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What does height tell us about the risk of dementia?
Abstract
Taller individuals might have a favourable dementia profile by an affluent background, higher social status and more education, less obesity and chronic illness as well as a nutritional advantage and less psychosocial stress (Russ et al., 2014). Stature remains relatively stable, as individuals get older and is a reliable marker in cohort studies (Russ et al., 2014). Our working hypothesis was based upon available empirical evidence on height and dementia, and aimed at examining the relationship between height and dementia-related mortality, adjusting for known risk factors of dementia as low education, physical inactivity, obesity, cardiovascular disease, diabetes, dyslipidemia, hypertension and smoking, assessed at middle age.
Aim
The association between adult height and follow-up cognition requires an update in China. We aimed to examine the association between baseline height and follow-up cognitive trajectories in Chinese subjects from the China Health and Retirement Longitudinal Study (CHARLS).
Methods
A total of 6508 adults aged 45 years or older from the CHARLS were included for analysis. Latent class growth modeling was used to determine cognitive trajectories of 2011, 2013 and 2015. Multivariable linear regression and logistic regression models were used to examine the association between baseline adult height and cognitive performance and trajectories, respectively.
Results
At baseline, an increment of 1 SD (8.3 cm) of height was associated with a higher global cognitive score (β = 0.492, 95% CI, 0.348–0.636), verbal episodic memory (β = 0.155, 95% CI, 0.086–0.224) and mental status (β = 0.337, 95% CI, 0.225–0.449). These associations were still observed even when stratified by sex. Prospectively, for females, the third quartile of height level (i.e., 155 to 158 cm) was associated with a better global cognitive function trajectory (OR = 1.627, P = 0.001, P for trend = 0.009) and mental status trajectory (OR = 1.456, P = 0.012, P for trend = 0.047); and the tallest height level (i.e., 159 cm or taller) was related to a better verbal episodic memory trajectory (OR = 1.574, P = 0.017). For males, no associations were observed.
Conclusion
Increased stature might be associated with better cognitive trajectories for subjects in China. Geriatr Gerontol Int 2021; ••: ••–••.
This chapter will consider the prevention of dementia. The often neglected distinction between Alzheimer’s disease and Alzheimer’s dementia (and the formal inclusion of this distinction in the 2011 diagnostic criteria) will form our main focus, and, in particular, the consequent relevance of the life course paradigm in epidemiology that influences from any stage of life could potentially increase or decrease one’s risk of dementia. We will consider a number of risk factors for Alzheimer’s disease (i.e., primary prevention) including early life factors, intelligence and education, proxies for early life factors, midlife risk factors, multiple risk factors, and environmental factors. In considering prevention of Alzheimer’s dementia (i.e., secondary prevention), we will consider the relevance of the theory of cognitive or brain reserve. We will briefly consider attempts at disease modification in dementia (i.e., tertiary prevention) and the multiple trial failures seen in recent decades. After outlining the policy context, we will consider two important prevention initiatives: the PREVENT program and the European Prevention of Alzheimer’s Dementia (EPAD) project.
This chapter will consider the prevention of dementia. The often neglected distinction between Alzheimer’s disease and Alzheimer’s dementia (and the formal inclusion of this distinction in the 2011 diagnostic criteria) will form our main focus, and, in particular, the consequent relevance of the life course paradigm in epidemiology that influences from any stage of life could potentially increase or decrease one’s risk of dementia. We will consider a number of risk factors for Alzheimer’s disease (i.e., primary prevention) including early life factors, intelligence and education, proxies for early life factors, midlife risk factors, multiple risk factors, and environmental factors. In considering prevention of Alzheimer’s dementia (i.e., secondary prevention), we will consider the relevance of the theory of cognitive or brain reserve. We will briefly consider attempts at disease modification in dementia (i.e., tertiary prevention) and the multiple trial failures seen in recent decades. After outlining the policy context, we will consider two important prevention initiatives: the PREVENT program and the European Prevention of Alzheimer’s Dementia (EPAD) project.
Background:
That risk factors measured in middle age may not fully explain future dementia risk implicates exposures acting earlier in life. Height may capture early-life illness, adversity, nutrition and psychosocial stress.
Aims:
To investigate the little-explored association between height and dementia death. Method Individual participant meta-analysis using 18 prospective general population cohort studies with identical methodologies (1994-2008; n = 181 800).
Results:
Mean follow-up of 9.8 years gave rise to 426 and 667 dementia deaths in men and women respectively. The mean heights were 174.4 cm (s.d. = 7.3) for men and 161.0 cm (s.d. = 6.8) for women. In analyses taking into account multiple covariates, increasing height was related to lower rates of death from dementia in a dose-response pattern (P ⩽ 0.01 for trend). There was evidence of a differential effect by gender (P = 0.016 for interaction). Thus, the association observed in men (hazard ratio per s.d. decrease in height 1.24, 95% CI 1.11-1.39) was markedly stronger than that apparent in women (HR = 1.13, 95% CI 1.03-1.24).
