Social Health and Cognitive Change in Old Age: Role of Brain Reserve.

OBJECTIVE: Individual aspects of social health (SH; eg, network, engagement, support) have been linked to cognitive health. However, their combined effect and the role of the structural properties of the brain (brain reserve [BR]) remain unclear. We investigated the interplay of SH and BR on cognitive change in older adults. METHODS: Within the Swedish National Study on Aging and Care-Kungsholmen, 368 dementia-free adults aged ≥60 years with baseline brain magnetic resonance imaging were followed over 12 years to assess cognitive change. A measure of global cognition was computed at each of the 5 waves of assessment by averaging domain-specific Z scores for episodic memory, perceptual speed, semantic memory, and letter and category fluency. An SH composite score was computed at baseline by combining leisure activities and social network. BR was proxied by total brain tissue volume (TBTV). Linear mixed models (adjusted for sociodemographic, vascular, and genetic factors) were used to estimate cognitive trajectories in relation to SH and TBTV. Interaction analysis and stratification were used to examine the interplay between SH and TBTV. RESULTS: Moderate-good SH (n = 245; vs poor, ß-slope = 0.01, 95% confidence interval [CI] = 0.002-0.02, p = 0.018) and moderate-to-large TBTV (n = 245; vs small, ß-slope = 0.03, 95% CI = 0.02-0.04, p < 0.001) were separately associated with slower cognitive decline. In stratified analysis, moderate-good SH was associated with higher cognitive levels (but not change) only in participants with moderate-to-large TBTV (ß-intercept = 0.21, 95% CI = 0.06-0.37, p < 0.01; interaction SH * TBTV, p < 0.05). INTERPRETATION: Our findings highlight the interplay between SH and BR that likely unfolds throughout the entire life course to shape old-age cognitive outcomes. ANN NEUROL 2023;93:844-855.

The Association between Education and Cognitive Performance Varies at Different Levels of Cognitive Performance: A Quantile Regression Approach.

INTRODUCTION: Educational differences in cognitive performance among older adults are well documented. Studies that explore this association typically estimate a single average effect of education on cognitive performance. We argue that the processes that contribute to the association between education and cognitive performance are unlikely to have equal effects at all levels of cognitive performance. In this study, we employ an analytical approach that enables us to go beyond averages to examine the association between education and five measures of global and domain-specific cognitive performance across the outcome distributions. METHODS: This cross-sectional study included 1,780 older adults aged 58-68 years from the Longitudinal Aging Study Amsterdam. Conditional quantile regression was used to examine variation across the outcome distribution. Cognitive outcomes included Mini-Mental State Examination (MMSE) score, crystallized intelligence, information processing speed, episodic memory, and a composite score of global cognitive performance. RESULTS: The results showed that the associations between education and different cognitive measures varied across the outcome distributions. Specifically, we found that education had a stronger association with crystallized intelligence, MMSE, and a composite cognitive performance measure in the lower tail of performance distributions. The associations between education and information processing speed and episodic memory were uniform across the outcome distributions. CONCLUSION: Larger associations between education and some domains of cognitive performance in the lower tail of the performance distributions imply that inequalities are primarily generated among individuals with lower performance rather than among average and high performers. Additionally, the varying associations across some of the outcome distributions indicate that estimating a single average effect through standard regression methods may overlook variations in cognitive performance between educational groups. Future studies should consider heterogeneity across the outcome distribution.

Cardiometabolic multimorbidity and incident dementia: the Swedish twin registry.

AIMS: Cardiometabolic diseases (CMDs), including diabetes, heart disease, and stroke, are established risk factors for dementia, but their combined impact has been investigated only recently. This study aimed to examine the association between mid- and late-life cardiometabolic multimorbidity and dementia and explore the role of genetic background in this association. METHODS AND RESULTS: Within the Swedish Twin Registry, 17 913 dementia-free individuals aged ≥60 were followed for 18 years. CMDs [including age of onset in mid (60) or late (≥60) life] and dementia were ascertained from medical records. Cardiometabolic multimorbidity was defined as having ≥2 CMDs. Cox regression was used to estimate the CMD-dementia association in (i) a classical cohort study design and (ii) a co-twin study design involving 356 monozygotic and dizygotic pairs. By comparing the strength of the association in the two designs, the contribution of genetic background was estimated. At baseline, 3,312 (18.5%) participants had 1 CMD and 839 (4.7%) had ≥2 CMDs. Over the follow-up period, 3,020 participants developed dementia. In the classic cohort design, the hazard ratio (95% confidence interval) of dementia was 1.42 (1.27-1.58) for 1 CMD and 2.10 (1.73-2.57) for ≥2 CMDs. Dementia risk was stronger with mid-life as opposed to late-life CMDs. In the co-twin design, the CMD-dementia association was attenuated among monozygotic [0.99 (0.50-1.98)] but not dizygotic [1.55 (1.15-2.09)] twins, suggesting that the association was in part due to genetic factors common to both CMDs and dementia. CONCLUSION: Cardiometabolic multimorbidity, particularly in mid-life, is associated with an increased risk of dementia. Genetic background may underpin this association.

