Upon hearing that Robert Edwards won the Nobel Prize in Physiology or Medicine last Monday for the biological studies and medical implementation of in vitro fertilization, an inkling of cynic in me thought about how this advance primarily serves the relatively wealthy nations of the world.
Not that this is terribly different from any other medicine prize that recognizes contributions to the richest segment of society. For example, malaria has not been the subject of the prize since 1902 and 1907 when Robert Ross won for demonstrating the insect-mammal lifecycle of Plasmodium and Alphonse Laveran won for originally identifying the protozal nature of the infectious agent (and as the founder of the field of medical protozoology), respectively. But even with that, the Nobel citation for Ross noted first the 76,000 members of the British army in India hospitalized for malaria in 1897 before it discussed the five million Indian civilians who died of the disease.
Of course, the 4 million individuals who owe their lives to IVF – and the parents who have the life experience they desired – may disagree as to the relative importance of Edwards’s work. But leave it to The Onion to put such cynicism into their inimitable style:
The Nobel Prize in Medicine was awarded Monday to Robert Edwards, the British in vitro fertilization pioneer who made it possible for shitloads more babies to be born on top of the half million or so daily births already dangerously stressing the planet’s dwindling resources.
But what equally caught my eye was their closing sentence that joked about awarding the Prize in Chemistry to “the inventor of Pepcid antacids, which allow people to eat twice as much goddamn food as anybody needs.”
In fact, it turns out that the Prize – in Physiology or Medicine – was actually awarded in 1988 in part for the discovery of the forerunner to Pepcid, cimetidine or Tagamet. In that case, one-third of the award went to the industrial and academic physiologist and pharmacologist, Sir James Black, for the discovery of “beta-blocker” drugs for coronary heart disease as well as the identity H2-histamine receptors and design of antagonists for peptic ulcers. Pepcid (famotidine) and Zantac (ranitidine) were second-generation structural analogs that lack the liability of cimetidine in inhibiting the metabolism of other drugs.
An aside – For the chemists and pharmacologists, this was accomplished by replacing the imidazole structure with a thiazol or furan, for famotidine and ranitidine, respectively. If this kind of thing excites you, I encourage you to read Sir James’s beautifully-written Nobel lecture, “Drugs from Emasculated Hormones: The Principles of Syntopic Antagonism” – PDF here. You may also care to read these recollections of Sir James Black published in the July 2010 issue of the British Journal of Pharmacology following his death this past summer. I was honoured – yes, “honoured” – to have my remembrance included in the compilation of reflections (full text, PDF.) In fact, I am grateful to Wiley and the British Pharmacological Society for making the entire BJP issue dedicated to Sir James open-access. It includes not only the personal reflections but several of his original papers and personal history of his work.
The remainder of the 1988 prize was shared with my chemotherapy heroes, Gertrude Elion and George Hitchings, for antimetabolite chemotherapeutics that also gave rise to treatments for gout and in organ transplantation.
Hence, my dear friends at The Onion, the Nobel Prize has already been awarded in reality for the science that gave rise to Pepcid, albeit not to the exact inventors at Merck. These drugs, however, were originally developed to treat peptic ulcer disease, a potentially lethal disease, especially for people over age 55 – not so that we could eat far more food than we need.
However, I have nothing to add on their joke about the Nobel Prize in Literature going to Twilight author Stephenie Meyer. I believe that one is still not true.
Compilation. (2010). Sir James Black (1924-2010) reflections British Journal of Pharmacology, 160: S5-S14 DOI: 10.1111/j.1476-5381.2010.00846.x
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