Skip to main content
NCBI home page
GeroScience logoLink to GeroScience
. 2024 Sep 30;47(2):1721–1733. doi: 10.1007/s11357-024-01365-z

Nut consumption is associated with a lower risk of all-cause dementia in adults: a community-based cohort study from the UK Biobank

Bruno Bizzozero-Peroni 1,2, Valentina Díaz-Goñi 1, Nuria Beneit 1,✉, Andreia Oliveira 3,4,5, Estela Jiménez-López 1,6, Vicente Martínez-Vizcaíno 1,7, Arthur Eumann Mesas 1
PMCID: PMC11979034  PMID: 39343863

Abstract

This cohort study aimed to analyze the relationship between nut consumption and the risk of all-cause dementia in adults from the United Kingdom (UK). Data from participants in the UK Biobank cohort between 2007–2012 (baseline) and 2013–2023 (follow-up) were analyzed. Baseline information on nut consumption was obtained using the Oxford WebQ 24-h questionnaire. All-cause dementia (i.e. Alzheimer’s disease, frontotemporal dementia, or vascular dementia) was assessed at baseline and follow-up through self-reported medical diagnosis, hospitalization, or death records. Hazard regression models were used to estimate the association between nut consumption and the risk of developing all-cause dementia, with adjustments made for sociodemographic, lifestyle, hearing problems, self-rated health, and the number of chronic diseases. Participants with all-cause dementia at baseline were excluded. A total of 50,386 participants (mean age 56.5 ± 7.7 years, 49.2% women) were included in the prospective analyses. The incidence of all-cause dementia was 2.8% (n = 1422 cases). Compared with no consumption, daily nut consumption (> 0 to 3 or more handfuls) was significantly associated with a 12% lower risk of all-cause dementia (hazard ratio = 0.88; 95% confidence interval, 0.77–0.99) after 7.1 mean years of follow-up, regardless of the potential confounders considered. No statistically significant interactions were observed between nut consumption and any of the covariates included in the hazard regression models. Stratified analyses revealed that nut consumption of up to 1 handful of 30 g/day and consumption of unsalted nuts were associated with the greatest protective benefits. The daily consumption of nuts may play a protective role in the prevention of dementia.

Supplementary Information

The online version contains supplementary material available at 10.1007/s11357-024-01365-z.

Keywords: Diet, Nuts, Healthy Lifestyle, Cognitive impairment, Mental disorders, Major neurocognitive disorder

Introduction

Dementia is a syndrome characterized by a significant loss of cognitive ability that interferes with the performance of daily activities such as occupational, domestic, or social functioning and has a negative impact on the quality of life of patients [1]. Currently, more than 50 million individuals worldwide are living with dementia (lifetime prevalence ranging from 0.59 to 0.79%) [2], and it is estimated that this number will reach 152 million by 2050 [3]. To date, pharmacological treatment for dementia has demonstrated only modest beneficial effects, especially in terms of preventing disease progression [4]. Emerging evidence indicates that reducing modifiable risk factors (e.g. smoking, excessive alcohol consumption, insufficient physical activity, social isolation) may prevent or delay the onset of up to 40% of dementias [5]. Therefore, public health systems should endorse strategies focused on lifestyle modification as a means of preventing dementia.

Dietary interventions have been proposed as promising strategies for preventing cognitive impairment and dementia [6]. In this context, Mediterranean dietary patterns have been consistently associated with a lower risk of dementia [7, 8]. These diets emphasize the consumption of plant-based foods with antioxidant and anti-inflammatory properties, which may play a key protective role in brain function and cognitive impairment [9]. A common aspect shared by these diets, among others, is the habitual consumption of nuts [8, 9]. In recent years, scientific research has examined the incorporation of nuts into dietary habits to maintain brain health throughout all stages of life [10, 11]. Specifically, tree nuts (i.e. walnuts, almonds, Brazil nuts, cashews, hazelnuts, and pistachios) and peanuts, from this point onwards referred to as ‘nuts’, are energy-dense foods with an optimal nutrient profile [12]. They are rich in essential nutrients and bioactive compounds such as mono- and polyunsaturated fatty acids, nonsodium minerals, polyphenols, and phytosterols, which may act synergistically to produce a wide range of neurocognitive health benefits [13, 14]. Bioavailable phytochemicals in nuts have shown anti-inflammatory and antioxidant properties that could play a beneficial role in delaying the progression of cognitive impairment [15].

Epidemiological evidence from prospective cohort studies indicates a beneficial association between nut consumption and cognitive function [16–19]. Furthermore, a 12-week randomized controlled trial (RCT) revealed that a regular diet enriched with high oleic peanuts (56–84 g/day) enhanced cognition (i.e. short-term memory and verbal fluency) in healthy middle-aged overweight adults when compared with a regular diet without nuts [20]. However, in an RCT with cognitively healthy older adults who were overweight and had a family history of dementia, no enhancements in brain health, such as global cognition and magnetic resonance imaging findings, were observed after a 3-year intervention involving a Mediterranean diet supplemented with nuts (142 g/week) [21]. In turn, a 2021 systematic review that synthesized observational and experimental studies concluded that the evidence is inconsistent as to whether nut consumption reduces the risk of neurocognitive disorders [10]. Therefore, the aim of this study was to evaluate the prospective association between nut consumption and the risk of all-cause dementia in a large sample of middle-aged and older adults from the United Kingdom (UK).

Methods

This community-based cohort study (project application number 72061) was conducted using the UK Biobank (UK-B) resource [22]. The UK-B project was approved by the North‒West Multicentre Research Ethics Committee (Ref: 16/NW/0274) in accordance with the principles of the Declaration of Helsinki. All participants provided signed consent forms. This study followed the Strengthening the Reporting of Observational Studies in Epidemiology reporting guidelines [23] (Supplementary Table S1).