Cognitive reserve, cortisol, and Alzheimer's disease biomarkers: A memory clinic study.

INTRODUCTION: Cognitive reserve might mitigate the risk of Alzheimer's dementia among memory clinic patients. No study has examined the potential modifying role of stress on this relation. METHODS: We examined cross-sectional associations of the cognitive reserve index (CRI; education, occupational complexity, physical and leisure activities, and social health) with cognitive performance and AD-related biomarkers among 113 memory clinic patients. The longitudinal association between CRI and cognition over a 3-year follow-up was assessed. We examined whether associations were influenced by perceived stress and five measures of diurnal salivary cortisol. RESULTS: Higher CRI scores were associated with better cognition. Adjusting for cortisol measures reduced the beneficial association of CRI on cognition. A higher CRI score was associated with better working memory in individuals with higher (favorable) cortisol AM/PM ratio, but not among individuals with low cortisol AM/PM ratio. No association was found between CRI and AD-related biomarkers. DISCUSSION: Physiological stress reduces the neurocognitive benefits of cognitive reserve among memory clinic patients. HIGHLIGHTS: Physiological stress may reduce the neurocognitive benefits accrued from cognitively stimulating and enriching life experiences (cognitive reserve [CR]) in memory clinic patients. Cortisol awakening response modified the relation between CR and P-tau181, a marker of Alzheimer's disease (AD). Effective stress management techniques for AD and related dementia prevention are warranted.

Social Health and Change in Cognitive Capability among Older Adults: Findings from Four European Longitudinal Studies.

INTRODUCTION: In this study, we examine whether social health markers measured at baseline are associated with differences in cognitive capability and the rate of cognitive decline over an 11-to-18-year period among older adults and compare results across studies. METHODS: We applied an integrated data analysis approach to 16,858 participants (mean age 65 years; 56% female) from the National Survey for Health and Development (NSHD), the English Longitudinal Study of Aging (ELSA), the Swedish National Study on Aging and Care in Kungsholmen (SNAC-K), and the Rotterdam Study. We used multilevel models to examine social health in relation to cognitive capability and the rate of cognitive decline. RESULTS: Pooled estimates show distinct relationships between markers of social health and cognitive domains, e.g., a large network size (≥6 people vs. none) was associated with higher executive function (0.17 standard deviation [SD] [95% CI: 0.00, 0.34], I2 = 27%) but not with memory (0.08 SD [95% CI: -0.02, 0.18], I2 = 19%). We also observed pooled associations between being married or cohabiting, having a large network size, and participating in social activities with slower decline in cognitive capability. However, estimates were close to zero, e.g., 0.01 SD/year (95% CI: 0.01, 0.02) I2 = 19% for marital status and executive function. There were clear study-specific differences: results for average processing speed were the most homogenous, and results for average memory were the most heterogeneous. CONCLUSION: Overall, markers of good social health have a positive association with cognitive capability. However, we found differential associations between specific markers of social health and cognitive domains and differences between studies. These findings highlight the importance of examining between-study differences and considering the context specificity of findings in developing and deploying interventions.

Associations between dietary patterns and dementia-related neuroimaging markers.

