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Psychological Bulletin 1991, Vol.110, No. 3,52i

Copyright 1991 by the American Psychological Association, Inc. 0033-2909/91/$3.00

The Nature of Environmental Influences on Weight and Obesity: A Behavior Genetic Analysis Carlos M. Grilo

Michael E Pogue-Geile

University of Pittsburgh

Department of Psychology and Department of Psychiatry University of Pittsburgh

The nature of environmental influences on individual diiferences in weight and obesity is presently unclear. To resolve this issue, behavior genetic studies are reviewed for their relevance to environmental influences on weight and obesity. Results are consistent in suggesting that environmental experiences are important for weight and obesity, although they account for much less variation than do the effects of genes. Furthermore, only environmental experiences that are not shared among family members appear to be important. In contrast, experiences that are shared among family members appear largely irrelevant in determining individual differences in weight and obesity. These conclusions are consistent with a growing body of evidence on the relative unimportance of such shared experiences for many psychological characteristics.

Obesity, a surplus of body fat that is generally diagnosed in individuals who are 20% over their ideal body weight for height (Jeffrey & Knauss, 1981), is a prevalent problem with serious

have emphasized both genetic influences (Foch & McClearn, 1980) and a range of environmental influences (Jeffrey &

health and psychological consequences (Bray, 1986; Brownell, 1982). It is very common in developed countries, with 34 mil-

influence on overweight has been excellently reviewed else-

lion Americans believed to be overweight (Van Itallie, 1985),

1987; Stunkard, 1988) and is not considered here in detail. Rather, our aim is to reconsider this behavior genetic evidence for its implications for environmental hypotheses.

Knauss, 1981). The evidence documenting a substantial genetic where (Epstein & Cluss, 1986; Foch & McClearn, 1980; Price,

and appears to be becoming more prevalent in both developed (Burton, Foster, Hirsch, & Van Itallie, 1985; Sonne-Holm & Sorensen, 1977) and developing countries (Lara-Pantin, 1987;

The documentation of a major role for genetic factors in

Salans, 1987). Obesity/overweight is also associated with increased risk of hypertension, hyperglycemia, hyperlipidemia, and non-insulin-dependent diabetes melh'tus (Bray, 1986;

weight does not rule out the importance of life experiences.

Brownell, 1982; Burton et al, 1985; Hubert, Feinleib, McNamara, & Castelli, 1983; Keys, 1979; Salans, 1987). Middle-aged

reports emphasized the possible role of family disturbances in the development of overweight (Bruch, 1964); more recent em-

people who are 50% overweight suffer a 90% increase in mortal-

pirical studies have examined a range of environmental factors

ity (Bray, 1976). Being overweight also has numerous negative psychological (Wadden & Stunkard, 1985) and social (Allon,

that are hypothesized to be relevant to overweight, such as rear-

Hypotheses of specific environmental contributors to weight have both a long history and an active present. Early clinical

ing practices (Birch, Zimmerman, & Hind, 1980), child-feed-

1982) consequences. Given the societal importance of obesity/overweight, it is critical to understand its causes, because they should inform efforts

nomic status (Sobal & Stunkard, 1989). Biologically oriented investigators have similarly hypothesized the importance of

at prevention. It is increasingly apparent that obesity/over-

diet fat content (Sclafani, 1980) and lack of exercise (Stern &

weight is a complex, multifactorial phenomenon (Brownell, 1981; Jeffrey & Knauss, 1981; Rodin, 1982). Only approxi-

Lowney, 1986). Apparent cohort effects for increasing rates of overweight in recent decades (Christensen, Sonne-Holm, & Sorensen, 1981; Sonne-Holm & S0rensen, 1977) also suggest

ing practices (Klesges et al, 1983), life stressors, and socioeco-

mately 5% of cases of obesity can be attributed to specific known physical causes, including endocrine dysfunction, brain

that environmental influences are important in its etiology.

damage, and hereditary diseases, such as Prader-Willi syndrome. Etiological models for the remaining cases of obesity

The depth of current interest in environmental contributors to this major health problem suggests the timeliness of a review of the environmental implications of behavior genetic research on weight and obesity. In many ways, behavior genetic designs provide the best evidence regarding the etiological importance

Preparation of this article was supported in part by National Institute of Mental Health Grant MH 43666 to Michael F. Pogue-Geile and National Heart, Lung, and Blood Institute Grant HL 40962. Carlos M. Grilo is now with the Eating and Weight Disorders Program, Department of Psychology, Yale University. Correspondence concerning this article should be addressed to Michael E Pogue-Geile, 4015 O'Hara Street, Department of Psychology, University of Pittsburgh, Pittsburgh, Pennsylvania 15260.

