HEALTH PROMOTION INTERNATIONALC Oxford University Press 1996

Vol. 11, No. IPrinted in Great Britain

Using theory to guide policy relevant health promotionresearch

KATHRYN DEANResearch and Training Consultant, Population Health Studies, Copenhagen, Denmark

SUMMARYThe concept of health promotion has evolved into astrategy for improving health that goes beyond indi-vidual behaviour to include the physical, social andeconomic environments in which health and behaviourare shaped. The core of the strategy is to stimulate actionagainst the root causes of ill health in communities. Aprerequisite for effective health promotion action is validknowledge about how forces protect or damage healthin daily life. Developing and using theory to guide thecollection, analysis and evaluation of empirical evidence

is a neglected aspect of obtaining the knowledge neededfor promoting health. Population interventions toreduce cholesterol provide an example that illustratesthe consequences of basing community health policyand programmes on findings from empirical researchwithout developing a logically sound theoretical basisfor identifying inconsistencies and contradictions in thefindings. The use of theory to guide research to supporthealth promotion action is discussed.

Key words: health promotion; informed action; theory

INTRODUCTION

The field of health promotion is infusing newthinking into population health research and thepolicy making process for health. Originating in acritique of traditional health education (Greenand Raeburn, 1988), the concept of healthpromotion has evolved into a strategy forimproving health that goes beyond individualbehaviour to include the physical, social andeconomic environments in which both health andbehaviour are shaped (World Health Organiza-tion (WHO), 1984; Kickbusch, 1986). The coreof the strategy is to stimulate action on the rootcauses of ill health in communities.

What then, it might be asked, has theory, a coreelement of 'basic' research, to do with healthpromotion? Since health promotion research issupposed to support action, it is, in the minds ofmany, limited to 'action' research. When focusedon community health, action research involvesattempts to change policies, environments,

professional services or the personal behaviour ofindividuals in order to improve health. Frequentlyit involves implementing and assessing the effectsof interventions. Clearly, action and/or actionresearch based on faulty 'basic research', will leadto uncertain problem identification or incorrectassumptions that misdirect policy (Orosz, 1994).

A prerequisite for action that addresses theroot causes of poor health in communities is validknowledge about the forces that protect anddamage health in daily life. Characterized as a'knowledge challenge' (Kickbusch and Dean,1992; Labonte, 1994), a health promotionstrategy involves assuring a valid knowledge baseto inform the action. Without entering the deepand muddy waters of debates about the differ-ences between basic and applied research, thispaper asserts that theory is essential to valid andmeaningful research, however conceptualized.Since the central concerns of theory building have

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20 K. Dean

to do with explaining phenomena in both the mostcomprehensive and the most precise way possible(Selltiz et al., 1976; Suppe, 1977a), it might beconcluded that theory is the most fundamentalprerequisite of a policy science, and that theabsence of theory and effective theory buildingare serious weaknesses of much of the existingresearch available for the policy making processfor improving the health of populations.

In order to explore these issues, a detailedexample will be used to illustrate the conse-quences of basing community health policy andprogrammes on findings from empirical researchwithout developing a logically sound theoreticalbasis for identifying inconsistencies and contra-dictions in the findings. Based on this example,the use of theory to guide basic and appliedresearch to support health promotion action willbe discussed.

COMMUNITY INTERVENTIONS TOREDUCE CHOLESTEROL

In the 1980s, major health policy initiativesdirected toward reducing cardiovascular diseaseinvolved population interventions to reducecholesterol blood levels. A well-documentedhigher risk of death from coronary heart diseaseamong persons with elevated levels of bloodcholesterol formed the basis of the policiesfocused on activating people to lower bloodcholesterol. The goal was to contribute to improv-ing public health by shifting the distribution ofblood cholesterol concentrations for entirepopulations (Consensus Conference, 1985;Study Group, 1987). Extensive public funds wereused in many countries on interventions andhealth education focused on getting people tochange their diets, obtain blood cholesterolmeasurements and even use drugs to reducecholesterol levels. After extremely costly popula-tion based programmes had been in place forsome time, it became known that not only high,but also low levels of blood cholesterol are asso-ciated with disease and death—that there is a'U-shaped curve' in the relationship betweenblood cholesterol and mortality.

