Statins, Colorectal Cancer Tie Examined
Long-term statin therapy did not protect against colorectal cancer in a large case-control study in the United Kingdom.
However, neither did statins promote colorectal cancer, as has been reported in the international PROSPER (Pravastatin in Elderly Individuals at Risk of Vascular Disease) trial, wrote Yana Vinogradova, a research statistician at the University of Nottingham (England), and her colleagues in the August 2007 issue of Gastroenterology. The results of trials on the risk of cancer in patients on statins “have been equivocal because of inadequate [statistical] power,” they noted.
The current study was designed to have greater statistical power and analyzed data on over 30,000 patients attending 454 general practices in the United Kingdom between 1995 and 2005. A total of 5,686 patients who developed colorectal cancer during the study period were matched to 24,982 control subjects, and their patterns of medication use were compared.
There was no significant association between statin use in general and risk of colorectal cancer, nor was there any association between the disease and any of five individual statins assessed. When colon and rectal cancers were considered separately, there also was no association between the risk of either type of cancer and statin use.
In contrast, the protective effect of NSAIDs reported in several previous studies was confirmed in this study, with prolonged use of NSAIDs being associated with a 25% or greater reduction in colorectal cancer risk, said the authors.
Exercise Pumps Up HDL Levels
Regular aerobic exercise increases HDL cholesterol levels to a modest but still highly significant degree, reported Dr. Satoru Kodama of Ochanomizu University, Tokyo, and associates.
In their meta-analysis of 35 randomized clinical trials that examined the effect of exercise training on serum levels of HDL cholesterol, every 10-minute increase in the duration of exercise beyond a minimum of 120 minutes per week corresponded to a 1.4-mg/dL rise in HDL cholesterol.
The meta-analysis comprised 35 clinical trials that included 1,404 subjects aged 23–75 years who performed at least 15 minutes a day of exercise such as walking, bicycling, or continuous swimming. They performed a mean of 3.7 exercise sessions each week.
The mean estimated relative intensity of activity was 65% of maximal aerobic capacity. The mean increase in HDL cholesterol levels was “modest although statistically significant” at 2.53 mg/dL, the authors said (Arch. Intern. Med. 2007;167:999–1008).
The findings also showed that there is a minimum amount of exercise—120 minutes a week—below which HDL cholesterol levels will not be affected. To raise HDL cholesterol, an increase in the time of each exercise session would be more effective than an increase in the intensity of the activity, because neither the intensity nor the frequency of exercise was found to correlate with cholesterol levels in this study.
Light Cigarettes Heavy on the Heart
Low-tar, low-nicotine cigarettes impede the coronary flow velocity reserve (CFVR) of smokers as much as do regular cigarettes, according to data from a small study.
The researchers found similar changes in other hemodynamic and coronary flow measurements, all of which contradict the belief that light cigarettes are less dangerous to coronary health.
Forty smokers—half of whom smoked light cigarettes (8 mg tar, 0.6 mg nicotine, and 9 mg CO) and half of whom smoked regular cigarettes (12 mg tar, 0.9 mg nicotine, and 12 mg CO)—had similarly, and significantly, reduced CFVR values, compared with 22 healthy nonsmokers. The mean age was 24–25 years, and smokers had steadily smoked the same kind of cigarette for at least 3 years (Heart 2007 May 15 [Epub doi: 10.1136/hrt.2006.100255]).
Coronary flow velocity reserve at the distal left anterior descending artery was measured using echocardiography, first after a 12-hour fasting and smokeless period and, 2 days later, after the tobacco users smoked two of their usual cigarettes within 15 minutes. Similar decreases in CFVR after smoking were seen in light (2.68 to 2.05) and regular cigarette smokers (2.65 to 2.18). The baseline values in both smoker groups were significantly lower than those of controls.
Similar impairments also were seen between the two smoker groups in mean systolic blood pressure, diastolic blood pressure, and heart rate. The impairment of vascular function was statistically significant, but not clinically disabling.