, 0.980) | 0.007 |
| Model2 | Ref. | 0.795 (0.598, 1.057) | 0.664 (0.525, 0.841) | 0.755 (0.596, 0.957) | 0.769 (0.597, 0.992) | 0.019 | |
| Model3 | Ref. | – | – | – | – | 0.056 | |
| Model4 | Ref. | – | – | – | – | 0.121 | |
| Total population | Model1 | Ref. | 0.798 (0.638, 0.997) | 0.695 (0.580, 0.834) | 0.729 (0.605, 0.877) | 0.804 (0.660, 0.979) | 0.002 |
| Model2 | Ref. | 0.783 (0.606, 1.010) | 0.699 (0.568, 0.860) | 0.748 (0.606, 0.923) | 0.782 (0.625, 0.978) | 0.017 | |
| Model3 | Ref. | 0.781 (0.596, 1.024) | 0.735 (0.592, 0.914) | 0.730 (0.584, 0.913) | 0.820 (0.648, 1.038) | 0.047 | |
| Model4 | Ref. | – | – | – | – | 0.125 | |
Model 1: adjusted for basic socio-demographic characteristics [age; sex; ethnicity; education level; occupation status; TDI; BMI].
Model 2: adjusted for Model 1 and lifestyle [smoking status; dietary patterns; alcohol consumption; physical activity; social contact; duration of sedentary behavior].
Model 3: adjusted for Model 2 and health-related issues [family history of dementia; APOE genotype; depression; history of cancer; history of cardiovascular disease].
Model 4: adjusted for Model3 and serum markers and drug use [Aspirin use status; lipid-lowering medications use status; dyslipidemia; hypertriglyceridemia; serum 25(OH)D status].
Association between interaction of coffee and tea consumption and dementia risk in the population with hypertension and without hypertension
After adjusting all covariates, the statistically significant associations were found between the interaction of coffee and tea consumption and the risk of all-cause dementia and Alzheimer’s disease in the hypertensive population (Fig. 6).Consuming four to five cups of coffee and six or more cups of tea daily is statistically significantly associated with the lowest risk of developing all-cause (HR = 0.541, 95% CI 0.311–0.939) dementia and Alzheimer’s disease(HR = 0.294, 95% CI 0.094–0.921) than those who drink six or more cups of coffee and don’t drink tea in hypertensive patients. Among them, we observed that with the increase in tea consumption, the relationship between coffee consumption and the risk of all-cause dementia in hypertensive patients gradually changed from a U-shaped to an inverted U-shaped (Fig. 7). In contrast, there was no statistically significant association between the interaction of coffee and tea and the risk of developing all-cause dementia, Alzheimer's disease and vascular dementia in the population without hypertension.
Fig. 6.
Association between interaction of coffee and tea consumption and the risk of all-cause dementia and Alzheimer’s disease in individuals with hypertension. We adjusted for socio-demographic characteristics (age, sex, ethnicity, education level, occupation status, TDI, BMI), lifestyle factors (smoking status, dietary patterns, alcohol consumption, physical activity, social contact, sedentary behavior duration), health-related issues (family history of dementia, APOE genotype, depression, cancer history, cardiovascular disease history), and serum markers and drug use (aspirin use, lipid-lowering medication use, dyslipidemia, hypertriglyceridemia, serum 25(OH)D status).
Fig. 7.

Correlation between interaction of coffee and tea consumption and risk of all-cause dementia in hypertensive patients. We adjusted for socio-demographic characteristics (age, sex, ethnicity, education level, occupation status, TDI, BMI), lifestyle factors (smoking status, dietary patterns, alcohol consumption, physical activity, social contact, sedentary behavior duration), health-related issues (family history of dementia, APOE genotype, depression, cancer history, cardiovascular disease history), and serum markers and drug use (aspirin use, lipid-lowering medication use, dyslipidemia, hypertriglyceridemia, serum 25(OH)D status).
Association between coffee type or hot drink temperature and dementia risk in the population with hypertension and without hypertension
After adjusting for all covariates, the statistically significant associations were found between coffee type and the risk of all-cause and vascular dementia in the population with and without hypertension, but no association with Alzheimer's disease. Ground coffee consumption revealed the lowest risk of the onset of all-cause dementia [(HR = 0.762, 95% CI 0.618–0.940) for non-hypertensive population and (HR = 0.682, 95% CI 0.588–0.791) for hypertensive population] and vascular dementia [(HR = 0.421, 95% CI 0.246–0.721) for non-hypertensive population and (HR = 0.655, 95% CI 0.478–0.898) for hypertensive population] compared with decaffeinated coffee consumption (Table 5). In addition, after adjusting for all covariates, no statistically significant association was identified between the temperature at which a hot drink was consumed and the risk of developing dementia (Table 6).
Table 5.
