- Email: [email protected]
CARBOXYMETHYLCELLULOSE, TAMPONS, AND STAPHYLOCOCCI
873 The second assumption again 13 raises the question of the primary goal of genetic counselling-is it to improve society’s "genetic health" by reducing the frequency of disease or is it to help individuals and families in making informed, autonomous decisions about their own health and reproduction? A recent US report14 on the ethical, social, and legal implications of genetic screening, counselling, and education programmes, by the President’s Commission for the Study of Ethical problems in Medicine and Biomedical and Behavioural Research, emphasises that "the very notions of ’genetic health’ and ’genetic normality’ are extremely vague and elastic slogans that attempt to disguise controversial ideals of human excellence as value-free medical categories" and that "sound public policy ... cannot be based on such loose and abusable notions". Society’s respect for the autonomy of the individual and the right to make informed decisions argue for mformative, non-directive counselling for anyone at risk for a genetic disease, including Huntington’s disease. If the goal of genetic counselling is an informed, autonomous individual, a measure of the effectiveness of such counselling should be an objective test of knowledge of the characteristics, distribution, prognosis, treatment, and heredity of Huntington’s disease and a subjective sense, on the part of those counselled, of support and understanding, rather than the somewhat removed measure of a noticeable decrease in reproduction. The President’s Commission warns that the attitudes and policies of health professionals may affect the choices individuals feel able or constrained to make. The purposes and goals of genetic counselling of those at risk for Huntington’s disease must be clarified so that a consistent policy can be established. Science, Technology, and Society, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA
STEPHANIE J. BIRD
SUGARS AND DENTAL DECAY
SIR,—It is not unexpected that correspondence (March 12 issue) :ommenting on my Feb 5 article should include letters from people linked to the sugar and confectionery industry. Their views are minority views whilst those expressed in the article are widely held. For example, Bowen has assessed the situation as follows: "Evidence incriminating sugars has continued to accumulate from the results of epidemiological and animal research and has now reached such proportions that no reasonable person would deny that frequent consumption of sugars by caries-susceptible humans will result in the development of dental caries". There is a consensus that sugars are the most important dietary cause of caries and that fluoride will reduce the effect by remineralising some of the lesions and increasing the resistance to aCld attack. It is not surprising, therefore, that there has been a dechne in caries in countries where fluoride has been widely available. But the amount and frequency of sugar consumption has also changed in the past decade. Despite Mr Hugill’s claim that per caput sugar consumption has remained virtually static, evidence from Britain, for example, shows that sugar consumption has decreased by 15% since 19712 and the sucrose consumed in confectionery by 13% since 1973 with no increase in glucose consumption.3In Sweden, Koch4in his report to the conference on the decline in caries which Hugill refers to, stated that the frequency of sugar intake has declined. De Paola et al,4 at the same conference, 13 Editorial Genetic counselling and the prevention of Huntington’s chorea. Lancet 1982, i 147 14 President’s Commission for the Study of Ethical Problems in Medicine and Biomedical
and Behavioural Research
Screening and counseling for Government Printing Office, Washington, 1983.
conditions. US
1 Bowen WH. Role of carbohydrates in dental caries. In: Wei S, ed Symposium on dental nutrition
Ames
University of Iowa,
2 National Food Survey
of Community Dental Health, Dental School, London Hospital Medical College, London E1 2AD
Department
A. SHEIHAM
CARBOXYMETHYLCELLULOSE, TAMPONS, AND STAPHYLOCOCCI
SIR,-Dr Tierno, Dr Hanna, and Dr Davies (March 19,
p 615) carboxymethylcellulose substrate is degraded by &bgr;-glucosidase to yield free glucose. Tiernol and Hanna2had independently reported similar findings previously. A second predictable observation is that Staphylococcus aureus multiplies in a dilute glucose solution. Tierno et al then invoke a broad literature of toxic shock syndrome (TSS) related microbiology to amplify their single observation. As someone engaged in TSS
report that a cellulase and
research I can affirm that the genesis of this significant illness is not yet understood. Tierno et al fail to alleviate our ignorance. The concentrations of glucose and other potential nutrients in vaginal secretions are significantly greater than can be derived from a minimal degradation of a relatively inert complex polysaccharide, and the conclusion that their finding "may very well explain the increased frequency of TSS among users of tampons" is unjustified. 5. US
Department of Health and Human Services. The prevalence of dental caries in United States children 1979-80 NIH publ no 82-2245. Bethesda, Maryland: NIH, 1981.
