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Are We Killing Ourselves or Not?

THE LANCET

PHYSICIANS have long recognised the influence ofpersonality, behaviour, and reactions on the outcomeof organic disease in a particular patient. Familiarcircumstances include exacerbations of anginapectoris, high blood-pressure, and epigastric pain.Good doctors feed such understanding into their

everyday clinical advice. However, the influence of"stress", life-style, and behaviour pattern on clinicalillness and specific disease processes has been onlymarginally examined by controlled scientific methods.Patients-to-be (who include most of us) cannot get astraight answer to the question "How much risk do Irun if I carry on like this?". This unsatisfactory state ofaffairs is a reflection not so much of a pedestrianapproach by researchers as of the complexity of thematter.

More than twenty years ago FRIEDMAN andROSENMAN reported that a certain type of

personality, in employed, middle-aged U.S. citizens,was associated with an increased risk of clinicallyapparent coronary heart disease. They had studiedthree groups of men. In group A the behaviour patternwas primarily characterised by intense ambition,competitive drive, constant preoccupation with

occupational deadlines, and a sense of urgency. Thesemen were contrasted with a second group, B, who had aconverse behaviour- pattern. Group C consisted oftotally blind, unemployed men who had little ambitionor drive but who were chronically insecure andanxious. Some very provocative conclusions werereached. Clinical coronary artery disease was seventimes more frequent, and arcus senilis over three timesmore frequent, in group A than in groups B or C. Dataon cigarette smoking, exercise, working hours, alcoholingestion, and heredity were studied but none of theseseemed to account for the extraordinary differencebetween group A and groups B and C. Group Aindividuals had a higher cholesterol than the otherswithout convincing evidence of dietary or otherrelevant differences. The hypothesis was that theirbehaviour pattern (designated type A) was of itselflargely responsible for their higher serum cholesteroland also, directly or indirectly, for their increasedsusceptibility to clinical coronary artery disease. The

1. Friedman M, Rosenman RH. Association of specific overt behaviour pattern withblood and cardiovascular findings. JAMA 1959; 169: 1286-96.

small size of group A, 83 men, raised the possibility ofselection, but concern on this score was largely allayedby the fact that, before the investigation, only 4 of 23persons with clinical coronary disease were aware that

they had it.If a definable personality and behaviour pattern does

indeed precipitate coronary artery disease then

rigorous scientific assessment is clearly worth while.Recently the U.S. National Institutes of Health

charged a panel of biomedical and behaviouralscientists with the task of critically evaluating allresearch and theory linking behaviour to coronaryartery disease.2 2 The task was divided into fiveareas-association of coronary-prone behaviour and

coronary artery disease; assessment of the type Abehaviour pattern; physiological mechanisms linkingbehaviour to coronary heart disease; cultural and

developmental factors; and intervention strategies.The panels of reviewers produced summary statementswhich "delineated the perceived strengths and

shortcomings of the theory and data for their respectivesections and provided recommendations to theNational Heart, Lung and Blood Institute". Thematters at issue are some of the most difficult to convertfrom reasonable philosophy to objective datamarshalled into scientific evidence. On the one handwe have the discrimination and measurement ofdifferent components of human reaction, and, on theother, the quantification of an adverse influence on theheart, blood vessels, and health. Lastly, any hypothesisbased on such analyses requires testing by controlledinterference or perturbation. Such testing has also toproceed to clinical trial if any conclusions are to besubsequently translated into treatment.Type A behaviour is a state of mental arousal

associated with a positive, competitive, ambitious,time-conscious, driving existence. It is not to beconfused with merely working hard, nor is it

necessarily associated with a tangible successful

outcome-rather, a mismatch between striving intentand accomplished results. The essence of type A couldconceivably be as fundamental as geneticdetermination, but it might equally include or be solelydue to the repeated conditioning of a particular life-style and environment. Its presence is relative and atpresent the degree can be ascertained only by interviewor questionnaire. How far such data quantitativelyrepresent a personal response characteristic is

uncertain, and conservative psychometricians wouldsettle for "present" or "absent". More accurate

definition and measurement is desirable, in variousdifferent social, occupational, racial, and nationalgroups.A better explanation of numerical quantification is

also necessary. Very few doctors, and fewer lay people,have a realistic perspective of what a risk factor impliesfor an individual. In the case of a single risk, such as

2. Coronary-prone behaviour and coronary heart disease: A critical review. Circulation1981, 63: 1199-1215.

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high blood-pressure, high cholesterol, or smoking, thestatistics seldom have much impact on the patientbecause of the long time-scale. Indeed the risks maywell be psychologically small when it is made clear that,even with a strong statistical association, only a verysmall proportion will come to grief.3 In this connectionthe type A phenomenon may be important from twopoints of view. Firstly, the magnitude of the type A riskhas been assessed as roughly equivalent to that ofhypertension or smoking.4 Because of the

multiplicatory behaviour of coexisting risk factors, thecombination of risks may be great enough to inspireimmediate fear. Secondly, absence of type A behaviourmay partly explain the survival of some people whohave a multiplicity of conventional risks.