Coffee type on the risk of dementia in a population.
| Coffee type | P-value | |||||
|---|---|---|---|---|---|---|
| Decaffeinated coffee | Instant coffee | Ground coffee | Other type of coffee | |||
| HR (95% CI) | HR (95% CI) | HR (95% CI) | HR (95% CI) | |||
| All-cause dementia | ||||||
| Participants without hypertension | Model1 | Ref. | 0.800 (0.700, 0.914) | 0.707 (0.605, 0.827) | 1.297 (0.882, 1.909) | < 0.001 |
| Model2 | Ref. | 0.786 (0.674, 0.916) | 0.773 (0.646, 0.924) | 1.176 (0.729, 1.898) | 0.004 | |
| Model3 | Ref. | 0.789 (0.671, 0.926) | 0.778 (0.644, 0.939) | 0.933 (0.533, 1.632) | 0.019 | |
| Model4 | Ref. | 0.792 (0.663, 0.946) | 0.762 (0.618, 0.940) | 1.021 (0.569, 1.831) | 0.017 | |
| Participants with hypertension | Model1 | Ref. | 0.918 (0.840, 1.003) | 0.700 (0.626, 0.784) | 1.055 (0.797, 1.395) | < 0.001 |
| Model2 | Ref. | 0.893 (0.805, 0.989) | 0.713 (0.627, 0.812) | 0.893 (0.628, 1.271) | < 0.001 | |
| Model3 | Ref. | 0.902 (0.810, 1.005) | 0.691 (0.603, 0.792) | 0.810 (0.549, 1.195) | < 0.001 | |
| Model4 | Ref. | 0.897 (0.798, 1.009) | 0.682 (0.588, 0.791) | 0.836 (0.554, 1.264) | 0.021 | |
| Total population | Model1 | Ref. | 0.880 (0.818, 0.947) | 0.706 (0.644, 0.773) | 1.123 (0.895, 1.409) | < 0.001 |
| Model2 | Ref. | 0.862 (0.791, 0.938) | 0.716 (0.645, 0.795) | 0.973. (0.733, 1.292) | < 0.001 | |
| Model3 | Ref. | 0.868 (0.794, 0.949) | 0.713 (0.639, 0.796) | 0.846 (0.615, 1.163) | < 0.001 | |
| Model4 | Ref. | 0.866 (0.786, 0.955) | 0.706 (0.625, 0.796) | 0.884 (0.631, 1.239) | < 0.001 | |
| Alzheimer disease | ||||||
| Participants without hypertension | Model1 | Ref. | 0.888 (0.727, 1.083) | 0.708 (0.558, 0.899) | 1.368 (0.759, 2.465) | 0.014 |
| Model2 | Ref. | – | – | – | 0.051 | |
| Model3 | Ref. | – | – | – | 0.230 | |
| Model4 | Ref. | – | – | – | 0.651 | |
| Participants with hypertension | Model1 | Ref. | 0.921 (0.806, 1.053) | 0.720 (0.608, 0.853) | 0.928 (0.590, 1.460) | 0.001 |
| Model2 | Ref. | 0.956 (0.817, 1.119) | 0.760 (0.623, 0.926) | 0.941 (0.548, 1.616) | 0.031 | |
| Model3 | Ref. | 0.971 (0.822, 1.147) | 0.768 (0.624, 0.947) | 0.915 (0.511, 1.640) | 0.049 | |
| Model4 | Ref. | – | – | – | 0.067 | |
| Total population | Model1 | Ref. | 0.908 (0.813, 1.015) | 0.709 (0.616, 0.814) | 1.043 (0.729, 1.494) | < 0.001 |
| Model2 | Ref. | 0.936 (0.822, 1.066) | 0.734 (0.625, 0.863) | 1.073 (0.703, 1.638) | 0.001 | |
| Model3 | Ref. | 0.976 (0.851, 1.120) | 0.763 (0.644, 0.905) | 0.962 (0.597, 1.549) | 0.005 | |
| Model4 | Ref. | 0.963 (0.828, 1.119) | 0.766 (0.636, 0.923) | 0.991 (0.597, 1.644) | 0.019 | |
| Vascular dementia | ||||||
| Participants without hypertension | Model1 | Ref. | 0.574 (0.421, 0.782) | 0.337 (0.219, 0.517) | 0.901 (0.329, 2.471) | < 0.001 |
| Model2 | Ref. | 0.594 (0.418, 0.845) | 0.364 (0.226, 0.588) | 0.320 (0.044, 2.313) | < 0.001 | |
| Model3 | Ref. | 0.667 (0.463, 0.961) | 0.424 (0.259, 0.695) | 0.000 (0.000, 1.774^43) | 0.004 | |
| Model4 | Ref. | 0.685 (0.462, 1.015) | 0.421 (0.246, 0.721) | 0.000 (0.000,3. 225^140) | 0.017 | |
| Participants with hypertension | Model1 | Ref. | 0.939 (0.780, 1.131) | 0.673 (0.528, 0.857) | 1.371 (0.818, 2.296) | 0.002 |
| Model2 | Ref. | 0.842 (0.682, 1.041) | 0.660 (0.502, 0.866) | 1.188 (0.640, 2.205) | 0.017 | |
| Model3 | Ref. | 0.844 (0.676, 1.053) | 0.639 (0.480, 0.853) | 1.095 (0.554, 2.163) | 0.019 | |
| Model4 | Ref. | 0.912 (0.715, 1.165) | 0.655 (0.478, 0.898) | 1.420 (0.715, 2.818) | 0.021 | |
| Total population | Model1 | Ref. | 0.823 (0.703, 0.964) | 0.570 (0.462, 0.703) | 1.213 (0.767, 1.918) | < 0.001 |
| Model2 | Ref. | 0.768 (0.641, 0.920) | 0.580 (0.457, 0.735) | 0.957 (0.533, 1.720) | < 0.001 | |
| Model3 | Ref. | 0.778 (0.644, 0.940) | 0.579 (0.451, 0.743) | 0.798 (0.407, 1.564) | < 0.001 | |
| Model4 | Ref. | 0.827 (0.672, 1.017) | 0.574 (0.437, 0.755) | 0.961 (0.489, 1.889) | 0.001 | |
Model 1: adjusted for basic socio-demographic characteristics [age; sex; ethnicity; education level; occupation status; TDI; BMI].
