Adherence to the MIND diet is associated with 12-year all-cause mortality in older adults

OBJECTIVE: To prospectively evaluate the association of three dietary patterns: the MIND (Mediterranean-DASH diet intervention for Neurodegenerative Delay) diet; a Mediterranean-type diet and a traditional diet, with all-cause mortality over a 12-year period in an older sample. DESIGN: A longitudinal birth cohort study. We ascertained dietary patterns using FFQ data at baseline (2004–2007) and mortality using linkage data. Cox regression was used to estimate mortality hazard ratios (HR) with adjustment for confounders. SETTING: The Lothian Birth Cohort 1936 (LBC1936) study in Edinburgh, Scotland. PARTICIPANTS: Dietary patterns were ascertained in 882 participants, mean age 69·5 (±0·8) years, at baseline. During the 12-year follow-up (to October 2019), 206 deaths occurred. RESULTS: In the basic-adjusted model, all three dietary patterns were significantly associated with mortality, the MIND diet and Mediterranean-type diet with a lower risk and the traditional diet with a higher risk. In fully adjusted models, MIND diet score was inversely related to all-cause mortality (HR 0·88; 95 % CI 0·79, 0·97) such that the risk of death was reduced by 12 % per unit increase in MIND diet score. Participants in the top compared with the bottom third of MIND diet score had a 37 % lower risk of death (HR 0·63; 95 % CI 0·41, 0·96). No significant associations with the Mediterranean-type or traditional dietary patterns were observed in the final multivariate model. CONCLUSIONS: Our findings suggest that closer adherence to the MIND diet is associated with a significantly lower risk of all-cause mortality, over 12 years of follow-up, and may constitute a valid public health recommendation for prolonged survival

Lifestyle factors and cognitive ageing in the Lothian Birth Cohort 1936: exploring the role of confounding by prior cognitive ability

With an increase in life expectancy, the number of older people affected by cognitive decline and dementia is rising, causing major, global public health concerns. However, there is substantial variation in the rate and magnitude of cognitive decline experienced among ageing individuals. Evidence suggests that many age-associated changes in cognitive functioning can be explained by modifiable lifestyle factors such as smoking, physical activity and diet choices. The weight of the evidence supports the promotion of a healthy lifestyle as an effective strategy for healthy cognitive ageing. Many epidemiological studies have drawn causal conclusions with regard to the positive and direct benefits of lifestyle, yet few have considered the possible confounding role of prior cognitive ability in explaining the lifestyle and cognition relationship in older age. Given the potential for reverse causation, whereby better prior cognitive functioning leads to a greater uptake of healthy behaviours rather than vice versa, it is a mechanism which should be studied, but rarely is. The present thesis focuses on the possible confounding effect of prior cognitive ability on the cross-sectional relationships between lifestyle factors and cognitive ability domains in later-life. The core of the thesis is a series of independent, peer-reviewed (six first-author and one co-author) journal articles in the public domain. Data were derived from the Lothian Birth Cohort 1936 study (n = 1091), a sample of relatively healthy, community-dwelling men and women aged 70 years from Edinburgh, Scotland, for whom childhood (age 11) mental test scores are available. The lifestyle factors investigated were caffeine consumption, alcohol consumption, dietary patterns, body mass index, smoking, serum cholesterol, and physical activity. Cognitive function was assessed across five major ageing-related domains: age 70 IQ (based on the same test that was taken in childhood), general cognitive ability (g), processing speed, memory, and verbal ability. General linear models (ANCOVA) were adjusted for the following covariates: age; sex; childhood cognitive ability; and socioeconomic status (SES). Other potential covariates were additionally adjusted for as necessary. Overall, the positive and significant associations observed between ‘healthy’ lifestyle factors and better cognitive functions at age 70 were consistent with previous research; their effect size was around 1% of the variance in cognitive tests scores. However, these relationships were markedly attenuated (by on average 80%) by a higher childhood cognitive ability and adult SES; for the most part, associations were reduced to non-significance. None of the lifestyle factors were consistent predictors of performance across cognitive domains, though smoking avoidance, a physically active lifestyle, and moderate intake of alcohol, appeared to have the most potential. The key novel finding of this thesis is that, in addition to having predictive value for lifestyle choices over 60 years later, cognitive ability at age 11 accounted for the majority of the cross-sectional associations between lifestyle factors and cognitive abilities in later-life. This finding is consistent with the theory of confounding or even reverse causation. That is, individuals with higher lifetime ‘trait’ cognitive ability may be more likely to adopt a lifestyle which protects against cognitive decline. Rather than a unidirectional or indirect effect of health behaviours on cognitive function, the present findings suggest there may be a dynamic cycle involving cognition, self-management of health and ultimate cognitive outcomes

