growing older but not happier

2
84 References continued at foot of next column our suggestion that idiopathic hyperaldosteronism is a variant of essential hypertension, not a variant of Conn’s syndrome. Why was Idiopathic Hyperaldosteronism Misclassified ? The reason may be historical. Low renin was first recognised as a feature of Conn’s syndrome,23 and thereafter renin was used as a marker for sodium retention resulting from mineralocorticoid excess. However, low renin was also found in approximately a quarter of all patients with essential hypertension;24 and, not surprisingly, these patients were suspected of having mineralocorticoid excess. A small number did have an excess of aldosterone, and since renin and angiotensin II were relatively low they were grouped with primary aldosteronism. They were not considered to have essential hypertension, probably because at that time it was not recognised that aldosterone excess was a feature of essential hypertension in the sodium-loaded state25,26 or that the response of aldosterone to infused angiotensin II was enhanced. Given the sequence in which observations were made, misclassification is not surprising. The cause of essential hypertension is not known. If abnormalities of renin and aldosterone are discovered in some patients it is to be expected that these will be classified separately. Having been misclassified and having received a name they come to be seen as an entity. The fault is well described by John Stuart Mill.27 "The tendency has always been strong to believe that whatever receives a name must be an entity or being, having an independent existence of its own; and if no real entity answering to the name could be found man did not for that reason suppose that none existed, but imagined that it was something peculiarly abstruse and mysterious, too high to be an object of sense." Requests for reprints should be addressed to the Secretary, MRC Blood Pressure Unit, Western Infirmary, Glasgow G11 6NT. REFERENCES 1. Conn JW. Primary aldosteronism. New clinical syndrome. J Lab Clin Med 1955; 45: 6-17. 2. Ferriss JB, Beevers DG, Brown JJ, et al. Clinical, biochemical and pathological features of low renin (’primary’) hyperaldosteronism Am Heart J 1978; 95: 375-88. 3 Biglieri EG Schambelan M, Slaton P, Stockigt JR. The intercurrent hypertension of primary aldosteronism Circulation Res 1970; 26 (suppl. 1)· 195-202. 4 Baer L, Brunner HR, Buhler F, Laragh JA. Pseudo-primary aldosteronism, a variant of low-renin essential hypertension? In: Genest J, Loiw E, eds. Hypertension ’72. Berlin: Spring Verlag, 1972: 459-72. 5. Ferriss JB, Beevers, DG, Boddy K, et al The treatment of low-renin (’primary’) hyperaldosteronism. Am Heart J 1979; 96: 97-109. 6. Editorial. Idiopathic aldosteronism: A diagnostic artifact. Lancet 1979; ii: 1221-22. 7. Neville AM. The nodular adrenal. Invest Cell Pathol 1978; 1: 99-111. 8. Weinberger MH, Grim CF, Hollifield JW, et al. Primary aldosteronism, diagnosis localisation and treatment Ann Intern Med 1979; 90: 386-95. 9. Kaplan NM. The steroid content of adrenal adenomas and measurements of aldosterone production in patients with essential hypertension and primary aldosteronism. J Clin Invest 1967; 45: 728-34. 10. Neville AM, O’Hare MJ The human adrenal gland: aspects of structure, function and pathology In. James VHT, ed. The human adrenal gland. London: Academic Press, 1979. 11. Gunnels JC, McGuffin WL, Robinson RR, Grim CE, Wells S, Silver D, Glenn JF. Hypertension, adrenal abnormalities, and alterations in plasma renin activity. Ann Intern Med 1970, 73: 901-11. 12. Davies DL, Beevers DG, Brown JJ, et al. Aldosterone and its stimuli in normal and hypertensive man: are essential hypertension and primary hyperaldosteronism without tumour the same condition? J Endocrinol 1979; 81: 79P-91P. 13. Ferris JB, Brown JJ, Fraser R, et al. Hypertension with aldosterone excess and low plasma-renin. preoperative distinction between patients with and without adrenocortical tumour. Lancet 1970; ii: 995-1000 14 Luetscher JA, Ganguly A, Melada GA, Dowdy AJ. Pre-operative differentiation of adrenal adenoma from idiopathic adrenal hyperplasia in primary aldosteronism. Circulation Res 1974, 34: (suppl. 1): 1-175-1-182. 15. Spark RF, Dale SL, Kahn PC, Melby JC. Activation of aldosterone secretion in primary aldosteronism. J Clin Invest 1969; 48: 96-104. 