Woodrow Wilson's hidden stroke of 1919: the impact of patient-physician confidentiality on United States foreign policy.

World War I catapulted the United States from traditional isolationism to international involvement in a major European conflict. Woodrow Wilson envisaged a permanent American imprint on democracy in world affairs through participation in the League of Nations. Amid these defining events, Wilson suffered a major ischemic stroke on October 2, 1919, which left him incapacitated. What was probably his fourth and most devastating stroke was diagnosed and treated by his friend and personal physician, Admiral Cary Grayson. Grayson, who had tremendous personal and professional loyalty to Wilson, kept the severity of the stroke hidden from Congress, the American people, and even the president himself. During a cabinet briefing, Grayson formally refused to sign a document of disability and was reluctant to address the subject of presidential succession. Wilson was essentially incapacitated and hemiplegic, yet he remained an active president and all messages were relayed directly through his wife, Edith. Patient-physician confidentiality superseded national security amid the backdrop of friendship and political power on the eve of a pivotal juncture in the history of American foreign policy. It was in part because of the absence of Woodrow Wilson's vocal and unwavering support that the United States did not join the League of Nations and distanced itself from the international stage. The League of Nations would later prove powerless without American support and was unable to thwart the rise and advance of Adolf Hitler. Only after World War II did the United States assume its global leadership role and realize Wilson's visionary, yet contentious, groundwork for a Pax Americana. The authors describe Woodrow Wilson's stroke, the historical implications of his health decline, and its impact on United States foreign policy.

Variation in plasma corticosterone in migratory songbirds: a test of the migration-modulation hypothesis.

Physiological mechanisms underlying migration remain poorly understood, but recent attention has focused on the role of the glucocorticoid hormone corticosterone (CORT) as a key endocrine regulator of migration. The migration-modulation hypothesis (MMH) proposes that baseline plasma CORT levels are elevated in migratory birds to facilitate hyperphagia and lipogenesis and that further elevation of CORT in response to acute stress is suppressed. Consequently, CORT may be a poor indicator of individual condition or environmental variation in migratory birds. We tested the MMH by measuring baseline and stress-induced CORT in common yellowthroats (Geothlypis trichas) during fall migration over 2 consecutive years in the Revelstoke Reach drawdown zone, a migratory stopover site affected by local hydroelectric operations. Birds had low baseline CORT at initial capture (<5 ng/mL) and then showed a robust stress response, with CORT increasing to ca. 50 ng/mL within 10-20 min. Our data therefore do not support the MMH. Baseline CORT did not vary with body mass, time of capture, Julian day, or year, suggesting that variable flooding regimes did not affect baseline CORT. Individual variation in the rate of increase in CORT was correlated with Julian day, being higher later in the migration period. Our data suggest that plasma CORT can be a useful metric in migration studies.