Model 2: adjusted for Model 1 and lifestyle [smoking status; dietary patterns; alcohol consumption; physical activity; social contact; duration of sedentary behavior].
Model 3: adjusted for Model 2 and health-related issues [family history of dementia; APOE genotype; depression; history of cancer; history of cardiovascular disease].
Model 4: adjusted for Model3 and serum markers and drug use [Aspirin use status; lipid-lowering medications use status; dyslipidemia; hypertriglyceridemia; serum 25(OH)D status].
Table 6.
Association btween hot drink temperature and risk of dementia in the participants.
| Hot drink temperature | P-value for trend | ||||
|---|---|---|---|---|---|
| Very hot | Hot | Warm | |||
| HR (95% CI) | HR (95% CI) | HR (95% CI) | |||
| All-cause dementia | |||||
| Participants without hypertension | Model1 | Ref. | 1.126 (0.979, 1.296) | 1.268 (1.060, 1.516) | 0.034 |
| Model2 | Ref. | – | – | 0.296 | |
| Model3 | Ref. | – | – | 0.338 | |
| Model4 | Ref. | – | – | 0.242 | |
| Participants with hypertension | Model1 | Ref. | – | – | 0.051 |
| Model2 | Ref. | – | – | 0.140 | |
| Model3 | Ref. | – | – | 0.154 | |
| Model4 | Ref. | – | – | 0.366 | |
| Total population | Model1 | Ref. | 1.105 (1.021, 1.197) | 1.192 (1.080, 1.314) | 0.002 |
| Model2 | Ref. | 1.103 (1.007, 1.209) | 1.151 (1.028, 1.289) | 0.042 | |
| Model3 | Ref. | – | – | 0.053 | |
| Model4 | Ref. | – | – | 0.111 | |
| Alzheimer disease | |||||
| Participants without hypertension | Model1 | Ref. | 1.257 (1.011, 1.564) | 1.446 (1.098, 1.903) | 0.029 |
| Model2 | Ref. | – | – | 0.128 | |
| Model3 | Ref. | – | – | 0.304 | |
| Model4 | Ref. | – | – | 0.416 | |
| Participants with hypertension | Model1 | Ref. | 1.208 (1.038, 1.406) | 1.268 (1.056, 1.523) | 0.026 |
| Model2 | Ref. | 1.270 (1.061, 1.521) | 1.230 (0.988, 1.531) | 0.034 | |
| Model3 | Ref. | – | – | 0.116 | |
| Model4 | Ref. | – | – | 0.223 | |
| Total population | Model1 | Ref. | 1.218 (1.075, 1.379) | 1.311 (1.126, 1.527) | 0.001 |
| Model2 | Ref. | 1.240 (1.073, 1.433) | 1.249 (1.044, 1.493) | 0.012 | |
| Model3 | Ref. | – | – | 0.051 | |
| Model4 | Ref. | – | – | 0.094 | |
| Vascular dementia | |||||
| Participants without hypertension | Model1 | Ref. | – | – | 0.228 |
| Model2 | Ref. | – | – | 0.437 | |
| Model3 | Ref. | – | – | 0.401 | |
| Model4 | Ref. | – | – | 0.591 | |
| Participants with hypertension | Model1 | Ref. | – | – | 0.640 |
| Model2 | Ref. | – | – | 0.640 | |
| Model3 | Ref. | – | – | 0.682 | |
| Model4 | Ref. | – | – | 0.694 | |
| Total population | Model1 | Ref. | – | – | 0.358 |
| Model2 | Ref. | – | – | 0.306 | |
| Model3 | Ref. | – | – | 0.351 | |
| Model4 | Ref. | – | – | 0.497 | |
Model 1: adjusted for basic socio-demographic characteristics [age; sex; ethnicity; education level; occupation status; TDI; BMI].
Model 2: adjusted for Model 1 and lifestyle [smoking status; dietary patterns; alcohol consumption; physical activity; social contact; duration of sedentary behavior].
Model 3: adjusted for Model 2 and health-related issues [family history of dementia; APOE genotype; depression; history of cancer; history of cardiovascular disease].
Model 4: adjusted for Model3 and serum markers and drug use [Aspirin use status; lipid-lowering medications use status; dyslipidemia; hypertriglyceridemia; serum 25(OH)D status].
Association between caffeine intake and dementia risk in the population with hypertension and without hypertension
After adjusting for all covariates, a statistically significant association was found between caffeine intake and the risk of all-cause and vascular dementia in the hypertensive population, but no association with Alzheimer's disease. There was a U-shaped association between daily caffeine intake and the risk of all-cause dementia (Fig. 8) and vascular dementia (Fig. 9) in the hypertensive population. Compared to those who consume Quintile 1 of daily caffeine, individuals with higher caffeine intake generally faced a lower risk of all-cause and vascular dementia. Notably, hypertensive patients consuming Quintile 2 of caffeine daily have the lowest risk of both types of dementia [(HR = 0.764, 95% CI 0.669–0.872) for all- cause dementia and (HR = 0.596, 95% CI 0.446–0.798) for vascular dementia]. In addition, there appears to be a W-shaped association between daily caffeine intake and the risk of all-cause dementia in the population without hypertension (Fig. 10). Interestingly, in the population without hypertension, no statistically significant association was observed between caffeine intake and the risk of Alzheimer's disease and vascular dementia (Table 7).
Fig. 8.

