Attenuating the mortality risk of high serum uric acid: the role of physical activity underused.

BACKGROUND: High serum uric acid (sUA) has been associated with increased mortality risks, but its clinical treatment varied with potential side effects. The role of physical activity has received limited attention. METHODS: A cohort, consisting of 467 976 adults, who went through a standard health screening programme, with questionnaire and fasting blood samples, was successively recruited between 1996 and 2008. High sUA is defined as uric acid above 7.0 mg/dL. Leisure time physical activity level was self-reported, with fully active defined as those with 30 min per day for at least 5 days a week. National death file identified 12 228 deaths with a median follow-up of 8.5 years. Cox proportional model was used to analyse HRs, and 12 variables were controlled, including medical history, life style and risk factors. FINDINGS: High sUA constituted one quarter of the cohort (25.6%). Their all-cause mortality was significantly increased [HR: 1.22 (1.15-1.29)], with much of the increase contributed to by the inactive (HR: 1.27 (1.17-1.37)), relative to the reference group with sUA level of 5-6 mg/dL. When they were fully active, mortality risks did not increase, but decreased by 11% (HR: 0.89 (0.82-0.97)), reflecting the benefits of being active was able to overcome the adverse effects of high sUA. Given the same high sUA, a 4-6 years difference in life expectancy was found between the active and the inactive. CONCLUSIONS: Physical activity is a valuable alternative to pharmacotherapy in its ability to reduce the increases in mortality risks from high sUA. By being fully active, exercise can extend life span by 4-6 years, a level greater than the 1-4 years of life-shortening effect from high sUA.

Motivating patients to exercise: translating high blood pressure into equivalent risk of inactivity.

OBJECTIVE: Even with the 2008 physical activity guidelines for Americans and the strong epidemiological evidence, physicians are not routinely emphasizing the importance of exercise. We try to explore an innovative way to communicate the benefits of physical activity in a term familiar to patients. METHODS AND RESULTS: A cohort of 470, 163 adults from a medical screening program in Taiwan were recruited between 1994 and 2008. Their vital status was followed up by matching with the National Death File. Individuals were classified as 'inactive', 'low active', or 'fully active', with 'fully active' meeting the current exercise recommendation of 150  min per week or more. Cox proportional model was used to calculate the hazard ratio. More than one-half of the cohort was inactive (54%), with one-quarter fully active (24%). One in seven was hypertensive (14%), defined as SBP at least 140  mmHg. Among the hypertensive individuals, mortality risks were increased by 37% for the inactive. Inactive individuals had higher all-cause mortality than active ones across all blood pressure (BP) levels. At 110-119  mmHg, the inactive had a risk as high as the risk at 155  mmHg, an increased mortality risk equivalent to a risk of BP increase of 41.2 mmHg. CONCLUSION: The mortality risk of being inactive was equivalent to an increase of around 40  mmHg in SBP or 20  mmHg in DBP, a number relevant to hypertensive patients. Appreciating this relationship may convince the inactive to start exercising, a behavior as important as controlling BP.

High serum iron is associated with increased cancer risk.

Epidemiologic studies linking high serum iron with cancer risks are limited and inconclusive, despite evidence implicating body iron in human carcinogenesis. A cohort of 309,443 adults in Taiwan who had no history of cancer had serum iron levels tested at the time of recruitment (1997-2008). Initially measured iron levels were associated with subsequent cancer risk by linking individuals with the National Cancer Registry and National Death File. HRs were calculated by the Cox model. One third of males (35%) and one fifth of females (18%) had high serum iron (≥120 µg/dL), which was associated with a 25% increase in risk for incidence of all cancers [HR, 1.25; 95% confidence interval (CI), 1.16-1.35] and with a 39% increase in risk for mortality from all cancers (HR, 1.39; 95% CI, 1.23-1.57). The relationship between serum iron and cancer risk was a J-shaped one, with higher cancer risk at both ends, either at lower than 60 µg/dL or higher than 120 µg/dL. At the higher end, cancer risk increased by 4% for every 10 µg/dL increment above 80 µg/dL, showing a dose-response relationship, with 60 to 79 µg/dL as a reference level. In a sensitivity analysis, the increases in risk were still observed after the first 5 years of cancer cases were excluded. Liver cancer risk was increased in HBV (-) non-hepatitis B carrier (3-fold) and HBV (+) hepatitis B carrier (24-fold). Lifestyle risks such as smoking, drinking, or inactivity interacted synergistically with high serum iron and significantly increased the cancer risks. The liver (HR, 2.49; 95% CI, 1.97-3.16) and the breast (HR, 1.31; 95% CI, 1.01-1.70) were the two major cancer sites where significant cancer risks were observed for serum iron either ≥120 µg/dL or ≥140 µg/dL, respectively. This study reveals that high serum iron is both a common disorder and a marker of increased risk for several cancers.