Food for inefficient thought

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COMMENTARIES

VOLUME 58 AUGUST 1976 . NUMBER 2

PEDIATRICS

Vol. 58 No. 2 August

1976

145

Pediatrics

in the on-going roniance between behaviorists

and food faddists.

THE POPULATION CONSIDERED

Food for inefficient

thought

“Not only other ages but also lytle cliyldren are oftentimes afflycted wit/i this gryecouse syckenes, some tyme by nature receyved of tile parents and than it is impossible or difficile to

cure, sometime by evil and unholsonie diet whereby there is

engendred many colde and moist humors in tile bra yne

wlierupon this infirmity procedeth, which if it be in one that is young and tender it is very hard to i.)e removed, but in them that are somewhat strong as of seven yeres and upwarde, it is more easye.”

THOMAS PHAER

The Boke of Ghildren

(1545)

The notion that “even an unwholesome diet”

may have an impact upon the function of the

central nervous system has been a recurring

theme in the history of medicine and the study of

human behavior. In the current issue of Pediatrics,

Conners et al.’ present an important exploration

of a comtemporary hypothesis regarding this

association. Ultimately, their and other studies on

the subject may modify our approach to the

inefficient school-age child, or, alternatively, such pursuits may form another unfulfilling flirtation

In recent years, there has been growing aware-ness that there exists a population of children whose performance in life is handicapped signifi-cantly by intrinsic or constitutional inefficiencies.

Poor control of activity and ineffective attention

with easy distractibility and impulsivity are the

most common behavioral manifestations.2 In

addition, there may be specific learning

handi-caps that involve one or more cognitive

modali-ties, such as visual perception, auditory-language

ftmction, memory, and communication skills.

Examination of such children may uncover

neuro-logic signs of inaturational delay.t

The study of the dysfunctioning school-age

child has been hampered by problems of

termi-nology. A bevy of labels have been applied,

including hyperactivity, hyperkinesis,

hperki-netic impulse disorder, minimal cerebral

dysfunc-tion, minimal brain damage, developmental

dyslexia, and a lengthy list of others. ‘ Semantic

ambiguities are confounded by the growing recognition that we are lumping togethei youngsters whose dysfunctions may be heterogen-eons in their origins and in whom close scrutiny may reveal a spectrum of manifestations. Despite the common denominators of poor activity

control and attentional weakness, there exist

multiple developmental pathways and associated

handicaps.

In a special

diagnostic

clinic

at the

Children’s

Hospital Medical Center, we perceive that

ineffi-cient attention is the common underlying

dysfunction in these children. They fail in the purposeful selection of stimuli and in the

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TABLE I

146 FOOD FOR THOUGHT

A GENERAL CLASSIFICATION OF CHRONIC INATTENTION IN SCHOOL-AGE CHILDREN#{176}

Subtypes Descriptions Frequently Observed Associations

. Primary attention Intrinsic inefficiencies of selective attention

- - .

disorder

Early onset of temperamental dysfunction

Perinatal stress events

.

-Signs of neuromaturational delay

Inattention in multiple settings and situations

Sleep disorders

Visual perceptual disabilities

Inattention secondary to deficits in information Developmental language disabilities

processing Deficits of sequential organization and short-term memory

Secondary attentional .

. Signs of neuromaturational delay

disorders

I

Family problems

Inattention secondary to psychosocial and

J

Emotional disturbance in other family

mem-emotional disturbances

]

bers

I..

Primary depression and anxiety

Ti -rtiary inattention Apparent inattention resulting from inappro- f Tendency toward inattention only in specific priate expectations, perceptions, or educa- settings or situations

tional circumstances extrinsic to the child Discrepant perceptions of child by adults

Mixed forms Two or more subtypes Relevant to subtypes

‘Common denominators of the subtypes: (1) Purposeless selection of stimuli; (2) weak resistance to distraction; (3) impersistence; (4) inefficiencies of motor activity; (5) insatiability; (6) impulsivity; (7) academic failure; (8) social failure; (9) performance inconsistency; and (10) diminished self-esteem. Some or all of these manifestations are seen in each subtype of attentional disorder.

moment-to-moment choice between sustained

attention and shift of focus. Often (but not always) such attentional deficits are accompanied by

inappropriate regulation of activity, for just as a

youngster may not select and adhere to an

appro-priate object of attention, he or she may be

relatively indiscriminate in the selection of and

adherence to an activity. In both instances, it is

clear that what deserves our scrutiny is not the

amount or span of attention and activity, but

rather the quality, efficiency, or purposefulness. In a youngster with the symptoms of chronic

inattention and inefficient activity, critical

differ-entiating questions need to be considered: Is the disordered attention and activity a primary

central nervous system handicap? Is the child

secondarily inattentive and fidgety because of specific cognitive disabilities which interfere with

learning such that good attention has no rewards

and is seldom reinforced with success? Or, is he or

she chronically drained of attention because of anxiety and emotional problems that are perva-sive distractions? Alternatively, is this a child whose poor activity control and distractibility result from a reaction to an educational setting or home environment that fails to match his or her

specific needs? Finally, is this “problem” a style

rather than a disease in a child who is difficult to

manage but highly exploratory and purposeful?