16 Fraser R, Beretta-Piccoli C, Brown JJ, Lever AF, Mason PA, Morton JJ, Robertson JIS. Response of aldosterone and 18-hydroxycorticosterone to angiotensin II in normal man and patients with essential hypertension, Conn’s syndrome and non- tumorous hyperaldosteronism. Hypertension (in press). Point of View GROWING OLDER BUT NOT HAPPIER THREE years ago the Department of Health and Social Security published a consultative document, A Happier Old Age. Many people responded to the questions posed in it expecting a definitive white-paper to be produced within twelve months. The white-paper has finally been published. Growing Older2 addresses itself to many of the questions posed earlier, but the answers leave much to be desired. After three years of waiting, the time is ripe for new enthusiasm, and the right document could have stimulated this, just as a past white-paper, Better Services for the Mentally Handicappe4’ 3 started the long process of change in that area. Growing Older is disappointing; it adds little new, and promises less. It does not even summarise the contributions received during consultation, which alone would have been valuable, since many good ideas are never published, and exchange of information on the grapevine is a slow and unreliable process. One of the themes in the white-paper is the role of voluntary work. The present Government has always placed an emphasis on such work, and here, whenever social clubs, home care, shopping, or holidays are mentioned, the suggestion is always the same: "voluntary bodies will be able to expand their activities;" "much can be done by voluntary workers;" and so on. A similar line was taken in another white-paper prepared by the D.H.S.S., Care m Action, 4 which set out priorities in the area of social services-namely, to expand the scope of voluntary activity. There is nothing basically wrong with this endeavour. Voluntary work has a long tradition in this country; the Wolfenden committee on voluntary organisations suggested in 1978 that 8% of the population were involved in some type of voluntary work, without counting individual, informal help. Voluntary work played an important part in Beveridge’s plans; and helping others promotes a sense of satisfaction and self-esteem. The theme is good, but if it is repeated too often, too loudly, it creates only cynicism. The Government must follow its message with active encouragement. 1. Department of Health and Social Security. A happier old age. H M. Stationery Office, 1978. 2. Department of Health and Social Security Growing older H.M. Stationery Office, 1981. See Lancet 1981; i: 793. 3 Department of Health and Social Security. Better services for the mentally handicapped. Cmnd 4683.H.M. Stationery Office, 1971. 4. Department of Health and Social Security. Care in action: a handbook of policies and priorities for the health and personal social services in England. H.M. Stationery Office, 1981. 17. Wisgerhof M, Carpenter PC, Brown RD. Increased adrenal sensititvity to angiotensin II in idiopathic hyperaldosteronism. J Clin Endocrinol Metab 1978; 47: 938-43 18. Kisch ES, Dluhy RG, Williams GH. Enhanced aldosterone response to angiotensin II in human hypertension. Circulation Res 1976; 38: 502-05. 19. Wisgerhof M, Brown RD. Increased adrenal sensitivity to angiotensin II in low renin hypertension J Clin Invest 1979; 64: 1456-62 20. Ganguly A, Melada GA, Leutscher JA, Dowdy AJ. Control of plasma aldosterone in primary aldosteronism: distinction between adenoma and hyperplasia J Clin Endocrinol Metab 1973; 37: 765-75. 21. Schambelan M, Brust NL, Chang B, Slater KL, Biglieri EG. Circadian rhythm and effect of posture on plasma aldosterone concentration in primary aldosteronism J Clin Endocrinol Metab 1976; 43: 115-31. 22. Espiner EA, Donald RA. Aldosterone regulation in primary aldosteronism: influence of salt balance, posture and ACTH. Clin Endocrinol 1980; 12: 277-86. 23. Brown JJ, Davies DL, Lever AF, Robertson JIS. Plasma renin in a case of Conn’s syndrome with fibrinoid lesions: use of spironolactone in treatment. Br Med J 1964; ii. 1636-37. 24. Dunn MJ, Tannen RL. Low-renin hypertension Kidney Int 1974; 5: 317-25. 25. Collins DR, Weinberger MH, Dowdy AJ, Nokes GW, Gonzales CM, Luetscher JA Abnormally sustained aldosterone secretion during salt loading in patients with various forms of benign hypertension: relation to plasma renin activity J Clin Invest 1970; 49: 1415-26. 26. Khokhar AM, Slater JDH, Jowett TP, Payne NN. Suppression of the remn- aldosterone system in mild essential hypertension. Clin Sci Mol Med 1976, 50: 269-76. 27. Mill JS. Analysis of the phenomenon of the human mind, by James Mill, vol. 2, London- 1869

