- Email: [email protected]
Percutaneous absorption of sunscreens
CORRESPONDENCE
transit and lowered oestrogen reabsorption. We are not aware of any such data and there is some evidence to the contrary, a history of stressful life events being associated with an increase in breast-cancer risk.1 Women with newly diagnosed breast cancer will be very anxious. While this may be a factor in reducing phytooestrogen excretion, as suggested, we did measure total urinary nitrogen excretion, as an index of overall intake/absorption of nutrients, and there was little difference between cases and controls. There is no ideal moment to undertake a case-control study of nutrition and cancer and we felt that the best time was before any treatment had started. If Heaton and Lewis believe that habitual slow intestinal transit is a risk factor for breast cancer they should do the study. However, it is always going to be difficult to separate the effect of phyto-oestrogens from transit because lignans are in the outer fibre coat of cereals2 and high fibre intake is also associated with more rapid intestinal transit. Punam Mangtani and Isabel dos Santos Silva discuss issues in relation to timing and possible biases in our study. The many studies of dietary records in relation to breast cancer all suffer from the fact that dietary recall is inaccurate. We did collect dietary questionnaires but did not use them in the analysis. We measured excretion, a much more reliable index of consumption and metabolism of phyto-oestrogens. This measures intake and metabolism at only one point in time and may not reflect intake in earlier years, so our study needs to be followed by a large prospective cohort study. If one of the cohort studies done elsewhere collected and stored urine samples, it might not require the usual long interval before results are available. Mangtani and dos Santos Silva also argue that the controls might have been influenced by publicity and so they consumed a diet containing more phyto-oestrogens. However, our controls did not know they were taking part in a study of breast cancer and phyto-oestrogens; they were invited to take part in a study of diet and health. Furthermore, in 1993 and 1994 soy and linseed breads were not available and phyto-oestrogens were not widely known. Publicity will, however, make similar studies more difficult in the future. Rafael Marques de Souza argues that family history should have been taken into account. In fact, there was no increase in the number of controls
THE LANCET • Vol 351 • January 10, 1998
with a first-degree family history of breast cancer (7·7%); as expected, there was a higher proportion in the cases (11·3%). We did not control for family history in the final model because preliminary analyses had shown this factor to have a nonsignificant effect on risk. If the cases had changed to a diet rich in phytooestrogens once the diagnosis was made, that would have brought urinary excretion of phyto-oestrogens closer to that of the controls. Furthermore, at the time of the study there was little information readily available to the public on phyto-oestrogens and breast cancer. Part of the reason this time period (ie, immediately after diagnosis) was chosen was so that the women would not have time to do any personal research into diet and breast cancer. Charles Humfrey makes the point that a 3-day urine tells us only about phyto-oestrogen consumption and metabolism at that time and not when the cancer was developing, many years earlier. The pooled 72 h urine gives an index of phyto-oestrogen consumption and metabolism over 4–5 days not 24–48 h, as Humfrey says. Nevertheless he is basically correct. A study such as ours proves nothing but it does provide one more piece in the jigsaw of the aetiology of breast cancer. It is probably more useful than the case-control studies on soy consumption and breast cancer because we measured excretion, a more accurate index of consumption and metabolism than dietary recall, and because it is the first such study in a western population, where breast cancer is such a major problem. Jan Tesarik and Carmen Mendoza make the point that there are several possible mechanisms by which phytooestrogens might reduce breast cancer risk other than by interactions with the nuclear oestrogen receptor. There are more than 150 publications of the inhibitory effect of genistein on tyrosine specific protein kinases and topoisomerases, a topic excellently reviewed by the “father” of the modern phyto-oestrogen hypothesis, Herman Adlercreutz.3 David Ingram Suite 44, Mount Vernon Medical Center, 146 Mounts Bay Road, Perth, WA 6000, Australia 1
2
3
Ginsberg A, Price SD, Ingram DM, Nottage E. Life events and the risk of breast cancer: a case-control study. Eur J Cancer 1996; 32A: 2049–52. Nilsson M, Aman P. Hankonen H, et al. Contents of nutrients and lignans in roller milled fractions of rye. J Sci Food Agr 1997; 73: 143–48. Adlercreutz H, Mazur W. Phyto-oestrogens and western diseases. Ann Med 1997; 29: 95–120.
