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Background: Social connections may impact the dynamic trajectory of frailty., Methods: Using data from the British Regional Heart Study (BRHS) in the UK (n = 715), and the US Health, Aging and Body Composition (Health ABC) Study (n = 1256), we conducted multinominal regression analyses to examine the association of baseline and change in social engagement and loneliness with progression to pre-frailty and frailty, as well as their association with reversal to pre-frailty and robust status among older adults., Results: A higher level of social engagement at baseline (BRHS: relative risk ratio (RRR) 0.69 [95%CI 0.55-0.85]; Health ABC: 0.56 [0.45-0.70]), as well as increase in social engagement (BRHS: 0.73, [0.59-0.90]; Health ABC: 0.51 [0.41-0.63]), were associated with a lower risk of developing frailty. In BRHS, a higher level of loneliness at baseline (1.42 [1.10-1.83]) and an increase in loneliness (1.50 [1.18-1.90]), increased the risk of developing frailty. For reversal of frailty, higher social engagement at baseline (Health ABC: 1.63 [1.08-2.47]) and an increase in social engagement (BRHS:1.74[1.18-2.50]; Health ABC: 1.79[1.17-.274]) were beneficial., Conclusion: Social connections maybe potentially important and modifiable factors in both preventing and reversing progression of frailty in older adults., (© The Author(s) 2024. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health.)

The trajectories of physical activity (PA) from midlife into old age and their associations with established and novel cardiovascular disease (CVD) risk factors in later life remain unclear. This study examined associations between 20-year nonoccupational PA trajectories and a range of CVD biomarkers at ages 60-79 years. We used data from a sample of 3,331 men (mean baseline age = 50.2 ± 5.8 years) recruited in 1978-1980, with follow-up after 12, 16, and 20 years, reporting habitual nonoccupational PA at each wave. At the 20-year follow-up, surviving men attended a physical examination and provided a fasting blood sample. Group-based trajectory modeling was used to identify trajectories. Adjusted regression analyses examined the association between trajectory-group membership and several cardiometabolic, cardiac, and inflammatory markers at follow-up. Three distinct 20-year trajectories were identified: low/decreasing (21.3%), light/stable (51.8%), and moderate/increasing (27.0%). Compared with the low/decreasing group, membership in the light/stable and moderate/increasing trajectory groups was associated with a more favorable cardiometabolic profile and lower levels of inflammation and endothelial dysfunction. Although following a moderate-increasing PA trajectory was most favorable, more modest but sustained doses of PA into old age may be sufficient to lower CVD risk.

Although body build is related to disability and mortality in older people, the independent contributions of adiposity and lean mass are not fully defined. The authors examined the relations of body composition (fat mass index, fat-free mass index) and adiposity (body mass index, waist circumference) to ill health and physical disability in a cross-sectional study of 4,252 British men aged 60-79 years in 1998-2000. Increased body mass index, waist circumference, and fat mass index were associated with increased prevalence of cardiovascular disease, overall ill health, and disability. Adjusted odds ratios of cardiovascular disease (top vs. bottom fifth) were 1.58 (95% confidence interval (CI): 1.23, 2.03) for fat mass index, 1.45 (95% CI: 1.14, 1.86) for body mass index, and 1.27 (95% CI: 0.99, 1.62) for waist circumference. For overall "poor/fair" health, the corresponding odds ratios were 1.71 (95% CI: 1.33, 2.21), 1.49 (95% CI: 1.17, 1.90), and 1.64 (95% CI: 1.28, 2.09) and, for mobility limitation, they were 1.56 (95% CI: 1.17, 2.06), 1.96 (95% CI: 1.48, 2.56), and 1.88 (95% CI: 1.42, 2.49). A high fat-free mass index was associated with only a decreased prevalence of respiratory problems and cancer (odds ratios=0.45 (95% CI: 0.33, 0.62) and 0.62 (95% CI: 0.42, 0.94), respectively). Body fatness, not fat-free mass, is associated with cardiovascular disease and disability in older men. Simple measures of overweight, such as body mass index and waist circumference, are good indicators of the likelihood of morbidity in older men. Prevention of weight gain with increasing age is likely to reduce morbidity and disability among older men.

