- Email: [email protected]
Management of hyperactive inattentive children
CORRESPONDENCE
(LDL)-cholesterol by 2% (BECAIT),2 and reduction of LDL-cholesterol alone by 30% in the MAAS 3 or REGRESS4 studies. LDL-cholesterol and fibrinogen act synergistically as predictors of cardiovascular events in patients with angina (see Nair). The relative importance of LDL and fibrinogen reduction in retarding the progression of coronary artery disease is unclear. We agree with your correspondents who believe that the effect of statins on other non-classic risk factors for cardiovascular disease including fibrinogen and Lp(a) requires further work. Unexpected actions need to be kept in mind when extrapolating results from studies using proven agents to those on which there is no endpoint data yet available. *Anthony S Wierzbicki, Martin A Crook Department of Chemical Pathology, St Thomas’ Hospital, London SE1 7EH, UK 1
2
3
4
Saloma V, Rasi V, Pekannen J, et al. Haemostatic risk factors and prevalent coronary heart disease: the FINRISK haemostasis study. Eur Heart J 1994; 15: 1293–99. Ericsson C-G, Hamsten A, Nilsson J, Grip L, Svane B, de Faire U. Angiographic assessment of the effects of bezafibrate on progression of coronary artery disease in young male post-infarction patients. Lancet 1996; 347: 849–53. MAAS Investigators. Effect of simvastatin on coronary athermoma: the Multicentre Anti-Atheroma Study (MAAS). Lancet 1994; 344: 633–38. Jukema JW, Bruschke AVG, van Boven AJ, on behalf of the REGRESS study group. Effect of lipid lowering by pravastatin on progression of coronary artery disease in symptomatic men with normal to moderately elevated serum cholesterol levels. The Regression Growth Evaluation Statin Study (REGRESS). Circulation 1995; 91: 2528–40.
Management of hyperactive inattentive children Sir—We were surprised that neither the seminar on hyperactivity by J M Swanson and colleagues (Feb 7, p 429)1 nor R Beach and R Proops’2 accompanying commentary mention the striking improvement that can be achieved by identification of hidden food allergies with an elimination diet and then avoidance of the trigger foods, or the need to check for micronutrient deficiencies. Since 1985, three trials of elimination dieting (with double-blind, placebo-controlled testing of a subgroup for confirmation) have now shown this strategy to be effective in
1432
73–76% of hyperactive children.3 In their review, Robinson and Ferguson4 concluded that both foods and food additives should be tested in these children with challenge with adequate amounts of food. They thought that foods were important only in a few affected children, but in fact a large proportion of children with hyperactivity respond well to an elimination diet.3 Children in Boris and Mandel’s5 study were consecutive referrals with primary hyperactivity, and we should therefore accept that nearly three-quarters of hyperactive children can be helped by detecting trigger foods and avoiding them in the short to medium term. We know of no evidence that there is any difference in the response of the various subgroups in the condition, although this cannot be ruled out. If the trigger foods are avoided, children may regain tolerance of some within months, allowing them to be eaten in moderation without relapse. Hyperactive children treated by specific prophylaxis regain tolerance of the trigger foods earlier than those managed by avoidance alone,3 suggesting an allergic mechanism. Our experience is in keeping with these reports, and we find it worrying that most children with hyperactivity are treated with drugs or psychological methods without investigation of the role of adverse food reactions. Triggers are often multiple3 and may include other types of chemical exposure— toothpaste, bubble bath, cleaning chemicals or cigarette smoke, for instance—and behaviour is often normal provided that all triggers are avoided. It would be interesting to know whether the abnormalities shown by the functional imaging techniques cited by Swanson and colleagues were present in such children. Even higher success rates might be achieved in studies which took all possible triggers into account, and attended to micronutrient nutrition, particularly of zinc and of essential fatty acids.3 In our experience, hidden food allergy provokes hyperactive behaviour over the whole range of severity, and improvement can be rapid and complete. Once the trigger substances have been identified, many of the children take an active part in avoidiing them, because they prefer to feel well. Sometimes, however, combined approaches are needed because family dynamics have been strained by longstanding hyperactive behaviour with the development of secondary psychological problems, and full improvement cannot be achieved until these have also been addressed; the
earlier that allergic identified, the better.
