EVOLUTION AND INFANT FEEDING

EVOLUTION AND INFANT FEEDING

1441 contraceptive pills to "treat" the menstrual problems associated with injectable progestagens negates their advantage of being oestrogen-free. I...

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1441

contraceptive pills to "treat" the menstrual problems associated with injectable progestagens negates their advantage of being oestrogen-free. In appendix ut I make the very same

point.

The value of oral oestrogens in the management of

bleeding problems is questionable-spotting or increased bleeding is usually self-limiting, and most women need no more than explanation and reassurance. She challenges my statement that injectable progestagens do not adversely affect lactation, but seems to be confusing this with the question of the possible effects of progestagen secreted in breast milk on the infant or young child. There is no evidence that progestagens reduce lactation, and WHO considers DMPA safe for use in lactating women. The reason for withholding injectable progestagens during the first 6 weeks after delivery is not the possible effects on breast-fed infants but the possibility of prolonged bleeding. She challenges my suggestion that injectables may protect against iron-deficiency anaemia. Bleeding is rarely severe enough to threaten health. We are not told the source of her statement that between 0-5% and 10% of women experience

"heavy bleeding". Ms Nair makes a serious allegation against SCF when she that ’Depo Provera’ "trials" were carried out at the SCF River Project in Bangladesh. This is not so. Nor was depo provera the only contraceptive offered by SCF staff. Government family planning workers also provide services in the River Project area. Furthermore, injectable progestagens are now being promoted in the Government family planning states

programme.

Save the Children Fund commissioned the report precisely because of widespread anxieties about injectable contraceptives. The prominence given to the emotive and frequently inaccurate propaganda against injectables had been distorting discussion of the issues, and it was felt that SCF was well placed to redress the balance. Inevitably the report’s conclusions will conflict with the views of some people, but I had hoped that it would at least receive a fair reading. 5 Brighton Court, 73 West Hill, London SW15 2UL

ELIZABETH ARCHER

Although the numbers of women are small, these results are relevant in assessing the place of family planning in reducing both high birth rates and high maternal mortality rates in poor communities in black Africa. Given the choice, women who will readily opt for family planning are those whose children from previous births are all likely to survive. In this Zaria study, women in such privileged position made up 37",, (654/1762) of those with three to six previous births, and a mere 8% (63/766) of those with more than six previous births. Because these advantaged women are a small minority, contraceptive use among them will most probably not succeed in checking population increase in the whole community. If, however, family planning is to be directed towards reducing high maternal mortality rate, then it would be reasonable to target contraceptive use to those at the highest risk of death during pregnancy. These are women in whom high parity (parity seven or more) and low child survival rate (50% or less) are combined. This is an unfortunate combination because Nigerian women who are not assured of the survival of their children will be most reluctant to practise effective contraception. The point here is that high parity is not always associated with poor maternal and child survival. Where it is, the chances are that the women affected are those who are already at risk for some other reason, this being the adverse conditions under which they live. Examined in this way, it is clear that in the prevailing sociocultural milieu, where the associated problems of severe socioeconomic deprivation exist on a very large scale, the promotion of family planning is unlikely to succeed in reducing maternal mortality. High maternal mortality has its roots in underdevelopment and mass illiteracy. 3-5 If we are looking for major decreases in maternal mortality we must first attack those social conditions which perpetuate underdevelopment, the most fundamental need being the eradication of mass illiteracy through universal formal education. At the same time, we should lay the foundations for a health service structure that can both prevent and deal promptly with the principal causes of maternal mortality, which in northern Nigeria are bacterial infections, severe anaemia, eclampsia, haemorrhage, and obstructed labour, together with its consequences. Department of Obstetrics and Gynaecology, University of Port Harcourt, PMB 5323, Port Harcourt,

FAMILY PLANNING AND MATERNAL MORTALITY IN THE THIRD WORLD

SIR,-Rosenfeld and Maine1 and

many others believe that and high maternal mortality are associated,

because high parity family planning, by reducing high parity, will lead to a fall in maternal mortality rate. This letter, drawing on data from the Zaria maternity survey2 in northern Nigeria, casts doubt on this concept. Pregnancy prevention for reasons other than high parity does not concern us here. The table shows the relation between child mortality, previous births, and maternal death rates. Maternal mortality rose as child survival worsened, particularly in women with over six previous births. Only where child survival was very poor did maternal mortality rise with increasing parity. In women with the best possible child survival record, the maternal death rate fell with increasing parity.