Study design and participants

The study design and methods of the UK-B are reported in detail elsewhere [22]. In brief, the UK-B is a large-scale epidemiological study established in 2006–2010 with UK adults recruited from 22 assessment centres. A total of ~ 9.2 million individuals registered with the UK National Health Service were invited, and ~ 5.5% participated in the initial assessment [24]. The sampling population is volunteer-based and therefore not representative of the UK population [24]. The UK-B dataset for this population-based study included 502,287 middle-aged and older adults aged 37–73 years. Of these, 58,947 participants had valid baseline data for nut consumption, all-cause dementia (i.e. Alzheimer’s disease, frontotemporal dementia, or vascular dementia), and the covariates studied. After the exclusion of 102 individuals with all-cause dementia at baseline and those who developed all-cause dementia within the first year of follow-up, along with 8459 individuals with missing data on any of the study variables, a total of 50,386 participants (40–70 years) were followed for a mean duration of 7.1 ± 2.9 years, ranging from 1.0 to 13.7 years (Fig. 1).

Fig. 1.

Fig. 1

Open in a new tab

Flow diagram of the study participants from the original UK-B cohort

Study variables

The variables and criteria used for defining nut consumption, all-cause dementia, and covariates on the basis of the UK-B data are detailed in Supplementary Tables S2 to S4. Baseline assessments (nut consumption, all-cause dementia, and covariates) were performed between 2007 and 2012, and longitudinal assessments (all-cause dementia) were conducted between 2013 and 2023.

Exposure: nut consumption

The UK-B employs the Oxford WebQ questionnaire, which is a validated online 24-h dietary recall tool that assesses self-reported nut consumption on the previous day [25]. The participants completed dietary assessments at the conclusion of the recruitment phase (2009–2010) and four additional rounds of questionnaires between 2011 and 2012. The dietary assessment tool was designed to be used on multiple occasions to reduce potential measurement error. In accordance with recommendations [25], baseline nut consumption was averaged across the five time points to estimate usual consumption. The Oxford WebQ obtained information on nut consumption by asking participants ‘Did you eat any crisps, nuts, or savoury snacks yesterday?’ with responses of (i) no or (ii) yes (Supplementary Table S2). For those who reported consuming, a list of different types of snack foods and nuts was presented, and the respondents were asked to specify the type (i.e. nuts and/or peanuts) and handfuls of nuts (i.e. 1/2, 1, 2, or ≥ 3) consumed over the previous day [26].

For the present study, the answers for ‘unsalted nuts (e.g. almonds, cashews, pistachios)’, ‘salted/roasted nuts (e.g. almonds, cashews, pistachios)’, ‘peanuts, unsalted (monkey nuts)’, and ‘peanuts, salted/roasted (monkey nuts)’ were considered valid for the estimation of total nut consumption [26]. Nuts were considered to include both nuts and peanuts [12]. For the primary analyses in this study, the original response options for nut consumption were dichotomized into two categories: (i) no consumption (reference category) and (ii) nut consumption (> 0 to 3 or more handfuls of nuts/day). These categories were proposed because the mean quantity of nut consumption across the five assessment time points indicated that the high consumption categories (i.e. 2 and 3 or more handfuls/day) included a limited sample of participants. Therefore, the proposed stratification not only facilitated the interpretation of the results but also increased the statistical power and provided a stable estimate of the study association.

Outcome: all-cause dementia

In the UK-B, all-cause dementia was determined using a validated algorithm, which included three subtypes of dementia (i.e. Alzheimer’s disease, frontotemporal dementia, and vascular dementia) [27]. Accordingly, for the present study, all-cause dementia was defined by at least one of the following criteria: (i) self-reported physician diagnosis of dementia, (ii) electronic health records on hospital admission, or (iii) death registry data. In the UK-B baseline assessments, individuals were asked, ‘Has a doctor ever told you that you have had any serious medical conditions or disabilities?’ with “yes” or “no” responses (touchscreen questionnaire). Those who responded affirmatively were subsequently interviewed by a trained nurse in a face-to-face setting. The research nurses inquired about the individual’s history of ‘dementia or Alzheimer’s or cognitive impairment’, to which they answered ‘yes’ or ‘no’. For cases of all-cause dementia identified from hospital admission or death records, diagnoses were based on Read codes (i.e. coded thesaurus of clinical terms used in the UK National Health Service) and the International Classification of Diseases, Ninth Revision (ICD-9) or ICD-10 codes, respectively [27] (Supplementary Table S3).

Covariates

Covariates were selected on the basis of recent evidence on the potential determinants of dementia and their associations with nut consumption [5]. The criteria used to define the UK-B covariates in the present study are detailed in Supplementary Table S4. In brief, information on potential confounders of the study associations was obtained from the touchscreen questionnaire, face-to-face interviews, the Oxford WebQ questionnaire, and physical measurements assessed at baseline [22]. Self-reported information was obtained for sex, age, educational or professional qualifications, tobacco use, frequency of alcohol consumption, fruit and vegetable consumption, physical activity, sleep duration, loneliness, hearing problems, and medical conditions. Body mass index (BMI) was calculated as weight divided by the square of the height (kg/m2), both of which were objectively measured under standardized conditions (Seca 202 device). Moreover, handgrip strength was quantified using a Jamar J00105 hydraulic hand dynamometer, with the means of the right and left values expressed in absolute units (kg). Finally, total energy intake was estimated from responses to 24-h dietary recall data obtained from the online Oxford WebQ survey and expressed in total kilocalories/day.

Statistical analysis

First, we examined the baseline characteristics of all the study participants and according to their dementia status (i.e. no dementia or incident all-cause dementia) in terms of absolute (n) and relative (%) frequency for categorical variables and mean ± standard deviation for continuous variables.

Second, Cox proportional hazard regression models were employed to estimate the hazard ratios (HRs) and their 95% confidence intervals (95% CIs) for incident all-cause dementia according to nut consumption categories (no consumption as the reference category = 1), with person-years of follow-up as the timeline variable. Participants were followed from the baseline UK-B assessments until the date of their first all-cause dementia diagnosis, death, or the conclusion of the follow-up period, whichever occurred first. To reduce the potential influence of reverse causality, Cox regression analyses were performed with the exclusion of events occurring within the first year. Three models were estimated to progressively assess the confounding effect of the following blocks of covariates: Model 1, adjusted for sociodemographic characteristics (i.e. sex, age, and educational or professional qualifications); Model 2, the previous model adjusted for BMI status, lifestyle behaviours (i.e. tobacco use, alcohol consumption, total energy intake, fruit and vegetable consumption, physical activity, and sleep duration), and handgrip strength; and Model 3, the previous model adjusted for loneliness, hearing problems, and the number of medical conditions.