triggers
are
D J Maberly, *H M Anthony, Sybil Birtwistle Airedale Allergy Centre, Keighley BD20 6SB, UK; and Fulbourn, Cambridge 1
2
3
4
5
Swanson JM, Sergeant JA, Taylor E, Sonuya-Barke EJS, Jensen PS, Cantwell DP. Attention-deficit hyperactivity disorder and hyperkinetic disorder. Lancet 1998; 351: 429–33. Beach R, Proops R. Management of hyperactive, inattentive children. Lancet 1998; 351: 387. Anthony HM, Birtwistle S, Eaton K, Maberly J. Environmental medicine in clinical practice. BSAENM Publications 1997, pages 259–60. Robinson J, Ferguson A. Food sensitivity and the nervous system: hyperactivity, addiction and criminal behaviour. Nutr Res Rev 1992; 5: 203–23. Boris M, Mandel FS. Foods and additives are common causes of the attention deficit hyperactive disorder in children. Ann Allergy 1994; 72: 462–68.
Sir—I think it is important to emphasise that attention-deficit hyperactivity disorder and hyperkinetic disorders are multifactorial disorders, and that prognosis is also multifactorial.1 It is too extreme, I believe, to state that followup studies in the USA have confirmed a poor prognosis for children with these disorders. The critical factor in prognosis is probably not whether the core symptoms are present in a particular child, but rather whether antisocial behaviour is absent2 and whether redemptive factors (for example, stable home, functioning school accommodations, extracurricular opportunities, &c) are present. Most children can have a good outcome. Ernest F Krug III Division Developmental-Behavioural Paediatrics,William Beaumont Hospital, Royal Oak, MI 48073, USA 1
2
Swanson JM, Sergeant JA, Taylor E, Sonuga-Barke EJS, Jensen PS, Cantwell DP. Attention-deficit hyperactivity disorder and hyperkinetic disorder. Lancet 1998; 351: 429–33. Weiss G, Hectman LT. Hyperactive children grown up. New York: Guildford Press, 1986.
Sir—Neither J M Swanson and colleagues1 nor R Beach and R Proops2 mention the role of food intolerance in hyperactive children, despite the fact that there have been two successful double-blind placebo-controlled trials3,4 of the food allergy hypothesis (any food in any combination can cause it). One trial was published in The Lancet, and one of the authors (E Taylor) of the seminar was an author of the other. The drug treatment Swanson and colleagues describe has been established
THE LANCET • Vol 351 • May 9, 1998
CORRESPONDENCE
by appropriate trials, but it is mere symptomatic treatment. Dietary treatment, at its best (and this is difficult in this disease) is curative, and so points to possible pathogenetic mechanisms. Our interest started in diet and hyperactivity when we noticed that some children with migraine whom we treated in this way5 also recovered from severe behaviour disorder. Swanson notes several associated symptoms, many of which we have seen also to respond to diet. Intellectual honesty would require extrapolation to investigate the possible role of diet treatment of these too. But that is difficult. It is easier, and ostrichlike, to pretend that diet treatment is not there. J F Soothill Pensylvania, Lodge Lane, Axminster, Devon EX13 5RT, UK 1
2
3
4
5
Swanson JM, Sergeant JA, Taylor E, Sonuga-Barke EJS, Jensen PS, Cantwell DP. Attention-deficit hyperactivity disorder and hyperkinetic disorder. Lancet 1998; 351: 429–33. Beach R, Proops R. Management of hyperactive, inattentive children. Lancet 1998; 351: 387. Egger J, Carter CM, Gumley D, et al. A controlled trial of oligoantigenic diet treatment in the hyperkinetic syndrome. Lancet 1985; i: 940–45. Carter CM, Urbanowicz M, Hemsley R, et al. Effect of a few food diet in attention deficit disorder. Arch Dis Childh 1995; 69: 564–68. Egger J, Carter CM, Wilson J, et al. Is migraine food allergy? Lancet 1983; ii: 865–69.