SIR—Just 1 month after your Sept 6 editorial, 1 “Meta-analysis under scrutiny”, you published David Ingram and colleagues’ case-control study of phyto-oestrogens and breast cancer (Oct 4, p 990),2 which refers to “the hypothesis that a diet rich in fats predisposes a woman to breast cancer . . . does not support this hypothesis.”. The World Cancer Research Fund and the American Institute for Cancer Research published an overall review entitled “Food, nutrition and the prevention of cancer; a global perspective”, on Sept 30, 1997, 3 which states that “total fat, saturated fat/animal fat, and meat increase the risk of cancer of the breast”, and that “diets high (sic) in red meat, total fat, and animal/saturated fat possibly increase the risk”. Whom does the non-specialist reader believe? A E Bender 2 Willow Vale, Fetcham, Leatherhead, Surrey KT22 9TE, UK 1 2
3
Editorial. Meta-analysis under scrutiny. Lancet 1997; 350: 675. Ingram D, Sanders K, Kolybaba M, Lopez D. Case-control study of phytooestrogens and breast cancer. Lancet 1997; 350: 990–94. World Cancer Research Fund/American Institute for Cancer Research. Food, nutrition, and prevention of cancer: a global perspective. Washington DC: American Institute for Cancer Research, 1977.
Percutaneous absorption of sunscreens SIR—Hayden and colleagues (Sept 20, p 863) 1 raise the issue of percutaneous absorption of sunscreens. Cosmetic manufacturers increasingly promote their products as containing sunscreens with sun protection factors of 15 or more. Since these creams are used throughout the year, particularly on the face, and since percutaneous absorption through facial skin is 2–13 times that through the forearm2,3,4 (on which Hayden’s study is based) a significant amount may be absorbed over time. However, the systemic effects of any drug depend on plasma concentration. Although we have information on urinary excretion, we know little about plasma concentration (which depends on the drug’s pharmacokinetics), the accumulation of oxybenzone (absorption in excess of metabolism and excretion), and its long-term biological effects. Clearly, more research is needed because sunscreens
139
CORRESPONDENCE
have a proven role in protecting against sunlight’s damaging effects. Colin S Ong University of Sydney, Sydney, New South Wales, Australia 1
2
3
4
Hayden CGJ, Roberts MS, Benson HAE. Systemic absorption of sunscreen after topical application. Lancet 1997; 350: 863–64. Rougier A, Lotte C, Maibach HI. In vivo percutaneous penetration of some organic compounds related to anatomic site in humans: predictive assessment by the stripping method. J Pharm Sci 1987; 76: 451–54. Guy RH, Maibach HI. Correction factors for determining body exposure from forearm percutaneous absorption data. J Appl Toxicol 1984; 4: 26–28. Feldman RJ, Maibach HI. Regional variation in percutaneous penetration of 14 C-cortisol in man. J Invest Dermatol 1967; 48: 181–83.
Health-care costs of ageing SIR—Chris van Weel and Joop Michels (Oct 18, p 1159)1 touch on a persistent misunderstanding about the relation between demography, population health, and health-care costs. They argue that the costs of health care are related to the process of dying, not to age-related illness and disability, and that these costs are difficult to control; they base their argument on epidemiological data from primary care, and on hospital costs. However, they are misled by their narrow focus on acute health care. General practice generates less than 4% of total health-care costs in the Netherlands, and hospital care (excluding psychiatric hospitals) only 32%. The picture changes dramatically when all health-care costs in the Netherlands are taken into account for 19882 or 1994.2,3 Contrary to what the investigators suggest, detailed data on the distribution of all health-care costs
(hospital care, long-term nursing care, medication, &c) by age, sex, diagnosis, and health-care sector are available,4 and were even published in the same report as cited by van Weel and Michels.4 From age 50 years and older, total costs per inhabitant rise exponentially by age until the oldest ages (⭓95 years).2 Costs of acute health care only decrease beyond age 85, which accords with findings cited by the investigators and elsewhere for acute health care. This decline may reflect the fact that many elderly people are already cared for in institutions or at home, and are too frail to undergo further medical procedures. However, whilst costs of acute care decline at the oldest ages, costs for long-term nursing care increase dramatically. The table shows the top 13 diagnostic