BACKGROUND: The exploration of associations between dietary patterns and dementia-related neuroimaging markers can provide insights on food combinations that may impact brain integrity. METHODS: Data were derived from the Swedish Gothenburg H70 Birth Cohort Study (n = 610). Three dietary patterns were obtained using principal component analysis. Magnetic resonance imaging markers included cortical thickness, an Alzheimer's disease (AD) signature score, small vessel disease, and white matter microstructural integrity. Adjusted linear/ordinal regression analyses were performed. RESULTS: A high-protein and alcohol dietary pattern was negatively associated with cortical thickness in the whole brain (Beta: -0.011; 95% confidence interval [CI]: -0.018 to -0.003), and with an Alzheimer's disease cortical thickness signature score (Beta: -0.013; 95% CI: -0.024 to -0.001). A positive association was found between a Mediterranean-like dietary pattern and white matter microstructural integrity (Beta: 0.078; 95% CI: 0.002-0.154). No associations were found with a Western-like dietary pattern. DISCUSSION: Dietary patterns may impact brain integrity through neurodegenerative and vascular pathways. HIGHLIGHTS: Certain dietary patterns were associated with dementia-related neuroimaging markers. A Mediterranean dietary pattern was positively associated with white matter microstructure. A high-protein and alcohol pattern was negatively associated with cortical thickness.

Trajectories of cognitive decline and dementia development: A 12-year longitudinal study.

INTRODUCTION: Mapping the preclinical dementia phase is important for early detection and evaluation of interventions. We assessed the trajectories of cognitive decline in preclinical dementia over 12 years and investigated whether being a fast decliner across 6 years is associated with increased risk of dementia the following 6 years. METHODS: Rates of cognitive decline were determined using mixed-effects models for 1646 participants from the Swedish National Study on Aging and Care in Kungsholmen (SNAC-K) cohort. Cox regression was used to assess the future likelihood of dementia for fast decliners (declining ≥1.5 standard deviations [SDs] faster than the age-specific rates). RESULTS: Participants in a preclinical phase of dementia showed increased rates of decline in all cognitive tests compared to the no-dementia group, particularly closer (0-6 years) to diagnosis. Participants declining fast in three or more cognitive tests 12-6 years before diagnosis demonstrated a high risk of dementia 6 years later (hazard ratio [HR] 3.90, 95% confidence interval [CI] 2.28-6.69). DISCUSSION: Being a fast decliner is linked to increased risk of future dementia.

Cardiometabolic multimorbidity accelerates cognitive decline and dementia progression.

INTRODUCTION: Cardiometabolic diseases (CMDs) have been individually associated with adverse cognitive outcomes, but their combined effect has not been investigated. METHODS: A total of 2577 dementia-free participants 60 years of age or older were followed for 12 years to observe changes in cognitive function and to detect incident cognitive impairment, no dementia (CIND) and dementia. CMDs (including type 2 diabetes, heart disease, and stroke) were assessed at baseline through medical records and clinical examinations. Cardiometabolic multimorbidity was defined as the presence of two or more CMDs. Data were analyzed using multi-adjusted linear mixed-effects models, Cox regression, and Laplace regression. RESULTS: CMD multimorbidity was associated with cognitive decline, CIND (hazard ratio [HR] 1.73; 95% confidence interval CI 1.23 to 2.44), and its progression to dementia (HR 1.86; 95% CI 1.17 to 2.97). CMD multimorbidity accelerated the onset of CIND by 2.3 years and dementia by 1.8 years. CONCLUSIONS: CMD multimorbidity accelerates cognitive decline and increases the risk of both CIND and its conversion to dementia. HIGHLIGHTS: We explored the combined impact of cardiometabolic diseases (CMDs) on cognition. An increasing number of CMDs dose-dependently accelerated cognitive decline. CMD multimorbidity increased the risk of both cognitive impairment and dementia. Co-morbid CMDs could be ideal targets for interventions to protect cognitive health.

Individual changes in anthropometric measures after age 60 years: a 15-year longitudinal population-based study.