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84

References continued at foot of next column

our suggestion that idiopathic hyperaldosteronism is a

variant of essential hypertension, not a variant of Conn’ssyndrome.

Why was Idiopathic Hyperaldosteronism Misclassified ?The reason may be historical. Low renin was first

recognised as a feature of Conn’s syndrome,23 and thereafterrenin was used as a marker for sodium retention resultingfrom mineralocorticoid excess. However, low renin was alsofound in approximately a quarter of all patients with essentialhypertension;24 and, not surprisingly, these patients weresuspected of having mineralocorticoid excess. A smallnumber did have an excess of aldosterone, and since renin andangiotensin II were relatively low they were grouped withprimary aldosteronism. They were not considered to haveessential hypertension, probably because at that time it wasnot recognised that aldosterone excess was a feature ofessential hypertension in the sodium-loaded state25,26 or thatthe response of aldosterone to infused angiotensin II was

enhanced. Given the sequence in which observations were

made, misclassification is not surprising.The cause of essential hypertension is not known. If

abnormalities of renin and aldosterone are discovered in some

patients it is to be expected that these will be classifiedseparately. Having been misclassified and having received aname they come to be seen as an entity. The fault is welldescribed by John Stuart Mill.27"The tendency has always been strong to believe that whatever

receives a name must be an entity or being, having an independentexistence of its own; and if no real entity answering to the namecould be found man did not for that reason suppose that none

existed, but imagined that it was something peculiarly abstruse andmysterious, too high to be an object of sense."

Requests for reprints should be addressed to the Secretary, MRC BloodPressure Unit, Western Infirmary, Glasgow G11 6NT.

REFERENCES

1. Conn JW. Primary aldosteronism. New clinical syndrome. J Lab Clin Med 1955; 45:6-17.

2. Ferriss JB, Beevers DG, Brown JJ, et al. Clinical, biochemical and pathological featuresof low renin (’primary’) hyperaldosteronism Am Heart J 1978; 95: 375-88.

3 Biglieri EG Schambelan M, Slaton P, Stockigt JR. The intercurrent hypertension ofprimary aldosteronism Circulation Res 1970; 26 (suppl. 1)· 195-202.

4 Baer L, Brunner HR, Buhler F, Laragh JA. Pseudo-primary aldosteronism, a variant oflow-renin essential hypertension? In: Genest J, Loiw E, eds. Hypertension ’72.Berlin: Spring Verlag, 1972: 459-72.

5. Ferriss JB, Beevers, DG, Boddy K, et al The treatment of low-renin (’primary’)hyperaldosteronism. Am Heart J 1979; 96: 97-109.

6. Editorial. Idiopathic aldosteronism: A diagnostic artifact. Lancet 1979; ii: 1221-22.7. Neville AM. The nodular adrenal. Invest Cell Pathol 1978; 1: 99-111.8. Weinberger MH, Grim CF, Hollifield JW, et al. Primary aldosteronism, diagnosis

localisation and treatment Ann Intern Med 1979; 90: 386-95.9. Kaplan NM. The steroid content of adrenal adenomas and measurements of

aldosterone production in patients with essential hypertension and primaryaldosteronism. J Clin Invest 1967; 45: 728-34.

10. Neville AM, O’Hare MJ The human adrenal gland: aspects of structure, function andpathology In. James VHT, ed. The human adrenal gland. London: AcademicPress, 1979.

