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<dc>
   <title>The red wine hypothesis: from concepts to protective signalling molecules</title>
   <creator>Lionel H. Opie</creator>
   <creator>Sandrine Lecour</creator>
   <date>2007</date>
   <description>We review evidence for and against the ‘red wine hypothesis’, whereby red wine is more likely to confer cardiovascular benefits than white. As background, there is a strong
      epidemiological and mechanistic evidence for J-shaped relation between alcohol intake and total mortality. However, epi- Resveratrol; Molecular mechanisms; Sirtuin demiological data favouring a
      specific benefit of red over white wine are not strong and the ‘French paradox’ could at least in part be explained by confounding factors. More convincing evidence is that human studies with
      de-alcoholized red but not white wine show short-term cardiovascular benefits. The specific components of the de-alcoholized wine that are active on cardiovascular endpoints, are the polyphenols
      found in red wine, especially resveratrol. The effects of resveratrol on isolated tissues or organs are well-described including molecular mechanisms leading to decreased arterial damage,
      decreased activity of angiotensin-II, increased nitric oxide, and decreased platelet aggregation. Anti-ischaemic effects include stimulation of prosurvival paths, decreased LDL-oxidation,
      atheroma, and on the ischaemic-beneficial metabolic changes. Most recently, the agonist effect of resveratrol on the anti-senescence factor sirtuin has lessened cell death in myocytes from
      failing hearts. Mechanistic feasibility strengthens the case for prospective therapeutic trials of alcohol vs. red wine vs. resveratrol, for example in those with heart failure. </description>
   <subject>wine</subject>
   <subject>alcohol</subject>
   <type>text</type>
</dc>