A U-shaped relationship exists between caffeine intake and all-cause dementia risk in hypertensive patients. Model 1: adjusted for basic socio-demographic characteristics [age; sex; ethnicity; education level; occupation status; TDI; BMI]. Model 2: adjusted for Model 1 and lifestyle [smoking status; dietary patterns; alcohol consumption; physical activity; social contact; duration of sedentary behavior]. Model 3: adjusted for Model 2 and health-related issues [family history of dementia; APOE genotype; depression; history of cancer; history of cardiovascular disease]. Model 4: adjusted for Model 3 and serum markers and drug use [Aspirin use status; lipid-lowering medications use status; dyslipidemia; hypertriglyceridemia; serum 25(OH)D status].
Fig. 9.

A U-shaped relationship exists between caffeine intake and all-cause dementia risk in hypertensive patients. Model 1: adjusted for basic socio-demographic characteristics [age; sex; ethnicity; education level; occupation status; TDI; BMI]. Model 2: adjusted for Model 1 and lifestyle [smoking status; dietary patterns; alcohol consumption; physical activity; social contact; duration of sedentary behavior]. Model 3: adjusted for Model 2 and health-related issues [family history of dementia; APOE genotype; depression; history of cancer; history of cardiovascular disease]. Model 4: adjusted for Model 3 and serum markers and drug use [Aspirin use status; lipid-lowering medications use status; dyslipidemia; hypertriglyceridemia; serum 25(OH)D status].
Fig. 10.

Caffeine intake and the risk of all-cause dementia in the population without hypertension is W-shaped. Model 1: adjusted for basic socio-demographic characteristics [age; sex; ethnicity; education level; occupation status; TDI; BMI]. Model 2: adjusted for Model 1 and lifestyle [smoking status; dietary patterns; alcohol consumption; physical activity; social contact; duration of sedentary behavior]. Model 3: adjusted for Model 2 and health-related issues [family history of dementia; APOE genotype; depression; history of cancer; history of cardiovascular disease]. Model 4: adjusted for Model 3 and serum markers and drug use [Aspirin use status; lipid-lowering medications use status; dyslipidemia; hypertriglyceridemia; serum 25(OH)D status].
Table 7.
Associaton between caffeine intake and risk of dementia in the participants.
| Coffeine consumption, mg/day | P-value | ||||||
|---|---|---|---|---|---|---|---|
| Quintile1 | Quintile2 | Quintile2 | Quintile4 | Quintile5 | |||
| HR (95% CI) | HR (95% CI) | HR (95% CI) | HR (95% CI) | HR (95% CI) | |||
| All-cause dementia | |||||||
| Participants without hypertension | Model1 | Ref. | 0.734 (0.629, 0.856) | 0.821 (0.708, 0.953) | 0.788 (0.677, 0.918) | 0.855 (0.734, 0.995) | 0.001 |
| Model2 | Ref. | 0.758 (0.636, 0.902) | 0.826 (0.697, 0.979) | 0.730 (0.612, 0.872) | 0.825 (0.693, 0.983) | 0.004 | |
| Model3 | Ref. | 0.767 (0.639, 0.920) | 0.797 (0.667, 0.953) | 0.729 (0.606, 0.876) | 0.807 (0.671, 0.971) | 0.007 | |
| Model4 | Ref. | 0.783 (0.640, 0.958) | 0.834 (0.685, 1.014) | 0.675 (0.547, 0.832) | 0.842 (0.688, 1.032) | 0.006 | |
| Participants with hypertension | Model1 | Ref. | 0.888 (0.807, 0.978) | 0.830 (0.751, 0.916) | 0.816 (0.738, 0.904) | 0.905 (0.817, 1.002) | < 0.001 |
| Model2 | Ref. | 0.860 (0.770, 0.960) | 0.763 (0.679, 0.856) | 0.785 (0.699, 0.882) | 0.845 (0.752, 0.951) | < 0.001 | |
| Model3 | Ref. | 0.845 (0.753, 0.950) | 0.740 (0.655, 0.835) | 0.759 (0.672, 0.858) | 0.851 (0.754, 0.962) | < 0.001 | |
| Model4 | Ref. | 0.870 (0.766, 0.989) | 0.764 (0.669, 0.872) | 0.799 (0.700, 0.913) | 0.880 (0.770, 1.005) | 0.001 | |
| Total population | Model1 | Ref. | 0.841 (0.775, 0.912) | 0.825 (0.760, 0.896) | 0.806 (0.741, 0.877) | 0.888 (0.815, 0.966) | < 0.001 |
| Model2 | Ref. | 0.828 (0.754, 0.908) | 0.780 (0.709, 0.858) | 0.767 (0.696, 0.845) | 0.837 (0.760, 0.923) | < 0.001 | |
| Model3 | Ref. | 0.821 (0.745, 0.905) | 0.757 (0.685, 0.837) | 0.751 (0.678, 0.832) | 0.839 (0.757, 0.929) | < 0.001 | |
| Model4 | Ref. | 0.844 (0.757, 0.939) | 0.786 (0.705, 0.877) | 0.763 (0.682, 0.854) | 0.868 (0.777, 0.970) | < 0.001 | |
| Alzheimer disease | |||||||
| Participants without hypertension | Model1 | Ref. | 0.722 (0.574, 0.908) | 0.786 (0.629, 0.983) | 0.750 (0.596, 0.945) | 0.862 (0.686, 1.082) | 0.037 |
| Model2 | Ref. | – | – | – | – | 0.172 | |
| Model3 | Ref. | – | – | – | – | 0.226 | |