6 Barmes DE Epidemiology of dental disease. J Clin Periodont 1977; 4: 80-93. 7. Newbrun E. Sucrose in the dynamics of the carious process Int Dent J 1982; 32: 13-23. 8. Symposium on Diet and Dental Caries (held at the University of Melbourne, Australia,
1982)
1978.
Food Facts Dec 14, 1981. Ministry of
sucrose consumption had decreased since 1971 and contributed have to the declining caries rate. may Despite the decline in caries reported in many industrialised countries, there is still a high caries rate. For example, in the USA the average 17-year-old had six teeth decayed (DMFT) in 19806 and in Norway, 16-year-olds had sixteen decayed surfaces (DMFTS) in 1981. In New Zealand, where the filling rate has declined by 41% since 1977, each schoolchild needed 1.5 fillings per year in 1980.5A contrasting pattern of caries to that found in industrialised countries is occurring in underdeveloped countries where sugar consumption is increasing. Here, the increase in caries is so rapid that Dr D. E. Barmes, chief of the oral health unit of WHO, has described it as "absolutely frightening". The reason for the rapid rise in caries is generally considered to be an increase in sugar consumption. Dr Bibby and Dr Curzon question whether there is a dose response relation between sugar and caries, without giving any evidence to substantiate their doubt. Newbrunhas summarised the relationship on the basis of available information as follows: "The relationship between sucrose and caries probably approximates to an S-shaped curve, rising steeply when the sucrose-containing food is eaten frequently, and when the immune response is immature, as in young children". Obviously the shape of the curve will be altered by the form in which the sugar is eaten. If eaten with highly refined starch, the effect will be worse. My views on the role of starch in caries are supported by a conclusion at a recent symposium on diet and caries.8 When discussing the cariogenicity of starch they concluded that the evidence in man suggests a low cariogenicity for starch despite the finding that starch caused prolonged drops in pH. The validity of the conclusions which Dr Walker draws from his data on dental caries and sugar in South African populations has been seriously questioned.9 Despite Walker’s reservations about the role of sugar in reducing caries prevalence it is heartening to read that he agrees with me and Newbrun that "the amount of sugar consumption and the frequency of ingesting between meal sugary snacks are related to caries in humans". The recommendations made in my article are all related to reducing the amount and frequency of eating sugars.
reported that
Agriculture, Fisheries and
Food, London 3 Cocoa, Chocolate and Confectionery Alliance. Annual report 1980-81 London: CCCA 4 The First International Conference of the Declining Prevalence of Dental Caries.J Dent Res 1982, 61 (spec issue). 1301-83
9 Newbrun E. Dental caries:
an overview
In: Conference on Foods Nutrition and Dental
(October, 1978). Chicago. American Dental Association, 1978: 25-36 PM Cellulase activity of microorganisms on carboxymethylcellulose from
Health 1. Tierno
tampons. Lancet 1981; ii: 746-47. 2. Hanna BA Microbial degradation of carboxymethylcellulose from tampons. Lancet 1982, i: 279
874 The title of this paper is Growth of Toxic Shock Syndrome Strain of Staphylococcus aureus after Enzymic Degradation of ‘Rely’ Tampon Component. A more accurate and unbiased title for this modest contribution might have been Enzymatic Degradation Product of Carboxymethylcellulose Supports the Growth of Staphylococcus aureus. I hope that Tierno and Hanna’s frequent roles as expert witnesses for plaintiffs in TSS related lawsuits against manufacturers is not beginning to cloud scientific objectivity. Department of Microbiology and Molecular Genetics, University of Cincinnati Medical Center, Cincinnati, Ohio 45267, USA
INCIDENCE OF ANTI-GLIADIN
(AGA) AND ANTI-RETICULIN (ARA)
ANTIBODIES IN CHILDREN WITH COELIAC DISEASE, OTHER GASTROINTESTINAL DISEASES AND NORMAL CHILDREN
PETER F. BONVENTRE
GLIADIN AND RETICULIN ANTIBODIES IN CHILDHOOD COELIAC DISEASE