categories in health-care costs for people aged 75 and older,2 the same age-group considered by van Weel and Michels. This age-group covers 5·5% of the Dutch population, but generates more than 28% of total health-care costs. The large share of non-fatal disorders in this ranking is remarkable: dementia, musculoskeletal disease, falls (hip fracture), and symptoms and ill-defined conditions. Dementia causes more than a sixth of all health-care costs among elderly women. The costs of cancer are strongly related to the end of life and terminal disease, but all cancers together are only the sixth cause of costs in this age-group, taking only a fifth of the costs of dementia alone. Also, contrary to what the researchers claim, the lifetime distribution of health-care costs has been published for the Netherlands.5 Of health-care costs (including hospital care, nursing homes, and medication) beyond age 50, only 15·5% can be attributed to the last year of life. Beyond age 75, the extra medical costs of dying decrease with age.5
Diagnostic category (ICD-9 code)
Men
Women
Total
Dementia (290) Stroke (430–38) Musculoskeletal (710–39) Falls (E880–888) Symptoms and ill-defined (780–99) Cancer (140–208) Heart failure (428–29) Other circulatory (390–98, 415–27, 440–59) Nervous (320–359) Other respiratory (460–87, 500–19) Other mental (293–94, 297–99, 301–02, 306–16) Eye (360–79) Coronary heart disease (410–14) All others
316 (12·8%) 199 (8·0%) 76 (3·1%) 59 (2·4%) 112 (4·5%) 148 (6·0%) 84 (3·4%) 97 (3·9%) 84 (3·4%) 79 (3·2%) 44 (1·8%) 48 (1·9%) 70 (2·8%) 1061 (42·8%)
1298 (19·2%) 477 (7·1%) 350 (5·2%) 339 (5·0%) 252 (3·7%) 179 (2·7%) 165 (2·4%) 142 (2·1%) 145 (2·1%) 104 (1·5%) 137 (2·0%) 117 (1·7%) 88 (1·3%) 2963 (43·9%)
1614 (17·5%) 676 (7·3%) 426 (4·6%) 398 (4·3%) 364 (3·9%) 327 (3·5%) 248 (2·7%) 239 (2·6%) 229 (2·5%) 183 (2·0%) 182 (2·0%) 164 (1·8%) 158 (1·7%) 4024 (43·6%)
Total
2476 (100·0%)
6756 (100·0%)
9232 (100·0%)
Exchange rate $1994=Fl 1·82.
Top 13 diagnostic categories (ICD-9 codes) by health-care costs for people aged 75 years and older in the Netherlands, 1994 (in $ millions)
140
Health-care costs among the elderly parallel the ageing process. Senescence is both a cause of death and a cause of disability, so the causes of senescencerelated costs are hard to attribute. Since only living people can consume health care, the non-fatal diseases of ageing that require long-term care are bound to dominate costs. We agree that costs are highest at the end of life, but not only because of impending death. Unfortunately, doctors too often observe cure only and disregard care, and end up making inaccurate conclusions on the relation between health care, demography, and population health. Thus, the title of their paper is inappropriate: all available data show that death is not to blame for health-care costs. Obviously, the elderly are not to blame for high health-care costs either, and the longterm nursing care that they require is the hallmark of a humane society. *Willem Jan Meerding, Johan Polder, Luc Bonneux, Marc Koopmanschap, Paul van der Maas *Department of Public Health and Institute for Medical Technology Assessment, Erasmus University Rotterdam, PO Box 1738, 3000 DR Rotterdam, Netherlands 1
2
3
4
5
van Weel C, Michels J. Dying, not ageing, to blame for costs of health care. Lancet 1997; 350: 1159–60. Polder JJ, Meerding WJ, Koopmanschap MA, Bonneux L, van der Maas PJ. Costs of diseases in the Netherlands, 1994 [in Dutch]: Department of Public Health, Institute for Medical Technology Assessment, Erasmus University Rotterdam, 1997. Koopmanschap MA, van Roijen L, Bonneux L, Bonsel GJ, Rutten FFM, van der Maas PJ. Costs of diseases in an international perspective. Eur J Public Health 1994; 4: 258–64. Ruwaard D, Kramers PGN. Public Health Status and Forecasts 1997 [in Dutch]. Utrecht: Elsevier/de Tijdstroom, 1997. Scientific Council for Government Policy. Population health care. Den Haag: Sdu Vitgevers, 1997.
Authors’ reply SIR—Willem Jan Meerding and colleagues challenge our report on age and costs of medical care. The demographic correlation they provide goes undisputed, in fact, we referred in our publication to the same study. This answers the question of when in a long life most health-care costs are made, but not what the degree of costs would be if most people died at a young age. It is time and again stated that the process of ageing in itself is responsible for the increase in health-care costs. Our calculations—based on insurance data, not “narrowly focused on primary care costs” as they suggest—point to a clustering during the final years of life.