Muldoon and his colleagues (1990), conducteda meta-analysis, a quantitative review of theevidence, on findings from primary preventiontrials of the type that had been used to justify thiscommunity health policy. The purpose of themeta-analysis was to determine the effects of

lowering blood cholesterol on total and casespecific mortality. In order to enhance thecomparability of the findings and reduce statis-tical effects from combining data from differentstudies, rigorous criteria were developed foraccepting experimental trials into the study. Eachproject had to have: (i) been a randomized clinicalprevention trial of serum cholesterol reduction;(ii) included a treatment group that receivedinstructions for a diet and/or drugs to reducecholesterol and a control group; (iii) resulted inthe lowering of cholesterol in the interventiongroup relative to the control group; and (iv)reported both total and cause specific mortality inthe results of the trial. Six randomized trials total-ling 24 847 male participants could be acceptedon the basis of these criteria.

The results of the meta-analysis showed thatwhile each trial reported evidence of success inlowering blood cholesterol levels, the evidence ofany reduced coronary heart disease (CHD)mortality was weak, and overall survival amongmen who underwent lipid lowering treatment wasnot improved. Furthermore, mortality not relatedto illness was nearly twice as high in the inter-vention groups as in the control groups, a findingconsistent for all six studies whether or not thecholesterol lowering treatment was carried outwith drugs or dietary education. These highlyconsistent and disturbing results were reportedabout the same time that other investigators wereuncovering similar findings (Holme, 1990;Strandberg etal., 1991).

The evidence from studies of cholesterolreduction was presented for evaluation in a USNational Heart, Lung and Blood Institute expertconference in 1990 (Conference Report, 1992).The experts reviewed and discussed existing dataon the left-hand limb (association between lowcholesterol and mortality) of the U-shaped curve,the term that is used to represent the greatermortality found among persons with both highand low blood cholesterol levels. Presentingresults of a statistical overview of available cohortstudies with findings involving 68 406 deaths, astudy of unprecedented size, it was documentedthat the higher mortality rates associated with lowblood cholesterol held both across studies and fora diverse range of causes. Especially high excessdeath rates from digestive system conditions andfrom less common diverse causes were found, butalso cancer, respiratory system and injury deathswere associated with low cholesterol.

The findings of higher risk of death from causes

other than CHD held for both men and women.At the same time, however, the second majorfinding of the conference report was the 'surpris-ing observation' that for women 'high bloodcholesterol is not associated with all-cause mor-tality nor even with cardiovascular mortality'(Hulley et al., 1992). Three major conclusionswere drawn from the findings presented in theexpert conference:

• the association between low blood cholesteroland noncardiovascular deaths indicated theneed to review policies aimed at shifting entirepopulation distributions of blood cholesterolto lower levels;

• the lack of association between high bloodcholesterol and cardiovascular deaths inwomen indicated that, except for those withcoronary disease or other high risk of CHDdeath, 'it no longer seems wise to screen for andtreat high blood cholesterol in women';

• the findings in primary prevention trials ofcholesterol intervention that the increase innon-CHD mortality rates is similar to thedecrease in CHD death rates indicated that,except for people who already have coronarydisease, it is unwise to treat high blood choles-terol with drugs.

IMPORTANCE OF KNOWING AND USINGRELEVANT RESEARCH LITERATURE

Actually, it turns out, as noted by Hulley and hiscolleagues (1992), that this 'U-shaped curve' hadbeen reported for two decades. Moreover,Muldoon and his colleagues (1990) had notedthat, although large primary prevention trials hadfound evidence suggesting that lowering serumcholesterol concentrations reduced the incidenceof coronary events, predominantly myocardialinfarction, only one had found mortality fromheart disease lowered significantly after choles-terol reduction.

