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Tms was the subject of the Heath Clark lectures,1972, given by Prof. V. Ramalingaswami at the LondonSchool of Hygiene and Tropical Medicine. Professor

Ramalingaswami is director of the All-India Instituteof Medical Sciences, New Delhi, and head of thedepartment of pathology there. The All-IndiaInstitute is remarkable in that it combines under oneroof a centre for research in clinical medicine andbasic sciences, a teaching hospital, and an under-graduate medical school. Thus, as Ramalingaswamihas said elsewhere, the work described in theselectures was done in an environment where teaching,research, and practice are in progress, and where

young teachers and investigators are in training.The first lecture was concerned with experimental

production of protein malnutrition in the rhesus

monkey. The results show that in some importantrespects the views held 25 years ago are not onlyuntrue but even the opposite of the truth. At aboutthat time Himsworth published his extremely stimu-lating monograph, Lectures on the Liver and its

Diseases, which married human and experimentalpathology. Fatty liver had been produced by dietarymeans in the rat, and there was no doubt whateverthat if prolonged and severe it went on to fibrosis.Naturally this led to expectation that the fatty liverof kwashiorkor might have something to do with thecirrhosis which is rather common in many tropicalcountries. Although many have tried, no-one hassucceeded in demonstrating this sequence in man. Itwas therefore well worth reopening the question in therhesus monkey-a better analogue for man than therat. The monkeys on a low-protein diet developedfatty livers, which began periportally, as in man. Itwas shown very elegantly that the cause of the fattyinfiltration was a decreased capacity of the liver tosecrete lipoprotein. However, no fibrosis, still less

cirrhosis, was produced. Quantitative measurementswere then made of the extent of the fibrous tissuereaction to the implantation of foreign material in theliver, and it was shown that the low protein dietgreatly reduced the fibrous response. A second elementin the pathogenesis of cirrhosis is nodular regeneration.A number of studies on different tissues-liver itself, bone, intestinal mucosa, lymph-glands-allled to the conclusion that another effect of proteindeficiency is to delay and prolong the process of celldivision. Thus we are forced to the conclusion that,far from protein deficiency causing cirrhosis, on thecontrary it produces conditions unfavourable to thedevelopment of both the main histopathologicalchanges-fibrous tissue proliferation and cellular

regeneration. Another series of experiments wasconcerned with the important problem of the inter-action of diet and aflatoxin in the production of liverinjury. No evidence was obtained that protein de-ficiency potentiates the effect of the toxin, contrary to abelief sometimes held. This fresh look at some of the

problems of dietary liver injury has therefore clearedaway many misconceptions.

In his second lecture Professor Ramalingaswamidescribed two forms of liver disease in man-idiopathic1. Ramalingaswami, V. Lancet, 1969, ii, 733.

portal hypertension and Indian childhood cirrhosis.The first of these conditions occurs predominantly inmale adults; the signs are those of portal hypertensionwith splenomegaly and oesophageal varices. Thecharacteristic morphological change is thickening ofthe walls of the intrahepatic portal vessels, leading toocclusion, without much primary change in the paren-chyma. The condition appears to be common through-out India; it is not the same as the big-spleen diseaseof Uganda, and its cause is quite unknown. Indianchildhood cirrhosis is another puzzle, and a tragic one,since it is uniformly fatal. The slides shown byProfessor Ramalingaswami illustrated very clearlythe extraordinary extent of piecemeal cell-destruction,with dense intercellular fibrosis and accumulation in

many degenerate cells of an eosinophilic hyalinematerial resembling that described by Mallory inalcoholic livers. It now seems quite certain that thisis not a nutritional disease. In many cases hepatitis-associated antigen is present, although the picture isnot in the least like that of viral hepatitis. The most

promising theory at present seems to be that thisdisease represents a distorted immunological responseto an injury not yet identified.These lectures on nutrition and liver disease were a

memorable experience for those who heard them. Theirrather paradoxical conclusion is that liver disease isvery important in India, but nutrition plays little or nopart in it. Because the team at the All-India Instituteis attacking these problems on a broad front, we canlook forward to another instalment in a few years’time.


No-oNE knows better than the population experts thehazards of extrapolation, but extrapolate they mustbecause there is no other way of achieving even remotelyrational economic and social plans. The latest projec-tion is for a U.K. population of 66 million by the year2010/ and this is nearly 5 million fewer than wasthought only a year ago. These latest figures havebeen greeted by sighs of relief, and derision is beingpoured on the " prophets of gloom ": the report hasdrawn from one newspaper 2 the comment that

population planning " is a subject on which politiciansshould be urged to display the utmost possible com-placency and individuals the greatest possible in-difference to instructions about their duty to societyat large ".The Government has not yet regarded the idea of

a population policy with much enthusiasm, perhapsbecause those who support zero population growth(or less) grossly overestimate the tools available toGovernment in a country where freedom of personalchoice in many matters, including family size, is

respected. But there are many reasons why Whitehallshould not propose a vote of thanks to the Government

Actuary and strike the item off its agenda papers.1. Office of Population Censuses and Surveys. Population Projections

No. 2, 1971-2011. H.M. Stationery Office. Pp. 115. £1.2. Daily Telegraph, Nov. 16.