K. A. HARRISON

Nigeria

Department of Occupational London School of Hygiene and Tropical Medicine, London WC1

Health,

C. E. ROSSITER HWEE TAN

1. Rosenfeld AL, Maine D, Maternal mortality: a neglected tragedy. Lancet 1985; ii: 83-85. 2. Harrison KA, Rossiter CE. Maternal mortality. In: Harrison KA, ed. Childbearing, health and social priorities. Br J Obstet Gynaecol 1985; 92: (suppl 5): 100-15. 3. Jaya Rao, KS. Attitudes to women and nutrition programmes in India. Lancet 1979; ii: 1357-58. 4. Forum interview. Prevention of maternal mortalilty. World Health Forum (in 5.

press). Harrison, KA, Rossiter CE, Chong H, et al. Antenatal care, formal education and child-bearing. In: Harrison KA, ed. Child-bearing, health and social priorities. Br J Obstet Gynaecol 1985; 92 (suppl 5): 14-22.

EVOLUTION AND INFANT FEEDING CHILD MORTALITY, PREVIOUS

BIRTHS, AND MATERNAL DEATH

RATES IN UNBOOKED WOMEN IN ZARIA

Reproduced, by

kind

of the editor, Bntish Journal 1985.

permission

Gynaecology, from Harnson

of Obstetrics

and

SiR,—Dr Latham (May 10, p 1089), commenting on my March 22 paper, questions the benefit of the caloric restriction of breast milk, but the example he uses implicitly assumes a linear response to changing energy balance. The data available for infants and children show that mortality does not increase linearly with decreasing intake; rather there is a large rise in mortality only when the weight-for-age reaches a critical level. Although evidence is scanty, it seems that the same pattern of response may apply to the mothers. We have suggested! that many peasant farmers, both male and female, who form a large part of the population of developing countries, are close to the

1442 critical level of nutrition below which they cannot successfully accomplish the heavy work of cultivation, planting, and harvesting. Under these conditions, the difference cited by Latham could be crucial for the survival of the mother and her family. One of the purposes of my paper was to alert professionals to the needs of the mother, both in energy and other resources, and so encourage research in this neglected area.

Latham’s letter ends by questioning the validity of my paper on the grounds that funds from Wyeth Pharmaceuticals were involved. He ignores my acknowledgement to the Nursing Mothers Association of Australia’s approval. When we were planning a large prospective study of infant health, growth, disease, and feeding, neither institutional funding agencies nor the Nursing Mothers Association could provide funds. I approached Wyeth, who agreed to support the study. Knowing that such funding would automatically make the results suspect in some quarters, I made it a condition that the research protocol should be approved by the Nursing Mothers Association of Australia, which has a long record of antiindustry activity. The association sent the protocol to referees. They approved the protocol. Some changes and improvements were suggested and incorporated. Data from this three-year project are now being analysed. Throughout, the association has cooperated in many ways, while Wyeth has provided scientific stimulus besides money. I have gone to considerable lengths to exclude bias in this research. To my knowledge, this is the first time that the baby food industry and a consumer group have both had significant inputs into a research project. All parties have gained understanding and knowledge. This pattern points the way to future cooperation. Human Nutrition Research Group, Department of Child Health, University of Queensland, St Lucia, Queensland 4067, Australia 1.

Dugdale AE, Payne PR. Food Nutr (in press).

A model of seasonal

A. E. DUGDALE changes

in energy balance. Ecol

SIR,-Your May 31 editorial (p 1255) states that calcitonin is the established treatment for osteolcytic lesions and that a dose of at least 100 IU daily is necessary for 12 months or more. We predict that you will soon be commissioning another editorial to mark the relegation of calcitonin (and etidronate) to the repository for therapeutic has-beens. As far as we know we are the major centre in the UK evaluating intravenous aminohydroxypropylidene-l,l-bisphosphonate (APD) for the sole management of Paget’s disease of bone, and we have already treated 50 patients. The clinical and biochemical response is impressive, with rapid healing of lytic disease after a course of twelve weekly infusions of 15 or 30 mg in saline over 2 h.l.2 The drug has no serious side-effects and induces prolonged remissions (time will tell whether it will effect a cure). By contrast calcitonin has severe side-effects and does not produce sustained remissions. Calcitonin is very expensive CC2700 a year at 100 IU per day) and APD is likely to be a lot cheaper. Because of erratic and poor absorption and gastrointestinal side-effects from APD when given orally, the intravenous route is likely to be the one of choice. We would urge other centres to evaluate intravenous APD for Paget’s disease, to hasten the day when this agent does become generally available.