Inflammation as a risk factor for the development of frailty in the Lothian Birth Cohort 1936

Background Research suggests that frailty is associated with higher inflammation levels. We investigated the longitudinal association between chronic inflammation and frailty progression. Methods Participants of the Lothian Birth Cohort 1936, aged 70 at baseline were tested four times over 12 years (wave 1: n = 1091, wave 4: n = 550). Frailty was assessed by; the Frailty Index at waves 1–4 and Fried phenotype at waves 1, 3 and 4. Two blood-based inflammatory biomarkers were measured at wave 1: Fibrinogen and C-reactive protein (CRP). Results Fully-adjusted, linear mixed effects models showed higher Fibrinogen was significantly associated with higher wave 1 Frailty Index score (β = 0.011, 95% CI[0.002,0.020], p < .05). Over 12 year follow-up, higher wave 1 CRP (β = 0.001, 95% CI[0.000,0.002], p < .05) and Fibrinogen (β = 0.004, 95% CI[0.001,0.007], p < .05) were significantly associated with increased Frailty Index change. For the Fried phenotype, wave 1 Pre-frail and Frail participants had higher CRP and Fibrinogen than Non-frail participants (p < .001). Logistic regression models calculated risk of worsening frailty over follow-up and we observed no significant association of CRP or Fibrinogen in minimally-adjusted nor fully-adjusted models. Conclusions Findings showed a longitudinal association of higher wave 1 CRP and Fibrinogen on worsening frailty in the Frailty Index, but not Fried Phenotype. A possible explanation for this disparity may lie in the conceptual differences between frailty measures (a biopsychosocial vs physical approach). Future research, which further explores different domains of frailty, as well the associations between improving frailty and inflammation levels, may elucidate the pathway through which inflammation influences frailty progression. This may improve earlier identification of those at high frailty risk

Can we spot deleterious ageing in two waves of data? The Lothian Birth Cohort 1936 from ages 70 to 73

‘Younger ’ old age (the late 60s through early 70s) is, for many, a period of stability of lifestyle and considerable freedom to pursue leisure activities. Despite the stability that many enjoy, the mortality rate is about 2 % per year in western nations. This increases to about 5 % by age 80. It would be useful to know if those most vulnerable can be identified through patterns of deleterious ageing, and especially if this could be accomplished with just two waves of data. The Lothian Birth Cohort 1936 was surveyed on a host of individual difference variables including cognition, personality, biomarkers of physical health, and activities at ages 70 and 73 years. Overall, the group showed the expected basic stability in mean levels for these variables, but some individuals had died and others did show substantial changes that could be considered statistically reliable. These presumably reliable changes were at least as likely to be positive (reflecting improved condition/ability) as negative (reflecting decline/ageing). Moreover, limitations in the estimated reliabilities of the measures meant that most of the observed changes could not be considered reliable. The changes clustered only weakly around general health to predict death over the next approximately two years. We concluded that two waves of longitudinal data were not sufficient to assess meaningful patterns of ageing, despite often being used to do so