BACKGROUND: weight loss is commonly observed with ageing. We explored the trajectory of body mass index (BMI) and two proxies of muscle mass-calf circumference (CC) and mid-arm circumference (MAC)-and identified their determinants. METHODS: within the SNAC-K cohort, 2,155 dementia-free participants aged ≥60 years were followed over 15 years. BMI, CC and MAC were measured at baseline and follow-ups. Baseline sociodemographic and lifestyle factors were collected through interviews. Diabetes and vascular disorders were diagnosed by physicians through clinical examination and medical records. Data were analysed using linear mixed-effect models stratified by age (younger-old [<78 years] vs. older-old [≥78 years]). RESULTS: over the 15-year follow-up, BMI remained stable among participants aged 60 years at baseline (ßslope = 0.009 [95% confidence interval -0.006 to 0.024], P = 0.234) and declined significantly among those aged ≥66 years, while CC and MAC declined significantly across all age groups. The decline over 15 years in BMI, CC and MAC separately was 0.435 kg/m2, 1.110 cm and 1.455 cm in the younger-old and was 3.480 kg/m2, 3.405 cm and 3.390 cm in the older-old. In younger-old adults, higher education was associated with slower declines in all three measures, while vascular disorders and diabetes were associated with faster declines. In older-old adults, vigorous physical activity slowed declines in BMI and CC, while vascular disorders accelerated declines in BMI and MAC. CONCLUSIONS: CC and MAC declined earlier and more steeply than BMI. Cardiometabolic disorders accelerated such declines, while higher education and physical activity could counteract those declines.

The impact of diabetes on cognitive impairment and its progression to dementia.

INTRODUCTION: Diabetes is a well-established risk factor for dementia, but its impact on the prodromal phase of dementia is unclear. METHODS: Cohorts of older adults who were cognitively healthy (n = 1840) or had cognitive impairment-no dementia (CIND; n = 682) were followed over 12 years to detect incident CIND and dementia, respectively. RESULTS: Poorly controlled diabetes (glycated hemoglobin [HbA1c] ≥7.5%; reference = normoglycemia) was associated with double the risk of CIND (Cox regression multi-adjusted hazard ratio [HR] 2.01, 95% confidence interval [CI] 1.13-3.58) and triple the risk CIND progressing to dementia (HR 2.87, 95% CI 1.20-6.85). Co-morbid diabetes and heart disease doubled the risk of incident CIND and dementia, although neither disease conferred a significant risk of either outcome alone. Elevated systemic inflammation contributed to the diabetes-associated increased dementia risk. CONCLUSIONS: Diabetes characterized by poor glycemic control or cardiovascular complications is related to a greater risk of the development and progression of cognitive impairment. Inflammation may play a role in these relationships.

Genetic risk of dementia mitigated by cognitive reserve: A cohort study.

OBJECTIVE: We investigated whether cognitive reserve modifies the risk of dementia attributable to apolipoprotein ε4 (APOE-ε4), a well-known genetic risk factor for dementia. METHODS: We followed 2,556 cognitively intact participants aged ≥60 years from the ongoing prospective community-based Swedish National Study on Aging and Care in Kungsholmen (SNAC-K). Dementia was ascertained through clinical and neuropsychological assessments and diagnosed according to Diagnostic and Statistical Manual of Mental Disorders, 4th edition criteria. Structural equation modeling was used to generate a cognitive reserve indicator from 4 previously validated contributors: early life education, midlife substantive work complexity, late life leisure activities, and late life social networks. Cox proportional hazard models estimated dementia risk in relation to cognitive reserve indicator. The interaction between the cognitive reserve indicator and APOE-ε4 was assessed on multiplicative and additive scales. RESULTS: After an average of 6.3 years (range = 2.1-10.7) of follow-up, 232 dementia cases were ascertained. Relative to individuals in the lowest tertile of cognitive reserve indicator, those with moderate and high reserve were at a reduced risk of dementia. There was no multiplicative interaction between APOE-ε4 status and cognitive reserve indicator (p = 0.113). Additive interaction was statistically significant. Relative to APOE-ε4 carriers with low cognitive reserve, ε4 carriers with high reserve had a reduced risk of dementia (hazard ratio [HR] = 0.28, 95% confidence interval [CI] = 0.13-0.59). The magnitude of risk reduction was similar in ε4 noncarriers with a high cognitive reserve indicator (HR = 0.24, 95% CI = 0.15-0.40). INTERPRETATION: Lifelong engagement in reserve-enhancing activities attenuates the risk of dementia attributable to APOE-ε4. Promoting cognitive reserve might be especially effective in subpopulations with high genetic risk of dementia. ANN NEUROL 2019.

Disability trajectories and mortality in older adults with different cognitive and physical profiles.