Third, stratified analyses were conducted to identify possible moderators of the study associations. Additionally, the likelihood ratio test was used to explore the possible first-order interactions between nut consumption and all covariates associated with incident all-cause dementia. For this purpose, the cross-products between nut consumption and the following covariate categorizations were individually included in Model 3: age (< 60 vs. ≥ 60 years), sex (male vs. female), educational or professional qualification (higher vs. lower) [28], BMI (obesity, BMI ≥ 30 kg/m2 vs. no obesity, BMI < 30 kg/m2), fruit and vegetable consumption (inadequate, consumers of < 5 portions/day vs. adequate, consumers of ≥ 5 portions/day) [29], physical activity (insufficiently active, < 600 MET-min/week vs. sufficiently active, ≥ 600 MET-min/week) [30], sleep duration (extreme, ≤ 6 and ≥ 9 h/day vs. adequate, 7–8 h/day) [31], handgrip strength (muscle weakness, < 26 kg for men and < 16 kg for women vs. no muscle weakness, ≥ 26 kg for men and ≥ 16 kg for women) [32], loneliness index (lonely vs. not lonely) [33], hearing problems (yes vs. no), and the number of medical conditions (worse health status, ≥ 2 medical conditions vs. better health status, < 2 medical conditions, including angina, anxiety, cancer, depression, diabetes, heart attack, hypertension, multiple sclerosis, osteoporosis, and Parkinson’s disease, among others).

In addition, the risk of developing all-cause dementia was explored in complementary analyses by grouping the exposure variable into three categories [34]: (i) no consumption (reference category), (ii) > 0 to 1 handful of 30 g/day, and (iii) > 1 to 3 or more handfuls of 30 g/day. Furthermore, stratified analyses were conducted according to the mode of nut preparation (i.e. unsalted, salted/roasted, or mixed [unsalted plus salted/roasted]) and dementia subtypes (i.e. Alzheimer’s disease, frontotemporal dementia, or vascular dementia). Finally, complementary analyses were performed excluding participants with all-cause dementia that developed within the first 2 years of follow-up.

All the statistical analyses were performed using IBM SPSS Statistics software (version 28.0; IBM Corp., Armonk, NY, USA). The threshold for statistical significance was set at p < 0.05.

Results

A total of 50,386 participants (mean age 56.5 ± 7.7 years, 49.2% female) were included in the analyses (Fig. 1). Table 1 presents the main baseline characteristics of all participants and according to all-cause dementia status. The mean age was greater among individuals with incident all-cause dementia (63.8 ± 4.8 years) than among those without this condition (56.3 ± 7.7 years). Additionally, in comparison with individuals without all-cause dementia, those with incident all-cause dementia were more likely to have a low level of education (6.5% vs. 17.4%, respectively), extreme sleep duration (27.7% vs. 33.0%, respectively), muscle weakness (5.6% vs. 11.7%, respectively), and hearing problems (25.8% vs. 35.4%, respectively). These characteristics are available separately for men and women in Supplementary Table S5.

Table 1.

Baseline characteristics of the UK Biobank cohort by dementia status

Baseline characteristics Total (n = 50,386) No all-cause dementia (n = 48,964) Incident all-cause dementia (n = 1422)
Women, n (%) 24,806 (49.2) 24,173 (49.4) 633 (44.5)
Age, mean (years) ± SD 56.5 ± 7.7 56.3 ± 7.7 63.8 ± 4.8
Age over 60 years, n (%) 21,092 (41.9) 19,867 (40.6) 1225 (86.1)
Lower educational/professional qualification, n (%) 3446 (6.8) 3198 (6.5) 248 (17.4)
BMI, mean (kg/m2) ± SD 26.7 ± 4.4 26.7 ± 4.4 27.1 ± 4.6
Obesity (BMI ≥ 30.0 kg/m2), n (%) 9,700 (19.3) 9375 (19.1) 325 (22.9)
Current smoking status, n (%) 3575 (7.1) 3472 (7.1) 103 (7.2)
Daily/almost daily alcohol intake, n (%) 12,327 (24.5) 11,956 (24.4) 371 (26.1)
Total energy intake, mean (kcal/d) ± SD 2146.5 ± 631.8 2146.3 ± 629.2 2153.6 ± 716.8
Fruit and vegetable consumption (< 5 portions/day)a, n (%) 21,133 (41.9) 20,599 (42.1) 534 (37.6)
No nut consumption, n (%) 37,959 (75.3) 36,842 (75.2) 1117 (78.6)
Nut consumption, mean (g/day) ± SD 5.8 ± 14.4 5.9 ± 14.3 5.7 ± 16.6
Insufficiently active (< 600 MET-min/week), n (%) 9515 (18.9) 9274 (18.9) 241 (17.0)
Extreme sleep durationb, n (%) 14,051 (27.9) 13,582 (27.7) 469 (33.0)
Muscle weaknessc, n (%) 2894 (5.7) 2758 (5.6) 166 (11.7)
Loneliness, n (%) 2531 (5.0) 2432 (5.0) 99 (7.0)
Hearing problems, n (%) 13,147 (26.1) 12,643 (25.8) 504 (35.4)
Two or more medical conditionsd, n (%) 13,711 (27.2) 13,395 (27.4) 316 (22.2)
Open in a new tab

The values are means ± standard deviations (SD) or n (%)

aNoncompliance with UK National Health Service guidelines on fruit and vegetables [29]

bExtreme sleep duration was defined as ≤ 6 and ≥ 9 h/day [31]

cMuscle weakness was defined as grip strength < 26 kg for men and < 16 kg for women [32]

dSelf-reported medical condition diagnosed by a doctor including cancer and other serious medical conditions or disabilities (e.g. angina, anxiety, depression, diabetes, heart attack, hypertension, multiple sclerosis, osteoporosis, or Parkinson’s disease, detailed in data-coding 6 of UK-B data-field 20,002, Supplementary Table S4)

At baseline, 75.3% of the individuals included in the study reported no nut consumption, with a mean nut consumption of 5.8 ± 14.4 g/day (Table 1). The prospective associations between nut consumption and all-cause dementia are presented in Table 2. The overall incidence of all-cause dementia was 2.8% (n = 1422 new cases), with a mean follow-up of 7.1 years. The minimally adjusted model (Model 1) indicated that daily nut consumption was significantly associated with a reduced risk of all-cause dementia (HR = 0.87; 95% CI, 0.76–0.98) compared with no nut consumption. This protective association remained statistically significant when covariates were added to the adjusted models. Specifically, the fully adjusted analysis (Model 3) revealed a significantly lower incidence of all-cause dementia in those who consumed nuts daily (HR = 0.88; 95% CI, 0.77–0.99).