If one examines research literature other thanthat from controlled clinical trials, evidence thatwould have foreseen these findings goes back to atleast 1962 (Groen et al). In an investigationconducted in Holland, cholesterol research wasplaced in a lifestyle context, with the result thatthe findings differed considerably from simplepredictive correlations between measures ofcholesterol and CHD mortality. The studyinvolved comparative analyses of behavioural

Using theory to guide policy 21

and health variables in populations of Benedic-tine and Trappist monks living in cloisteredmonasteries.

It was found that blood cholesterol levels weremuch higher in all age groups for the Benedictinemonks compared to the Trappist monks. Theessentially vegetarian diet of the Trappist monksis much stricter than that of the Benedictines. Thisis evidence that diet can affect blood cholesterol,also shown in the cholesterol intervention trials.Cardiovascular disease incidence was, however,in spite of the higher cholesterol levels of theBenedictines, the same in both monk populations,and much lower than in the general male popula-tion of comparable age in Holland. The findingsshow that even if blood cholesterol is a contrib-uting factor in cardiovascular disease, it is not asufficient cause. Social and psychosocial pro-cesses, as either component causes or modifiersof disease processes, appear to be the determininginfluences. This study illustrates that it is researchon lifestyle, understood as patterns and ways ofliving (Coreil et al., 1985), rather than cholesterolor any other risk factor that is needed for under-standing health and disease.

Geoffrey Rose (1985), in a discussion ofproblems and limitations of the risk factor modelof research on population health, unintentionally,but powerfully, illustrated the potential problemsthat would arise from action connecting choles-terol and heart disease in a simple causal model.He used findings from the Framingham Study, acomprehensive longitudinal investigation ofhealth outcomes in a US population sample, tojuxtapose the serum cholesterol curve of thepersons in the cohort study who developed CHDover the curve of those who did not develop heartdisease. The curves showed a comparable rangeand peak in the cholesterol values of those whodid and did not develop disease, rendering thepowerful relative risks produced from the dataunimpressive.

Rose felt that research focused on individualsconstrains knowledge about the causes ofdiseases. With roots in clinical practice, thepurpose of both case control and cohort epi-demiological studies, he noted, is to discover howsick and healthy individuals differ. He pointed outthat the use of relative risk as the measure ofaetiological force in this paradigm has almostexcluded the use of any other approach inepidemiology, even though relative risk 'is nomeasure at all of aetiological outcome or of publichealth importance' (p. 32). Rose reminded us

22 K. Dean

that, while considerable information is availableabout the characteristics of individuals suscep-tible to various diseases, 'most non-infectiousdiseases are still of largely unknown aetiology'.

These considerations led Rose to the conclu-sion that research should focus on populationsrather than individuals—ecological comparisonsin contrast to relative risk approaches. UsingCHD as an example, he pointed out that even withscreening to detect early disease, there is weakability to predict the future for individual patients.His suggested solution, looking at populationaverages and attempting to shift the curve ofwhole populations on specific risk factors is,however, the approach that was found to bedangerous in the overview of research findings onthe U-shaped curve with regard to cholesterolrelated mortality. Rose's recommendation, aimedat preventing cardiovascular disease in popula-tions instead of detecting disease at an early stagein individuals, was still centred in a risk factorcause and effect model of disease.

Both relative risk approaches to specific aetiol-ogy and ecological studies examining groupdifferences on specific phenomena look awayfrom the differential impact of causal influences inthe presence of other causes and over periods oftime. Rose's synthesis of findings pointing to thelimitations of the relative risk paradigm in a sensereplicate those of the research in Hollanddescribed above, but without the theoretical forceof the lifestyle study for suggesting contributingcauses.

THEORY, THE NEGLECTED COMPONENT

The evidence provided by the cholesterol studies,whether they stem from randomized trials, casecontrol, cohort or ecological studies, centre onstatistical effects and predictions. Detecting astatistical effect of a factor that remains afterother influences are removed by randomizationor statistical 'control' does not provide the infor-mation needed for understanding the statisticalconnection between the two variables. Relation-ships between variables that have been tested andreplicated may be true, but remain so unspecifiedthat they do not provide meaningful knowledge(Merton, 1949). It is necessary to learn theconditions under which statistical correlationshold, are modified or disappear to understandcausal processes determining health in the realworld. A theoretical logic for transferring statisti-

cal correlations into causal processes and forinvestigating inconsistencies and contradictionsin the findings, such as that developed by Rosen-berg (1968), is absent in the risk factor model ofdisease. This problem is a major barrier forunderstanding the meaning of statistical correla-tions between specific factors and disease.

