Cramer et al. reported less dementia and cognitive decline among statin users in the SALSA study participants. [1] This study implied that less cognitive decline may be a statin benefit yet the authors did not attribute the finding to the selection and prescribing bias.
The only on-label prescribing rationale for statin is elevated cholesterol, thereby unselecting those with lower levels of cholesterol. This was recently confirmed by a study asserting that, "Overall, the mean baseline cholesterol measurement of the statin-treated population is higher than that of the general population." [2]
The Framingham Heart study found that those with high cholesterol—defined as 240-380 mg/dL [6.1-9.7 mmol/L]—had significantly better cognition scores than those with lower levels of 150-199 mg/dL (3.85-5.1 mmol/L; P <_0.01 for="for" group="group" test="test" scores.="scores." _3="_3" p="p"/>Statin prescriptions naturally select a higher cholesterol population where cognitive status tends to be better. Cramer et al. should have conducted a simple cholesterol test as was done in the Framingham study. In the abstract, Cramer et al.’s conclusion suggests a protective effect of statin use on cognitive outcomes. However, this is not supported by other data and cannot be concluded from this patient selection study where baseline cholesterol pre-statin use is the one factor for which there was not adjustment. The authors, later in the article, mention that no randomized study to date has reported a cognitive benefit from statin use. This contradicts the assertion made in the abstract.
Cholesterol is vital to memory and the aging brain [4] and the message the authors convey may promote non evidence-based drug use. At an age where cognitive decline, low cholesterol, and heart failure become major health issues, a recent observational study found 2.6 times the in-hospital mortality from heart failure in those with lowest cholesterol, an effect that became highly significant among statin users. [5]
References
1. Cramer C, Haan MN, Galea S, Langa KM, Kalbfleisch JD. Use of statins and incidence of cognitive impairment without dementia in a cohort study. Neurology 2008;71:344-350.
2. Thompson R, O’Regan C, Morant A, Phillips B, Ong S. Measurement of baseline total cholesterol: new data from The Health Improvement Network (THIN) database. Prim Care Cardiovasc J 2008;1:107-111.
3. Elias PK, Elias MF, D'Agostino RB, Sullivan LM, Wolf PA. Serum cholesterol and cognitive performance in the Framingham Heart Study. Psychosom Med 2005;67:24-30.
4. West R, Beeri MS, Schmeidler J, et al. Better memory functioning associated with higher total and low-density lipoprotein cholesterol levels in very elderly subjects without the apolipoprotein e4 allele. Am J Geriatr Psychiatry 2008;16:781-785.
5. Horwich TB, Hernandez AF, Dai D, Yancy CW, Fonarow GC. Cholesterol levels and in-hospital mortality in patients with acute decompensated heart failure. Am Heart J 2008:0:1-7 (in press).
Cramer et al. reported less dementia and cognitive decline among statin users in the SALSA study participants. [1] This study implied that less cognitive decline may be a statin benefit yet the authors did not attribute the finding to the selection and prescribing bias.
The only on-label prescribing rationale for statin is elevated cholesterol, thereby unselecting those with lower levels of cholesterol. This was recently confirmed by a study asserting that, "Overall, the mean baseline cholesterol measurement of the statin-treated population is higher than that of the general population." [2]
The Framingham Heart study found that those with high cholesterol—defined as 240-380 mg/dL [6.1-9.7 mmol/L]—had significantly better cognition scores than those with lower levels of 150-199 mg/dL (3.85-5.1 mmol/L; P <_0.01 for="for" group="group" test="test" scores.="scores." _3="_3" p="p"/>Statin prescriptions naturally select a higher cholesterol population where cognitive status tends to be better. Cramer et al. should have conducted a simple cholesterol test as was done in the Framingham study. In the abstract, Cramer et al.’s conclusion suggests a protective effect of statin use on cognitive outcomes. However, this is not supported by other data and cannot be concluded from this patient selection study where baseline cholesterol pre-statin use is the one factor for which there was not adjustment. The authors, later in the article, mention that no randomized study to date has reported a cognitive benefit from statin use. This contradicts the assertion made in the abstract.
Cholesterol is vital to memory and the aging brain [4] and the message the authors convey may promote non evidence-based drug use. At an age where cognitive decline, low cholesterol, and heart failure become major health issues, a recent observational study found 2.6 times the in-hospital mortality from heart failure in those with lowest cholesterol, an effect that became highly significant among statin users. [5]
References
1. Cramer C, Haan MN, Galea S, Langa KM, Kalbfleisch JD. Use of statins and incidence of cognitive impairment without dementia in a cohort study. Neurology 2008;71:344-350.
2. Thompson R, O’Regan C, Morant A, Phillips B, Ong S. Measurement of baseline total cholesterol: new data from The Health Improvement Network (THIN) database. Prim Care Cardiovasc J 2008;1:107-111.
3. Elias PK, Elias MF, D'Agostino RB, Sullivan LM, Wolf PA. Serum cholesterol and cognitive performance in the Framingham Heart Study. Psychosom Med 2005;67:24-30.
4. West R, Beeri MS, Schmeidler J, et al. Better memory functioning associated with higher total and low-density lipoprotein cholesterol levels in very elderly subjects without the apolipoprotein e4 allele. Am J Geriatr Psychiatry 2008;16:781-785.
5. Horwich TB, Hernandez AF, Dai D, Yancy CW, Fonarow GC. Cholesterol levels and in-hospital mortality in patients with acute decompensated heart failure. Am Heart J 2008:0:1-7 (in press).
Disclosure: The authors report no disclosures.