Table 2.

Prospective associations between nut consumption and all-cause dementia after 7.1 mean years of follow-up

Total, n (incident cases of all-cause dementiaa) Model 1 Model 2 Model 3
Total 50,386 (1422)
No nut consumption 37,959 (1117) 1.00 1.00 1.00
Nut consumptionb 12,427 (305) 0.87 (0.76, 0.98) * 0.87 (0.76, 0.99) * 0.88 (0.77, 0.99) *
Open in a new tab

The values are hazard ratios (95% confidence intervals) for incident all-cause dementia. Bold values indicate statistically significant associations (p < 0.05). Model 1: adjusted for sex (female vs. male), age (< 60 years vs. ≥ 60 years), and educational or professional qualification (high vs. low); Model 2: previous model adjusted for BMI status (obesity vs. no obesity), tobacco use (current vs. never/former), alcohol consumption (daily/almost daily vs. never/occasionally), total energy intake (kcal/day), fruit and vegetable consumption (< 5 vs. ≥ 5 portions/day), physical activity (< 600 vs. ≥ 600 MET-min/week), sleep duration (≤ 6 and ≥ 9 vs. 7–8 h/day), and handgrip strength (< 26 vs. ≥ 26 kg for men and < 16 vs. ≥ 16 kg for women); and Model 3: previous model adjusted for loneliness (lonely vs. not lonely), hearing problems (yes vs. no), and self-reported medical conditions diagnosed by a doctor (≥ 2 medical conditions vs. < 2 medical conditions)

aIncident cases were defined as those participants without dementia at baseline assessment (including the first year of follow-up) and who reported all-cause dementia during the 7.1-year follow-up

bNut consumption was determined as > 0 to 3 or more handfuls/day

No statistically significant interactions between nut consumption and any of the covariates were observed for the association with the risk of all-cause dementia (Fig. 2). While a lower risk of all-cause dementia was observed among nut consumers who were women, older adults, nonsmokers, nondaily alcohol consumers, and those without obesity, extreme sleep duration, muscle weakness, or feelings of loneliness, no significant associations were found for men, middle-aged adults, current smokers, daily alcohol consumers, or individuals with obesity, extreme sleep duration, muscle weakness, or feelings of loneliness (Fig. 2).

Fig. 2.

Fig. 2

Open in a new tab

The associations between nut consumption and no consumption and the risk of all-cause dementia stratified by the covariates of the fully adjusted Cox regression model. The values are hazard ratios (95% confidence intervals) for incident all-cause dementia. Bold values indicate statistically significant associations (p < 0.05). Model 3: adjusted for sociodemographic factors (blue covariates), i.e. sex (female vs. male), age (< 60 years vs. ≥ 60 years), and educational or professional qualification (high vs. low); lifestyle factors (purple covariates), i.e. BMI status (obesity vs. no obesity), tobacco use (current vs. never/former), alcohol consumption (daily/almost daily vs. never/occasionally), total energy intake (kcal/day), fruit and vegetable consumption (< 5 vs. ≥ 5 portions/day), physical activity (< 600 vs. ≥ 600 MET-min/week), sleep duration (≤ 6 and ≥ 9 vs. 7–8 h/day), and handgrip strength (< 26 vs. ≥ 26 kg for men and < 16 vs ≥ 16 kg for women); and health-related factors (pink covariates), i.e. loneliness (lonely vs. not lonely), hearing problems (yes vs. no), and self-reported medical conditions diagnosed by a doctor (≥ 2 medical conditions vs. < 2 medical conditions)

When different categories of nut consumption were examined, a lower incidence of all-cause dementia was observed in middle-aged and older adults who consumed > 0 to 1 handful of 30 g/day of nuts than in their counterparts who did not consume nuts (Supplementary Table S6). Stratified analyses revealed that the consumption of unsalted nuts was the sole mode of nut preparation associated with a reduced risk of all-cause dementia (Supplementary Table S7). Furthermore, the results of additional complementary analyses were no longer significant when considering dementia subtypes (i.e. Alzheimer’s disease, frontotemporal dementia, or vascular dementia) as separate outcomes (Supplementary Table S8). Finally, after excluding participants who developed all-cause dementia within the first year or first 2 years of follow-up, the protective role of nut consumption remained significant (Supplementary Table S9).

Discussion

This cohort study analyzed the association between nut consumption and the incidence of all-cause dementia in a large sample of middle-aged and older UK adults. The main finding was that daily nut consumption was associated with a 12% lower risk of all-cause dementia than no nut consumption after a mean follow-up of 7.1 years, regardless of adjustment for sociodemographic, lifestyle, hearing problems, self-rated health, and the number of chronic diseases. Specifically, a nut consumption of up to 1 handful of 30 g/day was associated with a 16% lower incidence of all-cause dementia. Furthermore, although no statistically significant interactions were observed between nut consumption and any of the covariates included in the hazard regression models, in our results, the potential benefits of nut consumption for preventing major neurocognitive disorders were significant only in women, adults aged 60 years and older, and those without risk factors such as obesity, tobacco use, daily alcohol consumption, extreme sleep duration, muscle weakness, and feelings of loneliness. Finally, stratified analyses revealed that the consumption of unsalted nuts was associated with a 17% lower risk of all-cause dementia in adults.

