In this large, prospective cohort study of older US adults, lifestyle factors including physical activity level, dietary habits, smoking habits, alcohol use, and adiposity measures, assessed late in life, were each independently associated with risk of new-onset diabetes. In combination, these basic lifestyle risk factors strongly predicted diabetes incidence, with an approximately 50% lower risk with only physical activity level and dietary habits in the low-risk group and an approximately 80% lower risk with physical activity level, dietary habits, smoking habits, and alcohol use in the low-risk group. In sum, 8 in 10 cases of diabetes in this population of older adults appeared attributable to these 4 lifestyle factors, suggesting that, if these associations are causal, 8 in 10 new cases of diabetes might have been prevented if all older adults were in the low-risk group for these lifestyle factors. Adding either not being overweight or not having a high waist circumference, nearly 9 in 10 new cases of diabetes appeared attributable to not being in the low-risk group for these lifestyle factors. These findings provide an estimate of the public health burden of combined nonoptimal lifestyle risk factors for incidence of diabetes in older adults, the fastest growing segment of the US population.
We assessed incidence of diabetes defined by drug treatment alone; by drug treatment or abnormal fasting glucose level; or by drug treatment, abnormal fasting glucose level, or abnormal 2-hour postchallenge glucose level. Each of these different diagnostic classes may have different clinical implications and even potentially different underlying pathophysiological characteristics. Because fasting glucose and oral glucose tolerance testing were not available at each annual visit, our findings likely underestimate the incidence of diabetes defined by these criteria. Nevertheless, we observed similar relationships between lifestyle and incident diabetes by each of these definitions, suggesting robust effects of lifestyle factors on diabetes risk among older adults regardless of the methods for diagnosis.
Quantifying the impact of all of the different possible combinations of different lifestyle factors on diabetes incidence among older adults would be difficult or even unethical in randomized controlled trials. Our results provide evidence for a tremendous combined impact of lifestyle on diabetes risk in older adults. Notably, the magnitudes of diabetes prevention from intervening on only 2 lifestyle factors (diet and physical activity) in structured randomized trials among selected high-risk adults1,2
are quite consistent with our observed PAR% for these same 2 lifestyle factors. In the Diabetes Prevention Program trial, which included overweight or obese adults with both elevated fasting glucose levels and elevated 2-hour post-challenge glucose levels, structured advice to adopt a healthy low-calorie diet and be moderately active (eg, walking briskly on most days of the week) reduced incidence of diabetes by 58%.1
Similarly, in the Finnish Diabetes Prevention Study, which included overweight middle-aged adults with abnormal 2-hour postchallenge glucose levels, incidence of diabetes was reduced 58% by a structured program to increase physical activity to at least 30 min/d and to promote a healthy low-calorie diet that included whole-grain products, vegetables, fruits, low-fat milk and meat products, and soft margarines and vegetable oils.2
The magnitude of our findings—approximately 50% lower incidence of diabetes with only moderate physical activity and better dietary habits ()—are consistent with the magnitude of effect in these trials, suggesting that the substantial benefits of moderate physical activity and diet for preventing diabetes seen in the high-risk trials extend to a much broader and much less selected general population of older adults.
In the Finnish trial, no cases of diabetes occurred among individuals in either the control or intervention group who achieved at least 4 of 5 main activity, dietary, and weight loss goals.2
Although numbers were small (only 64 participants achieved 4 or more goals), these findings suggested that diabetes may be almost entirely preventable in this high-risk middle-aged population. Our observational findings in a large cohort of older men and women suggest, similarly, that diabetes may be largely preventable among older adults through adherence to a similar set of relatively modest lifestyle goals.
