An inverse relationship between educational level and dementia has been reported in several studies. In this study we investigated the relationship between educational level and dementia related deaths for cohorts of people all born during 1915-39. The cohorts were followed up from adulthood or old age, taking into account possible confounders and mediating paths. Our study population comprised participants in Norwegian health examination studies in the period 1974-2002; The Counties Study and Cohort of Norway (CONOR). Dementia related deaths were defined as deaths with a dementia diagnosis on the death certificate and linked using the Cause of Death Registry to year 2012. The study included 90,843 participants, 2.06 million person years and 2440 dementia related deaths. Cox regression was used to assess the association between education and dementia related deaths. Both high and middle educational levels were associated with lower dementia related death risk compared to those with low education when follow-up started in adulthood (35-49 years, high versus low education: HR=0.68, 95% confidence interval (CI) 0.50-0.93; 50-69 years, high versus low education: HR=0.52, 95% CI 0.34-0.80). However, when follow-up started at old age (70-80 years) there was no significant association between education and dementia related death. Restricting the study population to those born during a five-year period 1925-29 (the birth cohort overlapping all three age groups), gave similar main findings. The protective effects found for both high and middle educational level compared to low education were robust to adjustment for cardiovascular health and life style factors, suggesting education to be a protective factor for dementia related death. Both high and middle educational levels were associated with decreased dementia related death risk compared with low educational level when follow-up started in adulthood, but no association was observed when follow-up started at old age.
To investigate the association between random measured glucose levels in middle and old age and dementia-related death.
Population-based cohort study.
Norwegian Counties Study (middle-aged individuals; 35-49) and Cohort of Norway participants (older individuals; 65-80).
Individuals without (n=74,630) and with (n=3,095) known diabetes mellitus (N=77,725); 67,865 without and 2,341 with diabetes mellitus were included in the complete case analyses (nonmissing for all included covariates), of whom 1,580 without and 131 with diabetes mellitus died from dementia-related causes.
Dementia-related death was ascertained according to the Norwegian Cause of Death Registry. Cox regression was used to assess the relationship between random glucose levels (nonfasting) in individuals without and with diabetes mellitus and dementia-related death. Education, smoking, cardiovascular disease, body mass index, cholesterol, blood pressure, and physical activity were adjusted for.
Individuals without diabetes mellitus at midlife with glucose levels between 6.5 and 11.0 mmol/L had a significantly greater risk of dementia-related death than those with levels less than 5.1 mmol/L (hazard ratio=1.32, 95% confidence interval=1.04-1.67) in a fully adjusted model. A dose-response relationship (P=.02) was observed. No significant association between high glucose levels in individuals aged 65 to 80 and dementia-related death was detected.
High random glucose levels measured in middle-aged but not older age persons without known diabetes mellitus were associated with greater risk of dementia-related death up to four decades later.
It is not fully understood how subjective feelings of psychological distress prognosticate dementia. Our aim was to investigate the association between self-reported psychological distress and risk of dementia-related mortality.
We included 31,043 eligible individuals between the ages of 60 and 80 years, at time of examination, from the CONOR (Cohort of Norway) database. They were followed for a period of 17.4 years (mean 11.5 years). The CONOR Mental Health Index, a seven-item self-report scale was used. A cut-off score equal to or above 2.15 on the scale denoted psychological distress. Cox regression was used to assess the association between psychological distress and risk of dementia-related mortality.
Total number of registered deaths was 11,762 and 1118 (9.5%) were classified as cases of dementia-related mortality. We found that 2501 individuals (8.1%) had psychological distress, of these, 119 (10.6%) had concomitant dementia-related mortality. Individuals with psychological distress had an increased risk of dementia-related mortality HR = 1.52 (95% confidence interval (CI) 1.25-1.85) after adjusting for age, gender and education. The association remained significant although attenuated when implemented in a full adjusted model, including general health status, smoking, obesity, hypertension, diabetes and history of cardiovascular disease; hazard ratio, HR = 1.30 (95% CI 1.06-1.59).
Our results indicate that psychological distress in elderly individuals is associated with increased risk of dementia-related mortality. Individuals at increased risk of dementia may benefit from treatments or interventions that lessen psychological distress, but this needs to be confirmed in future clinical studies.
Our aims were two-fold: firstly, to investigate the association and interaction between apolipoprotein E (ApoE), lifestyle risk factors and dementia-related mortality and, secondly, to examine if using dementia-related mortality yielded comparable risk estimates for the ApoE genotypes as reported in studies using a clinical dementia diagnosis as the end point.