Previous systematic reviews and meta-analyses have supported significant associations between increased adherence to healthy diets and a reduced risk of dementia [35, 36]. One of the most extensively studied healthy dietary patterns is the Mediterranean diet, which is characterized by the consumption of plant-based foods, including nuts [37]. Nevertheless, the evidence on the role of nuts in the prevention of dementia remains inconclusive [10]. A study examined the preventive role of nut consumption on the incidence of dementia based on data from three cohorts of more than 8000 middle-aged and older adults and found that nut consumption (≥ 6 vs. < 1 serving/week) contributed to the protective role of high adherence to the Mediterranean dietary matrix in lowering the risk of dementia [8]. Consistently but extending beyond the adherence to a healthy or unhealthy dietary pattern (i.e. defined as < 5 vs. ≥ 5 portions/day of fruits and vegetables) [29], our findings showed a significant association between nut consumption (> 0 to 3 or more handfuls of 30 g/day) and a reduced risk of all-cause dementia in the fully multivariable-adjusted model.

Furthermore, our findings are consistent with those of previous studies that evaluated the association between nut consumption and cognitive function in middle-aged and older individuals. In a cohort of US women over 70 years of age, greater nut consumption (≥ 5 servings/week) was associated with better cognitive status after more than 6 years of follow-up [16]. In this cohort study, the mean difference in cognitive status between nut consumers and nonconsumers was equivalent to approximately 2 years of cognitive aging [16]. In addition, a crossover RCT was performed in apparently healthy Dutch adults (mean age 65 years) who received a 16-week nut intervention (i.e. 60 g/day of mixed nuts, including walnuts, pistachios, cashews, and hazelnuts) [14]. Compared to the control period without nuts, this intervention resulted in significant improvements in whole-brain cerebral blood flow and cognitive performance related to the memory domain [14]. Some authors have proposed a dose‒response relationship between nut consumption and a delay in cognitive impairment. In a cohort of 6630 Spanish adults aged 55–75 years, Ni et al. [38] reported that individuals who consumed greater amounts of nuts (i.e. ≥ 3 to < 7 and ≥ 7 servings/week) showed more favourable changes in general cognitive performance over a 2-year follow-up period than did those who consumed < 1 serving/week.

In our study, we explored the risk of all-cause dementia in middle-aged and older UK adults considering different categories of nut consumption. Our findings indicate a lower incidence of all-cause dementia in those who consumed up to 1 handful of 30 g/day of nuts. However, no association was observed for the highest nut consumers (i.e. those who consumed > 1 to 3 or more handfuls of 30 g/day), probably due to a limited statistical power. Additionally, subgroup analyses revealed that the consumption of unsalted nuts, but not other forms of nut preparation, was associated with a lower risk of all-cause dementia. These findings suggest that processed nuts may not exhibit the same beneficial effects as unsalted nuts in reducing cognitive impairment in adults.

The following main mechanisms have been proposed to explain cognitive impairment: reduced blood flow, which may contribute to the development of atherosclerosis; mitochondrial dysfunction, which results in increased oxidative stress in the brain; and inflammation, which leads to neurodegeneration and is involved in the aging process [39]. Thus, the enhancement of these mechanisms may elucidate the potential neuroprotective association between healthy dietary patterns and dementia. Current evidence suggests that the consumption of nuts may improve the blood lipid profile [40], endothelial function [41], blood pressure [42], oxidative stress, and inflammation [41]. These benefits may be attributed to the rich nutrient profile of the nuts and their content of bioactive compounds, including high concentrations of unsaturated fatty acids (e.g. α-linolenic acids) and antioxidant phytochemicals (e.g. carotenoids, polyphenols, phytosterols, and vitamin E) [13, 43, 44]. Indeed, a high intake of mono- and polyunsaturated fatty acids has been demonstrated to be a protective factor against dementia [45, 46]. Moreover, vitamin E may also play a neuroprotective role [47] and has been associated with a reduced risk of Alzheimer’s disease in advanced age [48]. Finally, the high-quality amino acids (e.g. L-arginine) and optimal mineral composition (e.g. magnesium) found in nuts may provide neuroprotective benefits through the main mechanisms between nuts and cognitive function [13, 15, 49].

Some limitations of the study should be noted. First, the UK-B is not representative of the sample population, and there is evidence of healthy volunteer selection bias [24], which could affect the magnitude and generalizability of the findings. Second, the data on nut consumption were self-reported. In addition, nut consumption was assessed on a daily basis, which may have resulted in an underestimation of cases of low or moderate weekly consumption. Third, establishing a definitive causal relationship between dietary habits and the risk of developing dementia is difficult because emerging cognitive impairment may affect participants’ dietary and behavioural choices. To reduce the potential confounding effect of reverse causality, in addition to including individuals without dementia at baseline, we performed a complementary analysis excluding participants who developed all-cause dementia within the first year and first 2 years of follow-up. Fourth, although our analyses were adjusted for relevant covariates, residual confounding cannot be completely ruled out since potentially modifiable (e.g. traumatic brain injury) or genetic (e.g. apolipoprotein E gene variants) risk factors for dementia were not available in our UK-B database.

The strengths of this study include its prospective design, large sample size, and relatively long follow-up with a mean of 7.1 years, excluding participants with all-cause dementia within the first year of follow-up. Although some dementias have a long preclinical phase before diagnosis, previously proposed diagnostic criteria for probable dementia, such as Alzheimer’s disease, suggest a minimum symptom duration of 6 months [50]. Additionally, the study employed a previously validated dietary questionnaire to assess nut consumption during the previous day on multiple occasions. Moreover, to the best of our knowledge, this is the first study to provide evidence on potential moderators between nut consumption and the risk of developing all-cause dementia according to sociodemographic, lifestyle, hearing problems, self-rated health, and the number of chronic diseases. Finally, we were able to perform complementary analyses according to the mode of nut preparation and dementia subtypes.

Conclusions

In this cohort study with repeated measures of diet and dementia, UK adults who consumed nuts daily had a reduced risk of all-cause dementia compared with nonconsumers after 7.1 years of follow-up, regardless of adjustment for sociodemographic, lifestyle, hearing problems, self-rated health, and the number of chronic diseases. In addition, benefits in all-cause dementia prevention were observed specifically in adults who consumed > 0 to 1 handful of 30 g/day (16% lower risk) or unsalted nuts (17% lower risk). While significant associations were found only in women, older adults, nonsmokers, nondaily alcohol consumers, and individuals without obesity, extreme sleep duration, muscle weakness, or feelings of loneliness, there were no significant interactions between nut consumption and factors such as sex, age, BMI, tobacco use, alcohol consumption, sleep duration, handgrip strength, and loneliness for the risk of all-cause dementia. Future long-term follow-up studies, both observational and clinical trials, should evaluate the efficacy of nut consumption as a strategy for preventing dementia in adults.