The cholesterol example is illustrative becauseresults available in the research literaturecontained theoretical insight suggesting alterna-tive directions long before the costly and perhapsdangerous interventions led those responsible forthem to conclude that the policy needed to bechanged. One wonders at the power given statisti-cal predictions in this body of work, as if thestatistical connections between two factors hadreal meaning for the health outcomes of individ-ual people.

Even without an awareness of research findingssuch as those from the investigation in Hollandand those presented by Rose, or without stoppingto think about the reality constraints of statisticalcorrelations, one wonders why cholesterol wasgiven such unique power as a cause of CHD.Should not cholesterol be regarded as a biologicalmarker expressing a state of physicochemicalprocesses in the individual at a given time, anoutcome or at least an intermediate outcome,rather than a cause? What theoretical logic waspresented and tested that could grant cholesterolthe causal status justifying intervention affectingthe health of general populations and the use ofhuge amounts of limited public health resources?

The purpose of scientific theory and methods isto expand knowledge about causal processes. Allresearch designs and statistical models havelimitations for testing theories. The details of howscientific methods fall short fill numerous texts onresearch methodology. Research granting amethodological approach a primacy that hides itslimitations, and without theoretical frameworksto illuminate the limitations, should never be thebasis of health policy and action. The over-whelming consensus is that methods appropriatefor given research questions (fallible as they are)should be used to test theories (Stolzenberg andLand, 1983). This means that both action andbasic research in pursuit of knowledge to informhealth policy would always be an interplaybetween expanding theory and improvingmethods (Dean, 1993).

Using theory to guide policy 2 3

CHANGING VIEWS ABOUT THE ROLE OFTHEORY

The meaning and importance of theory havechanged periodically throughout the history ofscience. Long traditions of separating theory fromempirical observations had serious consequenceson scientific research, including that conducted inpopulation based sciences (Bernert, 1983). Theweaknesses of atheoretical empirical work arenow widely recognized (Faust, 1984; Maclure,1985; Dean, 1993). Suppe (1977b) discussingmajor contemporary views on theory building,reached the conclusion that only in primitivescience, where the development of theories isneglected, does the verification of empirical pre-dictions maintain a central position. A majorfunction of theory is to organize and integrateinformation for discovery (Shapere, 1977).

The above observations do not mean thatdeveloping and using theory guarantees 'truth' oreven necessarily the advancement of knowledge.Theory, an aid to human cognitive limitations,helps to organize information in the body ofknowledge for further inquiry (Faust, 1984).When not tested and modified appropriately,theory can become transformed from a scientificthesis about reality relationships into a rationalefor a belief system.

Competing theories are also important forgaining new knowledge. The interpretation ofobservations considered true within the frame-work of a particular theory will be only partialtruths, or even false, in the context of anothertheory. Gillett (1994) illustrates this with theexample of the corpuscular theory of light beingconsidered false when wave theory becamedominant, but regaining importance with quan-tum theory. The revived importance of corpuscu-lar theory was not, however, considered todiscredit wave theory. Both became part of a newunderstanding of particles and the developmentof a new theory of light. This example is usefulbecause it illustrates that different theories, some-times opposing or contradictory and sometimescomplimentary, as well as the modification oftheory, are core aspects of advancing scientificknowledge. Referring back to the cholesterolexample, the point is that empirical observationsare always partial representations conveyingcertain truths and concealing others.