Authors’ reply Sir—D J Maberly and colleagues and J F Soothill remind us of the possible value of elimination diets. This approach has a place—but it is smaller, more controversial, and less specific than they suggest. Much research in the past, on elimination of artificial colours and preservatives and natural salicylates, has shown that this approach is effective in a few individual children but is not generally effective in the clinical population of children with attention-deficit hyperactivity disorder and hyperkinetic disorders. The modern approach, described in the references provided by Soothill, applies more comprehensive elimination diets that remove many foods to which children may have developed an intolerance (not necessarily an allergy, because immune mechanisms have not yet been found). Some small randomised clinical trials1 provide limited support for this approach. The challenge studies cited by Maberly and co-workers (in which the suspected substance is removed from
THE LANCET • Vol 351 • May 9, 1998
and then reintroduced into the diet) are promising, but they have methodological limitations and are not yet definitive. The high response rates cited are based on non-blind outcome and selected series, and other evidence2 suggests that most treated children do not show a clinically meaningful response. Some of the strengths and weaknesses of the dietary approach are summarised in a review by Robinson and Ferguson on which your correspondents rely: the actual conclusions of the review were: that the evidence gives no support to elimination diets as primary therapy for hyperactivity; that the association between certain foods and hyperkinetic disorders holds only for a few affected children; and that elimination diets can benefit carefully selected children. We agree with all these findings. In addition, we are aware of disadvantages of the diets (excessive preoccupation, restriction of activities, suboptimum nutrition, coercive interactive cycles between parents and children in the effort to maintain diet, neglect of other adverse influences), and of difficulties in selection of who should be treated. Ernest Krug rightly emphasises the multifactorial nature of the disorder and the heterogeneity of outcome. The clear finding, documented in our seminar, is that the core symptoms of the disorder are indeed an adverse influence on children’s psychological development— even in the absence of other risks.3,4 Nevertheless, this substantial group risk is compatible with a good outcome in many individual children.3 Individual case analyses are always required for clinical treatment. Research now in progress, referenced in the seminar, should provide information about moderators and mediators of outcome, as well as about niches in which individuals with the disorder are likely to succeed. We take the research on diet seriously, and in addition to the trial mentioned by Soothill another of us has contributed some evidence about possible mechanisms of action of elimination diets.5 Further research is definitely needed on these interesting approaches, but, given present knowledge of inconsistent effects, it is not prudent to give broad recommendations for the widespread application of dietary treatment to the clinical population defined by a diagnosis of attention-deficit hyperactivity disorder and hyperkinetic disorders. *Eric Taylor, James Swanson, Joseph Sergeant, Edmund Sonuga-Barke, Peter Jensen
MRC Child Psychiatry Unit, Institute of Psychiatry, London SE5 8AF, UK 1
2
3
4
5
Young E, Patel S, Stoneham M, Rona R, Wilkinson JD. The prevalence of reaction to food additives in a survey population. J R Coll Phys Lond 1987; 21: 241–47. Schulte-Koerne G, Diemel W, Gutenbrunner C, et al. Effect of an oligoantigen diet on the behaviour of hyperkinetic children. Zeitschrift fuer Kinder-und Jugendpsychiatrie 1996; 24: 176–83. Taylor E, Chadwick O, Heptinstall E, Danckaerts M. Hyperactivity and conduct problems as risk factors for adolescent development. J Am Acad Child Adol Psychiatry 1996; 35: 1213–26. Satterfield J, Swanson JM, Schell A, Lee F. Prediction of antisocial behavior in attentiondeficit hyperactivity disorder boys from aggressive/defiance scores. J Am Acad Child Adol Psychiatry 1994; 33: 185–90. Swanson JM, Kinsbourne M. Food dyes impair performance of hyperactive children on a laboratory learning test. Science 1980; 207: 533–41.
Antiretroviral therapy in countries with low health expenditure Sir—Olaf Müller and colleagues (Jan 3, p 68)1 argue against future public investments in the triple-combination antiretroviral therapy against HIV-1 in sub-Saharan Africa. They feel that such countries’ meagre resources should be used to improve existing health services and ensure care of the increasing number of cases of tuberculosis, pneumonia, and other opportunistic infections. Furthermore, lack of laboratory facilities to quantify HIV RNA or CD4 lymphocyte counts, poor compliance, and severe sideeffects would lead to rapid development of drug resistance in the community. These arguments are just as applicable to some Asian countries—particularly, Vietnam, Laos, Bangladesh, and Nepal, where less than US$10 per person per year is spent on health care.2 Asian, African, and Latin American countries have both public and private health-care systems.3 In some countries that spend such a small amount on health, a greater proportion of available funds is spent in the private than the public sector (table).3 Antiretroviral therapy is available in the private sector in Madras, India, but the drugs have to be procured through black-market sources: the government is reluctant to encourage general use because of the three million or so HIV1-positive people in our country.4 The use of anti-HIV-1 multidrug cocktails that consist of poor quality drugs will surely lead to the emergence of multidrug-resistant strains.