SIR,—Dr Savilahti and colleagues (Feb 12, p 320) found an association between circulating antigliadin antibodies of IgA class (IgA-AGA) and the mucosal lesion in active, untreated childhood coeliac disease. Surprisingly, they had no disease controls; nor did they look for IgA antibodies to non-wheat food antigens in their patients’ sera. Patients with untreated coeliac disease tend to have serum antibodies to a wide range of food antigens, 1-3 and this has been taken as indicating non-specific antibody development as a result of damage to the small-intestinal mucosa. Over the past four years we have screened 821 sera from 369 infants aged two years or less at initial presentation who were under investigation4for gastrointestinal disease, looking for AGA both by an enzyme-linked immunosorbent assay essentially the same as that used by Savilahti et al and by a new immunofluorescent methodand for anti-reticulin antibodies of R1 pattern (Rl-ARA) by indirect immunofluorescence on cryostat tissue sections.Our results are given in the table. All children with untreated coeliac disease were AGA positive, but 20% of the 249 disease controls were also positive. RI-ARAwas far more disease specific, being found in only 3 disease controls; however, it was much less sensitive. Although IgA-AGA was most likely to be found in active coeliac disease (85% positive) this class of KG, Walker-Smith JA. Immunoglobulins and dietary protein antibodies in childhood coeliac disease Gut 1970; 11: 635-40 2 Ferguson A, Carswell F. Precipitins to dietary proteins in serum and upper intestinal secretions of coeliac children Br Med J 1972; i: 75-77. 3 Kumar PJ, Ferguson A, Lancaster-Smith M, Clark MJ. Food antibodies in patients with dermatitis herpetiformis and adult coeliac disease-relationship to jejunal morphology. Scand J Gastroenterol 1976; 11: 5-10 4. Walker-Smith JA. Diseases of the small intestine in childhood, 2nd ed. London: Pitman Medical, 1979. 5. Unsworth DJ, Leonard JN, McMinn RMH, Swain AF, Holborow EJ, Fry L. Antigliadin antibodies and small intestinal mucosal damage in dermatitis herpetiformis. Br J Dermatol 1981; 105: 653-58. 6. Unsworth DJ, Manuel PD, Walker-Smith JA, Campbell CA, Johnson GD, Holborow EJ. A new immunofluorescent blood test for gluten sensitivity. Arch Dis Child 1981; 1. Kenrick
antibody was also found in 7 (14%) of the 50 AGA-positive disease controls-3 with untreated cow’s milk sensitive enteropathy, 3 with Crohn’s disease (affecting both small and large bowel in each case), and 1 with autoimmune disease of the small intestine. All the AGApositive sera contained AGA of IgA class and all but 2 contained normal levels of IgM antibody. Sera from 43 infants were selected at random from the above to cover untreated coeliac disease, non-coeliac gastrointestinal disease, and children for whom gastrointestinal disease had been excluded, and tested for IgA, IgG, and IgM antibody to wheat gliadin, ovalbumin, and &bgr;-lactoglobulin (figure). Patients with circulating IgG-AGA tended to have IgG antibody to ovalbumin and &bgr;-lactoglobulin as well; in contrast, patients with 7 Walker-Smith
JA, Unsworth DJ, Hutchins P, Phillips AD, Holborow EJ. Autoantibody against gut epithelium in a child with small-intestinal enteropathy
Lancet
56: 864-68
ELISA titres of serum antibodies to
1982; i: 566-67.
ovalbumin (0), and
&bgr;-lactoglobulin (B). serum dilution of 1/50, 2= serum dilution of 1/100, and so on. IgM antibody titres were
ELISA titre given as I = all in the normal range and are
not
gliadin (G),
shown.
STEPHANIE J. BIRD
SUGARS AND DENTAL DECAY
SIR,—It is not unexpected that correspondence (March 12 issue) :ommenting on my Feb 5 article should include letters from people linked to the sugar and confectionery industry. Their views are minority views whilst those expressed in the article are widely held. For example, Bowen has assessed the situation as follows: "Evidence incriminating sugars has continued to accumulate from the results of epidemiological and animal research and has now reached such proportions that no reasonable person would deny that frequent consumption of sugars by caries-susceptible humans will result in the development of dental caries". There is a consensus that sugars are the most important dietary cause of caries and that fluoride will reduce the effect by remineralising some of the lesions and increasing the resistance to aCld attack. It is not surprising, therefore, that there has been a dechne in caries in countries where fluoride has been widely available. But the amount and frequency of sugar consumption has also changed in the past decade. Despite Mr Hugill’s claim that per caput sugar consumption has remained virtually static, evidence from Britain, for example, shows that sugar consumption has decreased by 15% since 19712 and the sucrose consumed in confectionery by 13% since 1973 with no increase in glucose consumption.3In Sweden, Koch4in his report to the conference on the decline in caries which Hugill refers to, stated that the frequency of sugar intake has declined. De Paola et al,4 at the same conference, 13 Editorial Genetic counselling and the prevention of Huntington’s chorea. Lancet 1982, i 147 14 President’s Commission for the Study of Ethical Problems in Medicine and Biomedical
and Behavioural Research
Screening and counseling for Government Printing Office, Washington, 1983.