THE LANCET • Vol 351 • January 10, 1998
transit and lowered oestrogen reabsorption. We are not aware of any such data and there is some evidence to the contrary, a history of stressful life events being associated with an increase in breast-cancer risk.1 Women with newly diagnosed breast cancer will be very anxious. While this may be a factor in reducing phytooestrogen excretion, as suggested, we did measure total urinary nitrogen excretion, as an index of overall intake/absorption of nutrients, and there was little difference between cases and controls. There is no ideal moment to undertake a case-control study of nutrition and cancer and we felt that the best time was before any treatment had started. If Heaton and Lewis believe that habitual slow intestinal transit is a risk factor for breast cancer they should do the study. However, it is always going to be difficult to separate the effect of phyto-oestrogens from transit because lignans are in the outer fibre coat of cereals2 and high fibre intake is also associated with more rapid intestinal transit. Punam Mangtani and Isabel dos Santos Silva discuss issues in relation to timing and possible biases in our study. The many studies of dietary records in relation to breast cancer all suffer from the fact that dietary recall is inaccurate. We did collect dietary questionnaires but did not use them in the analysis. We measured excretion, a much more reliable index of consumption and metabolism of phyto-oestrogens. This measures intake and metabolism at only one point in time and may not reflect intake in earlier years, so our study needs to be followed by a large prospective cohort study. If one of the cohort studies done elsewhere collected and stored urine samples, it might not require the usual long interval before results are available. Mangtani and dos Santos Silva also argue that the controls might have been influenced by publicity and so they consumed a diet containing more phyto-oestrogens. However, our controls did not know they were taking part in a study of breast cancer and phyto-oestrogens; they were invited to take part in a study of diet and health. Furthermore, in 1993 and 1994 soy and linseed breads were not available and phyto-oestrogens were not widely known. Publicity will, however, make similar studies more difficult in the future. Rafael Marques de Souza argues that family history should have been taken into account. In fact, there was no increase in the number of controls
THE LANCET • Vol 351 • January 10, 1998
with a first-degree family history of breast cancer (7·7%); as expected, there was a higher proportion in the cases (11·3%). We did not control for family history in the final model because preliminary analyses had shown this factor to have a nonsignificant effect on risk. If the cases had changed to a diet rich in phytooestrogens once the diagnosis was made, that would have brought urinary excretion of phyto-oestrogens closer to that of the controls. Furthermore, at the time of the study there was little information readily available to the public on phyto-oestrogens and breast cancer. Part of the reason this time period (ie, immediately after diagnosis) was chosen was so that the women would not have time to do any personal research into diet and breast cancer. Charles Humfrey makes the point that a 3-day urine tells us only about phyto-oestrogen consumption and metabolism at that time and not when the cancer was developing, many years earlier. The pooled 72 h urine gives an index of phyto-oestrogen consumption and metabolism over 4–5 days not 24–48 h, as Humfrey says. Nevertheless he is basically correct. A study such as ours proves nothing but it does provide one more piece in the jigsaw of the aetiology of breast cancer. It is probably more useful than the case-control studies on soy consumption and breast cancer because we measured excretion, a more accurate index of consumption and metabolism than dietary recall, and because it is the first such study in a western population, where breast cancer is such a major problem. Jan Tesarik and Carmen Mendoza make the point that there are several possible mechanisms by which phytooestrogens might reduce breast cancer risk other than by interactions with the nuclear oestrogen receptor. There are more than 150 publications of the inhibitory effect of genistein on tyrosine specific protein kinases and topoisomerases, a topic excellently reviewed by the “father” of the modern phyto-oestrogen hypothesis, Herman Adlercreutz.3 David Ingram Suite 44, Mount Vernon Medical Center, 146 Mounts Bay Road, Perth, WA 6000, Australia 1
2
3
Ginsberg A, Price SD, Ingram DM, Nottage E. Life events and the risk of breast cancer: a case-control study. Eur J Cancer 1996; 32A: 2049–52. Nilsson M, Aman P. Hankonen H, et al. Contents of nutrients and lignans in roller milled fractions of rye. J Sci Food Agr 1997; 73: 143–48. Adlercreutz H, Mazur W. Phyto-oestrogens and western diseases. Ann Med 1997; 29: 95–120.
