There are two major pathways by which atherosclerosis progresses: excess lipids in blood, which end up in atherosclerotic plaque, and inflammatory forces. Much recent research has demonstrated the association of chronic low‐level inflammation (microinflammation) with both diabetes and cardiovascular disease. It appears that microinflammation is not only a result of these diseases but also exhibits “positive feedback,” causing the disease process to accelerate. This downward spiral has a slope that is modified by genetic architecture and environmental variables, and may prove difficult to interrupt or modify effectively, since the pathways involved represent not only pathophysiology but also normal homeostatic physiology. We currently have some medications that do seem to work to modify this process, such as aspirin and statins. The role of the environment is clearly important, but the role of genetic architecture is only now emerging. There is a need for more effective public health efforts in education and behavior modification, as well as economic and political approaches to arrest the burgeoning global epidemic of obesity. We already know that if the lipid burden is decreased, atherosclerosis will decrease. If we can understand the microinflammatory pathways in enough detail, and learn how to modify these activities, we may be able to decrease atherosclerosis through this mechanism as well, and also affect the development of the other chronic diseases of old age. By attacking both major arms we may finally be able to limit chronic progressive atherosclerosis, and possibly the other chronic diseases of old age as well.