conditions. US
1 Bowen WH. Role of carbohydrates in dental caries. In: Wei S, ed Symposium on dental nutrition
Ames
University of Iowa,
2 National Food Survey
of Community Dental Health, Dental School, London Hospital Medical College, London E1 2AD
Department
A. SHEIHAM
CARBOXYMETHYLCELLULOSE, TAMPONS, AND STAPHYLOCOCCI
SIR,-Dr Tierno, Dr Hanna, and Dr Davies (March 19,
p 615) carboxymethylcellulose substrate is degraded by &bgr;-glucosidase to yield free glucose. Tiernol and Hanna2had independently reported similar findings previously. A second predictable observation is that Staphylococcus aureus multiplies in a dilute glucose solution. Tierno et al then invoke a broad literature of toxic shock syndrome (TSS) related microbiology to amplify their single observation. As someone engaged in TSS
report that a cellulase and
research I can affirm that the genesis of this significant illness is not yet understood. Tierno et al fail to alleviate our ignorance. The concentrations of glucose and other potential nutrients in vaginal secretions are significantly greater than can be derived from a minimal degradation of a relatively inert complex polysaccharide, and the conclusion that their finding "may very well explain the increased frequency of TSS among users of tampons" is unjustified. 5. US
Department of Health and Human Services. The prevalence of dental caries in United States children 1979-80 NIH publ no 82-2245. Bethesda, Maryland: NIH, 1981.
6 Barmes DE Epidemiology of dental disease. J Clin Periodont 1977; 4: 80-93. 7. Newbrun E. Sucrose in the dynamics of the carious process Int Dent J 1982; 32: 13-23. 8. Symposium on Diet and Dental Caries (held at the University of Melbourne, Australia,
1982)
1978.
Food Facts Dec 14, 1981. Ministry of
sucrose consumption had decreased since 1971 and contributed have to the declining caries rate. may Despite the decline in caries reported in many industrialised countries, there is still a high caries rate. For example, in the USA the average 17-year-old had six teeth decayed (DMFT) in 19806 and in Norway, 16-year-olds had sixteen decayed surfaces (DMFTS) in 1981. In New Zealand, where the filling rate has declined by 41% since 1977, each schoolchild needed 1.5 fillings per year in 1980.5A contrasting pattern of caries to that found in industrialised countries is occurring in underdeveloped countries where sugar consumption is increasing. Here, the increase in caries is so rapid that Dr D. E. Barmes, chief of the oral health unit of WHO, has described it as "absolutely frightening". The reason for the rapid rise in caries is generally considered to be an increase in sugar consumption. Dr Bibby and Dr Curzon question whether there is a dose response relation between sugar and caries, without giving any evidence to substantiate their doubt. Newbrunhas summarised the relationship on the basis of available information as follows: "The relationship between sucrose and caries probably approximates to an S-shaped curve, rising steeply when the sucrose-containing food is eaten frequently, and when the immune response is immature, as in young children". Obviously the shape of the curve will be altered by the form in which the sugar is eaten. If eaten with highly refined starch, the effect will be worse. My views on the role of starch in caries are supported by a conclusion at a recent symposium on diet and caries.8 When discussing the cariogenicity of starch they concluded that the evidence in man suggests a low cariogenicity for starch despite the finding that starch caused prolonged drops in pH. The validity of the conclusions which Dr Walker draws from his data on dental caries and sugar in South African populations has been seriously questioned.9 Despite Walker’s reservations about the role of sugar in reducing caries prevalence it is heartening to read that he agrees with me and Newbrun that "the amount of sugar consumption and the frequency of ingesting between meal sugary snacks are related to caries in humans". The recommendations made in my article are all related to reducing the amount and frequency of eating sugars.