| Model4 | Ref. | – | – | – | – | 0.292 | |
| Participants with hypertension | Model1 | Ref. | – | – | – | – | 0.202 |
| Model2 | Ref. | – | – | – | – | 0.142 | |
| Model3 | Ref. | – | – | – | – | 0.274 | |
| Model4 | Ref. | – | – | – | – | 0.777 | |
| Total population | Model1 | Ref. | 0.845 (0.747, 0.956) | 0.828 (0.731, 0.938) | 0.818 (0.720, 0.929) | 0.880 (0.773, 1.001) | 0.010 |
| Model2 | Ref. | 0.839 (0.727, 0.967) | 0.800 (0.692, 0.926) | 0.821 (0.708, 0.951) | 0.894 (0.771, 1.037) | 0.020 | |
| Model3 | Ref. | 0.866 (0.745, 1.007) | 0.829 (0.711,0.966) | 0.807 (0.690, 0.943) | 0.919 (0.785, 1.076) | 0.049 | |
| Model4 | Ref. | – | – | – | – | 0.328 | |
| Vascular dementia | |||||||
| Participants without hypertension | Model1 | Ref. | – | – | – | – | 0.211 |
| Model2 | Ref. | – | – | – | – | 0.346 | |
| Model3 | Ref. | – | – | – | – | 0.432 | |
| Model4 | Ref. | – | – | – | – | 0.690 | |
| Participants with hypertension | Model1 | Ref. | 0.953 (0.782, 1.160) | 0.718 (0.580, 0.888) | 0.818 (0.664, 1.007) | 0.900 (0.730, 1.109) | 0.019 |
| Model2 | Ref. | 0.924 (0.739, 1.154) | 0.638 (0.497, 0.818) | 0.791 (0.624, 1.002) | 0.825 (0.650, 1.048) | 0.006 | |
| Model3 | Ref. | 0.881 (0.697, 1.114) | 0.589 (0.453, 0.767) | 0.781 (0.610, 1.001) | 0.827 (0.644, 1.061) | 0.002 | |
| Model4 | Ref. | 0.945 (0.732, 1.220) | 0.596 (0.446, 0.798) | 0.800 (0.610, 1.050) | 0.823 (0.624, 1.083) | 0.006 | |
| Total population | Model1 | Ref. | 0.906 (0.762,1.079) | 0.714 (0.593, 0.861) | 0.774 (0.644, 0.931) | 0.875 (0.729, 1.051) | 0.004 |
| Model2 | Ref. | 0.875 (0.718, 1.066) | 0.664 (0.536, 0.822) | 0.747 (0.606, 0.921) | 0.812 (0.659, 1.000) | 0.002 | |
| Model3 | Ref. | 0.847 (0.688, 1.043) | 0.625 (0.499, 0.784) | 0.748 (0.601, 0.930) | 0.825 (0.664, 1.026) | 0.001 | |
| Model4 | Ref. | 0.917 (0.730, 1.153) | 0.651 (0.506, 0.836) | 0.784 (0.616, 0.997) | 0.865 (0.680, 1.100) | 0.011 | |
Model 1: adjusted for basic socio-demographic characteristics [age; sex; ethnicity; education level; occupation status; TDI; BMI].
Model 2: adjusted for Model 1 and lifestyle [smoking status; dietary patterns; alcohol consumption; physical activity; social contact; duration of sedentary behavior].
Model 3: adjusted for Model 2 and health-related issues [family history of dementia; APOE genotype; depression; history of cancer; history of cardiovascular disease].
Model 4: adjusted for Model3 and serum markers and drug use [Aspirin use status; lipid-lowering medications use status; dyslipidemia; hypertriglyceridemia; serum 25(OH)D status].
Subgroup analysis and sensitivity analysis
When determining the association between the risk of all-cause dementia and coffee and tea consumption, types of coffee, and caffeine intake in hypertensive individuals, a stratified analysis was performed considering age, sex, and socioeconomic status. The findings suggest a higher risk of all-cause dementia in hypertensive patients aged over 65, male, and with a higher socioeconomic status (Supplementary Figs. 1–2). Overall, the subgroup analyses were consistent with the main results. We conducted four sensitivity analyses, and all associations remained significant and in line with the overall findings, demonstrating the robustness of the results, as presented in Supplementary Tables S4–S7.
Discussion
In this study, individuals with hypertension had a higher likelihood of developing dementia compared to the population without hypertension. There was an association between the risk of dementia and coffee and tea consumption in the total population, and the relationship between the risk of all-cause dementia and the consumption of coffee and tea in hypertensive people showed J-shaped and U-shaped patterns respectively. People who drink 0.5–1 cup of coffee or 4–5 cups of tea per day have the lowest risk of dementia. The significant association between the amount of coffee and tea consumed and the risk of all-cause and vascular dementia were more likely to be found in the hypertensive population than in the non-hypertensive population. Consumers of ground coffee have the lowest risk of all-cause dementia and vascular dementia. There is no correlation between the temperature of hot beverages and the risk of dementia. Furthermore, a U-shaped relationship was observed between daily caffeine consumption and the risk of developing all-cause dementia and vascular dementia in individuals with hypertension.
