CORRESPONDENCE
COMMENTARY
CORRESPONDENCE
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Insurance agreement to facilitate genetic testing Sir—A major objection to communitywide introduction of predictive genetic screening for serious diseases is the potential for discrimination by insurance companies.1 If discrimination is likely to result, many people will refuse genetic testing even if it is in their clinical interest. Most cases of haemochromatosis, a genetically inherited iron-overload disease, are due to homozygosity for one mutation, C282Y, in the HFE gene.2 People at high risk of developing the disease (up to one per 200 population in Australia)3 can be identified by DNA testing. In C282Y homozygous individuals, venesection prevents the iron accumulation that causes pathology, as well as providing donor blood to the community.4 Despite this successful treatment, concerns have been raised that if a person has this genetic predisposition, they may be subject to insurance premium loading.1,5 In Australia, unlike in the USA, insurance companies are bound by law to provide health insurance at one rate to all (community loading), and, therefore, only life insurance is open to discrimination. We were concerned about this issue when introducing a pilot genetic screening programme for haemochromatosis in Melbourne, Australia. We approached the umbrella organisation for life and disability insurance companies in Australia, the Investment and Financial Services Association. They agreed to the following assurances for life-insurance policies for people undergoing genetic screening for haemochromatosis. People who are not C282Y homozygous are guaranteed to have no insurance loadings on the basis of this genetic test. For C282Y homozygotes, those with normal iron indices will obtain insurance at baseline rates with no
conditions on the policy based on the genetic result; those with raised iron indices but no evidence of organ damage will be required to show evidence that steps are being taken to normalise iron indices and the policy will be issued at baseline rates when iron indices become normal; and those with raised iron indices and existing organ damage will be penalised if obtaining new policies, but insurance companies will comment that testing is desirable since treatment will keep disease progress to a minimum. We believe that this agreement represents a major step forward in dealing with the issue of genetic testing and insurance. Agreement between the medical and scientific community and the insurance industry is in the best interest of people who choose to have genetic testing and will be of increasing importance as more genetic markers that indicate predisposition to preventable disorders are described. *Martin Delatycki, Katrina Allen, Robert Williamson Murdoch Children’s Research Institute and Genetic Health Services Victoria, Royal Children’s Hospital, Parkville, Victoria 3052, Australia (e-mail:
[email protected]) 1
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Barash CI. Genetic discrimination and screening for hemochromatosis: then and now. Genet Test 2000; 4: 213–18. Powell LW, Subramaniam VN, Yapp TR. Haemochromatosis in the new millennium. J Hepatol 2000; 32: 48–62. Olynyk JK, Cullen DJ, Aquilia S, Rossi E, Summerville L, Powell LW. A populationbased study of the clinical expression of the hemochromatosis gene. N Engl J Med 1999; 341: 718–24. Niederau C, Fischer R, Purschel A, Stremmel W, Haussinger D, Strohmeyer G. Long-term survival in patients with hereditary hemochromatosis. Gastroenterology 1996; 110: 1107–19. Motulsky AG, Beutler E. Population screening in hereditary hemochromatosis. Ann Rev Public Health 2000; 21: 65–79.
THE LANCET • Vol 359 • April 20, 2002 • www.thelancet.com
Treatment of insomnia Sir—In his review of insomnia, Charles George (Nov 10 p 1623)1 writes as if the disorder is a clinical entity in its own right; it may be, but only rarely. Pharmacological treatment has an important role, but that role is limited and, in my view, that should have been stated. George writes that insomnia may also be associated with tiredness, lack of energy, difficulty in concentrating, and irritability and mood change. In fact, insomnia with all these symptoms (any one of which may be more prominent than the others) constitutes a syndrome for which the cause must be sought before treatment can be given. The most common causes are mood disorders, either primary or the result of adverse events, or of excessive alcohol consumption, most frequently not amounting to alcohol abuse. It is these disorders that probably cost the quoted figure of US$13 billion per year and their treatment should be that of the cause, not of the insomnia. George states that pharmacological therapy in the treatment of insomnia is widely used, but he neither defends this practice nor criticises it. It should not be widely used if the cause is carefully considered. Later, George quotes a report in which an increased number of awakenings was reported on the second and third nights after discontinuation of zaleplon,2 and he goes on to say, as if to lessen this finding, that other symptoms of rebound insomnia were not seen. What other symptoms of rebound insomnia are there apart from awakenings? This is the only reference to rebound in the article although the difficulty of rebound arousal is central to the use of all sedative substances. Samuel I Cohen Department of Psychiatry, London Hospital Medical College, Jerusalem 93108, Israel
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