Alzheimer's disease (AD) accounts for a significant proportion of long-term care costs. The recent discovery that the e4 allele of the ApoE gene indicates a predisposition to earlier onset of AD raises questions about the potential for adverse selection in long-term care insurance, about long-term care costs in general, and about the potential effects on costs of gene therapy, or better targetted treatments for AD. This paper describes a simple Markov model for AD, and the estimation of the transition intensities from the medical and epidemiological literature.

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The UK Biobank project is a proposed large-scale investigation of the combined effects of genotype and environmental exposures on the risk of common diseases. It is intended to recruit 500,000 subjects aged 40-69, to obtain medical histories and blood samples at outset, and to follow them up for at least 10 years. This will have a major impact on our knowledge of multifactorial genetic disorders, rather than the rare but severe single-gene disorders that have been studied to date. What use may insurance companies make of this knowledge, particularly if genetic tests can identify persons at different risk? We describe here a simulation study of the UK Biobank project. We specify a simple hypothetical model of genetic and environmental influences on the risk of heart attack. A single simulation of UK Biobank consists of 500,000 life histories over 10 years; we suppose that case-control studies are carried out to estimate age-specific odds ratios, and that an actuary uses these odds ratios to parameterise a model of critical illness insurance. From a large number of such simulations we obtain sampling distributions of premium rates in different strata defined by genotype and environmental exposure. We conclude that the ability of such a study reliably to discriminate between different underwriting classes is limited, and depends on large numbers of cases being analysed.

The UK Biobank project is a proposed large-scale investigation of the combined effects of genotype and environmental exposures on the risk of common diseases. It is intended to recruit 500,000 subjects aged 40-69, to obtain medical histories and blood samples at outset, and to follow them up for at least 10 years. This will have a major impact on our knowledge of multifactorial genetic disorders, rather than the rare but severe single-gene disorders that have been studied to date. What use may insurance companies make of this knowledge, particularly if genetic tests can identify persons at different risk? We describe here a simulation study of the UK Biobank project. We specify a simple hypothetical model of genetic and environmental influences on the risk of heart attack. A single simulation of UK Biobank consists of 500,000 life histories over 10 years; we suppose that case-control studies are carried out to estimate agespecific odds ratios, and that an actuary uses these odds ratios to parameterise a model of critical illness insurance. From a large number of such simulations we obtain sampling distributions of premium rates in different strata defined by genotype and environmental exposure. We conclude that the ability of such a study reliably to discriminate between different underwriting classes is limited, and depends on large numbers of cases being analysed.