First, extrapolation is not simply a matter of drawinga graph of what has gone before and continuing itwith a dotted line, for the projections are a compoundof many items and even some guesses. The 1955-

based estimates grossly underestimated what actuallyhappened; so, to a lesser extent, did the ones for 1960.The figures based on 1965 look like major overstate-ments, and we cannot yet tell how right the ones for1970 and 1971 will be or even in which direction theywill err. Did those who now react so complacentlyto last week’s report throw up their hands in dismaywhen the 1965 projections were published ? Thebirth-rate has been falling, but it will not contractfor ever; and, just as the fall has not been fullyexplained, nor can a future rise be safely ruled out.Secondly, no post-war projection has suggestedthat the population of the U.K. will fall, and thereare those who believe that population stability isnot enough and that a total well below the presentfigure of almost 56 million is all that can be supported.And, thirdly, complacency tends to be infectious:experience in a Western country should not beallowed to divert attention from the persisting problemsof overpopulation in the Third World.

STATUS QUO IN SCHIZOPHRENIASOME 400 psychiatrists from all over the world

gathered in London between Nov. 13 and Nov. 15at a World Psychiatric Association symposium onschizophrenia. Little was heard to challenge the veryconcept of this somewhat nebulous disease-entity,though the still small voice of Dr. Joshua Bierer washeard at one point saying that billions of dollars hadbeen spent studying a disease that did not exist. If

schizophrenia does not exist, however, something does,for there are some 60,000 patients in hospital inBritain carrying the label, at a cost of nearly a millionpounds a year for hospital care alone, and in 1969 therewere apparently 180,000 such in the U.S.A., 98% ofthem in public hospitals.The problem of interpreting the American data was

highlighted by Prof. J. E. Cooper (U.K.), who sum-marised work which showed American East-CoastState-hospital psychiatrists twice as likely to makethis diagnosis as their British colleagues. The reasonsfor the difference were not certain, but part of theexplanation might be the Kraepelinian influence onBritish psychiatry and the Bleulerian influence onAmerican, furthered by the writings of Adolf Meyer.The one-to-one private-psychotherapy model oftreatment tended towards a conclusion that a patientwas schizophrenic where " rapport " was not estab-lished ; and one speaker pointed out the kudos attachedto success in psychotherapy where an initial diagnosisof schizophrenia had been made. Diagnostic practicesapparently approximated closer to the British thefurther West in the U.S.A. one went, a trend whichanother speaker attributed to the special social stressesof the East due to immigration, drugs, overcrowding,unemployment, and crime. In Canada it seemed thatdiagnostic practice depended more on the academic

origins of the professor, but was generally intermediatebetween Britain and the U.S.A. An interesting pointwas that the use of lithium in manic states had led toan American reappraisal of the situation such that" a wave of hypomania " seemed to have swept down the

East Coast-a rare example of diagnostic techniquesfollowing therapeutic advances, rather than the reverse.Rather more congruent, multicentre, internationalresults were reported from the W.H.O. studies ofDr. N. Sartorius (Switzerland) and his colleagues, andthere was no substantial challenge to internationalacceptance of a nucleus of symptoms including im-pairment of associations and of affect, autism, anddisturbed relation to reality. Round the edges, how-ever, international, not to say interpsychiatrist,evaluation becomes somewhat blurred.

Differences in diagnostic labels may account for thewidely differing emphasis placed on genetic factors.The work of Heston on schizophrenia in the adoptedchildren of a schizophrenic parent seemed to leave noroom for environmental factors; but, as Sir MartinRoth among others pointed out, identical twins fellshort of 100% in concordance for schizophrenia. Howfar they fell short was disputed, and no speaker sup-ported the older figures reaching 80-90% concordancelevels, since the populations were highly selectedand of uncertain zygosity. There was surprise,however, at the very low level of 15% for mono-zygotes and half this for dizygotes in Prof. P. Tienari’ssurvey of all surviving twin pairs living in Finlandwho had been born during 1920-29. Had he under-selected, perhaps, and, in particular, were schizo-phrenic twins more likely to have had a partnerwho had died or gone abroad, and thus been ex-cluded from the series ? The role of genetic elementsin causation seemed generally accepted. Even allowingfor a conservative 30-40% concordance for identicaltwins, there remained at least 60% of the astiology tobe accounted for by environment, and Prof. FiniSchulsinger (Denmark) presented a cogent case for theharmful effects of early parental separation andperinatal complications. He and Dr. Sarnoff Mednickhad applied psychophysiological techniques to identifyhigh-risk cases and, with others, felt the basic disorperto be a form of " learned avoidance thinking " ingenetically predisposed children. The need to showthis kind of thought correlated well with Bateson’sconcept of the

" double-bind " parental relationship.The extent to which a genetically predisposed childmight be especially likely to be separated, and hismother therefore be least likely to care for him, ledto a complex of interlacing variables which made itextremely hard to disentangle cause from effect.This is an area of research, however, of which a greatdeal more will be heard.

Another potentially crucial area of study was out-lined by Prof. M. Vartanian, who read a paper for Dr.Galina Kolyaskina (U.S.S.R.) on the immunopatho-logical reactions of schizophrenic patients and theirrelatives. Antibrain antibodies appeared in directcorrelation with the expression of the disease, with thehighest frequency in the

" progressive-juvenile malig-nant group ", amounting to 32%. After cessation ofneuroleptic drugs, these antibodies increased signifi-