BMJ 2004;328:500-501 (28 February), doi:10.1136/bmj.328.7438.500
Primary care
Effect of statin treatment for familial hypercholesterolaemia on life assurance: results of consecutive surveys in 1990 and 2002
H A W Neil, honorary consultant physician1,
T Hammond, research assistant2,
D Mant, professor of general practice2,
S E Humphries, professor of cardiovascular genetics3
1 Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, Oxford OX3 7HJ,
2 Division of Public Health and Primary Health Care, Institute of Health Sciences, University of Oxford, Oxford OX3 7LF,
3 Centre for Cardiovascular Genetics, British Heart Foundation Laboratories, Royal Free and University College London Medical School, London WC1E 6JJ
Correspondence to: H A W Neil andrew.neil{at}wolfson.ox.ac.uk
Introduction
One of the concerns often raised about genetic testing is the
possibility that a positive result (or even disclosing that
the test has been taken) may result in difficulty in obtaining
life assurance. Currently the UK insurance industry has declared
a moratorium on requiring genetic tests from applicants,
1 but
since DNA based tests offer a definitive, highly specific diagnosis
they are likely eventually to replace less specific clinical
diagnostic criteria for many inherited disorders. Early, presymptomatic
treatment may increase life expectancy by preventing or reducing
the risk of developing the disease or associated complications.
However, if life assurance policy premiums do not adequately
reflect the reduction in mortality with treatment relatives
of affected probands may be deterred from being tested. We examined
how life assurance companies have responded to the improvement
in the prognosis of heterozygous familial hypercholesterolaemia
with statin treatment.
2
Familial hypercholesterolaemia is an autosomal dominant disorder, inherited on average by one in two children of an affected parent. The prevalence in the United Kingdom is about 1:500, but at least three quarters of cases remain undiagnosed.3 It is usually caused by mutations in the gene for the low density lipoprotein (LDL) receptor that result in accumulation of plasma cholesterol and substantially increased coronary mortality. Without effective treatment the cumulative risk of a coronary event is at least 50% in men and 30% in women by the age of 60 years.4 With statin treatment, however, the standardised mortality ratio for coronary heart disease for such patients aged 20-59 years has more than halved over the past decade.2
Participants, methods, and results
We conducted a survey of 41 life assurance companies in 1990
5 and repeated it in 2002 by sending the same questionnaire to
26 companies still underwriting term life assurance. They were
asked to assess a fictional proposal for a 20 year policy (paying
benefit only on death) by applying an excess mortality rating
defined as the percentage increase over the assumed rate of
mortality. In the follow up survey companies were asked to assess
the rating before and after statin treatment. The applicant
was a normotensive (120/80 mm Hg), non-smoking, 30 year old
man taking no medication, with a body mass index of 22.1 kg/m
2 and a normal resting electrocardiogram, whose father had had
a non-fatal myocardial infarction aged 45 years. He had no other
family history of heart disease, other medical history of note,
or tendon xanthomata on examination. The results of the lipid
profile (mmol/l) were total cholesterol 11.4, high density lipoprotein
(HDL) cholesterol 1.7, triglycerides 1.3, and calculated LDL
cholesterol 9.1; and the presumptive diagnosis was familial
hypercholesterolaemia. On treatment with atorvastatin 80 mg
daily his total cholesterol concentration was 6.2 mmol/l (compared
with 10.7 mmol/l on cholestyramine prescribed in 1990).
The figure shows the excess mortality ratings applied. Because two companies would assess proposals only from patients receiving statin treatment statistical comparisons were restricted to 24 companies. The mean excess rating increased from 89% (SD 52) in 1990 to 158% (SD 40) in 2002 (difference 69%, 95% confidence interval 41 to 97; P < 0.000, paired t test), but fell to 56% (SD 43) on treatment (102%, 79 to 126; P < 0.000), which was 33% lower (5 to 61; P = 0.022) than the original rating in 1990.

View larger version (38K):
[in this window]
[in a new window]
|
Percentage excess mortality ratings applied by life assurance companies in 1990 and 2002, before and after starting statin treatment
|
|
Comment
The increase in mortality rating in the second survey, together
with the substantial reduction in the excess applied to patients
taking statins show that underwriters now assess risk more realistically
and recognise that the prognosis for familial hypercholesterolaemia
has improved with more effective treatment.