of environmental events, because only in designs such as twin and adoption studies can the effects of family environment and genes be disentangled. A further major advantage of many behavior genetic strategies is their ability to detect unspecified environmental effects (Pogue-Geile & Rose, 1987). By comparing resemblance for

520

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ENVIRONMENTAL INFLUENCES ON WEIGHT AND OBESITY

521

degree of family physical and social contact, these designs are

consequences of these different concepts are discussed in more detail below.

sensitive to the effects of life experiences on weight that are associated with degree of contact. An example of this approach is the comparison of resemblance for weight shown between

etiological effects of both unspecified and specified shared environmental influences on weight and obesity. This is followed by

weight among family members across samples that vary in their

biological siblings who are either reared together or reared apart. An advantage of such an approach is that hypotheses regarding specific life experiences (e.g., modeling of specific parental behaviors) are not required. Although a finding of significant unspecified environmental influence in such a design cannot point to which specific experiences are etiologicalry important, it can demonstrate that something is important

The present review focuses first on evaluating the potential

a review of behavior genetic findings relevant to estimating and characterizing nonshared environmental influences. Before reviewing the studies, a methodological note on the definitions and measurements of obesity and overweight is in order. First, note the distinction between obesity and overweight (Bray, 1986). Obesity refers to a surplus of adipose tissue in proportion to lean body mass, whereas overweight refers to excess weight with reference to weight for height tables devel-

enough to justify further research. A final contribution of behavior genetic strategies to the

oped by insurance companies (e.g., Metropolitan Life Insurance

study of environmental effects is the increasingly important

Company, 1984). Although most obese individuals are over-

distinction between unspecified environmental influences that are shared among family members versus those that are nonshared (Jinks & Fulker, 1970; Plomin & Daniels, 1987; Rowe & Plomin, 1981). To the extent that resemblance among family

weight, not all individuals who are overweight are obese (Bray,

members for weight is increased in samples that have a greater degree of family contact, then some specific life experiences that are shared among family members must be important in determining individual differences in weight. For instance, to

used is 20% over ideal weight for height (Jeffrey & Knauss, 1981); this cutoff is associated with significant increases in morbidity and mortality (Bray, 1986). Few studies cited in this re-

the degree that adoptive siblings (Le, biologically unrelated individuals who are reared together) resemble each other in weight,

1986). Because body weight and body fat composition are continuous distributions in the population, such cutoffs are to some extent arbitrary. The most common criterion of obesity

view investigated this dichotomy; instead, most used a variety of continuous measures of weight, weight-fbr-height ratios, and

some life experiences that are shared by them must be etiologically important in determining individual differences in

skinfold thicknesses at different body sites. Second, with any of these measures, it is important to control in some fashion for stature or height. Weight/height and the body mass index (BMI;

weight, although which specific experiences are important is not resolved. Examples of specific experiences that tend to be

weight divided by height squared) are commonly used ratios that correlate highly with body fat (Bray, 1986). Third, because

shared among family members include parental physical and behavioral characteristics, some parental rearing practices, socioeconomic status, some family mealtime practices, and overall family emphasis on physical fitness. However, the precise

many of the studies cited assessed children, adolescents, and adults, corrections for age and sex differences are crucial and can have important effects on behavior genetic findings

degree that such experiences correlate within families is an em-

for further discussion of measurement issues specific to overweight and obesity.

pirical issue. In contrast, nonshared environmental effects reflect the ac-

(McGue & Bouchard, 1984). Readers are referred to Bray (1986)

tion of life experiences that are not shared among family members. For example, the only reason that genetically identi-

Shared Environmental Influences

cal monozygotic (MZ) twins who are reared together differ from each other is the effect of life experiences that they do not share. Nonshared environmental effects reflect the conse-

Unspecified

quences of unknown specific life experiences that are not

sensitive to the effects of any experiences that may be shared

shared among family members, which thus tend to reduce resemblance among family members. Examples of specific experiences that tend not to be shared among family members include

among people. In these designs, individuals are compared whose degree of social contact varies (e.g, reared together or apart) but whose genetic similarity remains constant (e.g, all

