Many patients with type 2 diabetes require insulin therapy for improved gly
cemic control after beta-cell failure. However, many physicians are relucta
nt to institute insulin therapy in type 2 diabetes for fear of accelerating
atherosclerosis. The epidemiological evidence is reasonably sound that hyp
erinsulinism correlates with increased cardiovascular disease in nondiabeti
c people and those with early type 2 diabetes. II is much less clear, howev
er, that insulin concentration plays a negative role when less well control
led diabetes is considered. The data are more consistent, in fact, with the
glucose hypothesis, i.e., that hyperglycemia is a risk factor, although th
e magnitude of the glucose effect is not well defined. Certainly the dysmet
abolism associated with poor glycemic control could increase the risk of ma
crovascular events through well-known mechanisms. There is direct evidence
that insulin therapy can reduce the risk of macrovascular events by improvi
ng glycemic control and diabetes-associated dyslipidemias, although the ben
eficial effects may be significantly compromised by excessive weight gain.
Insulin therapy does not appear to induce hypertension independent of chang
es in body weight. It is concluded that optimal glycemic control confers a
known benefit and can only be achieved with insulin therapy in some people
with type 2 diabetes. In these circumstances, the use of insulin has a net
benefit on cardiovascular risk, mediated primarily through improvement in d
yslipidemia and glycemia itself.