USING THEORY IN HEALTH PROMOTIONRESEARCH

A great deal of health promotion research hasbeen limited to the health related behaviour ofindividuals. When some form of theoreticalframework is used in research on behaviour andhealth, it is generally based on theories developedby social psychologists. These theories are usedquite loosely and rarely modified or rejectedwhen very little of the 'variance' in the behaviouralpractice is explained. It has been argued that thesemodels are more 'idea-sets' than the type oftheories usually developed to provide scientificexplanation (Research Unit in Health and Beha-vioural Changes (RUHBC), 1989). Influencedboth by risk factor epidemiology and socialpsychology, this work provided the knowledgebase for health education. In recent years, morestudies have focused on social environments andstructural determinants of health (Milio, 1986).Starting slowly as a critique of traditional healtheducation, the shift gained force with the evolu-tion of the field of health promotion.

The term 'health promotion', generally tracedto the Lalonde Report (1974), remained for sometime a vaguely conceived umbrella term veryoften used in relation to quite traditional researchand programmes (McQueen, 1994). It was afterthe WHO (1984), Health Promotion: A Discus-sion Document on the Concept of Principles, andthe Ottawa Charter (WHO, 1986), launched 2years later at the first International Conference onHealth Promotion, that the process of estab-lishing research, education and publication struc-tures moved rapidly forward.

Much has been done to shift the health pro-motion research agenda. Still, a great deal of theresearch conducted in the field continues to relyon the risk factor tradition, methodologicalapproaches and the social psychological thinkingfrom which the field emerged. New theoreticalthinking is present in the field conceptually andimplicitly, but making theory explicit and a strongforce guiding research and explanation has notyet occurred. While health promotion cannot layclaim to well-developed theories of its own, evenin its infancy, this young field developed a strongconceptual base that provides a framework fortheory development. Theories embedded in theconcepts and principles of health promotion(WHO, 1984) and the Ottawa Charter (WHO,1986) can guide the various types of research oninstitutions, populations and individuals that are

24 K. Dean

needed to provide knowledge for health pro-moting action.

The health field concept (Lalonde, 1974),modified on the basis of the Ottawa Charter (Rae-burn and Rootman, 1989), summarizes domainsfor research and action. Other models and con-ceptual frameworks have been put forward aswell. The characteristics that best describe thetypes of research needed to provide the know-ledge for health promoting action are contextual-ism and dynamism (Dean et al., 1993). Theemphasis on environments, communities andpolicy opens the way for theories of multilevelinfluences that can expand knowledge about thecausal processes that people are exposed to in thecontexts of daily living.

Bringing together theory and knowledge fromdiverse sources is a central idea in Shapere's(1977) concept of theoretical domains. In histhinking, theory and empirical research aremutually interdependent. The development of atheoretical domain in research to promote healthwould entail discovering causal processes byexploring and then fitting together moderatinginfluences instead of trying to reduce complexityto a simple connection between two factors. Astatistical relationship between two variables canonly be a starting point for understanding thecontext in which the two variables relate to eachother, and for identifying the conditions thatmodify the relationship.

Developing the context in a theoretical domainexamining how lifestyles affect health wouldinvolve fitting together findings from differenttypes of studies, as well as integrating differentlevels of influence into investigations of lifestyleand health. The contexts in which people live theirdaily lives involve social conditions and oppor-tunities for learning and practising life skills.Social norms and formal legal statutes, as well asthe resources that shape both personal skills andsupportive environments, make up the domain inwhich lifestyles are formed and maintained. It isnecessary to study the formal and informal rulesgoverning the context in a research domain(Gillett, 1994).

Specific health related behaviours would havelimited meaning or relevance in a lifestyleresearch domain. Theories would postulate howways of living protect or damage health. Trans-lated into empirical research, patterns of behav-iour (their separate, joint and interactive effectson health) in the context of daily life, would bestudied with complementary types of research

methodologies. Cholesterol levels might bestudied to obtain knowledge about the causal pro-cesses leading some people with high cholesterolto develop heart disease while others remainhealthy. This would involve identifying how inter-vening influences such as general behaviouralpatterns, stress, supportive environments andavailable resources affect the health of peoplewith family histories of high cholesterol and/orheart disease.