This study found that there was an association between the risk of dementia and coffee and tea consumption in the total population. However, previous studies on the relationship between personal coffee or tea consumption and dementia risk have mostly been observational studies, with no experimental research evidence, so the research conclusions have been controversial. For example, a cohort study spanning 25 years did not find a significant link between midlife coffee consumption and the risk of cognitive decline and dementia21. Regular tea consumption does not demonstrate a significant correlation with the risk of Alzheimer’s disease22. Short-term associations between coffee intake and cognition were observed, but no long-term effects were noted23,24. Fortunately, our findings have been supported by several previous studies. The previous study found that the risk of dementia and Alzheimer’s disease was reduced by 60% by drinking one to two cups of coffee a day25. In addition, drinking one cup of tea a day reduced the risk of dementia or mild cognitive impairment by 6% and two cups by 11%26. There are several possible reasons for the inconsistency of these studies. Firstly, most studies primarily relied on self-reported coffee and tea consumption, which is susceptible to information bias. Secondly, the diagnosis of dementia varied among studies, and some level of misclassification of dementia may have occurred in most studies. Thirdly, inconsistent sample size and follow-up time in each study, along with excessive category combinations. Fourthly, there may be variability in the daily consumption of coffee and tea, making the exact amount and strength of coffee and tea consumption difficult to measure through questionnaires. Fifthly, the association between coffee and the risk of dementia varies depending on the type of coffee20. Most of the studies did not distinguish between types of coffee and tea, and did not look at the consumption of a particular type of coffee or tea in isolation to see if it was associated with the risk of developing dementia. In addition, this study found that the relationship between the risk of all-cause dementia and the consumption of coffee and tea in hypertensive people showed J-shaped and U-shaped patterns respectively, which is consistent with previous studies25,27,28. Among them, the study found that people who drink 0.5–1 cup of coffee or 4–5 cups of tea per day have the lowest risk of dementia, which is consistent with previous studies6. One possible reason is that coffee and tea ingredients, such as caffeine, may reduce the risk of dementia by decreasing neuroinflammation or providing neuroprotective benefits8–10. However, excessive drinking of coffee and tea will lead to a large amount of caffeine intake in the body, disturb sleep patterns, and diminish internal antioxidant effects in the body29. Excessive caffeine consumption can selectively and competitively bind to adenosine receptors, stimulating catecholamine secretion from the adrenal glands. This can lead to morphological changes in the brain7, increasing the risk of dementia and decreasing cognitive function30. In addition, taking more than 500 mg of high caffeine into the body makes it more difficult for the body to eliminate caffeine30. This can cause caffeine intoxication, leading to symptoms like anxiety, insomnia, and psychiatric disorders31, all of which are risk factors for dementia32–34. The study also found that the association between caffeine intake and risk of dementia was U-shaped, suggesting that moderate coffee and tea drinkers are more likely to find a significant association between coffee and tea consumption and risk of dementia.
In this study, the statistically significant association between coffee and tea consumption and the risk of dementia was more likely to found in people with hypertension than in people without hypertension. The possible reason for this is that the active compounds in coffee and tea not only reduce the risk of hypertension (an independent risk factor for dementia)17,18, but also inhibit acetylcholinesterase (a key enzyme in the pathogenesis of Alzheimer's disease), reduce lipid peroxidation and prevent neuronal damage19. Therefore, patients with hypertension who drink these drinks may get greater health benefits in delaying the development of neurodegenerative diseases such as dementia. Moreover, in addition to the separate links between coffee and tea consumption and the risk of dementia in hypertensive individuals, our study also found that there was a significant statistical significance between the interaction of coffee and tea the lower risk of developing all-cause dementia and Alzheimer's disease, aligning with previous studies6. This could be attributed to several factors. Firstly, coffee and tea share similar bioactive compounds like caffeine and chlorogenic acid, which work together to provide anti-inflammatory11, antioxidant35, blood pressure-lowering17,18, and reduction of cerebral lipid peroxidation19 effects, thus helping prevent the onset of oxidative neurodegenerative diseases in the brain. Secondly, certain polyphenols in coffee and tea play a joint protective role in the pathogenesis of dementia6. Thirdly, coffee and tea help reduce the risk of cardiovascular metabolic diseases like diabetes36 and hypertension37, thus lowering the chances of dementia38.
Prior research has shown that the link between coffee consumption and dementia risk differs based on the type of coffee consumed20, which aligns with our discovery that the type of coffee has a notable impact on the risk of developing all-cause dementia and vascular dementia. The risk of developing all-cause dementia and vascular dementia was lowest among those who consumption of ground coffee. The likely reason for this is that different types of coffee have different levels of caffeine, with ground coffee having the highest caffeine content, instant coffee the second highest, and decaffeinated coffee the lowest39. Caffeine is currently the most widely used psychostimulant in the world and has neuroprotective properties in the fight against neurodegenerative diseases5. Long-term consumption of caffeinated water not only slows the progression of memory deficits in mice with Tau pathology of Alzheimer's disease40, but also reverses their memory deficits that occur with age41. Secondly, the preference for coffee varies among individuals42, and there are variations in chemical composition between different types of coffee43,44. For example, ground coffee has the highest chlorogenic acid content43. In addition, the benefits of chlorogenic acid in instant coffee may be offset by the harmful effects of added sugar, creamer and other ingredients45. Therefore, we should pick the most suitable coffee and tea to drink in our normal life.
In this study, the statistically significant association between coffee and tea consumption, coffee type, caffeine intake, and the risk of dementia was more likely to be found in hypertensive patients over 65 years old, males, and those of high socioeconomic status. This may be because the prevalence of dementia rises sharply with age38. While coffee25 and tea26 consumption can lower the risk of dementia, these rich caffeinated versions cannot offset age-related cognitive decline46,47. Men seem to derive greater benefits from consuming coffee and tea than women, in line with previous research27,28. Gender variations in brain structure and function could affect how coffee and tea consumption impact their protective advantages48. In addition, regular tea consumption helped reduce Tauopathy and notably lowered the risk of dementia in males, while it did not have the same effect on Tauopathy in females20. Higher income groups are more likely to drink coffee and tea, which leads to a more significant reduction in their risk of developing dementia. Lower-income groups might have more cases of undiagnosed dementia49, while higher-income groups are more likely to receive a dementia diagnosis50.