Supplementary information

Below is the link to the electronic supplementary material.

Supplementary file1 (DOCX 112 KB) (112.8KB, docx)

Author contribution

B.B.-P: conceptualization, formal analysis, methodology, visualization, writing—original draft, writing—review and editing. V.D.-G: data curation, writing—review and editing. N.B: writing—original draft, writing—review and editing. A.O: methodology, visualization, writing—review and editing. E.J.-L.: data curation, writing—review and editing. V.M.-V: project administration, writing—review and editing. A.E.M: conceptualization, funding acquisition, methodology, project administration, visualization, writing—original draft, supervision. All authors approved the final version of this manuscript.

Funding

he research group leading this study was awarded on the call for the creation of Health Outcomes-Oriented Cooperative Research Networks (RD21/0016/0025) from the Ministry of Economy and Competitiveness of Spain and is supported by the Carlos III Health Institute, FEDER funds and the European Union’s NextGenerationEU initiative. The present study is a part of the “Nuts4Brain Project: The relationship between nut consumption and mental health outcomes throughout adulthood” (grant number PI21/01898), which is funded by the Ministry of Science and Innovation of Spain, the European Union NextGenerationEU program, the Instituto de Salud Carlos III in Spain, and the FEDER Funds. This work was also supported by supported by grants from the University of Castilla-La Mancha, Spain, co-financed by the European Social Fund (2020-PREDUCLM-16746) and the National Agency for Research and Innovation, Uruguay (POS_EXT_2023 _1_175630). The funders played no role in the study design, the data collection or analysis, the decision to publish, or the preparation of the manuscript.

Data availability

This research was conducted using the UK Biobank Resource under Application Number 72061. The data supporting this study’s findings are available from the UK-B website (http://www.ukbiobank.ac.uk). Restrictions apply to the availability of these data, which were used under license for the current study (Application Reference Number: 72061. Last dataset update: May 5, 2023; last update date for withdrawal of participants: November 15, 2023; statistical analyses performed between November 15, 2023 and February 15, 2024). The data described in the manuscript and analytic code will be made available upon request pending approval by the authors and the UK-B team.

Declarations

Ethics approval and consent to participate

The UK-B project was approved by the North‒West Multicentre Research Ethics Committee (Ref: 16/NW/0274) in accordance with the principles of the Declaration of Helsinki. All participants provided signed consent forms. Details of the study design, method, variables, and ethics governance/framework are available on the UK-B website (http://www.ukbiobank.ac.uk).

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.