SIR—Just 1 month after your Sept 6 editorial, 1 “Meta-analysis under scrutiny”, you published David Ingram and colleagues’ case-control study of phyto-oestrogens and breast cancer (Oct 4, p 990),2 which refers to “the hypothesis that a diet rich in fats predisposes a woman to breast cancer . . . does not support this hypothesis.”. The World Cancer Research Fund and the American Institute for Cancer Research published an overall review entitled “Food, nutrition and the prevention of cancer; a global perspective”, on Sept 30, 1997, 3 which states that “total fat, saturated fat/animal fat, and meat increase the risk of cancer of the breast”, and that “diets high (sic) in red meat, total fat, and animal/saturated fat possibly increase the risk”. Whom does the non-specialist reader believe? A E Bender 2 Willow Vale, Fetcham, Leatherhead, Surrey KT22 9TE, UK 1 2
3
Editorial. Meta-analysis under scrutiny. Lancet 1997; 350: 675. Ingram D, Sanders K, Kolybaba M, Lopez D. Case-control study of phytooestrogens and breast cancer. Lancet 1997; 350: 990–94. World Cancer Research Fund/American Institute for Cancer Research. Food, nutrition, and prevention of cancer: a global perspective. Washington DC: American Institute for Cancer Research, 1977.
Percutaneous absorption of sunscreens SIR—Hayden and colleagues (Sept 20, p 863) 1 raise the issue of percutaneous absorption of sunscreens. Cosmetic manufacturers increasingly promote their products as containing sunscreens with sun protection factors of 15 or more. Since these creams are used throughout the year, particularly on the face, and since percutaneous absorption through facial skin is 2–13 times that through the forearm2,3,4 (on which Hayden’s study is based) a significant amount may be absorbed over time. However, the systemic effects of any drug depend on plasma concentration. Although we have information on urinary excretion, we know little about plasma concentration (which depends on the drug’s pharmacokinetics), the accumulation of oxybenzone (absorption in excess of metabolism and excretion), and its long-term biological effects. Clearly, more research is needed because sunscreens
139
CORRESPONDENCE
have a proven role in protecting against sunlight’s damaging effects. Colin S Ong University of Sydney, Sydney, New South Wales, Australia 1
2
3
4
Hayden CGJ, Roberts MS, Benson HAE. Systemic absorption of sunscreen after topical application. Lancet 1997; 350: 863–64. Rougier A, Lotte C, Maibach HI. In vivo percutaneous penetration of some organic compounds related to anatomic site in humans: predictive assessment by the stripping method. J Pharm Sci 1987; 76: 451–54. Guy RH, Maibach HI. Correction factors for determining body exposure from forearm percutaneous absorption data. J Appl Toxicol 1984; 4: 26–28. Feldman RJ, Maibach HI. Regional variation in percutaneous penetration of 14 C-cortisol in man. J Invest Dermatol 1967; 48: 181–83.
Health-care costs of ageing SIR—Chris van Weel and Joop Michels (Oct 18, p 1159)1 touch on a persistent misunderstanding about the relation between demography, population health, and health-care costs. They argue that the costs of health care are related to the process of dying, not to age-related illness and disability, and that these costs are difficult to control; they base their argument on epidemiological data from primary care, and on hospital costs. However, they are misled by their narrow focus on acute health care. General practice generates less than 4% of total health-care costs in the Netherlands, and hospital care (excluding psychiatric hospitals) only 32%. The picture changes dramatically when all health-care costs in the Netherlands are taken into account for 19882 or 1994.2,3 Contrary to what the investigators suggest, detailed data on the distribution of all health-care costs
(hospital care, long-term nursing care, medication, &c) by age, sex, diagnosis, and health-care sector are available,4 and were even published in the same report as cited by van Weel and Michels.4 From age 50 years and older, total costs per inhabitant rise exponentially by age until the oldest ages (⭓95 years).2 Costs of acute health care only decrease beyond age 85, which accords with findings cited by the investigators and elsewhere for acute health care. This decline may reflect the fact that many elderly people are already cared for in institutions or at home, and are too frail to undergo further medical procedures. However, whilst costs of acute care decline at the oldest ages, costs for long-term nursing care increase dramatically. The table shows the top 13 diagnostic categories in health-care