The magnitudes of our findings are further supported by the effects of diet and physical activity evaluated singly or together in controlled trials and cohort studies, often with lifestyle assessment occurring in midlife. In controlled trials of intermediate endpoints, physical activity improves fasting and postprandial glucose-insulin homeostasis, induces and maintains weight loss, raises high-density lipoprotein cholesterol levels, lowers low-density lipoprotein cholesterol and triglyceride levels, lowers blood pressure, and probably lowers inflammation and improves endothelial function.6,30
These benefits are achieved with moderate activity, eg, 30 minutes of brisk walking on most days.4–7,30,31
Several dietary factors have been associated with lower incidence of diabetes, including higher consumption of dietary fiber and polyunsaturated fats and lower consumption of trans
fats and easily digestible (higher glycemic index) carbohydrates.8,9
In controlled trials, dietary habits affect fasting and postprandial glucose-insulin homeostasis, inflammatory pathways, and satiety; benefits may be greatest in persons most predisposed to diabetes.32
In the Diabetes Prevention Program trial, advice to improve dietary habits and physical activity improved multiple cardio-metabolic risk factors, including lowering of systolic and diastolic blood pressure, improving heart rate variability, lowering of triglyceride levels and raising of high-density lipoprotein cholesterol levels, and reducing prevalence of hypertension and hyperlipidemia.3,33
In comparison, metformin treatment reduced glucose levels and slightly raised high-density lipoprotein cholesterol levels, but produced none of these other additional benefits.3,33
We also found smoking and alcohol habits to be independently associated with diabetes incidence among older adults. In a meta-analysis of prospective cohort studies with a total of 1.2 million participants, current and former smokers had a higher incidence of diabetes compared with those who had never smoked.15
Based on the estimates in this meta-analysis and the weighted mean of former and current smokers in our cohort, our participants who had never smoked would have been expected to have a 22% lower risk of diabetes—very similar to the observed 23% lower risk. Smoking is proinflammatory34,35
and may also induce insulin resistance36–38
and increase visceral adiposity,39–41
each of which is strong risk factor for diabetes. Consistent with the time course of our results for diabetes incidence, several years of smoking cessation are required among older men and women for C-reactive protein levels to approach those of individuals who never smoked.35
Modest alcohol consumption is also associated with lower diabetes risk: 2 meta-analyses of prospective observational studies13,14
found an approximately 30% lower diabetes incidence with modest consumption (eg, 0.5–2.5 drinks per day14
) compared with nonconsumers. In contrast, high consumption (≥3 drinks per day) was not associated with lower diabetes risk.13,14
The observed lower risk (approximately 30%) in the present study of older adults (mean age, 73 years at baseline) is consistent with these previous findings in predominantly middle-aged populations. In our population, few individuals (6%) consumed more than 2 drinks per day, and thus the observed lower risk should be interpreted as that largely associated with modest intake (≤2 drinks per day). In a meta-analysis of controlled trials, alcohol improved lipid levels associated with diabetic dyslipidemia, with approximately 2 drinks per day increasing high-density lipoprotein cholesterol by 4 mg/dL and decreasing triglyceride levels by 5.7 mg/dL (to convert to millimoles per liter, multiply by 0.0113).42
In patients with type 2 diabetes mellitus, randomization to 1 glass of wine vs nonalcoholic beer with dinner for 3 months lowered fasting glucose from 140 to 118 mg/dL (P
=.02); glycosylated hemoglobin levels also decreased (from 7.4% to 7.1%; P
<.05), although this decrease was not significantly different from the control group.43
Metabolism of alcohol increases the hepatic cytosolic ratio of NADH to NAD+ (NADH dehydrogenase/nicotinamide adenine dinucleotide) and may inhibit gluconeogenesis, increase antioxidant capacity, and lower advanced glycation end products,44
suggesting potential biological mechanisms whereby modest alcohol intake may lower diabetes risk.
