Executive Authority to Reform Health: Options and Limitations

Presidential power has provoked increasingly vigorous debate since the turn of this century. In recent years, scholars and lawyers have been grappling with how Congress\u27s dictates may limit the President\u27s Commander-in-Chief power to detain enemy combatants at Guantanamo Bay, to fight wars abroad, and to conduct intelligence activities at home. But policymakers have not yet explored the many possibilities for invoking the President\u27s Take Care power to change health care policy. This paper explores the scope and limits of President Barack Obama\u27s ability to invoke his executive authority to reform health care. Specifically, it identifies ways the Obama Administration can use directives to: (1) expand Medicaid and SCHIP coverage through section 1115 waivers; (2) test quality initiatives through Medicare demonstration authority; (3) expand health information technology; (4) allow drug reimportation and experiment with contracting power under Medicare; (5) enhance patient protections and private coverage requirements; (6) lift coverage restrictions on Medicaid and SCHIP; and (7) build on the health insurance program for federal employees. Consistent with the mission of the Legal Solutions in Health Reform project, this paper does not endorse a particular policy. Instead of recommending what, it explains how

Legal Solutions in Health Reform: Executive Authority to Reform Health: Options and Limitations

Examines which healthcare reforms the president can implement without congressional approval and how. Identifies options for promoting and directing agency actions on specific policy goals, as well as legal, budgetary, and legislative constraints

Candidate genes for alcohol dependence: A genetic association study from India

Background & objectives: Search for candidate genes for alcohol dependence (AD) has been inconsistent and inconclusive. Moreover, most of the research has been confined to a few specific ethnic groups. Hence, the aim of our study was to explore specific candidate genes for AD in north Indian male population. Methods: In this clinic-based genetic association study, 210 males with AD and 200 controls matched for age, gender and ethnicity were recruited from the clinic and the general population, respectively. Cases were diagnosed with Semi-structured Assessment for Genetics of Alcoholism-II (SSAGA-II). Single-nucleotide polymorphism genotyping was done by real-time quantitative-polymerase chain reaction (PCR) using Taq Man assay (ABI 7500) fast real-time PCR system. Results: Both at the genotypic level and at allelic frequency, Met158 variant of catechol-O-methyl transferase (COMT) showed significant increase in cases as compared to controls. The frequency of heterozygous genotype (A/G) of gamma-aminobutyric acid receptor A1 (GABRA1) was significantly lower in cases as compared to controls. Likewise, for GABRA2, the frequency of homozygous recessive genotype (G/G) was significantly higher in the control group. With respect to the 5-hydroxytryptamine (5HT) transporter long promoter region (5HTTLPR), cholinergic receptor muscarinic (CHRM2) and alcohol dehydrogenase 1B (ADH1B) genes, there was no significant difference between the cases and the controls. Aldehyde dehydrogenase (ALDH2) gene was found to be monomorphic in our study population. Interpretation & conclusions: Our study findings showed COMT polymorphism conferring risk and GABRA polymorphism as a protective genotype for Indian male with AD. Genes for alcohol metabolism, serotonin transporter and cholinergic receptor gene polymorphism were perhaps not contributory to AD for Indian population