Moderate alcohol consumption is associated with a decreased risk of cardiovascular disease. However, the impact of variation in alcohol intake over time on estimated risk relations has not been adequately addressed. In this study, 6,544 middle-aged British men without previous cardiovascular disease were followed for cardiovascular events and all-cause mortality over 20 years from 1978/1980 to 1998/2000. Alcohol intake was ascertained at regular points throughout the study. A total of 922 men had a major coronary event within 20 years, 352 men had a stroke, and 1,552 men died of all causes. Baseline alcohol intake displayed U-shaped relations with cardiovascular disease and all-cause mortality, with light drinkers having the lowest risks and nondrinkers and heavy drinkers having similarly high risks. However, the nature of these relations changed after adjustment for intake variation; risks associated with nondrinking were lowered, and risks associated with moderate and heavy drinking increased. Regular heavy drinkers had a 74% higher risk of a major coronary event, a 133% higher risk of stroke, and a 127% higher risk of all-cause mortality than did occasional drinkers (these estimates were 8%, 54%, and 44% before adjustment for intake variation). The findings suggest that considerable caution may be needed before any recommendations regarding acceptable limits of alcohol consumption are made.

Variability of angina symptoms over a 5-year period was examined in a prospective study, in which 7,109 British middle-aged men completed two chest pain questionnaires, Q1 (1978-1980) and Q5 (1983-1985), and were classified as having no chest pain, nonexertional chest pain, or angina (Q) (exertional chest pain) on each occasion. Within persons, there was considerable variability in response to the chest pain questions at Q1 and Q5. Angina (Q) persistence showed marked associations with previous myocardial infarction, diagnosed angina, electrocardiogram ischemia, and subsequent major ischemic heart disease events from Q5 onward. Compared with men without angina (Q), the age-adjusted hazard ratios were 1.5 (95% confidence interval (CI): 1.1, 2.2) for angina (Q) at Q1 only, 2.6 (95% CI: 2.1, 3.2) for angina (Q) at Q5 only, and 3.4 (95% CI: 2.8, 4.3) for angina (Q) on both occasions. For men without diagnosed ischemic heart disease, for whom apparent remission of angina (Q) was particularly frequent, a similar pattern of association was found between angina (Q) persistence and subsequent major events. In middle-aged men, exertional chest pain is a strong indicator of major coronary risk but frequently appears transient in the longer term. Persistently reported symptoms are associated with severe disease and a poor prognosis.

In most prospective studies involving older subjects, weight loss is associated with increased mortality. The authors examined the characteristics and health status of middle-aged men from 24 towns (the British Regional Heart Study), who reported that they had lost weight intentionally or unintentionally as they aged. Questionnaires were completed at screening (1978-1980), 5 years later, and in 1992 and 1996. This paper concerns the 4,713 men who reported their weight in 1992 and 1996 and their perceived weight change over this period. Weight loss was reported by 847 men (18%), of whom 39% stated that it was intentional. Compared with intentional weight loss, unintentional weight loss was associated with lower social class, more smoking, less obesity, and less physical activity and with the highest rates of "poor health,"long-standing disability, cancer, and respiratory diseases. The rates of recalled heart attack, stroke, diabetes, and cardiovascular hospitalization were higher than among men whose weight was stable. Men who lost weight intentionally had been more obese than those who lost weight unintentionally and had high rates of obesity-related conditions. Thus, both intentional and unintentional weight loss may follow the development of disease. These findings probably account for the lack of benefit and the increased mortality associated with weight loss observed in most large-scale prospective studies.

An inverse relation between adult height and risk of coronary heart disease (CHD) has been reported in many studies, but the association between adult height and stroke remains uncertain. The authors examined the relation between adult height and risk of stroke and CHD in a prospective study of 7,735 men drawn from general medical practices in 24 towns in England, Wales, and Scotland. The men were followed up for an average of 16.8 years (range, 15.5-18.0 years) between 1978 and 1995. During this period, there were 351 major stroke events (63 fatal, 288 nonfatal) and 1,093 major CHD events (465 fatal, 628 nonfatal). The mean height of the men was 173.3 cm. Total stroke risk was increased only in the men who fell into the lowest quintile of the height distribution (<167.7 cm), with little difference being seen between the other groups. When data were examined separately for fatal and nonfatal events, no relation was seen with nonfatal stroke. An apparent inverse association was seen with fatal stroke, even after adjustment for a wide range of confounding variables, but the number of deaths was small and the trend was not statistically significant (p = 0.17). By contrast, a significant inverse relation was seen between height and risk of major CHD events: Risk decreased progressively with increasing height, even after full adjustment (highest quintile vs. lowest: relative risk (RR) = 0.74, 95% confidence interval (CI) 0.59-0.91; test for trend: p < 0.001). A stronger inverse association was seen with nonfatal CHD events (RR = 0.64, 95% CI 0.49-0.84) than with fatal CHD events (RR = 0.82, 95% CI 0.60-1.11). This study confirms the finding of an inverse association between height and CHD. The inverse association seen for fatal stroke but not nonfatal stroke suggests that height may be related to specific subtypes of stroke. There are different patterns of association between height and stroke and height and CHD. If the apparent association between short stature and increased risk of fatal stroke is confirmed in other prospective studies, this would suggest that different mechanisms underlie the effects of height on stroke and CHD.