The strong associations and likely causal effects of adiposity, particularly central adiposity, for diabetes risk do not require further elaboration.7,10
Comorbidity and frailty are common among older adults, and changes in lean body mass may reduce the precision of BMI and waist circumference for assessing central adiposity later in life.45
Nevertheless, we found that both adiposity measures were independently associated with diabetes risk among older adults. However, even adjusting for the adiposity measures, differences in other lifestyle factors including physical activity, diet, smoking, and alcohol use together explained much of the incidence of diabetes. This is likely because many effects of these lifestyle factors are independent of effects on adiposity. Because some other effects of these lifestyle habits are mediated through effects on adiposity, adjustment for adiposity when evaluating these lifestyle habits would also in part represent overadjustment.
Our analysis had several strengths. Information on sociodemographic factors, lifestyle risk factors, and diabetes incidence were prospectively collected in a well-established multicenter cohort study with little loss to follow-up. Repeated assessments over time allowed updating of lifestyle factors during follow-up, minimizing misclassification. Adequate numbers of events provided sufficient power to detect modest associations with risk. Participants were randomly selected and enrolled from Medicare eligibility lists in several US communities, providing a population-based sample of older adults and increasing generalizability.
Potential limitations should also be considered. Although we adjusted for major sociodemographic characteristics and lifestyle factors simultaneously, residual confounding by unknown or unmeasured factors may be present. Conversely, given the magnitude of many of the risk estimates (including several RRs <0.20) and consistency of our results with prior controlled trials of some lifestyle factors, it is improbable that all of the observed risk differences are owing to residual confounding. Data on fasting and postchallenge glucose levels were available at limited time points, and thus diabetes incidence based on these criteria might be misclassified. This could partly account for the somewhat less pronounced associations between lifestyle factors and diabetes by laboratory criteria; it is also possible that lifestyle factors have greater effect on incidence of medically treated, and presumably more severe, diabetes. The diagnosis of medically treated diabetes could also relate to lifestyle. Individuals with poor lifestyle could receive closer medical attention, causing overestimation of diabetes incidence among those with less healthy lifestyles; alternatively, individuals with healthier lifestyles might be more likely to have access to or seek medical care, causing overestimation of diabetes incidence among those with more healthy lifestyles. Some effects of dietary and physical activity habits are likely mediated through changes in adiposity, and, therefore, adiposity-adjusted analyses might underestimate the full impact of diet and physical activity. Some misclassification of lifestyle factors, particularly diet and physical activity, is probable, which would likely attenuate findings toward the null and underestimate the true magnitude of the associations. Dichotimization of different lifestyle variables (diet, activity, adiposity, etc) that have graded effects on risk would also attenuate the magnitude of association compared with other comparisons (eg, continuous or across quintiles). Therefore, our findings likely underestimate the importance of each of the individual lifestyle factors and their combined effects on disease risk; even small changes are likely to have an important effect on a population level. Finally, although the Cardiovascular Health Study represents a population-based survey from 4 US communities, the least healthy individuals are often less likely to participate in long-term studies. Thus, prevalence of healthier lifestyles may be overestimated and extremes of poor lifestyle habits underestimated, so that the RRs and PAR%s may be underestimates of the true effects.
Our findings suggest that, even later in life, the great majority of cases of diabetes are related to lifestyle factors. Our results support the need for emphasizing healthy and achievable physical activity and dietary goals among older adults, including moderate leisure-time activity and walking pace, higher intake of dietary fiber and polyunsaturated fat, and lower intake of trans fats and easily digestible carbohydrates. Although public health complexities and competing risks do not support recommending alcohol use to reduce diabetes incidence among older adults, our findings are consistent with recommendations that do not prohibit moderate alcohol use among older adults having no contraindications. Given low risk among nonsmokers or former smokers who quit at least 20 years ago or smoked for no more than 5 pack-years, our findings also support the importance of reducing smoking, and preventing initiation of smoking, earlier in life. Most of these moderate lifestyle behaviors will also reduce central obesity and its adverse metabolic consequences, further contributing to reduced incidence of diabetes in older adults.