Editorial
658 www.thelancet.com Vol 376 August 28, 2010
For Donald Barr’s essay see Perspectives page 678
What makes a good doctor?
The attributes of a good doctor vary according to the population surveyed. Patients value communication and care, colleagues seek competence and camaraderie, medical students prize cheerfulness. By contrast, admission panels focus on chemistry grades, as if knowledge of ionic bonds is somehow a proxy for the complex human and organisational bonds between doctors, their patients, and colleagues. As a result, most people seeking a career in medicine must fi rst master chemistry; those who cannot do so are unlikely to become doctors. This ritual was played out on Aug 19, when university applicants in the UK, including those aspiring to medicine, received examination results and wondered breathlessly if their chemistry (or other) grades would be satisfactory. In today’s The Art of Medicine, Donald Barr questions whether medical schools’ scientifi c bias actually selects the best doctors.
The tyranny of basic science over admissions dates from the Flexner Report 100 years ago, which redefi ned medical education in the USA. By emphasising the importance of
scientifi c study before medical school, and then a science- based medical curriculum, Abraham Flexner improved the quality of medical education, practice, and research. But at what cost? The measures transformed medical schools into the exclusive and expensive institutions they remain today, and by 1925, Flexner himself worried that the pendulum had swung too far towards science and away from the humanitarian aspects of medicine.
To their credit, many medical schools seek balanced intakes from a diverse pool of highly talented applicants.
But at a time when universities prefer to be known for their research rather than their education, there is a danger that scientifi c in-breeding will produce cadres of doctors who are neither content nor emotionally competent to provide the daily clinical care that underpins health systems. To get the chemistry right for future generations, a more holistic and sophisticated approach to selection—based on predictors of care that are both valid and patient-relevant—needs to be developed and applied. ■ The Lancet
Why are drug trials in Alzheimer’s disease failing?
Last week, semagacestat added itself to the phase 3 scrapheap of other disease-modifying hopefuls for Alzheimer’s disease. This drug is a γ-secretase inhibitor of the fi nal step in amyloid-β protein synthesis, aggregates of which form plaques, the hallmark of the disease.
A recent review in The Lancet Neurology summarises the problems for drug development in Alzheimer’s disease.
Other drugs also failed phase 3 trials. Hopes were high for latrepirdine, but its CONNECTION study did not reveal a signifi cant diff erence from control in March this year.
Similarly, tramiprosate and tarenfl urbil were abandoned.
These studies join trials for other neurological diseases, including stroke, multiple sclerosis, and Parkinson’s disease, which, while showing promise in animal studies and early human trials, were discontinued at late stages.
How do these drugs manage to progress to this stage?
Meta-analysis suggested that some animal models inaccurately predict drug effi cacy. The failure of the translation of research could be attributable to poor methodology in animal studies, or the use of models that do not accurately refl ect human pathogenesis.
Another meta-analysis showed that neutral or non- signifi cant animal studies are less likely to be published—
such publication bias can overestimate effi cacy.
Current treatment targets patients with symptomatic Alzheimer’s disease. But perhaps the disease is being treated too late, when damage is irreparable? The best time to treat Alzheimer’s disease is likely to be before memory loss and tissue destruction occurs, but this is hard to model in animals. That means identifying people at risk of developing the disease, perhaps because of a genetic predisposition or by measuring biomarkers, such as the recently reported cerebrospinal fl uid measurement of a mix of amyloid β1–42 and phosphorylated τ protein.
Drug-industry scientists are failing themselves if their animal studies are poorly done or use the wrong model, and their companies are failing academics who do their phase 3 trials with them, trial participants, and shareholders. Perhaps the problem is “translational research” itself: a phrase much bandied around, but does anyone know what it really means, let alone how to do it? ■ The Lancet
For the Review on drug development see Lancet Neurol 2010; 9: 702–16 For the meta-analyses see PLoS Med 2010; 7: e1000245 and PLoS Biol 2010; 8: e1000344 For genetic predisposition see Lancet Neurol 2010; 9: 850–51 For the biomarker study see Arch Neurol 2010; 67: 949–56
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