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Biomedical subjects

S Tonstad

Publications and source records attributed to S Tonstad.

95 records · Page 6Linked to original sources
PubMed1991

[Dietary supplementation in the treatment of hyperlipidemia].

While dietary and pharmacological therapies are the mainstay of treatment of hyperlipidemia, there has been a surge of interest for nonpharmacological treatments such as dietary fibre and food flavourings. In placebo-controlled studies, oat bran in relatively large doses of 56-95 grams per day have been shown to reduce serum cholesterol by 5-9%. Psyllium has caused a 5-15% reduction of serum cholesterol with doses of 10.2 grams per day, and guar gum a reduction of 5-17% with doses of 15 grams per day. Documentation of long-term effects is inadequate. Fresh garlic contains over 70 compounds containing sulphur, which may be biologically active. In animal experiments cholesterol is reduced by supplementing the diet with large doses of fresh, boiled, or dried products. Human studies are poor methodologically, and none has documented constancy of diet during the study.

Cholesterol↗
PubMed1991

Self-report of physical activity and patterns of mortality in Seventh-Day Adventist men.

The Adventist Mortality Study provides 26-year follow-up through 1985 for 9484 males who completed a lifestyle questionnaire in 1960. The relationship of self-reported physical activity and all cause and disease-specific mortality was examined by survival analysis and with the Cox proportional hazards model, controlling for demographic and lifestyle characteristics. Moderate activity was associated with a protective effect on cardiovascular and all cause mortality in both analyses. In the Cox model, age-specific estimates of relative risk (RR) were obtained for several endpoints due to a significant interaction between level of physical activity and attained age (age at death or end of follow-up). This model permits calculation of the age at which the RR = 1.0, or the age at crossover of risk. For moderate activity, this age was 95.6 years (95% confidence intervals, 81.7-109.4 years) for all cause mortality and 91.5 years (95% confidence intervals, 79.0-104.0 years) for cardiovascular mortality. While the protective effect on mortality associated with moderate activity decreased with increasing age, it remained significant to the verge of the present life span.

Adult↗
PubMed1991

Body mass index and patterns of mortality among Seventh-day Adventist men.

This study examines the relationship between body mass index (BMI) and 26-year mortality among 8828 nonsmoking, nondrinking Seventh-day Adventist men, including 439 who were very lean (BMI less than 20 kg/m2). The adjusted relative risk comparing the lowest BMI quintile (less than 22.3) to the highest (greater than 27.5 kg/m2) was 0.70 (95 percent CI 0.63-0.78) for all cause mortality, 0.60 (95 percent CI 0.43-0.85) for cerebrovascular mortality, and 0.80 (95 percent CI 0.61-1.04) for cancer mortality. Very lean men did not show increased mortality. To assess whether the protective effect associated with low BMI is modified by increasing age, the product term between BMI and attained age (age at the end of follow-up or at death) was included as a time-dependent covariate. For ischemic heart disease mortality, age-specific estimates of the relative risk for the lowest quintile relative to the highest ranged from 0.32 (95 percent CI, 0.19-0.52) at age 50 to 0.71 (95 percent CI, 0.56-0.89) at age 90. Interaction was also seen for the next lowest quintile (22.4-24.2). There was a significant trend of increasing mortality with increasing BMI for all endpoints studied. For cancer and cerebrovascular mortality the P-values for trend were 0.0001 and 0.001 respectively. For the other endpoints the P-values were less than 0.0001. Thus, there was no evidence for a J-shaped relationship between BMI and mortality in males. While the protective effect associated with the lowest BMI quintile decreased with increasing age for ischemic heart disease mortality, it remained greater than one at all ages. The relatively large number of subjects who were lean by choice, rather than as a result of preclinical disease or smoking, may explain these findings.

Adult↗
PubMedDate not supplied

Role of lipid-lowering pharmacotherapy in children.

For patients with coronary artery disease and healthy middle-aged or older individuals with elevated cholesterol levels, treatment with cholesterol-lowering drugs reduces morbidity and sometimes mortality. Treatment reverses established atherosclerotic lesions within a relatively short period of time, suggesting that starting cholesterol-lowering drugs in adulthood is adequate for most people at risk. Children with genetic lipid disorders, including familial hypercholesterolaemia and familial combined hyperlipidaemia, may be candidates for earlier therapy. A complete assessment of risk factors should be undertaken to determine which children are at highest risk. Treatment should start with diet, because diet is an important independent protective factor for disease. The bile acid sequestrants (resins) are the only drugs approved for children and may reduce low density lipoprotein (LDL)-cholesterol levels by 15 to 20% at best. Long term tolerability is good, but many children will not take the resins because they find them unpalatable. Tablet formulations have higher acceptability. Some children require supplementation with fat soluble vitamins or folate. Although hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors have not been tested in long term studies in children, safety records are excellent in adults. Short term studies show that HMG-CoA reductase inhibitors reduce LDL-cholesterol levels similarly in children and in adults. Thus, the drugs may be used in low dosages to treat some adolescents with exceptional risk of disease.

Arteriosclerosis↗