1433
(LDL)-cholesterol by 2% (BECAIT),2 and reduction of LDL-cholesterol alone by 30% in the MAAS 3 or REGRESS4 studies. LDL-cholesterol and fibrinogen act synergistically as predictors of cardiovascular events in patients with angina (see Nair). The relative importance of LDL and fibrinogen reduction in retarding the progression of coronary artery disease is unclear. We agree with your correspondents who believe that the effect of statins on other non-classic risk factors for cardiovascular disease including fibrinogen and Lp(a) requires further work. Unexpected actions need to be kept in mind when extrapolating results from studies using proven agents to those on which there is no endpoint data yet available. *Anthony S Wierzbicki, Martin A Crook Department of Chemical Pathology, St Thomas’ Hospital, London SE1 7EH, UK 1
2
3
4
Saloma V, Rasi V, Pekannen J, et al. Haemostatic risk factors and prevalent coronary heart disease: the FINRISK haemostasis study. Eur Heart J 1994; 15: 1293–99. Ericsson C-G, Hamsten A, Nilsson J, Grip L, Svane B, de Faire U. Angiographic assessment of the effects of bezafibrate on progression of coronary artery disease in young male post-infarction patients. Lancet 1996; 347: 849–53. MAAS Investigators. Effect of simvastatin on coronary athermoma: the Multicentre Anti-Atheroma Study (MAAS). Lancet 1994; 344: 633–38. Jukema JW, Bruschke AVG, van Boven AJ, on behalf of the REGRESS study group. Effect of lipid lowering by pravastatin on progression of coronary artery disease in symptomatic men with normal to moderately elevated serum cholesterol levels. The Regression Growth Evaluation Statin Study (REGRESS). Circulation 1995; 91: 2528–40.
Management of hyperactive inattentive children Sir—We were surprised that neither the seminar on hyperactivity by J M Swanson and colleagues (Feb 7, p 429)1 nor R Beach and R Proops’2 accompanying commentary mention the striking improvement that can be achieved by identification of hidden food allergies with an elimination diet and then avoidance of the trigger foods, or the need to check for micronutrient deficiencies. Since 1985, three trials of elimination dieting (with double-blind, placebo-controlled testing of a subgroup for confirmation) have now shown this strategy to be effective in
1432
73–76% of hyperactive children.3 In their review, Robinson and Ferguson4 concluded that both foods and food additives should be tested in these children with challenge with adequate amounts of food. They thought that foods were important only in a few affected children, but in fact a large proportion of children with hyperactivity respond well to an elimination diet.3 Children in Boris and Mandel’s5 study were consecutive referrals with primary hyperactivity, and we should therefore accept that nearly three-quarters of hyperactive children can be helped by detecting trigger foods and avoiding them in the short to medium term. We know of no evidence that there is any difference in the response of the various subgroups in the condition, although this cannot be ruled out. If the trigger foods are avoided, children may regain tolerance of some within months, allowing them to be eaten in moderation without relapse. Hyperactive children treated by specific prophylaxis regain tolerance of the trigger foods earlier than those managed by avoidance alone,3 suggesting an allergic mechanism. Our experience is in keeping with these reports, and we find it worrying that most children with hyperactivity are treated with drugs or psychological methods without investigation of the role of adverse food reactions. Triggers are often multiple3 and may include other types of chemical exposure— toothpaste, bubble bath, cleaning chemicals or cigarette smoke, for instance—and behaviour is often normal provided that all triggers are avoided. It would be interesting to know whether the abnormalities shown by the functional imaging techniques cited by Swanson and colleagues were present in such children. Even higher success rates might be achieved in studies which took all possible triggers into account, and attended to micronutrient nutrition, particularly of zinc and of essential fatty acids.3 In our experience, hidden food allergy provokes hyperactive behaviour over the whole range of severity, and improvement can be rapid and complete. Once the trigger substances have been identified, many of the children take an active part in avoidiing them, because they prefer to feel well. Sometimes, however, combined approaches are needed because family dynamics have been strained by longstanding hyperactive behaviour with the development of secondary psychological problems, and full improvement cannot be achieved until these have also been addressed; the
earlier that allergic identified, the better.