Conclusions:
Early-life circumstances, indexed by adult height, may influence later dementia risk.
Importance:
Young-onset dementia (YOD), that is, dementia diagnosed before 65 years of age, has been related to genetic mutations in affected families. The identification of other risk factors could improve the understanding of this heterogeneous group of syndromes.
Objective:
To evaluate risk factors in late adolescence for the development of YOD later in life.
Design:
We identified the study cohort from the Swedish Military Service Conscription Register from January 1, 1969, through December 31, 1979. Potential risk factors, such as cognitive function and different physical characteristics, were assessed at conscription. We collected other risk factors, including dementia in parents, through national register linkage.
Participants:
All Swedish men conscripted for mandatory military service (n=488,484) with a mean age of 18 years.
Setting:
Predominantly Swedish men born from January 1, 1950, through December 31, 1960.
Exposure:
Potential risk factors for dementia based on those found in previous studies, data available, and quality of register data.
Main outcomes and measure:
All forms of YOD.
Results:
During a median follow-up of 37 years, 487 men were diagnosed as having YOD at a median age of 54 years. In multivariate Cox regression analysis, significant risk factors (all P< .05) for YOD included alcohol intoxication (hazard ratio, 4.82 [95% CI, 3.83-6.05]); population-attributable risk, 0.28), stroke (2.96 [2.02-4.35]; 0.04), use of antipsychotics (2.75 [2.09-3.60]; 0.12), depression (1.89 [1.53-2.34]; 0.28), father's dementia (1.65 [1.22-2.24]; 0.04), drug intoxication other than alcohol (1.54 [1.06-2.24]; 0.03), low cognitive function at conscription (1.26 per 1-SD decrease [1.14-1.40]; 0.29), low height at conscription (1.16 per 1-SD decrease [1.04-1.29]; 0.16), and high systolic blood pressure at conscription (0.90 per 1-SD decrease [0.82-0.99]; 0.06). The population-attributable risk associated with all 9 risk factors was 68%. Men with at least 2 of these risk factors and in the lowest third of overall cognitive function were found to have a 20-fold increased risk of YOD during follow-up (hazard ratio, 20.38 [95% CI, 13.64-30.44]).
Conclusions and relevance:
In this nationwide cohort, 9 independent risk factors were identified that accounted for most cases of YOD in men. These risk factors were multiplicative, most were potentially modifiable, and most could be traced to adolescence, suggesting excellent opportunities for early prevention.
There is growing evidence that midlife risk factors for vascular disease also are risk factors for dementia, but there is still need for long-term observational studies to address this. Our objective was to investigate the association of midlife vascular disease risk factors with dementia death. Participants were included in The Norwegian Counties Study (NCS) in the period 1974-78, aged 35-50years at baseline. Information from NCS was linked with the Cause of Death Registry through the year 2009 using the unique personal identification number. The study included 48,793 participants, 1.5million person years and 486 dementia deaths (187 Alzheimer's; 299 non-Alzheimer's dementia). Cox regression for cause-specific hazards was used. Dementia death was associated with increased total cholesterol levels (>7.80 vs. <5.20mmol/l: HR=2.01, 95% confidence interval 1.37-2.93); diabetes (HR=2.43, 95% CI 1.40-4.32) and low body mass index (<20kg/m(2) vs. 20-25kg/m(2): HR=1.76, 95% CI 1.15-2.68) in midlife. The associations remained after adjustment for other vascular risk factors and educational level. Smoking status or blood pressure in midlife was not significantly associated with risk of dementia death, although the results indicate a possible increased risk in heavy smokers. People suffering from high cholesterol levels, diabetes or underweight in midlife are at increased risk of dying from or with dementia later in life. Our findings add to previous results suggesting that intervention in midlife may be important. To better understand the mechanisms involved in the associations between midlife underweight, diabetes, and elevated cholesterol level and late-life dementia death, these links need to be further investigated.
The relation between body mass index (BMI) and mortality is not clear in the literature. An inverse relation between height and mortality has been suggested. We explore these relations in a very large cohort in Norway.
We studied two million men and women, age 20-74 years, who were measured during 1963-2000. These persons were followed for an average of 22.1 years. We used Cox proportional hazard models in the analyses. Also, the optimal BMI (the BMI at the time of measurement that was subsequently related to the lowest mortality) was estimated.
Over the study period, 723,000 deaths were registered. The relative risk of death by BMI showed a J- or U-shaped curve, with the lowest rates of death at BMI between 22.5 and 25.0. In men, the optimal BMI increased from 21.6 when measured at age 20-29 to 24.0 when measured at age 70-74. In women, the optimal BMI was consistently higher, increasing from 22.2 to 25.7. Mortality decreased with increased height in men; in women, mortality decreased with height only up to heights of about 160-164 cm and then increased among the tallest women.
The relation between BMI and mortality was J- or U-shaped, with the "optimal" BMI varying by age and sex. Height was inversely related to mortality in men and in women up to a height of 165 cm.