reported that
Agriculture, Fisheries and
Food, London 3 Cocoa, Chocolate and Confectionery Alliance. Annual report 1980-81 London: CCCA 4 The First International Conference of the Declining Prevalence of Dental Caries.J Dent Res 1982, 61 (spec issue). 1301-83
9 Newbrun E. Dental caries:
an overview
In: Conference on Foods Nutrition and Dental
(October, 1978). Chicago. American Dental Association, 1978: 25-36 PM Cellulase activity of microorganisms on carboxymethylcellulose from
Health 1. Tierno
tampons. Lancet 1981; ii: 746-47. 2. Hanna BA Microbial degradation of carboxymethylcellulose from tampons. Lancet 1982, i: 279
874 The title of this paper is Growth of Toxic Shock Syndrome Strain of Staphylococcus aureus after Enzymic Degradation of ‘Rely’ Tampon Component. A more accurate and unbiased title for this modest contribution might have been Enzymatic Degradation Product of Carboxymethylcellulose Supports the Growth of Staphylococcus aureus. I hope that Tierno and Hanna’s frequent roles as expert witnesses for plaintiffs in TSS related lawsuits against manufacturers is not beginning to cloud scientific objectivity. Department of Microbiology and Molecular Genetics, University of Cincinnati Medical Center, Cincinnati, Ohio 45267, USA
INCIDENCE OF ANTI-GLIADIN
(AGA) AND ANTI-RETICULIN (ARA)
ANTIBODIES IN CHILDREN WITH COELIAC DISEASE, OTHER GASTROINTESTINAL DISEASES AND NORMAL CHILDREN
PETER F. BONVENTRE
GLIADIN AND RETICULIN ANTIBODIES IN CHILDHOOD COELIAC DISEASE
SIR,—Dr Savilahti and colleagues (Feb 12, p 320) found an association between circulating antigliadin antibodies of IgA class (IgA-AGA) and the mucosal lesion in active, untreated childhood coeliac disease. Surprisingly, they had no disease controls; nor did they look for IgA antibodies to non-wheat food antigens in their patients’ sera. Patients with untreated coeliac disease tend to have serum antibodies to a wide range of food antigens, 1-3 and this has been taken as indicating non-specific antibody development as a result of damage to the small-intestinal mucosa. Over the past four years we have screened 821 sera from 369 infants aged two years or less at initial presentation who were under investigation4for gastrointestinal disease, looking for AGA both by an enzyme-linked immunosorbent assay essentially the same as that used by Savilahti et al and by a new immunofluorescent methodand for anti-reticulin antibodies of R1 pattern (Rl-ARA) by indirect immunofluorescence on cryostat tissue sections.Our results are given in the table. All children with untreated coeliac disease were AGA positive, but 20% of the 249 disease controls were also positive. RI-ARAwas far more disease specific, being found in only 3 disease controls; however, it was much less sensitive. Although IgA-AGA was most likely to be found in active coeliac disease (85% positive) this class of KG, Walker-Smith JA. Immunoglobulins and dietary protein antibodies in childhood coeliac disease Gut 1970; 11: 635-40 2 Ferguson A, Carswell F. Precipitins to dietary proteins in serum and upper intestinal secretions of coeliac children Br Med J 1972; i: 75-77. 3 Kumar PJ, Ferguson A, Lancaster-Smith M, Clark MJ. Food antibodies in patients with dermatitis herpetiformis and adult coeliac disease-relationship to jejunal morphology. Scand J Gastroenterol 1976; 11: 5-10 4. Walker-Smith JA. Diseases of the small intestine in childhood, 2nd ed. London: Pitman Medical, 1979. 5. Unsworth DJ, Leonard JN, McMinn RMH, Swain AF, Holborow EJ, Fry L. Antigliadin antibodies and small intestinal mucosal damage in dermatitis herpetiformis. Br J Dermatol 1981; 105: 653-58. 6. Unsworth DJ, Manuel PD, Walker-Smith JA, Campbell CA, Johnson GD, Holborow EJ. A new immunofluorescent blood test for gluten sensitivity. Arch Dis Child 1981; 1. Kenrick
antibody was also found in 7 (14%) of the 50 AGA-positive disease controls-3 with untreated cow’s milk sensitive enteropathy, 3 with Crohn’s disease (affecting both small and large bowel in each case), and 1 with autoimmune disease of the small intestine. All the AGApositive sera contained AGA of IgA class and all but 2 contained normal levels of IgM antibody. Sera from 43 infants were selected at random from the above to cover untreated coeliac disease, non-coeliac gastrointestinal disease, and children for whom gastrointestinal disease had been excluded, and tested for IgA, IgG, and IgM antibody to wheat gliadin, ovalbumin, and &bgr;-lactoglobulin (figure). Patients with circulating IgG-AGA tended to have IgG antibody to ovalbumin and &bgr;-lactoglobulin as well; in contrast, patients with 7 Walker-Smith
JA, Unsworth DJ, Hutchins P, Phillips AD, Holborow EJ. Autoantibody against gut epithelium in a child with small-intestinal enteropathy
Lancet
56: 864-68
ELISA titres of serum antibodies to
1982; i: 566-67.
ovalbumin (0), and
&bgr;-lactoglobulin (B). serum dilution of 1/50, 2= serum dilution of 1/100, and so on. IgM antibody titres were
ELISA titre given as I = all in the normal range and are
not
gliadin (G),
shown.