To our knowledge, few studies have looked at both coffee and tea consumption and caffeine intake in relation to the risk of dementia in people with hypertension. In addition, the reliability and validity of the study are strengthened by the large sample size, long-term follow-up and rigorously defined variables. However, this study has some limitations. Firstly, self-report of coffee and tea consumption at baseline may be subject to information bias. In addition, these kinds of measurements at baseline may not accurately reflect the long-term consumption since these behaviors are very likely to change with time. Secondly, estimates from higher intakes involved fewer participants, potentially resulting in imprecision in the dementia observed at these levels of coffee and tea consumption. Thirdly, UK Biobank is affected by a ‘healthy volunteer’ selection bias, as participants tend to be more health-conscious, resulting in an underestimation of dementia incidence and prevalence51. Fourthly, since the majority of UK Biobank participants were white UK citizens, our results may only be applicable to similar demographic groups. Finally, although we adjusted for many potential confounders, residual confounding from unmeasured or unknown variables may still affect our analyses.
Conclusions
There was an association between the risk of dementia and coffee and tea consumption in the total population, and the relationship between the risk of all-cause dementia and the consumption of coffee and tea in hypertensive people showed J-shaped and U-shaped patterns respectively. The significant association between the amount of coffee and tea consumed and the risk of all-cause and vascular dementia were more likely to be found in the hypertensive population than in the non-hypertensive population. Furthermore, a U-shaped relationship was observed between daily caffeine consumption and the risk of developing all-cause dementia and vascular dementia in individuals with hypertension.
Methods
Study design and population
The UK Biobank is a vast population-based study that recruited more than 500,000 participants (aged 39–74) at 22 assessment centers in England, Wales, and Scotland from 2006 to 201052. Participants underwent physical examinations conducted by trained staff and completed touchscreen questionnaires. The cohort ensures continuous tracking of health-related outcome data of participant by establishing links with electronic records from primary care, hospitalization, and death registries. It has gathered a broad array of genetic and health data to explore genetic and lifestyle influences on various common diseases in middle-aged and older adults53. All participants signed the informed consent form. In addition, UK Biobank adheres to the ethical principles of the 1975 Helsinki Declaration and has been approved by the North West Multi-Centre Research Ethics Committee (MREC) as a Research Tissue Bank (RTB), enabling researchers to operate within the approved scope without requiring additional ethical clearance. Among 502,370 UK Biobank participants collected at baseline, those with any of the following conditions were also excluded: (1) 4 people were excluded from the initial analysis for missing baseline data. (2) 45,536 participants who lacked baseline blood pressure measurement information were excluded. (3) 277 participants with secondary hypertension were excluded. (4) 2,428 participants who lacked baseline coffee and tea consumption information were excluded. (5) 212 subjects with a baseline diagnosis of dementia were excluded. A final cohort of 453,913 subjects who were followed until April 1, 2024, with an average follow-up of 15.12 years were included in this study (Fig. 1).
Assessment of Hypertension
The baseline information for the normal and hypertensive population was determined using a combination of self-reported data from the UK Biobank, hospital registry data, and the collection of two blood pressure measurements using an Omron HEM 7015-T automated sphygmomanometer. In this study, the baseline hypertensive population was defined by meeting one of the following criteria: (1) self-reported doctor diagnosis of hypertension; (2) self-reported use of antihypertensive medication; (3) measured systolic blood pressure ≥ 140 mmHg or diastolic blood pressure ≥ 90 mmHg. The third criterion cut-off aligns with global hypertension definition54.
Exposure assessment
Data on coffee and tea consumption were gathered through the Food Frequency Questionnaire (FFQ) to evaluate the type and intake of coffee and tea in an initial survey of the UK Biobank database55. Participants were asked how many cups of coffee and tea they drank per day and what type of coffee and tea they typically consumed. We then looked at the relationship between different types of coffee and tea and consumption and the risk of developing dementia in people with diabetes. Caffeine intake (mg/d) was determined using self-reported coffee and tea consumption in the survey, with an assumption of 75 mg of caffeine per cup of coffee and 40 mg of caffeine per cup of tea56–58 (See Table S1).
Assessment of outcome
We diagnosed dementia by utilizing health-related outcomes defined by the UK Biobank preprocessing algorithm59, based on primary care, hospitalization, and death registry data during follow-up. Health-related outcome data were published in 2018, and data were dynamically updated to the end of this study in April 2024. Subsequently, dementia was classified according to the International Classification of Diseases (ICD) 9th and 10th editions. The dependent variable was dementia, including all-cause dementia, Alzheimer's disease and vascular dementia. The accuracy of UK Biobank in utilizing routinely collected healthcare datasets to detect dementia events showed high positive predictive value, sensitivity, and specificity60,61 (See Table S2).