Thus in a lifestyle framework, meaningfulresearch would seek to understand the influenceof living situations, and of cultural and subgrouplearning and expectations on behavioural prac-tices. Another important area of inquiry would bethe progressive nature of health damaging habitsfor some people. 'Addiction' research needs tostudy environmental demands and the moder-ating effects of personal skills and of supportavailable in social networks.

Time, generally neglected in population healthresearch, is another major force determining thecontextual nature of causation. Lifestyle theory,developing the interplay of environmental con-text and behavioural patterns would need to betested with methods capable of disentangling theeffects of age, period and cohort aspects of causalprocesses (Riley, 1993). The contribution of anyspecific influence is not necessarily stable overtime, and there may be social group differences inthe relative stability of influences. Take, forexample, the impact of diet at different periods oflife. A deficiency in childhood of nutrients neededfor normal development will have far moreserious consequences for health, functioning andlongevity than the same deficiency in late life(Barker, 1988).

For other influences, the impact at differentperiods of the life course may reverse. Thephysiological caustic effects of a substance suchas alcohol may be far less for young active peoplewith rapid metabolism than for old people whoare less active and whose metabolic processeshave altered character. At the same time, alcoholpresents other dangers to young people relative toolder people. The role of peer pressure isespecially strong in youth, and may contribute tooveruse or dangerous use of alcohol or othermood altering substances among young peoplerelative to mature adults. Accidents, especiallythose involving alcohol and/or speeding in motorvehicles, are a major cause of death and disabilityfor young males. Variations in how influencesaffect outcomes need to be understood for effec-

Using theory to guide policy 25

tive health promotion. It is not possible to infusethe time dimension into studies of causalprocesses without theory to organize existingknowledge for the development of plausibleexplanations.

MOVING FORWARD

The field of health promotion has already takengreat strides in shifting the research agenda tosubjects more in tune with real community healthneeds. It is now important to assure that the some-times heavily rhetorical discussions on the subjectof health promotion do not impede progress. Inorder to continue and build on the contributionsalready made to public health, the field of healthpromotion 'must now move beyond the rhetoricof its developmental years' (McQueen, 1994).'Action' research and other forms of research toinform health policy are not new. They havealways existed in the field of public health.Throughout an extended period in this century,research became dominated by the biologicalexperimental paradigm, and indeed actionresearch in that tradition did form the basis ofcommunity health policy. The policies focused onshifting the cholesterol curves of general popula-tions resulted from action research accepted inthe policy making process.

Changing the focus of the health debate and therenewed emphasis on the environmental deter-minants of health are important contributions ofthe field. Community health programmes have,however, received high priority in the past only tobe dismantled, and even within the field of healthpromotion research and programmes have notalways risen above the individualized risk factorapproaches (Green, 1994).

Research simply shifting the focus from 'riskfactors' to 'risk conditions' is not sufficient forimproving knowledge. The risk factor model itselfhas built in limitations. Like so many dysfunc-tional dichotomies that are being challenged incontemporary science, arguments about themicro-macro determinants of health, and theircounterpart, the nature-nurture division, areboth reductionistic approaches (Lewontin et al,1984; Lewontin, 1991). Both fail to acknowledgethe multidimensional and interactive nature of thecausal processes that shape health and func-tioning.

CONCLUSION

Theory for guiding health promotion researchneeds to build in the complexity involved in realcausal processes that shape health over time.Relationships among influences can then beexplored with the range of research designs,qualitative as well as quantitative, for studyingresearch issues, and with analytic approaches thatare capable of studying direct, indirect andmoderating relationships.

'The 1990s represent the watershed for healthpromotion. Now health promotion must show itsutility to the skeptics, as well as those who havehad their consciousness raised by its rhetoric'(McQueen, 1994, p. 336). Action that is not basedon valid knowledge will discredit the field. Theorybased in the concepts and principles of healthpromotion can guide research to new knowledgeabout health and health related quality of life.

Address for correspondenceKathryn DeanPopulation Health StudiesRibegade 6 st.tvDK-2100 CopenhagenDenmark

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