11. Gunnels JC, McGuffin WL, Robinson RR, Grim CE, Wells S, Silver D, Glenn JF.Hypertension, adrenal abnormalities, and alterations in plasma renin activity. AnnIntern Med 1970, 73: 901-11.

12. Davies DL, Beevers DG, Brown JJ, et al. Aldosterone and its stimuli in normal andhypertensive man: are essential hypertension and primary hyperaldosteronismwithout tumour the same condition? J Endocrinol 1979; 81: 79P-91P.

13. Ferris JB, Brown JJ, Fraser R, et al. Hypertension with aldosterone excess and lowplasma-renin. preoperative distinction between patients with and withoutadrenocortical tumour. Lancet 1970; ii: 995-1000

14 Luetscher JA, Ganguly A, Melada GA, Dowdy AJ. Pre-operative differentiation ofadrenal adenoma from idiopathic adrenal hyperplasia in primary aldosteronism.Circulation Res 1974, 34: (suppl. 1): 1-175-1-182.

15. Spark RF, Dale SL, Kahn PC, Melby JC. Activation of aldosterone secretion inprimary aldosteronism. J Clin Invest 1969; 48: 96-104.

16 Fraser R, Beretta-Piccoli C, Brown JJ, Lever AF, Mason PA, Morton JJ, RobertsonJIS. Response of aldosterone and 18-hydroxycorticosterone to angiotensin II innormal man and patients with essential hypertension, Conn’s syndrome and non-tumorous hyperaldosteronism. Hypertension (in press).

Point of View

GROWING OLDER BUT NOT HAPPIER

THREE years ago the Department of Health and Social Securitypublished a consultative document, A Happier Old Age. Manypeople responded to the questions posed in it expecting a definitivewhite-paper to be produced within twelve months. The white-paperhas finally been published. Growing Older2 addresses itself to manyof the questions posed earlier, but the answers leave much to bedesired. After three years of waiting, the time is ripe for newenthusiasm, and the right document could have stimulated this, justas a past white-paper, Better Services for the Mentally Handicappe4’ 3started the long process of change in that area.Growing Older is disappointing; it adds little new, and promises

less. It does not even summarise the contributions received duringconsultation, which alone would have been valuable, since manygood ideas are never published, and exchange of information on thegrapevine is a slow and unreliable process.One of the themes in the white-paper is the role of voluntary work.

The present Government has always placed an emphasis on suchwork, and here, whenever social clubs, home care, shopping, orholidays are mentioned, the suggestion is always the same:

"voluntary bodies will be able to expand their activities;" "muchcan be done by voluntary workers;" and so on. A similar line wastaken in another white-paper prepared by the D.H.S.S., Care mAction, 4 which set out priorities in the area of social

services-namely, to expand the scope of voluntary activity.There is nothing basically wrong with this endeavour. Voluntary

work has a long tradition in this country; the Wolfenden committeeon voluntary organisations suggested in 1978 that 8% of the

population were involved in some type of voluntary work, withoutcounting individual, informal help. Voluntary work played animportant part in Beveridge’s plans; and helping others promotes asense of satisfaction and self-esteem. The theme is good, but if it isrepeated too often, too loudly, it creates only cynicism. TheGovernment must follow its message with active encouragement.

1. Department of Health and Social Security. A happier old age. H M. Stationery Office,1978.

2. Department of Health and Social Security Growing older H.M. Stationery Office,1981. See Lancet 1981; i: 793.

3 Department of Health and Social Security. Better services for the mentallyhandicapped. Cmnd 4683.H.M. Stationery Office, 1971.

4. Department of Health and Social Security. Care in action: a handbook of policies andpriorities for the health and personal social services in England. H.M. StationeryOffice, 1981.

17. Wisgerhof M, Carpenter PC, Brown RD. Increased adrenal sensititvity to angiotensinII in idiopathic hyperaldosteronism. J Clin Endocrinol Metab 1978; 47: 938-43

18. Kisch ES, Dluhy RG, Williams GH. Enhanced aldosterone response to angiotensin IIin human hypertension. Circulation Res 1976; 38: 502-05.