The relation between serum potassium level and all-cause mortality was examined in a prospective study of 7,636 middle-aged British men followed for 11.5 years (1978-1991). Men being treated for hypertension had a significantly lower mean (+/- standard error) potassium level than men not in treatment (4.24 +/- 0.03 mmol/liter vs. 4.32 +/- 0.01 mmol/liter; p < 0.01). During the follow-up period of 11.5 years, after exclusion of the 374 men under antihypertensive treatment, there were 771 deaths from all causes in the remaining 7,262 men. A low potassium level (< 3.7 mmol/liter) was not associated with increased mortality. Elevated potassium levels > or = 5.2 mmol/liter were associated with a significant increase in mortality, particularly noncardiovascular deaths, even after adjustment for potentially confounding factors. However, serum potassium was strongly related to smoking, and the increased risk of mortality associated with elevated potassium was seen only among current smokers. In current smokers with raised potassium levels (> or = 5.2 mmol/liter) compared with smokers with levels under 5.2 mmol/liter, the relative risks of mortality were 1.7 (95% confidence interval (CI) 1.2-2.5) for deaths from all causes, 1.8 (95% CI 1.0-3.2) for all cancer deaths, and 2.5 (95% CI 1.1-5.6) for lung cancer deaths. In the 374 men receiving regular antihypertensive treatment, a low potassium level was not associated with excess mortality; those with raised potassium levels had excess risks for both cardiovascular and noncardiovascular deaths. The findings suggest that either raised potassium levels in association with smoking have an influence on the risk of death from noncardiovascular disease, particularly lung cancer, or a raised serum potassium level is a marker for some other risk factor associated with smoking. The prognostic and therapeutic implications of these observations warrant further exploration.

Earlier studies have not resolved the question of whether elevated circulating insulin levels are independently related to the development of coronary heart disease. Previous studies have not used a specific insulin assay and in all but a minority of studies that have addressed this issue it has not been possible to adjust for possible confounding due to high density lipoprotein (HDL) cholesterol. The authors examined the relation between serum insulin concentration and major coronary disease events (fatal and non-fatal myocardial infarction) in the British Regional Heart Study. The data are based on 5,550 men (aged 40-59 years) in 18 towns whose baseline, non-fasting serum samples were analyzed for insulin using a specific enzyme-linked immunoadsorbent assay (ELISA) method. Known diabetics were excluded. At 11.5 years of follow-up, 521 major coronary disease events had occurred, 261 fatal and 260 non-fatal. A nonlinear relation between serum insulin and coronary disease events was observed with an almost twofold increased relative risk in the 10th decile of the serum insulin distribution (> or = 33.8 mU/liter) relative to the 1st to the 9th deciles combined (age-adjusted relative risk (RR) = 1.9, 95% confidence interval (CI) 1.6-2.4). There was some attenuation of this association on cumulative adjustment for a wide range of biologic and life-style coronary disease risk factors, including HDL cholesterol, though it remained significant in the fully adjusted proportional hazards model (RR = 1.6, 95% CI 1.1-2.3). Similar associations between insulin and coronary disease events were seen in men with and without evidence of coronary disease at screening and in men with baseline serum glucose below the 80th percentile. These data are consistent with the hypothesis that a high level of serum insulin (hyperinsulinemia) is atherogenic, with a threshold effect. However, the markedly nonlinear form of the association and the attenuation in multivariate analysis strongly suggest that elevated insulin levels may only be a marker for common etiologic factors in the development of both coronary disease and non-insulin-dependent diabetes mellitus.