Such a youngster may be mislabelled as

dysfunc-tional by the traditional parent and teacher

questionnaires that are utilized, but be destined

for success, productivity, and happiness.

All of these forms of hyperkinesis or attentional

disorder exist. Mixed types are common. Table I

shows a simplified basic classification system that is used in our clinic. These subtypes tend to be

grouped homogeneously in studies of treatment

that are based largely on behavioral symptoms. ‘

Subtype associations are often but not always

relevant in individual cases. Likewise, the

common denominators vary in their degree of

expression from child to child. Such formulations

need to be supplemented with specific data in

each case with regard to maturational status,

developmental attainment, the presence or

absence of specific learning disabilities,

educa-tional performance, and psychosocial and cultural

information. The emphasis is placed on attention

rather than activity. This allows for the possibility

that one child may be overactive and yet

produc-tive and efficient, while another may be lethargic

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COMMENTARIES

147

and yet inattentive, distractible, and inefficient.

The latter have been called “hypoactive-hyperac-tive” children.7 They may be the last to receive help in a diagnostic system in which high activity level is the cardinal symptom of dysfunction! Future studies of treatment intervention need to offer a sample description more explicit than that in the report by Conners et a!.

THE DIET

The Feingold diet is timely. It comes at a moment in history when the constitutionally dysfunctioning child presents a major treatment challenge. It coincides with a public outcry against stimulant medication for such youngsters. It is also coincident with a tidal wave of enthu-siasm throughout the country flowing toward “physiophilia” or naturalism in life style and diet (another leit motif in history), with its accompanying antitechnology thrust. Such ex-quisite timeliness may elicit a priori cynicism in some readers.

In the present study, the Feingold diet, said to be free of possibly harmful food additives, has been tried on a small sample of “hyperkinetic” youngsters. There is not an extensive description of the sample. Subtypes or forms of dysfunction are not considered. This might be of special interest here, since Feingold himself has stated that his diet does not help all children. It would be useful to know which children allegedly bene-fit.

This is not exclusively a study of the effects of food additives; rather, it is an investigation of an experimental diet, which, as the authors point out, differs from the control diet in ways other than the absence of food additives (e.g., a differ-ence in carbohydrate intake is observed by the authors).

After scrutiny of this study, other justifications for caution emerge. First, a sample of 15 is small and ought not to have a major impact on the way pediatricians manage children with these symp-toms. Second, one has to wonder about how this sample was chosen. Were the parents who volun-teered for this study particularly motivated and interested in its outcome? Were they insightful enough to penetrate all of the allegedly blind safeguards? There is no way the investigators could shield parents totally from knowledge of the Feingold diet and from reflection on the foods their children were eating. Moreover, there were only minimal precautions against illicit detours to the cupboard! It may be that the study of this diet should occur in a well-controlled inpatient

popu-lation, although ethical standards for such an investigation might be difficult to develop.

There are some perplexing inconsistencies in

this report that need further elaboration. Why

were the effects of the two diets related so

strongly to the order in which they were admin-istered to the children? Why did the control diet produce an increase in hyperkinesis that was observed only by teachers and not by parents? How adequate are the outcome measures that were used in this study? How valid in general are

outcome indices that depend largely on parental

and teacher reports or perceptions and are vulnerable to contamination by halo effects?

More direct measurement of outcome may be

crucial.

The Feingold hypothesis bears further study. It

is possible that ingested chemicals may comprise

one of many factors known to aggravate the

dysfunction of children with attentional disorders. The precedent of heavy metal intoxication is well established. It is clear that continued pediatric input into the investigation of the failing school age child will be crucial. It is likely that there will

be no easy answers to the treatment of such

children. Careful controlled studies, such as this

one, set a precedent that is positive in studying a

series of disorders whose treatments commonly are supported only by anecdotal accounts and

ardent parental testimonials. We need to work to

define and refine our notions of disordered

atten-tion in childhood. Even well-designed trials of

drugs or diets will be fraught with intellectual hazards until we have identified more precisely the ecology of constitution and development in inefficient children.

In the iiieantime, caution should be advised with regard to the Feingold diet. The widespread popularization of the hypothesis is regrettable. As the authors note, more data irnist be sought. At present, there is no substitute for describing a child well and avoiding labels. Assessments need

to focus on a child’s cognitive style,

develop-mental status, and neuromaturational level, as well as psychosocial, educational, and family evaluation. The premature endorsement of “food subtractives, “ like the im pulsive recoin mendation

of drugs, may mask underlying cognitive deficien-cies or emotional maladjustments while risking

toxic effects and malnutrition. This is the danger

we face in craving easy answers to a complex,

fundamental, and widespread form of failure in

childhood. Just as Thomas Phaer notes in

discussing “The Fallynge Evyll,” this infirmity “is very hard to be removed.” Simplistic cures are

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148 ENDURANCE

OF UNCERTAINTY

unlikely; in contrast to the comforting prognosis offered by Phaer, the cure may not be “easye”

after “seven yeres and upwarde.”