References

  • 1.Gale SA, Acar D, Daffner KR. Dementia. Am J Med. 2018;131(10):1161–9. 10.1016/j.amjmed.2018.01.022. [DOI] [PubMed] [Google Scholar]
  • 2.Institute of Health Metrics and Evaluation. Global Health Data Exchange (GHDx) 2019. Washington, D.C.: University of Washington; 2022. Available from: https://vizhub.healthdata.org/gbd-results/. Accessed 8 Apr 2024.
  • 3.Lancet T. Dementia burden coming into focus. Lancet. 2017;390(10113):2606. 10.1016/S0140-6736(17)33304-4. [DOI] [PubMed] [Google Scholar]
  • 4.Gerlach LB, Kales HC. Pharmacological management of neuropsychiatric symptoms of dementia. Curr Treat Options Psychiatry. 2020;7(4):489–507. 10.1007/s40501-020-00233-9. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 5.Livingston G, Huntley J, Sommerlad A, Ames D, Ballard C, Banerjee S, et al. Dementia prevention, intervention, and care: 2020 report of the Lancet Commission. Lancet. 2020;396(10248):413–46. 10.1016/S0140-6736(20)30367-6. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 6.Scarmeas N, Anastasiou CA, Yannakoulia M. Nutrition and prevention of cognitive impairment. Lancet Neurol. 2018;17(11):1006–15. 10.1016/S1474-4422(18)30338-7. [DOI] [PubMed] [Google Scholar]
  • 7.Tangney CC, Kwasny MJ, Li H, Wilson RS, Evans DA, Morris MC. Am J Clin Nutr. 2011;93(3):601–7. 10.3945/ajcn.110.007369. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 8.Chen H, Dhana K, Huang Y, Huang L, Tao Y, Liu X, et al. Association of the Mediterranean dietary approaches to stop hypertension intervention for neurodegenerative delay (MIND) diet with the risk of dementia. JAMA Psychiat. 2023;80(6):630–8. 10.1001/jamapsychiatry.2023.0800. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 9.Petersson SD, Philippou E. Mediterranean diet, cognitive function, and dementia: a systematic review of the evidence. Adv Nutr. 2016;7(5):889–904. 10.3945/an.116.012138. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 10.Theodore LE, Kellow NJ, Mcneil EA, Close EO, Coad EG, Cardoso BR. Nut consumption for cognitive performance: a systematic review. Adv Nutr. 2021;12(3):777–92. 10.1093/advances/nmaa153. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 11.Fernández-Rodríguez R, Ortolá R, Martínez-Vizcaíno V, Bizzozero-Peroni B, Rodríguez-Artalejo F, García-Esquinas E, et al. Nut consumption and depression: cross-sectional and longitudinal analyses in two cohorts of older adults. J Nutr Health Aging. 2023;27(6):448–56. 10.1007/s12603-023-1927-8. [DOI] [PubMed] [Google Scholar]
  • 12.George ES, Daly RM, Tey SL, Brown R, Wong THT, Tan SY. Perspective: is it time to expand research on “nuts” to include “seeds”? Justifications and key considerations. Adv Nutr. 2022;13(4):1016–27. 10.1093/advances/nmac028. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 13.Ros E, Singh A, O’Keefe JH. Nuts: natural pleiotropic nutraceuticals. Nutrients. 2021;13(9):3269. 10.3390/nu13093269. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 14.Nijssen KMR, Mensink RP, Plat J, Joris PJ. Longer-term mixed nut consumption improves brain vascular function and memory: a randomized, controlled crossover trial in older adults. Clin Nutr. 2023;42(7):1067–75. 10.1016/j.clnu.2023.05.025. [DOI] [PubMed] [Google Scholar]
  • 15.Gorji N, Moeini R, Memariani Z. Almond, hazelnut and walnut, three nuts for neuroprotection in Alzheimer’s disease: a neuropharmacological review of their bioactive constituents. Pharmacol Res. 2018;129:115–27. 10.1016/j.phrs.2017.12.003. [DOI] [PubMed] [Google Scholar]
  • 16.O’Brien J, Okereke O, Devore E, Rosner B, Breteler M, Grodstein F. Long-term intake of nuts in relation to cognitive function in older women. J Nutr Health Aging. 2014;18(5):496–502. 10.1007/s12603-014-0014-6. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 17.Bishop NJ, Zuniga KE. Investigating walnut consumption and cognitive trajectories in a representative sample of older US adults. Public Health Nutr. 2021;24(7):1741–52. 10.1017/S1368980020001287. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 18.Jiang Y-W, Sheng L-T, Feng L, Pan A, Koh W-P. Consumption of dietary nuts in midlife and risk of cognitive impairment in late-life: the Singapore Chinese Health Study. Age Ageing. 2021;50(4):1215–21. 10.1093/ageing/afaa267. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 19.Li F, Jiang W, Wang J, Zhang T, Gu X, Zhai Y, et al. Beneficial effects of nut consumption on cognitive function among elderly: findings from a 6-year cohort study. Front Aging Neurosci 2022;14. 10.3389/fnagi.2022.816443 [DOI] [PMC free article] [PubMed]
  • 20.Barbour JA, Howe PRC, Buckley JD, Bryan J, Coates AM. Cerebrovascular and cognitive benefits of high-oleic peanut consumption in healthy overweight middle-aged adults. Nutr Neurosci. 2017;20(10):555–62. 10.1080/1028415X.2016.1204744. [DOI] [PubMed] [Google Scholar]
  • 21.Barnes LL, Dhana K, Liu X, Carey VJ, Ventrelle J, Johnson K, et al. Trial of the MIND diet for prevention of cognitive decline in older persons. N Engl J Med. 2023;389(7):602–11. 10.1056/NEJMoa2302368. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 22.Sudlow C, Gallacher J, Allen N, Beral V, Burton P, Danesh J, et al. UK biobank: an open access resource for identifying the causes of a wide range of complex diseases of middle and old age. PLoS Med. 2015;12(3):1–10. 10.1371/journal.pmed.1001779. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 23.von Elm E, Altman DG, Egger M, Pocock SJ, Gøtzsche PC, Vandenbroucke JP. The Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) statement: guidelines for reporting observational studies. J Clin Epidemiol. 2008;61(4):344–9. 10.1016/j.jclinepi.2007.11.008. [DOI] [PubMed] [Google Scholar]
  • 24.Fry A, Littlejohns TJ, Sudlow C, Doherty N, Adamska L, Sprosen T, et al. Comparison of sociodemographic and health-related characteristics of UK Biobank participants with those of the general population. Am J Epidemiol. 2017;186(9):1026–34. 10.1093/aje/kwx246. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 25.Greenwood DC, Hardie LJ, Frost GS, Alwan NA, Bradbury KE, Carter M, et al. Validation of the Oxford WebQ online 24-hour dietary questionnaire using biomarkers. Am J Epidemiol. 2019;188(10):1858–67. 10.1093/aje/kwz165. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 26.Perez-Cornago A, Pollard Z, Young H, van Uden M, Andrews C, Piernas C, et al. Description of the updated nutrition calculation of the Oxford WebQ questionnaire and comparison with the previous version among 207,144 participants in UK Biobank. Eur J Nutr. 2021;60(7):4019–30. 10.1007/s00394-021-02558-4. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 27.Wilkinson T, Schnier C, Bush K, Rannikmäe K, Henshall DE, Lerpiniere C, et al. Identifying dementia outcomes in UK Biobank: a validation study of primary care, hospital admissions and mortality data. Eur J Epidemiol. 2019;34(6):557. 10.1007/s10654-019-00499-1. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 28.Yip JLY, Muthy Z, Peto T, Lotery A, Foster PJ, Patel P. Socioeconomic risk factors and age-related macular degeneration in the UK Biobank study. BMJ Open Ophthalmol. 