It will not be easy to sort out the correlations between

type A, the established risk factors, and sudden death,myocardial infarction, and angina, but there are nofundamental reasons to prevent a reasonably goodscientific job. There are many patterns of mentalstate which have been thought to predispose to acutecardiovascular disease. Widowhood, retirement, jobloss, and divorce are all fruitful sources for

psychometric analysis. But there are more seriousdifficulties. If the type A hypothesis is correct, thenobviously the links between behaviour and the

pathophysiological processes causing disease must befurther explored. It is in this area of analysis that thereal troubles begin. There is a possibility that a genetictrait might be expressed in dual fashion-for example,there might be a factor common to behaviourdetermination and arterial wall degeneration.Alternatively, adverse biochemical changes might ariseonly during a phase of type A behaviour. FRIEDMAN etal. alluded to this possibility in a report on accountantswho had. higher serum cholesterol when they wereparticularly oppressed by deadlines. In either case weare thrown back to the basic mechanisms ofatherosclerosis, thrombosis, and adrenergic drive, allof which have proved difficult enough without theadded complication of behaviour studies. At a lessfundamental level, we may get some information fromthose individuals who are obliged to undergo severalcoronary arteriograms; a selected group, admittedly,but one in which a higher proportion of type Acharacteristics may be expected. In such research,improved angiographic techniques giving better smallvessel definition are important for the future.

Optimistically we must suppose that practicalmedicine will be the better for such knowledge.Through the eyes of the individual the key question is swhether the quality or length of life can be improved byintervention, whether with advice or with drugs.

3. Rose G. Strategy of prevention: Lessons from cardiovascular disease. Br Med J 1981;282: 1847-51.

4. Rosenman RH, Brand RJ, Sholtz RI, Friedman M. Multivariate prediction of coronaryheart disease during 8· 5 year follow up in Western Collaborative Group Study. AmJ Cardiol 1976; 37: 903-09.

5. Friedman M, Rosenman RH, Carroll V. Changes in serum cholesterol and bloodclotting time in men subjected to cyclic variation of occupational stress. Circulation1958; 17: 852-61

Behaviour modification is a sensitive matter. We maynot wish to mend our ways. We may live and work in anenvironment that has encouraged and rewarded thetype A attitude. Our immediate world may or may notwish to change. A substantial loss of type A behaviourcould mean demotion in status, in job function, in theregard of colleagues and possibly in personal income.None of these prospects is very enticing. But, for ahigh-risk individual, the long-term view may offer littlechoice; and with good personal counselling the pricemay not be too high. Such counselling demands muchskill, and the family doctor may have to make anunusual effort.To what degree can behavioural modification alter

the health and lif expectation of the individual? It is alltoo easy to assume that there is a simple link, and thatmodification of the one will alter the other. Given theneed for scientific demonstration, the most rewardingstatistical circumstances are those in which the highestincidence of test points occurs in the shortest period oftime. Thus, hypertensive smokers with unfavourablelipid profiles should be a first focus. In thesecircumstances remoulding of a patient’s life-style mayprove an ethically defensible activity. In type Aindividuals with risk factors of a lower order ofmagnitude, the prospect of a useful result is small:there is scant chance of collecting enough "events," ina manageable number of people. At present there seemsno good reason to advise lower-risk individuals to mendtheir ways. Indeed, devil’s advocates have been heardto argue that, in some quarters, a small infusion of typeA would be beneficial all round.

To Sleep, Perchance to Breathe.ABNORMALITIES in breathing during sleep have

attracted increased attention with the identification,firstly, of sleep apnoea syndromes, in which breathingstops for over 10 seconds an average of more than tentimes per hour of night-time sleep;2 and, secondly, ofthe much more common disturbances of breathingpattern and arterial oxygenation during sleep in

patients with chronic lung disease.3-6 Two types ofsleep apnoea are distinguished-central apnoea, wherechest wall movement and diaphragmatic contractionscease when airflow stops at the nose and mouth; andobstructive apnoea, where transient upper-airwayobstruction is revealed by persistent chest wall

1 Guilleminault C, Tilian A, Dement WC Sleep apnea syndromes. Annu Rev Med 1976,27: 465-85.

2. Guilleminault C, Dement WC, eds. Sleep apnea syndromes. New York: A. R. Liss.1978.

3. Flick MR, Block A. Continuous in vivo monitoring of arterial oxygenation in chronicobstructive lung disease Ann Intern Med 1977; 86: 725-30

4. Wynne JW, Block AJ, Hemenway J, et al Disordered breathing and oxygendesaturation during sleep in patients with chronic obstructive pulmonary diseaseChest 1978; 73: suppl 301-03.

5. Douglas NJ, Calverley PMA, Leggett RJ, et al Transient hypoxaemia during sleep inchronic bronchitis and emphysema. Lancet 1979; i: 1

6 Fleetham JA, Mezon B, West P, Bradley CA, et al. Chemical control of ventilation andsleep arterial oxygen desaturation in patients with COPD. Am Rev Resp Dis 1980.122: 586-89.