triggers
are
D J Maberly, *H M Anthony, Sybil Birtwistle Airedale Allergy Centre, Keighley BD20 6SB, UK; and Fulbourn, Cambridge 1
2
3
4
5
Swanson JM, Sergeant JA, Taylor E, Sonuya-Barke EJS, Jensen PS, Cantwell DP. Attention-deficit hyperactivity disorder and hyperkinetic disorder. Lancet 1998; 351: 429–33. Beach R, Proops R. Management of hyperactive, inattentive children. Lancet 1998; 351: 387. Anthony HM, Birtwistle S, Eaton K, Maberly J. Environmental medicine in clinical practice. BSAENM Publications 1997, pages 259–60. Robinson J, Ferguson A. Food sensitivity and the nervous system: hyperactivity, addiction and criminal behaviour. Nutr Res Rev 1992; 5: 203–23. Boris M, Mandel FS. Foods and additives are common causes of the attention deficit hyperactive disorder in children. Ann Allergy 1994; 72: 462–68.
Sir—I think it is important to emphasise that attention-deficit hyperactivity disorder and hyperkinetic disorders are multifactorial disorders, and that prognosis is also multifactorial.1 It is too extreme, I believe, to state that followup studies in the USA have confirmed a poor prognosis for children with these disorders. The critical factor in prognosis is probably not whether the core symptoms are present in a particular child, but rather whether antisocial behaviour is absent2 and whether redemptive factors (for example, stable home, functioning school accommodations, extracurricular opportunities, &c) are present. Most children can have a good outcome. Ernest F Krug III Division Developmental-Behavioural Paediatrics,William Beaumont Hospital, Royal Oak, MI 48073, USA 1
2
Swanson JM, Sergeant JA, Taylor E, Sonuga-Barke EJS, Jensen PS, Cantwell DP. Attention-deficit hyperactivity disorder and hyperkinetic disorder. Lancet 1998; 351: 429–33. Weiss G, Hectman LT. Hyperactive children grown up. New York: Guildford Press, 1986.
Sir—Neither J M Swanson and colleagues1 nor R Beach and R Proops2 mention the role of food intolerance in hyperactive children, despite the fact that there have been two successful double-blind placebo-controlled trials3,4 of the food allergy hypothesis (any food in any combination can cause it). One trial was published in The Lancet, and one of the authors (E Taylor) of the seminar was an author of the other. The drug treatment Swanson and colleagues describe has been established
THE LANCET • Vol 351 • May 9, 1998
CORRESPONDENCE
by appropriate trials, but it is mere symptomatic treatment. Dietary treatment, at its best (and this is difficult in this disease) is curative, and so points to possible pathogenetic mechanisms. Our interest started in diet and hyperactivity when we noticed that some children with migraine whom we treated in this way5 also recovered from severe behaviour disorder. Swanson notes several associated symptoms, many of which we have seen also to respond to diet. Intellectual honesty would require extrapolation to investigate the possible role of diet treatment of these too. But that is difficult. It is easier, and ostrichlike, to pretend that diet treatment is not there. J F Soothill Pensylvania, Lodge Lane, Axminster, Devon EX13 5RT, UK 1
2
3
4
5
Swanson JM, Sergeant JA, Taylor E, Sonuga-Barke EJS, Jensen PS, Cantwell DP. Attention-deficit hyperactivity disorder and hyperkinetic disorder. Lancet 1998; 351: 429–33. Beach R, Proops R. Management of hyperactive, inattentive children. Lancet 1998; 351: 387. Egger J, Carter CM, Gumley D, et al. A controlled trial of oligoantigenic diet treatment in the hyperkinetic syndrome. Lancet 1985; i: 940–45. Carter CM, Urbanowicz M, Hemsley R, et al. Effect of a few food diet in attention deficit disorder. Arch Dis Childh 1995; 69: 564–68. Egger J, Carter CM, Wilson J, et al. Is migraine food allergy? Lancet 1983; ii: 865–69.