2 Nevertheless variability
in the rating applied was considerable, and patients could usefully
be advised to shop around for the most competitive premium.
The results of the survey, however, are reassuring and should
encourage relatives of probands to be tested rather than being
deterred by concerns about life assurance.
We thank the life assurance companies for participating in the
study.
Contributors: HAWN and DM designed the study, TH conducted the survey, HAWN undertook the analysis, SEH and HAWN wrote the paper. All authors participated in the interpretation and critical revision of the paper. HAWN is the guarantor.
Funding: This work was supported by a grant from the British Heart Foundation (PG2000/015) and was carried out in part with support from the Department of Health and the Department of Trade and Industry for the IDEAS Genetics Knowledge Park.
Competing interests: None declared.
References
- Mayor S. UK insurers agree five-year ban on using genetic tests. BMJ
2001;323: 1021.[Free Full Text]
- Scientific Steering Committee on behalf of the Simon Broome Register Group. Mortality in treated heterozygous familial hypercholesterolaemia: implications for clinical management. Atherosclerosis
1999;142: 105-12.[CrossRef][Web of Science][Medline]
- Neil HAW, Hammond T, Huxley R, Matthews DR, Humphries SE. Extent of underdiagnosis of familial hypercholesterolaemia in routine practice: prospective registry study. BMJ
2000;321: 148.[Free Full Text]
- Stone NJ, Levy RI, Fredrickson DS, Verter J. Coronary artery disease in 116 kindred with familial type II hyperlipoproteinaemia. Circulation
1974;49: 476-488.[Abstract/Free Full Text]
- Neil HAW, Mant D. Cholesterol screening and life assurance. BMJ
1991;302: 891-3.
(Accepted 2 October 2003)

CiteULike
Complore
Connotea
Del.icio.us
Digg
Reddit
StumbleUpon
Technorati What's this?
Relevant Article
-
Efficacy of statins in familial hypercholesterolaemia: a long term cohort study
- Jorie Versmissen, Daniëlla M Oosterveer, Mojgan Yazdanpanah, Joep C Defesche, Dick C G Basart, Anho H Liem, Jan Heeringa, Jacqueline C Witteman, Peter J Lansberg, John J P Kastelein, and Eric J G Sijbrands
BMJ 2008 337: a2423.
[Abstract]
[Full Text]
[PDF]
This article has been cited by other articles:
-
Chowdhury, T. A, Hitman, G. A
(2009). NICE guidance for identification and treatment of familial hypercholesterolaemia: Commentary 1. Heart
95: 587-589
[Full text]
-
Hadfield, S G, Horara, S, Starr, B J, Yazdgerdi, S, Marks, D, Bhatnagar, D, Cramb, R, Egan, S, Everdell, R, Ferns, G, Jones, A, Marenah, C B, Marples, J, Prinsloo, P, Sneyd, A, Stewart, M F, Sandle, L, Wang, T, Watson, M S, Humphries, S E, on behalf of the Steering Group for the Department,
(2009). Family tracing to identify patients with Familial Hypercholesterolaemia: the second Audit of the Department of Health Familial Hypercholesterolaemia Cascade Testing Project. Ann Clin Biochem
46: 24-32
[Abstract]
[Full text]
-
Versmissen, J., Oosterveer, D. M, Yazdanpanah, M., Defesche, J. C, Basart, D. C G, Liem, A. H, Heeringa, J., Witteman, J. C, Lansberg, P. J, Kastelein, J. J P, Sijbrands, E. J G
(2008). Efficacy of statins in familial hypercholesterolaemia: a long term cohort study. BMJ
337: a2423-a2423
[Abstract]
[Full text]
-
Austin, M. A., Hutter, C. M., Zimmern, R. L., Humphries, S. E.
(2004). Genetic Causes of Monogenic Heterozygous Familial Hypercholesterolemia: A HuGE Prevalence Review. Am J Epidemiol
160: 407-420
[Abstract]
[Full text]