Salford M6 8HD

DAVID C. ANDERSON HELEN M. BUCKLER JUDITH A. CANTRILL

JA, Buckler HM, Anderson DC. Low dose intravenous 3-amino-1 hydroxypropylidine-1-1 bisphosphonate (APD) for the treatment of Paget’s disease of bone Ann Rheum Dis (in press). 2. Bucker HM, Cantrill JA, Anderson DC. The use of intravenous 3-amino-1hydroxypropylidene-1-1-bisphosphonate (APD) in forty patients with Paget’s disease of bone. Bone and Tooth Society meeting (April 11, 1986); abstr p3 1. Cantrill

SIR,-We fully support the plea from our colleagues (May 24, p 1216) for the treatment of sexual partners of men with non-specific urethritis, or non-gonococcal urethritis (NGU). Because

Chlamydia trachomatis has been shown to cause at least

40% of cases of NGU (and 60% in some series1), it has, for the past seventeen years, been routine practice in our department of genitourinary medicine to treat all female contacts of these

patients. For the past six years we have been fortunate in having a chlamydia culture service. This now examines about 12 000 specimens a year, of which 97% originate from the department of genitourinary medicine. Provided that correct techniques are used for sampling and transportation, isolation of C trachomatis is straightforward. It is essential that the specimen contains columnar epthelial cells; samples of pus and high vaginal swabs unsuitable. Female contacts of men with NGU need to be seen and examined before treatment so that other coexisting sexually transmitted diseases can be diagnosed and treated. The risk of pregnancy should also be assessed, since pregnant women should be given erythromycin instead of tetracycline. Further contact tracing may also be appropriate. Much salpingitis will be prevented if all doctors dealing with sexually active women are made aware of the aetiological role of chlamydia in this condition and learn how to diagnose and treat this infection correctly. As with any chlamydial infection, the management of a woman with salpingitis includes examination and treatment of her contacts. Her male partner may be infected even if he is symptomless, and he may reinfect her, causing recurrent salpingitis and infertility. Patients would benefit from increased liaison between gynaecologists, the laboratory, and the department of genitourinary medicine in the management of C trachomatis infection. are

Departments of Genitourinary Medicine and Virology,

NEW DRUGS FOR PAGET’S DISEASE

Department of Medicine, University of Manchester, Clinical Sciences Building, Hope Hospital,

TREATMENT FOR SEXUAL PARTNERS OF MEN WITH NON-SPECIFIC URETHRITIS

St Thomas’ Hospital, London SE1 7EH

CAROLINE BRADBEER JAN WELCH R. N. THIN

Ridgway GL. Genital infection by C trachomatis. In: Current topics in infection: Series 2. London: Arnold, 1982.

1. Oriel JD,

REDUCED EXPRESSION OF INTERLEUKIN-2 RECEPTORS IN HYPOGAMMAGLOBULINAEMIA: A POSSIBLE CAUSE OF HIGHER CANCER INCIDENCE

SiR,—The highly significant increase in the incidence of malignancies in patients with common variable (late onset) hypogammaglobulinaemia (CVH) has not been explained. The function of lymphokine-activated killer (LAK) cells, which display very efficient tumour-eliminating activity in ViVo,l,2 is impaired in CVH.3 Since this might, at least partly, be responsible for the increased tumour incidence, we have investigated the mechanism for the reduced LAK-cell function. To exclude a reduction in the frequency of LAK-cell precursors, we developed a limiting dilution assay based on that used for specific cytotoxic T-cell precursors.’ We isolated peripheral blood mononuclear cells and prepared 24-well replicates of two-fold dilutions of the cells, beginning with 150 000 cells per round-bottomed microwell, and incubated them in a final volume of 0-15 ml per well in the presence of 500 units/ml of human recombinant interleukin-2 (IL-2). Cultures without IL-2 were set up in parallel. After 6 days, the IL-2-induced LAK activity in individual wells was measured in a 5 h 5’Cr-release assay using T24 target cells.3 Wells were considered positive when the chromium release was more than 3 standard deviations above the mean for spontaneous release. We investigated 14 healthy volunteers and 6 CVH patients. The LAK-cell precursor frequencies in healthy controls were in the range 1 per 7053 to 1 per 61 001. 5 CVH patients had