costs for people aged 75 and older,2 the same age-group considered by van Weel and Michels. This age-group covers 5·5% of the Dutch population, but generates more than 28% of total health-care costs. The large share of non-fatal disorders in this ranking is remarkable: dementia, musculoskeletal disease, falls (hip fracture), and symptoms and ill-defined conditions. Dementia causes more than a sixth of all health-care costs among elderly women. The costs of cancer are strongly related to the end of life and terminal disease, but all cancers together are only the sixth cause of costs in this age-group, taking only a fifth of the costs of dementia alone. Also, contrary to what the researchers claim, the lifetime distribution of health-care costs has been published for the Netherlands.5 Of health-care costs (including hospital care, nursing homes, and medication) beyond age 50, only 15·5% can be attributed to the last year of life. Beyond age 75, the extra medical costs of dying decrease with age.5
Diagnostic category (ICD-9 code)
Men
Women
Total
Dementia (290) Stroke (430–38) Musculoskeletal (710–39) Falls (E880–888) Symptoms and ill-defined (780–99) Cancer (140–208) Heart failure (428–29) Other circulatory (390–98, 415–27, 440–59) Nervous (320–359) Other respiratory (460–87, 500–19) Other mental (293–94, 297–99, 301–02, 306–16) Eye (360–79) Coronary heart disease (410–14) All others
316 (12·8%) 199 (8·0%) 76 (3·1%) 59 (2·4%) 112 (4·5%) 148 (6·0%) 84 (3·4%) 97 (3·9%) 84 (3·4%) 79 (3·2%) 44 (1·8%) 48 (1·9%) 70 (2·8%) 1061 (42·8%)
1298 (19·2%) 477 (7·1%) 350 (5·2%) 339 (5·0%) 252 (3·7%) 179 (2·7%) 165 (2·4%) 142 (2·1%) 145 (2·1%) 104 (1·5%) 137 (2·0%) 117 (1·7%) 88 (1·3%) 2963 (43·9%)
1614 (17·5%) 676 (7·3%) 426 (4·6%) 398 (4·3%) 364 (3·9%) 327 (3·5%) 248 (2·7%) 239 (2·6%) 229 (2·5%) 183 (2·0%) 182 (2·0%) 164 (1·8%) 158 (1·7%) 4024 (43·6%)
Total
2476 (100·0%)
6756 (100·0%)
9232 (100·0%)
Exchange rate $1994=Fl 1·82.
Top 13 diagnostic categories (ICD-9 codes) by health-care costs for people aged 75 years and older in the Netherlands, 1994 (in $ millions)
140
Health-care costs among the elderly parallel the ageing process. Senescence is both a cause of death and a cause of disability, so the causes of senescencerelated costs are hard to attribute. Since only living people can consume health care, the non-fatal diseases of ageing that require long-term care are bound to dominate costs. We agree that costs are highest at the end of life, but not only because of impending death. Unfortunately, doctors too often observe cure only and disregard care, and end up making inaccurate conclusions on the relation between health care, demography, and population health. Thus, the title of their paper is inappropriate: all available data show that death is not to blame for health-care costs. Obviously, the elderly are not to blame for high health-care costs either, and the longterm nursing care that they require is the hallmark of a humane society. *Willem Jan Meerding, Johan Polder, Luc Bonneux, Marc Koopmanschap, Paul van der Maas *Department of Public Health and Institute for Medical Technology Assessment, Erasmus University Rotterdam, PO Box 1738, 3000 DR Rotterdam, Netherlands 1
2
3
4
5
van Weel C, Michels J. Dying, not ageing, to blame for costs of health care. Lancet 1997; 350: 1159–60. Polder JJ, Meerding WJ, Koopmanschap MA, Bonneux L, van der Maas PJ. Costs of diseases in the Netherlands, 1994 [in Dutch]: Department of Public Health, Institute for Medical Technology Assessment, Erasmus University Rotterdam, 1997. Koopmanschap MA, van Roijen L, Bonneux L, Bonsel GJ, Rutten FFM, van der Maas PJ. Costs of diseases in an international perspective. Eur J Public Health 1994; 4: 258–64. Ruwaard D, Kramers PGN. Public Health Status and Forecasts 1997 [in Dutch]. Utrecht: Elsevier/de Tijdstroom, 1997. Scientific Council for Government Policy. Population health care. Den Haag: Sdu Vitgevers, 1997.
Authors’ reply SIR—Willem Jan Meerding and colleagues challenge our report on age and costs of medical care. The demographic correlation they provide goes undisputed, in fact, we referred in our publication to the same study. This answers the question of when in a long life most health-care costs are made, but not what the degree of costs would be if most people died at a young age. It is time and again stated that the process of ageing in itself is responsible for the increase in health-care costs. Our calculations—based on insurance data, not “narrowly focused on primary care costs” as they suggest—point to a clustering during the final years of life.
THE LANCET • Vol 351 • January 10, 1998