BACKGROUND: Cognitive and physical deficits independently raise the risk for negative events in older adults. Less is known about whether their co-occurrence constitutes a distinct risk profile. This study quantifies the association between cognitive impairment, no dementia (CIND), slow walking speed (WS) and their combination and disability and mortality. METHODS: We examined 2546 dementia-free people aged ≥ 60 years, part of the Swedish National study on Aging and Care in Kungsholmen (SNAC-K) up to 12 years. The following four profiles were created: (1) healthy profile; (2) isolated CIND (scoring 1.5 SD below age-specific means on at least one cognitive domain); (3) isolated slow WS (< 0.8 m/s); (4) CIND+ slow WS. Disability was defined as the sum of impaired activities of daily living and trajectories of disability were derived from mixed-effect linear regression models. Piecewise proportional hazard models were used to estimate mortality rate [hazard ratios (HRs)]. Population attributable risks of death were calculated. RESULTS: Participants with both CIND and slow WS had the worst prognosis, especially in the short-term period. They experienced the steepest increase in disability and five times the mortality rate (HR 5.1; 95% CI 3.5-7.4) of participants free from these conditions. Similar but attenuated results were observed for longer follow-ups. Co-occurring CIND and slow WS accounted for 30% of short-term deaths. CONCLUSIONS: Co-occurring cognitive and physical limitations constitute a distinct risk profile in older people, and account for a large proportion of short-term deaths. Assessing cognitive and physical function could enable early identification of people at high risk for adverse events.

Quality of life outcomes in patients undergoing knee replacement surgery: longitudinal findings from the QPro-Gin study.

BACKGROUND: Many patients report postoperative pain, limited improvement in physical function and poor quality of life (QOL) after knee replacement surgery. Our study uses baseline predictors of change to investigate the QOL of patients with knee osteoarthritis 3-months after knee replacement surgery. METHODS: A prospective observational study was designed to evaluate patients (n = 132) scheduled for uni-compartmental or total knee replacement surgery who were assessed at baseline (preoperatively) and 3-months after. Physical and mental endpoints based on the component scores of the SF-12 and on the Western Ontario and McMaster Universities Arthritis (WOMAC) index were used to investigate patients' QOL. Generalised estimating equation methodology was used to assess patients' baseline characteristics (age, sex, education, body mass index (BMI), comorbidity, depressive symptoms, cognitive impairment, smoking/alcohol and type of surgery), the study endpoints and their changes over a 3-month post-surgery period. Stratified analyses by rehabilitation status after discharge were performed. RESULTS: Longitudinal data analysis showed that the baseline factors associated with improvement in general QOL at the 3-month post-surgery assessment were higher BMI, a high comorbidity, total (as opposed to unicompartmental) knee replacement and low education level. Data analysis of the patients who underwent rehabilitation after discharge revealed that the current smokers' physical QOL worsened over time. The general QOL was unchanged over time in the presence of depressive symptomatology. CONCLUSIONS: These findings underline the importance of using comprehensive assessment methods to identify factors affecting functionality and QOL, and developing interventions to improve the health/wellbeing of patients after knee replacement.

Leisure activity and social integration mitigate the risk of dementia related to cardiometabolic diseases: A population-based longitudinal study.

INTRODUCTION: The effect of comorbid cardiometabolic diseases (CMDs), including diabetes, heart diseases, and stroke, on dementia remains unclear. METHODS: A cohort of 2648 dementia-free adults aged ≥60 years was followed up for 12 years. An active lifestyle was defined in accordance with the engagement in leisure activities and/or a social network. Cox models were used in data analysis. RESULTS: The multiadjusted hazard ratio (HR, 95% confidence interval) of dementia was 1.41 (1.07-1.86) for one, 2.38 (1.58-3.59) for two, and 4.76 (2.04-11.13) for three CMDs. In joint exposure analysis, the HR of dementia was 3.36 (2.14-5.30) for participants with CMDs plus an inactive lifestyle and 1.32 (0.95-1.84) for those with CMDs plus an active lifestyle (reference: no CMDs plus active lifestyle). An active lifestyle delayed dementia onset by 3.50 years in people with CMDs. DISCUSSION: CMDs, especially when comorbid, are associated with increased dementia risk; however, leisure activities and social integration mitigate this risk.

Can active life mitigate the impact of diabetes on dementia and brain aging?