Authors’ reply Sir—D J Maberly and colleagues and J F Soothill remind us of the possible value of elimination diets. This approach has a place—but it is smaller, more controversial, and less specific than they suggest. Much research in the past, on elimination of artificial colours and preservatives and natural salicylates, has shown that this approach is effective in a few individual children but is not generally effective in the clinical population of children with attention-deficit hyperactivity disorder and hyperkinetic disorders. The modern approach, described in the references provided by Soothill, applies more comprehensive elimination diets that remove many foods to which children may have developed an intolerance (not necessarily an allergy, because immune mechanisms have not yet been found). Some small randomised clinical trials1 provide limited support for this approach. The challenge studies cited by Maberly and co-workers (in which the suspected substance is removed from
THE LANCET • Vol 351 • May 9, 1998
and then reintroduced into the diet) are promising, but they have methodological limitations and are not yet definitive. The high response rates cited are based on non-blind outcome and selected series, and other evidence2 suggests that most treated children do not show a clinically meaningful response. Some of the strengths and weaknesses of the dietary approach are summarised in a review by Robinson and Ferguson on which your correspondents rely: the actual conclusions of the review were: that the evidence gives no support to elimination diets as primary therapy for hyperactivity; that the association between certain foods and hyperkinetic disorders holds only for a few affected children; and that elimination diets can benefit carefully selected children. We agree with all these findings. In addition, we are aware of disadvantages of the diets (excessive preoccupation, restriction of activities, suboptimum nutrition, coercive interactive cycles between parents and children in the effort to maintain diet, neglect of other adverse influences), and of difficulties in selection of who should be treated. Ernest Krug rightly emphasises the multifactorial nature of the disorder and the heterogeneity of outcome. The clear finding, documented in our seminar, is that the core symptoms of the disorder are indeed an adverse influence on children’s psychological development— even in the absence of other risks.3,4 Nevertheless, this substantial group risk is compatible with a good outcome in many individual children.3 Individual case analyses are always required for clinical treatment. Research now in progress, referenced in the seminar, should provide information about moderators and mediators of outcome, as well as about niches in which individuals with the disorder are likely to succeed. We take the research on diet seriously, and in addition to the trial mentioned by Soothill another of us has contributed some evidence about possible mechanisms of action of elimination diets.5 Further research is definitely needed on these interesting approaches, but, given present knowledge of inconsistent effects, it is not prudent to give broad recommendations for the widespread application of dietary treatment to the clinical population defined by a diagnosis of attention-deficit hyperactivity disorder and hyperkinetic disorders. *Eric Taylor, James Swanson, Joseph Sergeant, Edmund Sonuga-Barke, Peter Jensen
MRC Child Psychiatry Unit, Institute of Psychiatry, London SE5 8AF, UK 1
2
3
4
5
Young E, Patel S, Stoneham M, Rona R, Wilkinson JD. The prevalence of reaction to food additives in a survey population. J R Coll Phys Lond 1987; 21: 241–47. Schulte-Koerne G, Diemel W, Gutenbrunner C, et al. Effect of an oligoantigen diet on the behaviour of hyperkinetic children. Zeitschrift fuer Kinder-und Jugendpsychiatrie 1996; 24: 176–83. Taylor E, Chadwick O, Heptinstall E, Danckaerts M. Hyperactivity and conduct problems as risk factors for adolescent development. J Am Acad Child Adol Psychiatry 1996; 35: 1213–26. Satterfield J, Swanson JM, Schell A, Lee F. Prediction of antisocial behavior in attentiondeficit hyperactivity disorder boys from aggressive/defiance scores. J Am Acad Child Adol Psychiatry 1994; 33: 185–90. Swanson JM, Kinsbourne M. Food dyes impair performance of hyperactive children on a laboratory learning test. Science 1980; 207: 533–41.
Antiretroviral therapy in countries with low health expenditure Sir—Olaf Müller and colleagues (Jan 3, p 68)1 argue against future public investments in the triple-combination antiretroviral therapy against HIV-1 in sub-Saharan Africa. They feel that such countries’ meagre resources should be used to improve existing health services and ensure care of the increasing number of cases of tuberculosis, pneumonia, and other opportunistic infections. Furthermore, lack of laboratory facilities to quantify HIV RNA or CD4 lymphocyte counts, poor compliance, and severe sideeffects would lead to rapid development of drug resistance in the community. These arguments are just as applicable to some Asian countries—particularly, Vietnam, Laos, Bangladesh, and Nepal, where less than US$10 per person per year is spent on health care.2 Asian, African, and Latin American countries have both public and private health-care systems.3 In some countries that spend such a small amount on health, a greater proportion of available funds is spent in the private than the public sector (table).3 Antiretroviral therapy is available in the private sector in Madras, India, but the drugs have to be procured through black-market sources: the government is reluctant to encourage general use because of the three million or so HIV1-positive people in our country.4 The use of anti-HIV-1 multidrug cocktails that consist of poor quality drugs will surely lead to the emergence of multidrug-resistant strains.
1433