2021;6(1):e000585. 10.1136/bmjophth-2020-000585. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 29.Chudasama YV, Khunti K, Gillies CL, Dhalwani NN, Davies MJ, Yates T, et al. Healthy lifestyle and life expectancy in people with multimorbidity in the UK Biobank: a longitudinal cohort study. PLoS Med. 2020;17(9):e1003332. 10.1371/journal.pmed.1003332. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 30.Chudasama YV, Khunti KK, Zaccardi F, Rowlands AV, Yates T, Gillies CL, et al. Physical activity, multimorbidity, and life expectancy: a UK Biobank longitudinal study. BMC Med. 2019;17(1):1–13. 10.1186/s12916-019-1339-0. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 31.Fan M, Sun D, Zhou T, Heianza Y, Lv J, Li L, et al. Sleep patterns, genetic susceptibility, and incident cardiovascular disease: a prospective study of 385 292 UK biobank participants. Eur Heart J. 2020;41(11):1182–9. 10.1093/eurheartj/ehz849. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 32.Studenski S, Peters K, Alley D, Cawthon P, McLean R, Harris, TBFerrucci L, et al. The FNIH sarcopenia project: rationale, study description, conference recommendations, and final estimates. J Gerontol A Biol Sci Med Sci. 2014;69(5):547–58. 10.1093/gerona/glu010. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 33.Elovainio M, Hakulinen C, Pulkki-Råback L, Virtanen M, Josefsson K, Jokela M, et al. Contribution of risk factors to excess mortality in isolated and lonely individuals: an analysis of data from the UK Biobank cohort study. Lancet Public Health. 2017;2(6):e260–6. 10.1016/S2468-2667(17)30075-0. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 34.Bizzozero-Peroni B, Fernández-Rodríguez R, Martínez-Vizcaíno V, Garrido-Miguel M, Medrano M, Jiménez-López E, et al. Nut consumption is associated with a lower risk of depression in adults: a prospective analysis with data from the UK Biobank cohort. Clin Nutr. 2023;42(9):1728–36. 10.1016/j.clnu.2023.07.020. [DOI] [PubMed] [Google Scholar]
  • 35.Liu Y-H, Gao X, Na M, Kris-Etherton PM, Mitchell DC, Jensen GL. Dietary pattern, diet quality, and dementia: a systematic review and meta-analysis of prospective cohort studies. J Alzheimers Disease. 2020;78:151–68. 10.3233/JAD-200499. [DOI] [PubMed] [Google Scholar]
  • 36.Fu J, Tan L-J, Lee JE, Shin S. Association between the mediterranean diet and cognitive health among healthy adults: a systematic review and meta-analysis. Front Nutr. 2022;9. 10.3389/fnut.2022.946361. [DOI] [PMC free article] [PubMed]
  • 37.Willett WC, Sacks F, Trichopoulou A, Drescher G, Ferro-Luzzi A, Helsing E, et al. Mediterranean diet pyramid: a cultural model for healthy eating. Am J Clin Nutr. 1995;61(6):1402S-1406S. 10.1093/ajcn/61.6.1402S. [DOI] [PubMed] [Google Scholar]
  • 38.Ni J, Nishi SK, Babio N, Ros E, Basterra-Gortari FJ, Corella D, et al. Higher versus lower nut consumption and changes in cognitive performance over two years in a population at risk of cognitive decline: a cohort study. Am J Clin Nutr. 2023;118(2):360–8. 10.1016/j.ajcnut.2023.05.032. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 39.Yankner BA, Lu T, Loerch P. The aging brain. Annu Rev Pathol. 2008;3:41–66. 10.1146/annurev.pathmechdis.2.010506.092044.  [DOI] [PubMed] [Google Scholar]
  • 40.Gunathilake M, Van NTH, Kim J. Effects of nut consumption on blood lipid profile: a meta-analysis of randomized controlled trials. Nutr Metab Cardiovasc Dis. 2022;32(3):537–49. 10.1016/j.numecd.2022.01.006. [DOI] [PubMed] [Google Scholar]
  • 41.Neale EP, Tapsell LC, Guan V, Batterham MJ. The effect of nut consumption on markers of inflammation and endothelial function: a systematic review and meta-analysis of randomised controlled trials. BMJ Open. 2017;7(11):e016863. 10.1136/bmjopen-2017-016863. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 42.Mohammadifard N, Salehi-Abargouei A, Salas-Salvadó J, Guasch-Ferré M, Humphries K, Sarrafzadegan N. The effect of tree nut, peanut, and soy nut consumption on blood pressure: a systematic review and meta-analysis of randomized controlled clinical trials. Am J Clin Nutr. 2015;101(5):966–82. 10.3945/ajcn.114.091595. [DOI] [PubMed] [Google Scholar]
  • 43.Rusu ME, Mocan A, Ferreira ICFR, Popa D-S. Health benefits of nut consumption in middle-aged and elderly population. Antioxidants. 2019;8(8). 10.3390/antiox8080302. [DOI] [PMC free article] [PubMed]
  • 44.López-Uriarte P, Bulló M, Casas-Agustench P, Babio N, Salas-Salvadó J. Nuts and oxidation: a systematic review. Nutr Rev. 2009;67(9):497–508. 10.1111/j.1753-4887.2009.00223.x. [DOI] [PubMed] [Google Scholar]
  • 45.Morris MC, Evans DA, Bienias JL, Tangney CC, Bennett DA, Aggarwal N, et al. Dietary fats and the risk of incident Alzheimer disease. Arch Neurol. 2003;60(2):194–200. 10.1001/archneur.60.2.194. [DOI] [PubMed] [Google Scholar]
  • 46.Solfrizzi V, Frisardi V, Capurso C, D’Introno A, Colacicco AM, Vendemiale G, et al. Dietary fatty acids in dementia and predementia syndromes: epidemiological evidence and possible underlying mechanisms. Ageing Res Rev. 2010;9(2):184–99. 10.1016/j.arr.2009.07.005. [DOI] [PubMed] [Google Scholar]
  • 47.Khanna S, Parinandi NL, Kotha SR, Roy S, Rink C, Bibus D, et al. Nanomolar vitamin E α-tocotrienol inhibits glutamate-induced activation of phospholipase A2 and causes neuroprotection. J Neurochem. 2010;112(5):1249–60. 10.1111/j.1471-4159.2009.06550.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 48.Mangialasche F, Kivipelto M, Mecocci P, Rizzuto D, Palmer K, Winblad B, et al. High plasma levels of vitamin E forms and reduced Alzheimer’s disease risk in advanced age. J Alzheimers Dis. 2010;20:1029–37. 10.3233/JAD-2010-091450. [DOI] [PubMed] [Google Scholar]
  • 49.Nishi SK, Sala-Vila A, Julvez J, Sabaté J, Ros E. Impact of nut consumption on cognition across the lifespan. Nutrients. 2023;15(4). 10.3390/nu15041000. [DOI] [PMC free article] [PubMed]
  • 50.Dubois B, Feldman HH, Jacova C, Dekosky ST, Barberger-Gateau P, Cummings J, et al. Research criteria for the diagnosis of Alzheimer’s disease: revising the NINCDS-ADRDA criteria. Lancet Neurol. 2007;6(8):734–46. 10.1016/S1474-4422(07)70178-3. [DOI] [PubMed] [Google Scholar]

Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

Supplementary file1 (DOCX 112 KB) (112.8KB, docx)

Data Availability Statement

This research was conducted using the UK Biobank Resource under Application Number 72061. The data supporting this study’s findings are available from the UK-B website (http://www.ukbiobank.ac.uk). Restrictions apply to the availability of these data, which were used under license for the current study (Application Reference Number: 72061. Last dataset update: May 5, 2023; last update date for withdrawal of participants: November 15, 2023; statistical analyses performed between November 15, 2023 and February 15, 2024). The data described in the manuscript and analytic code will be made available upon request pending approval by the authors and the UK-B team.

Articles from GeroScience are provided here courtesy of Springer

RESOURCES