INTRODUCTION: We investigated whether lifelong exposure to stimulating activities (active life, AL) mitigates diabetes-associated dementia risk and brain aging. METHODS: In the Swedish National Study on Aging and Care-Kungsholmen, 2286 dementia-free older adults (407 with MRI volumetric measures) were followed over 12 years to detect incident dementia. AL index (low, moderate, high) combined education, work complexity, leisure activities, and social network. RESULTS: Participants with diabetes and low AL had higher dementia risk (hazard ratio [HR] = 2.36, 95% confidence interval [CI] 1.45-3.87) than patients who were diabetes-free with moderate-to-high AL (reference). Dementia risk in participants with diabetes and moderate-to-high AL did not differ from the reference. People with diabetes and low AL had the smallest brain volume, but those with diabetes and moderate-to-high AL exhibited total brain and gray-matter volumes that were similar to those of diabetes-free participants. AL did not modify the diabetes microvascular lesions association. DISCUSSION: AL could mitigate the deleterious impact of diabetes on dementia, potentially by limiting the loss of brain tissue volume.

Association of diabetes with stroke and post-stroke dementia: A population-based cohort study.

INTRODUCTION: The impact of prediabetes and diabetes on stroke and the development of dementia after a stroke remain unclear. METHODS: A total of 2655 dementia-free participants (including a stroke-free cohort and a prevalent stroke cohort) were followed-up for 12 years. Dementia and post-stroke dementia were determined by clinical examinations and national registry data. Diabetes was ascertained via medical examination, medication use, medical records, or glycated hemoglobin (HbA1c) ≥6.5%. Prediabetes was defined as HbA1c ≥5.7% in diabetes-free participants. RESULTS: In the stroke-free cohort, 236 participants developed ischemic stroke, and 47 developed post-stroke dementia. Diabetes was associated with ischemic stroke (hazard ratio [HR] 1.76, 95% confidence interval [CI] 1.16 to 2.67) and post-stroke dementia (HR 2.56, 95% CI 1.04 to 6.25). In the prevalent stroke cohort, diabetes was also related to dementia risk. Prediabetes was not significantly related to stroke or post-stroke dementia. DISCUSSION: Diabetes, but not prediabetes, is associated with an increased risk of ischemic stroke and post-stroke dementia.

Cognitive and physical markers of prodromal dementia: A 12-year-long population study.

INTRODUCTION: The aim is to test whether adding a simple physical test such as walking speed (WS) to the neuropsychological assessment increases the predictive ability to detect dementia. METHODS: The 2546 dementia-free people from the SNAC-K study were grouped into four profiles: (1) healthy profile; (2) isolated cognitive impairment, no dementia (CIND, scoring 1.5 standard deviation below age-specific means on ≥1 cognitive domains); (3) isolated slow WS (<0.8 m/s); (4) CIND+ slow WS. The hazard of dementia (Cox regression), the positive and negative predictive values (PPV, NPV), and the area under the curve (AUC) were estimated. RESULTS: Participants with CIND +slow WS demonstrated the highest hazard of dementia (3.4; 95% confidence interval [CI]: 2.5-4.8). The AUC increased from 0.69 for isolated CIND to 0.83 for CIND+ slow WS. Such an increase was due to the improvement of the PPV, the NPV remaining optimal. DISCUSSION: Adding WS to the cognitive assessment dramatically increases the diagnostic accuracy of prodromal dementia.

Specific nutrient patterns are associated with higher structural brain integrity in dementia-free older adults.