We used a nested case-control study with 561 cases drawn from dementia deaths in the Cohort of Norway (CONOR) and 584 alive controls.
ApoE e4 carriers were at increased risk of dementia-related mortality compared to noncarriers [odds ratio (OR) 2.46, 95% confidence interval (CI) 1.93-3.13], and e4 homozygotes were at particularly high risk (OR 7.86, 95% CI 3.80-13.8), while the e2 type was associated with a lower risk. The highest risk of dementia-related mortality was found among e4 carriers with more lifestyle risk factors (e4 carriers who were smokers, hypertensive, physically inactive and diabetics) versus e4 noncarriers without lifestyle risk factors (OR 15.4, 95% CI 4.37-52.4). The increased risk was additive, not multiplicative.
Ensuring a healthy lifestyle is important to be able to prevent dementia in populations at large, but especially for e4 carriers. Using dementia mortality gives comparable results for the ApoE-dementia association as studies using clinical dementia diagnoses.
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 35-50 years 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, 1.5 million 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.
Alzheimer's disease patients are reported to have higher survival rate compared to patients with vascular dementia or dementia with Lewy bodies. There is a paucity of studies investigating survival including persons with cognitive decline and dementia of various aetiologies.
We aimed to compare survival for patients with subjective cognitive decline, mild cognitive impairment, Alzheimer's disease, vascular dementia, mixed Alzheimer's/vascular dementia, dementia with Lewy bodies/Parkinson's disease, and other dementias compared to the general Norwegian population, taking into account the role of gender, cognitive function, function in everyday activities, comorbidity and education.
Patients (N = 4682), =65 years, in the The Norwegian register of persons assessed for cognitive symptoms (NorCog) during 2009-2017 were followed for mortality in the National Registry until January 2018. Flexible parametric survival models were applied to estimate relative survival, life expectancy and years of life lost for diagnostic groups compared with the general population.
Patients with vascular dementia or dementia with Lewy bodies/Parkinson's had the shortest survival, followed by mixed dementia, Alzheimer's disease, unspecified dementia, mild cognitive impairment and subjective cognitive decline. At age 70 years, men with vascular dementia or dementia with Lewy bodies/Parkinson's had life expectancy of 4.7 years, which corresponded to 10.3 years of life lost compared to the general population. Years of life lost for other diagnoses were 10.0 years for mixed dementia, 9.2 years for Alzheimer's disease, 9.3 years for other dementias, 5.2 years for mild cognitive impairment and 2.2 years for subjective cognitive decline. Corresponding years of life lost in women were: 12.7 years, 10.5 years, 9.8 years, 10.6 years, 7.8 years, and 2.6 years. Poor relative survival among dementia patients was associated with male gender, comorbidity, low cognitive function, and low function in activities of daily living.
Compared with the general population, patients with subjective cognitive decline had no significant loss in life expectancy, while patients with mild cognitive impairment and all dementia subtypes had large losses, especially those with a diagnosis of vascular dementia or dementia with Lewy bodies/Parkinson's.
The relationship between body mass index (BMI) and dementia is complex and controversial. This study investigates the association of weight change during midlife and later dementia-related mortality.
Two BMI measurements (average of 9.0 years apart) were available for 43,721 participants in the Norwegian Counties Study (NCS), with mean age 42 years at first BMI measurement and 51 at the final measurement. NCS was linked with the Cause of Death Registry until year 2015 (mean follow-up time 25.9 years). Cox regression with a conditional growth model was used.
Our study comprised 1,205 dementia-related deaths. Weight loss was associated with increased dementia-related mortality, irrespectively of baseline BMI and confounders; those with 10% or more loss had hazard ratio (HR) = 1.52 (95% confidence interval [CI]: 1.09, 2.12) compared to those being stable (0%-2.5% BMI gain), and those with 5%-10% loss had HR = 1.38 (95% CI: 1.08, 1.76). Gaining weigh was associated with reduced dementia-related mortality. Associations with BMI change did not vary by baseline BMI.
Weight loss during midlife was associated with increased dementia-related mortality risk more than 3 decades later, while weight gain was associated with reduced risk. These associations held both for low and high baseline BMI. Weight loss was an independent risk factor for dementia-related mortality and more strongly related with dementia-related mortality than stable BMI (stable high or low). Overweight and obesity were associated with an increased risk for nondementia-related mortality, which was far more common than dementia-related mortality.