From a story on statins in the New York Times discussing the fact that statins increase risk of diabetes:
"Exactly how statins may increase diabetes risk isn’t entirely clear, though animal studies suggest that statins can increase muscle resistance to insulin, resulting in higher levels of circulating blood sugar. Dr. Kausik notes that the patients in the studies were diagnosed with diabetes because of elevated blood sugar levels, but that the long-term consequences of higher blood sugar levels triggered by statin use aren’t known.
" 'Diabetes is defined by blood glucose levels, but none of us are absolutely certain if this is going to carry the same risk as if you traditionally developed diabetes,' Dr. Kausik said.
["Dr. Kausik" is Dr. Kausik Ray, professor of cardiovascular disease prevention at St. George’s University of London and senior author on the paper. Apparently the reporter couldn't even get the name right, so perhaps she also misquoted the doctor. Or maybe she refers to doctors as "Dr. Bob" or "Dr. Mary."]
A high blood glucose level is a high blood glucose level. It doesn't matter what caused it. The good doctor's statement makes as much sense as saying that high blood pressure caused by some drug has different consequences from high blood pressure caused by stress or genetics. It's the high blood pressure, or the high blood glucose, that causes the complications.
One could argue that high blood glucose levels caused by insulin resistance were riskier than high blood glucose levels caused by autoimmunity if you think it's the insulin resistance rather than the high blood glucose levels that are harmful in type 2.
But Dr. Ray said statins increase insulin resistance, so the diabetes they cause is like type 2.
With stupid reasoning like this, it's a miracle any of us survive our doctors' treatments! Remind me to avoid St. George's University of London.
I found it interesting that Dr. Steven Nissen, the one who pressed to have Avandia removed from the market because it increases heart disease risks, is arguing that people shouldn't stop taking statins even though they increase diabetes risks, and diabetes increases heart disease risks.
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See Lancet 2010. Among those with diabetes even after adjustment for risk factors including glucose (in 600 000 people studied, the largest study ever)the is about a 70% excess risk from "diabetes". i.e. glucose alone or in combination with other factors does not explain how diabetes increases CVD risk. Per SD change in glucose, vs LDL, vs BP glucose is a much weaker risk factor . So per 1000 pt years a 4 mmHg lowerig of BP reduces about 12.5 events, a 1 mmol/L lowering of LDL-C 8.5 events and a 1 % lowering of HbA1c 2 events. For every 1000 tx with a statin one extra case where glucose levels increase sufficiently to define someone as diabetic but about 9 first CVD events prevented. Finally as with anti hypertensives that also induce dysglycaemia , this appears reversible, unlike diabetes which is there although glucose levels may be controlled. As with all things it is good to look at the totally of the data.
ReplyDeleteAnonymous, there are a lot of articles in Lancet in 2010, so I'm not clear what you're referring to.
ReplyDeleteTry looking at this and web data. Diabetes mellitus, fasting blood glucose concentration, and risk of vascular disease: a collaborative meta-analysis of 102 prospective studies. Lancet. 375(9733): p. 2215-22.
ReplyDeletealso look at this esp the discussion comparing the benefits of different interventions
Effect of intensive control of glucose on cardiovascular outcomes and death in patients with diabetes mellitus: a meta-analysis of randomised controlled trials. Lancet, 2009. 373(9677): p. 1765-72.
Also look at
Impact of diabetes on cardiovascular disease risk and all-cause mortality in older men: influence of age at onset, diabetes duration, and established and novel risk factors. Arch Intern Med. 171(5): p. 404-10.
Predictors of new-onset diabetes in patients treated with atorvastatin: results from 3 large randomized clinical trials. J Am Coll Cardiol. 57(14): p. 1535-45.