Influences

As mentioned above, certain behavior genetic designs are

perinatal insult, some peer relationships, differential rearing

MZ twins). If, for example, when genetic similarity is held con-

practices, and accidents. Random measurement error also con-

stant, increased social contact is associated with increased resemblance for weight, then it can be concluded that some expe-

tributes to estimates of nonshared environmental effects. In this article, it is important to keep clear the differences

riences that are shared among individuals with increased social

between the concepts of shared unspecified environmental effects and specific family environmental influences. A specific family experience could be etiologicalty important in the ab-

contact are influential in determining individual differences in weight. However, because no aspect of the shared environment

sence of any evidence for shared environmental effects to the extent that it is not shared among family members. For example, if parental rearing strategies were important in determining individual differences in weight but these strategies differed

is actually measured, one cannot know which specific experiences are important. Among these designs, we have made a further distinction between those that use relatives of the same generation, collat-

substantially across offspring within a family, then there might

erals (i£., twins or siblings) versus different generations, ascendants/descendants (i.e, parents and offspring). We have termed

be no evidence of shared environmental influences despite the presence of an important family influence. The meaning and

the former studies of unspecified shared environmental influence because resemblance between collateral relatives is presumed

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522

CARLOS M. GRILO AND MICHAEL F. POGUE-GEILE

to be particularly sensitive to the host of unspecified experiences that they share during their early years. Of course, in addition to these unmeasured "third variables," any observed correlation among collateral relatives could also arise because of direct-modeling or competition effects between siblings or

nary estimate of the importance of shared environment. More direct estimates of this effect are considered below.

Adoptive Siblings Reared Together

twins (e.g, Carey, 1986; Eaves, 1976). In contrast is the nature of

A more direct estimate of the importance of shared rearing

the experiences that are shared between parents and offspring, which we term specified shared environment. Because of age

environment in the absence of shared genes is provided by the correlation between unrelated individuals who are reared to-

displacement, this relationship is often hypothesized to be espe-

gether. In the absence of selective placement, any resemblance

cially sensitive to direct-modeling effects from specific parent behavior to offspring (or vice versa) rather than to the indirect

among these individuals is attributable to shared environmental experiences. The presence of selective placement, in which

effects of unspecified shared experiences. Although not entirely distinct, this differentiation of collateral and ascendant/descen-

adoptees are not randomly paired, would serve to artifactually inflate the estimates of shared environmental effects in this

dant environmental relationships seeks to highlight the poten-

design. Although this is a crucially valuable strategy, there are few such studies available.

tial experiential differences between them. We first consider studies of unspecified shared experiences shared among collaterals.

Table 2 contains the available adoptive sibling correlations for weight, weight/height, and skinfold measures. Biron, Mongeau, and Bertrand (1977) and C. Bourchard, Savard, Depres, Tremblay, and Leblanc (1985) reported nonsignificant

Overall Familiality: Biological Siblings Reared Together Estimates of shared environmental influences may be derived from a number of different behavior genetic designs. However, before reviewing these, we present an examination of the total degree of resemblance among nuclear family members for weight and obesity to provide a context for understanding the more specific estimates. Because genetic and shared family experience both contribute to total familial resemblance and

adoptive sibling correlations for each of these measures, suggesting no effect of shared family experience. This is even the case with these relatively young adoptive siblings, who were likely to be currently living together. In contrast, Gam and colleagues, who included stepsiblings in their analyses reported significant correlations from the Tecumseh project. Inclusion of stepsiblings would tend to increase these correlations due to the effects of assortative mating and thus confounds any direct estimation of shared environmental effects. In summary, then,

given that the majority of the total familial aggregation of weight and obesity has been documented to be due to genetic influences (e.g., Stunkard, Harris, Pedersen, & McClearn,

the two available studies of true adoptive siblings found little evidence of shared environmental influences on weight and fatness, even in a young sample in which many of the adoptive

1990), the total degree of familiality provides a rough upper-

siblings were likely to be currently living together.

bound estimate of the potential importance of shared family environment. For this purpose, we examine sibling resemblance. Table 1 contains the major family studies that have reported

Twins: Reared Together Versus Reared Apart

sibling correlations for weight, BMI, or skinfold measures. Overall, across sexes and across all ages, same-sex sibling correlations average .30 for weight, .28 for BMI, .29 for tricep skinfolds, and .38 for subscapular skinfolds. The correlations among siblings under 18 years old (who are likely to live together currently) are not appreciably larger than those for older siblings (who are likely to live apart currently). Thus, correlations of these multiple measures of weight and obesity among samesex siblings average approximately .30, suggesting only a moderate degree of total family resemblance. It has been estimated that approximately 70% of total variation in weight is due to genetic influences (e.g., Stunkard et al., 1990); because siblings share on average 50% of their genes, this predicts a sibling correlation for weight of approximately .35, assuming only genetic causes (heritability, .70, multiplied by coefficient of genetic relationship between siblings, .50, = .35). The difference between this predicted correlation, which is based on only genetic expectations, and the observed sibling correlation provides a preliminary rough estimate of the likely importance of experiences shared among siblings who were reared together and probably currently live together. As can be seen, the observed correlation (.30) minus the expected correlation, which is based on only genetic effects (,35), yields an essentially zero (-.05) prelimi-