19. Wisgerhof M, Brown RD. Increased adrenal sensitivity to angiotensin II in low reninhypertension J Clin Invest 1979; 64: 1456-62

20. Ganguly A, Melada GA, Leutscher JA, Dowdy AJ. Control of plasma aldosterone inprimary aldosteronism: distinction between adenoma and hyperplasia J ClinEndocrinol Metab 1973; 37: 765-75.

21. Schambelan M, Brust NL, Chang B, Slater KL, Biglieri EG. Circadian rhythm andeffect of posture on plasma aldosterone concentration in primary aldosteronism JClin Endocrinol Metab 1976; 43: 115-31.

22. Espiner EA, Donald RA. Aldosterone regulation in primary aldosteronism: influenceof salt balance, posture and ACTH. Clin Endocrinol 1980; 12: 277-86.

23. Brown JJ, Davies DL, Lever AF, Robertson JIS. Plasma renin in a case of Conn’ssyndrome with fibrinoid lesions: use of spironolactone in treatment. Br Med J 1964;ii. 1636-37.

24. Dunn MJ, Tannen RL. Low-renin hypertension Kidney Int 1974; 5: 317-25.25. Collins DR, Weinberger MH, Dowdy AJ, Nokes GW, Gonzales CM, Luetscher JA

Abnormally sustained aldosterone secretion during salt loading in patients withvarious forms of benign hypertension: relation to plasma renin activity J Clin Invest1970; 49: 1415-26.

26. Khokhar AM, Slater JDH, Jowett TP, Payne NN. Suppression of the remn-aldosterone system in mild essential hypertension. Clin Sci Mol Med 1976, 50:269-76.

27. Mill JS. Analysis of the phenomenon of the human mind, by James Mill, vol. 2,London- 1869

85

Volunteer groups need support in order to develop and carry ontheir work. Society’s attitude has often been disparaging, and publicauthorities have even been hostile towards working with voluntarygroups. Professionalism is almost synonymous with the cold-

shouldering of the volunteer.

The growth of self-help groups over the past ten years probablyreflects this exclusion, but it has given greater benefit to thoseinvolved than has been provided by the more traditional services.The new white-paper does little to overcome any of this: its tone isone of "it’s all up to you, we’re not doing any more". More positivetactics could have been employed. A partnership with the nationalcharitable associations-Age Concern, for example-could be

helpful. Beveridge even talked about a minister for voluntary work.Another task is the production of a compendium of good practicesfor guidance of both public and voluntary organisations. It is no usesuggesting that local authorities can give grant aid to local groups oroffer rent-free accommodation and rate reductions, when directhelp is one of the first casualties of a reduction in publicexpenditure. Let us recognise the importance of voluntary workersin the care of old people, not abandon them to struggle as best as theycan.

The white-paper skims the surface of the issues raised by itspredecessor: it discusses the desirability of a flexible retirement age,"but not yet"; it talks about housing needs, but generally fails tooffer any solutions except where they have already been foundelsewhere. There is a short summary of the current situation

regarding hospital services, and the opportunity is taken for self-congratulation over pensions and supplementary benefit. The onlypositive statement is that the concept of euthanasia is unacceptable,although no reasons are offered. The value of private residentialcare is emphasised, but the fact that local authorities usually financethis care is forgotten. Employers could do more to provide pre-retirement courses, post-retirement clubs, and residential

accommodation, as they do in other countries; sponsorship couldhelp, but it is wrong to suggest that the public would not have topay. One short sentence acknowledges the need to revitalise the lawconcerning the registration of private accommodation in order toprotect residents and improve their quality of life.The opportunity to give guidance on two important areas of

overlap between health and social services has been ignored. Care ofpeople in their own homes by statutory agencies, as opposed torelatives and neighbours, is largely performed by home-helps anddistrict nurses. The former are supposed to perform only domestictasks, preparing meals, shopping, and washing linen, while thelatter attend to basic personal needs, dressing, washing, andtoiletting (these nursing duties are often performed by nursingauxiliaries rather than trained district nurses). In practice, however,home helps perform many personal tasks, and nurses feed peopleand wash dirty linen. This happens so regularly that there is muchto commend combining these two functions in a single careassistant. The idea is being tested successfully in West Sussex,Avon, and Oxfordshire. The role of the district nurse, relieved ofbasic nursing care, can then be redefined, perhaps embracing thework of the health visitor caring for old people.The other area of confusion lies in the provision of residential