MELVIN D. LEVINE, M.D.

CRAIG B. LIDEN, M.D.

Medical Outpatient Department, The Children’s Hospital

Medical Center

Boston, Massachusetts 02115

REFERENCES

1. Conners CK, Goyette CH, Southwick DA, et a!: Food additives and hyperkinesis: A controlled double-blind experiment. Pediatrics 58: 154, 1978. 2. Tarver SC, Hallahan DP: Attention deficits in children

with learning disabilities: A review. J Learn Disabil 7:36, 1974.

3. Peters JE, Romine JS, Dykeman RA: A special neuro-logic examination of children with learning disabil-ities. Dev Med Child Neurol 17:63, 1975. 4. Gofman HF, Ailmond BW: Learning and language

disorders in children. Curr Probl Pediatr 1:5, 1971.

5. Stroufe LA: Drug treatment of children with behavior problems. In, Horowitz FD (ed): Review of Child Development Research. Chicago, University of Chicago Press, 1975, pp 347-407.

6. Myers GJ, Pless IB: Where’s the hyperactive child going? Pediatrics 57: 1, 1976.

7. Browning RM: Hypo-responsiveness as a behavioral correlate of brain-damage in children. Psychol Rep

20:251, 1967.

The endurance

of uncertainty

In the debate about cholesterol and coronary heart disease (CHD), the score seems perpetually

tied. In 1972, the Intersociety Commission for

Heart Disease Resources recommended pervasive

dietary changes to lower cholesterol levels for all Americans.’ In the same year, partially in

response, the Committee on Nutrition of the

American Academy of Pediatrics published its

opinion that “dietary intervention, at present, is

experimental and . . . [the committee

recom-mends] . . .against dietary changes for all

chil-dren.” Contradictory recommendations about

pediatric intervention issue from two equally

prestigious oracles.

This issue of Pediatrics contains two additions

to the weighty files of evidence on the

relation-ships between cholesterol and CHD.’ As

intriguing as we find the papers by Hennekens et a!. and by Savage et a!. to be, however, we are

nonetheless disquieted to realize how little they

are likely to settle the cholesterol debate. The

reason could be simple: perhaps the debate is not

so much about what we do not know as it is about how to use what we do know.

Sackett and Holland’ have caricatured the

polarization of preventive medicine as an argu-ment between “evangelists” and “snails. ‘ ‘ The

former, activists, would risk action despite

uncer-tainty’, supporting, for example, attempts to

reduce population cholesterol levels. Snails

disagree; they point to the circumstantial quality of the evidence linking cholesterol and CHD, and

insist that we should know more (that is, through

controlled, prospective, longitudinal clinical trials) before trying to alter population-wide

behaviors. Snails prefer inaction to uncertain

action.

The web of circunistantial evidence does have

some strands securely in place, among them

these:

(1) Epidemiological Studies: Observational

studies in Framingham, Stockholm, Chicago, and

other “Westernized’ ‘ areas find cholesterol level

to be a strong predictive risk factor for CHD in individuals;

(2)

Retroectite Studies of CHD Victims and Families: Victims of CHD, especially younger

victims, have a higher prevalence of

hypercholes-terolemia than their well contemporaries, and

their close relatives have both higher cholesterol

levels3 and higher risk of CHD than the rest of

the population;

(3)

Cross-Cultural Studies: With few

excep-tions, the more affluent and highly

“\Vestern-ized” a culture is, the higher is its observed

burden of CHD,7 and the higher is its mean

cholesterol level at ages beyond infancy;

(4) Comparisons of Westernized Nations:

Among industrialized societies, CHD burden

correlates positively with average serum

choles-terol level, and with the percentage of dietary

calories eaten as saturated fat:

(

5) Animal Models: In numerous animals, including primates, coronary atherosclerosis can

be produced by diets resembling American table

diets, and the plaques regress when diet is altered

to lower serum cholesterol’;

(6)

Pathophysiologic Observations: As the ma-jor lipid component of the atherosclerotic plaque,

cholesterol is implicated by association as a

par-ticipant in the occlusive process.

As Cornfield and Mitchell concluded in their review,” what we lack, despite reams of such

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1976;58;145

Pediatrics

Melvin D. Levine and Craig B. Liden

Food for inefficient thought

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(6)

Food for inefficient thought

PEDIATRICS

Vol. 58 No. 2 August

1976

Pediatrics

Food for inefficient

thought

handicaps.

In a special

diagnostic

clinic

at the

Children’s

I

J

]

I..

COMMENTARIES

147

crucial.

148

ENDURANCE

OF UNCERTAINTY

The endurance

of uncertainty

(2)

(3)

(

(6)

1976;58;145

Pediatrics

Melvin D. Levine and Craig B. Liden

Food for inefficient thought

Services

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including high resolution figures, can be found at:

Permissions & Licensing

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entirety can be found online at:

Information about reproducing this article in parts (figures, tables) or in its

Reprints

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Information about ordering reprints can be found online:

1976;58;145

Pediatrics

Melvin D. Levine and Craig B. Liden

Food for inefficient thought

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