Assessment of covariates
The baseline survey obtained potential confounders such as corresponding socio-demographic, lifestyle and health-related issues through questionnaires. Confounders included age, sex (male and female), ethnicity (White, Asian, Black, and Other), education level (college or university degree, A level/AS levels or equivalent, O level/GCSEs or equivalent, CSEs or equivalent, NVQ or HND or HNC or equivalent, and other professional qualifications), occupation (employed, unemployed, and retired), Townsend Poverty Index(TDI) (low, medium, and high), body mass index (BMI) (< 18.5, 18.5–24.9, 25–29.9, and ≥ 30, kg/m2), smoking status (never, former, and current), dietary patterns (healthy dietary pattern, intermediate dietary pattern, and poor dietary pattern), alcohol consumption (IQRs, and quartiles), physical activity ((low, moderate, and high), social contact (active, moderately, isolated), Duration of sedentary behavior (< 2, 2–3.9, 4–5.9, and ≥ 6, hours/day), family history of dementia, APOE genotype, depression, history of cancer, history of cardiovascular disease, aspirin use status, lipid-lowering medications use status, dyslipidemia, hypertriglyceridemia, and serum 25(OH)D status (severely deficient, moderately deficient, and insufficient and above).
Socioeconomic status is evaluated through the Townsend Deprivation Index (TDI), where a higher TDI suggests a greater degree of deprivation62,63. The UK Biobank database uses the APOE single nucleotide polymorphisms rs7412 and rs429358 for genotyping to identify carriers of the APOE ε4 allele64,65. We establish a healthy dietary pattern based on the recommended intake of a heart-healthy diet in the United States66. Physical activity intensity was determined by analyzing information from the International Physical Activity Questionnaire20. Using the social connection index, determine the quality of the social relationship67. Evaluate the duration of sedentary behavior based on activities like driving, computer usage, and television watching68. Participants' serum 25(OH)D status was evaluated using baseline serum 25(OH)D data69. Information on cancer, depression, cardiovascular, and other related diseases was gathered from medical records, self-reports, and death records. Definitions of each component of covariates in this study are described in Additional file: Table S3.
Statistical analyses
In the descriptive analyses of the normal and hypertension populations, a one-way ANOVA determined the mean (standard deviation (SD)) of continuous variables among the two groups, while a Pearson test identified any statistical differences in the proportions of categorical variables. The person-years at risk for each participant were computed starting from the recruitment date until the occurrence of dementia report, date of decease, loss to follow-up, or 01 April 2024, whichever event transpired first. The proportional risk assumption was validated with Schoenfeld residuals, and Cox proportional risk regression models were utilized to compute estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for the link between coffee and tea consumption and dementia risk in individuals with hypertension. Non-linear relationships between coffee, tea, and caffeine intake and all-cause dementia were assessed using restricted cubic spline curves with three knots. In Model 1, we adjusted for basic socio-demographic characteristics [age; sex; ethnicity; education level; occupation status; TDI; BMI]. In Model 2, we further adjusted for lifestyle [smoking status; dietary patterns; alcohol consumption; physical activity; social contact; duration of sedentary behavior]. In Model 3, we further adjusted for health-related issues [family history of dementia; APOE genotype; depression; history of cancer; history of cardiovascular disease]. In Model 4, we additionally adjusted for serum markers and drug use [Aspirin use status; lipid-lowering medications use status; dyslipidemia; hypertriglyceridemia; serum 25(OH)D status].
This study investigated whether the risk of developing dementia could be reduced in hypertensive and non-hypertensive populations by improving the consumption of caffeine-containing beverages such as coffee and tea. First, to explore the link between coffee and tea consumption and the risk of dementia in hypertension patients, risk ratios and 95% confidence intervals were computed separately. The relationship between different types of coffee (such as decaffeinated coffee, instant coffee, ground coffee, and other types of coffee) and the temperature of hot drinks (including very hot, hot, and warm) in relation to the risk of developing dementia in patients with hypertension was also examined. In addition, we also calculated the intake level of caffeine according to the intake of coffee and tea to further analyze the influence of caffeine on the risk of dementia in hypertension patients.
To assess whether age, sex, and socioeconomic status affected the association between coffee and tea consumption and dementia, subgroup analyses were performed by age (≤ 65 years and > 65 years), sex, and socioeconomic status (low, medium, high). In addition, to assess the robustness of our findings, we conducted four sensitivity analyses. First, we excluded participants who developed dementia within 2 years to minimize the chance of observing reverse causality in the associations. Secondly, we excluded outliers in coffee and tea consumption, like consuming 13 or more hot beverages daily. Thirdly, participants who had experienced a stroke at baseline were excluded. Furthermore, we also accounted for weight reduction and grip strength, taking into consideration the potential impact of frailty on dementia.
All statistical analyses were performed using Stata software version 17 and R version 4.0.2, and statistical significance (two-sided) was defined as a P value < 0.055.
Supplementary Information
Acknowledgements
This research was conducted using the UK Biobank resource. We are grateful to the UK Biobank participants.
Author contributions
B.W: Conceptualization, Methodology, Software, Formal analysis, Writing-Original Draft, Data Curation, Writing-Review & Editing. T.M: Investigation, Data Curation. L.Y: Investigation, Visualization. S.H: Methodology, Supervision. J.L:Methodology, Supervision. X.S: Writing-Review & Editing, Supervision, Funding acquisition, Project administration. All authors read and approved the final manuscript.
Data availability
The data underlying this article are available in UK Biobank, at https://www.ukbiobank.ac.uk/. This research has been conducted using the UK Biobank Resource under Application Number 98124. The datasets analyzed during the current study available from the corresponding author on reasonable request.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher's note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Supplementary Information
The online version contains supplementary material available at 10.1038/s41598-024-71426-y.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Data Availability Statement
The data underlying this article are available in UK Biobank, at https://www.ukbiobank.ac.uk/. This research has been conducted using the UK Biobank Resource under Application Number 98124. The datasets analyzed during the current study available from the corresponding author on reasonable request.



