Stanford Health Policy is a joint effort of the Freeman Spogli Institute for International Studies and the Stanford School of Medicine
FSI’s researchers assess health and medicine through the lenses of economics, nutrition and politics. They’re studying and influencing public health policies of local and national governments and the roles that corporations and nongovernmental organizations play in providing health care around the world. Scholars look at how governance affects citizens’ health, how children’s health care access affects the aging process and how to improve children’s health in Guatemala and rural China. They want to know what it will take for people to cook more safely and breathe more easily in developing countries.
FSI professors investigate how lifestyles affect health. What good does gardening do for older Americans? What are the benefits of eating organic food or growing genetically modified rice in China? They study cost-effectiveness by examining programs like those aimed at preventing the spread of tuberculosis in Russian prisons. Policies that impact obesity and undernutrition are examined; as are the public health implications of limiting salt in processed foods and the role of smoking among men who work in Chinese factories. FSI health research looks at sweeping domestic policies like the Affordable Care Act and the role of foreign aid in affecting the price of HIV drugs in Africa.
A growing body of evidence suggests that managed care can reduce overall health care costs but provides little insight into how this could happen. One possibility is that managed care influences the adoption of new medical technologies. In examining the relationship between health maintenance organization (HMO) activity and market-level availability and use of magnetic resonance imaging (MRI), we find that high HMO market share is associated with low levels of MRI availability and use. This suggests that managed care may be able to reduce health care costs by influencing the adoption and use of new medical equipment and technologies.
Signs of a managed care backlash in California are increasing. This paper reports and interprets the recently completed work of the California Managed Health Care Improvement Task Force, focusing on the managed care backlash and the state's regulatory response. Although cost containment was a contributing factor, the causes of and solutions to the backlash differ among consumers, physicians, health care workers, politicians, and health plans. The recommendations of the task force could improve the market for health insurance. However, lasting solutions to the profound problems causing the backlash will require fundamental cultural and systemic change.
Signs of a managed care backlash in California are increasing. This paper reports and interprets the recently completed work of the California Managed Health Care Improvement Task Force, focusing on the managed care backlash and the state's regulatory response. Although cost containment was a contributing factor, the causes of and solutions to the backlash differ among consumers, physicians, health care workers, politicians, and health plans. The recommendations of the task force could improve the market for health insurance. However, lasting solutions to the profound problems causing the backlash will require fundamental cultural and systemic change.
Background & Aims: It is not known why some people with Helicobacter pylori infection develop gastric cancer whereas others do not. Whether the CagA phenotype of H pylori infection affected risk for cancer independently of other posited risk factors was evaluated.
Subjects: 242 persons who participated in a previous nested case-control study of gastric cancer. 179 (90 cases and 89 controls) were infected with H pylori as determined by enzyme linked immunosorbent assay (ELISA) in serum and 63 (13 cases and 50 controls) were uninfected.
Methods: Serum samples from cases and controls, obtained a mean of 14.2 years before diagnosis of cancer in the cases, were tested by ELISA for IgG antibodies against the CagA gene product of H pylori. They had previously been tested for pepsinogen I. Using logistic regression analysis, risk for cancer was compared among infected persons with CagA antibodies, infected persons without CagA antibodies, and uninfected persons.
Results: Subjects infected with H pylori who had CagA antibodies were 5.8-fold more likely than uninfected subjects to develop gastric cancer (95% confidence interval (95% CI) = 2.6-13.0). This was true for both intestinal (odds ratio (OR) 5.1, 95% CI = 2.1-12.2) and diffuse type (OR 10.1, 95% CI = 2.2-47.4) cancers. By contrast, H pylori infected subjects without CagA antibodies were only slightly, and not significantly, at increased risk for cancer (OR 2.2, 95% CI = 0.9-5.4) and any possible association was restricted to diffuse type carcinoma (OR 9.0, 95% CI = 1.2-65.8). Pepsinogen 1 50 ng/ml significantly increased risk for both cancer types in H pylori infected persons and lessened the magnitude of association between CagA and cancer. Educational attainment, cigarette smoking, and ABO blood group were not associated with malignancy.
Conclusions: When compared with uninfected subjects, persons infected with CagA positive H pylori are at considerably increased risk of gastric cancer. CagA negative H pylori are less strongly linked to malignancy and may only be associated with diffuse type disease.