care. The proportion of old people in residential care has alteredlittle since the beginning of the century. The homes were conceivedof as residential hotels for the working classes, according to AneurinBevan in a speech in the Commons in 1947. The characteristics ofthe residents have changed, however, so that many of them are nowhandicapped and highly dependent. It is not unusual for 20% ofresidents in Oxfordshire homes to be in wheelchairs, not includingthose who move about only with the aid of walking frames.Residents are frequently more de endent than long-stay patients inhospital, where staff/patient ratios are usually better, and theequipment and layout assists in the caring process. The white-papermentions an N.H.S. nursing home, which appears to be merely thelong-stay hospital under a different name, with no change in thestyle of care or the number of places. The nursing home is to betested in several areas. The difference between such types ofresidential care and sheltered housing is unclear. There exist many

experiments in special housing schemes where, with increasedlevels of domiciliary support, an elderly disabled person can remainin his or her own home. Warwickshire County Council is one of thepioneers in this area. Other authorities are experimenting, but thereis no co-ordination or guidance from the Government, despite threeyears of research. The Black report, Inequalities in Health,recognised the urgent need to review such issues, but that documentwas, of course, dismissed.

All in all, the white-paper is a sad affair which must be a source ofembarrassment to many in the Department of Health. It might havebeen better to have forgotten the whole thing, rather than churn outsuch an uninspiring paper after three years. It is a greatdisappointment to those working with older people. Growing olderappears to mean getting slower, run down, depressed, and

dependent on the good will of others, a stereotype many have beentrying to eradicate. Our elders deserve better than this; if centralgovernment cannot produce ideas, perhaps others can. Professionalgroups and the national bodies will have to take the initiative.

Oxfordshire Area Health

Authority (Teaching)Manor House, Off Headley Way,Headington, Oxford OX3 9OZ

J. S. RODGERSCommunity Physician

Medical Education

Joint Preclinical School of London and StBartholomew’s Hospital Medical Colleges

A working party* was appointed by the University of London inApril to examine the likely capital and recurrent costs of alternativeschemes for the siting of the joint preclinical departments of theLondon and St Bartholomew’s Hospital Medical Colleges either ona site adjacent to Queen Mary College (University of London) (theBLQ scheme) or at Charterhouse Square by extending the existingpreclinical accommodation of St Bartholomew’s Hospital MedicalCollege.

The working party has concluded:

A WORKING PARTY* was appointed by the University of London inApril to examine the likely capital and recurrent costs of alternativeschemes for the siting of the joint preclinical departments of theLondon and St Bartholomew’s Hospital Medical Colleges either ona site adjacent to Queen Mary College (University of London) (theBLQ scheme) or at Charterhouse Square by extending the existingpreclinical accommodation of St Bartholomew’s Hospital MedicalCollege.

(b) The difference in estimated annual running costs between thetwo schemes is insignificant. But both show savings of150 000 a year over retaining the two existing preclinicalschools.

(c) That the choice between the two schemes should be made bythe University not on financial grounds but in the light ofacademic and other wider considerations.

*The membership of the working party was: Prof. L. C. B. Gower (formerVice-Chancellor, University of Southampton), chairman; Sir Kenneth Berrill(former Head of the Central Policy Review Staff; Chairman of the UniversityGrants Committee, 1969-73); Sir John Butterfield (regius professor ofphysic, University of Cambridge); Sir John Ellis (dean , London HospitalMedical College); Prof. H. D. Ritchie (dean-elect, London Hospital MedicalCollege); Prof. R. A. Shooter (dean, St Bartholomew’s Hospital MedicalCollege); Dr 1. Kelsey Fry (dean-elect, St Bartholomew’s Hospital MedicalCollege); Sir James Menter (Principal, Queen Mary College); Prof K. W.Sykes (Vice-Principal, Queen Mary College).