Optimal nutrition may play a beneficial role in maintaining a healthy brain. However, the relationship between nutrient intake and brain integrity is largely unknown. We investigated the association of specific nutrient dietary patterns with structural characteristics of the brain. Within the population-based Swedish National study on Aging and Care-Kungsholmen (SNAC-K), a cross-sectional study of 417 dementia-free participants aged ≥60 years who underwent structural magnetic resonance imaging (MRI) scans during 2001-2003, was carried-out. Data on dietary intake were collected using a food frequency questionnaire, from which intake of 21 nutrients was estimated. By principal component analysis, five nutrient patterns were extracted: (1) NP1 was characterized by fiber, vitamin C, E, ß-carotene, and folate [Fiber&Antioxidants], (2) NP2 by eicosapentaenoic (EPA, 20:5 ω-3) and docosahexaenoic (DHA, 22:6 ω-3) polyunsaturated fatty acids (PUFAs), proteins, cholesterol, vitamin B3, B12, and D [long chain (LC) ω-3PUFAs&Proteins], (3) NP3 by α-linoleic (18:2 ω-6) and α-linolenic (18:3 ω-3) PUFAs, monounsaturated fatty acids (MUFAs), and vitamin E [MUFAs&ω-3,6PUFAs], (4) NP4 by saturated fatty acids (SFAs), trans fats, MUFAs, and cholesterol [SFAs&Trans fats], (5) NP5 by B-vitamins, retinol, and proteins [B-Vitamins&Retinol]. Nutrient patterns scores were tertiled with the lowest tertile as reference, and were related to total brain volume (TBV) and white matter hyperintensities volume (WMHV) using linear regression models adjusting for potential confounders. In the multi-adjusted model, compared to the lowest intake for each pattern, the highest intake of NP1 (ß = 11.11, P = 0.009), NP2 (ß = 7.47, P = 0.052), and NP3 (ß = 10.54, P = 0.005) was associated with larger TBV whereas NP5 was related to smaller TBV (ß = -12.82, P = 0.001). The highest intake of NP1 was associated with lower WMHV (ß = -0.32, P = 0.049), whereas NP4 was associated with greater WMHV (ß = 0.31, P = 0.036). In sum, our results suggest that the identified brain-health specific nutrient combinations characterized by higher intake of fruit, vegetables, legumes, olive and seed oils, fish, lean red meat, poultry and low in milk and dairy products, cream, butter, processed meat and offal, were strongly associated with greater brain integrity among older adults.

Prediabetes and diabetes accelerate cognitive decline and predict microvascular lesions: A population-based cohort study.

INTRODUCTION: The impact of prediabetes and diabetes on cognitive decline and the potential underlying mechanisms remain unclear. We investigated whether prediabetes and diabetes accelerate cognitive decline and brain aging, and the initial pathological changes linked to microvascular processes. METHODS: Nine-year longitudinal data from the Swedish National Study on Aging and Care-Kungsholmen (n = 2746, age ≥60 years) and the magnetic resonance imaging subsample (n = 455) were used. Cognitive function was assessed with Mini-Mental State Examination. Brain magnetic resonance imaging markers included total brain tissue, white matter, gray matter, white matter hyperintensities, and hippocampal volumes. RESULTS: Compared with diabetes-free status, prediabetes and diabetes were independently associated with accelerated cognitive decline. Prediabetes was cross-sectionally associated with smaller total brain tissue volume (P < .01), particularly smaller white matter volume. Diabetes was associated with larger white matter hyperintensities volume. Longitudinally, diabetes was associated with faster white matter hyperintensities accumulation. No associations between prediabetes or diabetes and hippocampal volume were found. DISCUSSION: Diabetes and prediabetes accelerate cognitive decline and might predict microvascular lesions among dementia-free older adults.

Diabetes in midlife and risk of cancer in late life: A nationwide Swedish twin study.

The association between diabetes and cancer risk remains controversial. Hence, we examined whether midlife diabetes is related to the risk of cancer in late-life, and whether genetic and early-life environmental factors play a role in this association. This study included 25,154 twin individuals born in 1958 or earlier from the Swedish Twin Registry. Information on cancer diagnosis in late life (aged ≥ 65) during 1998-2014, was derived from the National Patient and Cancer Registries. Diabetes was ascertained based on self- or informant-reported history, patient registry and antidiabetic medication use. Midlife diabetes was defined when diabetes was diagnosed before 65 years. Data were analyzed following two strategies: (i) unmatched case-control analysis for all participants using generalized estimating equation (GEE) models, and (ii) co-twin control analysis for cancer-discordant twin pairs using conditional logistic regression. Overall, 1,766 (7.0%) had midlife diabetes and 5,293 (21.0%) had cancer in late-life. In multiadjusted GEE models, the odds ratios (95% CIs) of diabetes were 10.55 (2.95-37.67) for pharynx cancer, 5.78 (1.72-19.40) for small intestine cancer, 2.37 (1.14-4.91) for liver cancer and 0.48 (0.35-0.67) for prostate cancer. In people with diabetes, diabetes duration was dose-dependently associated with cancer risk. In conditional logistic regression analysis of 176 prostate cancer-discordant twin pairs, the association between midlife diabetes and prostate cancer in later life became stronger. Midlife diabetes increases the risk of pharynx, small intestine and liver cancers, but reduces prostate cancer risk in late life. Genetic and early-life environmental factors may partially contribute to the diabetes-prostate cancer association.