The adoption studies reviewed above examined the effect of sharing a rearing environment without sharing any genes. Methods also exist that may shed light on the effects of a shared rearing environment but within the context of shared genes. Such designs compare relationships in which both genes and rearing environments are shared with relationships in which only genes are shared. One example of this behavior genetic design is the comparison of MZ twins reared together (MZT) with the rare MZ twins reared apart (MZA). MZA twin resemblance is attributable only to their shared genes because they share no environmental experience (assuming no selective placement), whereas MZT twin resemblance may be attributable to both shared genes and shared experiences. In such designs, the presence of selective placement for the reared-apart pairs would tend to underestimate the importance of shared environmental effects. The extent to which the resemblance of MZTs is greater than that of MZAs serves as an estimate of shared environmental influence within the context of shared genes. This is important to the extent that some family environments might be presumed to act only on genetically susceptible individuals. As presented in Table 3, MZT correlations average .80 for weight and .74 for BMI across studies. These figures do not differ appreciably between male and female pairs. Further-

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ENVIRONMENTAL INFLUENCES ON WEIGHT AND OBESITY

523

Table 1 Same- and Opposite-Sex Biological Siblings Reared Together Correlations for Weight and Obesity Measures Skinfold

Age range

Reference

n pairs

AgB/sex corrected

Wt

Wt/ht

BMI

Tricep

Subscap

.29

.28

.18 .18

.24 .26

.28

.28

Combined same- and opposite-sex biological siblings Tecumseh project Garn, Cole, & Bailey (1979)' Longini, Higgins, Hinton, Moll, & Keller (1984)' Biron, Mongeau, & Bertrand (1977) Savard, Bouchard, Leblanc, & Tremblay (1983) C. Bouchard, Savard, Depres, Tremblay, & Leblanc (1985) Province* Rao (1985) Total'

5-18 6-19 1-21 10-50 8-26

3,401 1,189

NA

2,813

Y N Y Y Y Y

1-21 1-21 6-19 5-50

2,893 80 4,002 3,771

Y Y Y Y

.34

Y Y Y Y Y Y N Y

.29 .49

7-62 6-12 18-39 20-62

12,002 194 4,720 204 168 101 74 1,204

3-62 7-62 1-62 1-62

12,743 1,372 17,065 5,063

N Y N N

.30

.53

7-62 6-12 18-39 20-49

190 145 112 84 429

Y Y N Y Y N Y

3-62 7-62 1-62

637 574 4,332

N Y N

80 NA 370

.36 .39

.37

.34

.30 .37 .32

Same-sex biological siblings Martin, Kurczynski, & Steinberg (1973) Susanne (1975) Gam & Clark (1976) Russell (1976) Mueller (1977) Mueller &Malina( 1 980) Kaur& Singh (1981) Heller, Garrison, Havlik, Feinleib, & Padget (1984) Total*

15-59 17-35 1-18

3

.39 .47 .45 .41

.25

.42

.39

.38

.38 .37 .23

.40 .24 .31

.26 .28 .29 .38

Opposite-sex biological siblings Susanne (1975) Garn & Clark ( 1976) Russell (1976) Mueller (1977) Mueller &Malina( 1980) Kaur& Singh (1981) Heller etal. (1984) 11

Total

17-35 1-18

3

106 3,991

.38 .53 .42 .35

.38

.37

.35

.38 .41 .17

.39 .32 .16

.37

.35

.09 .44 .16

Note. Studies with sample sizes less than 20 were omitted, as were reports earlier than 1970. Wt = weight, ht = height, BMI = body mass index, subscap = subscapular, N = no, Y = yes, NA = not available. The totals reported for each study represent averages computed across ages. • Based on overlapping samples. * Overall total denotes the average correlation across studies weighted by sample size. In the special case of longitudinal studies, an average correlation was calculated across ages for each study. This figure was then weighted by the average sample size (across ages) for each study. As a consequence of this procedure, some derived sample sizes and correlations may not total.

more, twins under 18 years old and those over 18 yield similar correlations. This is important as regards potential effects of shared experience, because although younger and older twins differ in their probability of currently living together, they do not differ in resemblance for weight. MZA twins are very rare; representative samples are difficult

1937; Price & Gottesman, 1991; Shields, 1962; Stunkard et al, 1990). Of particular importance is the recent large study reported by Stunkard et al. (1990) of BMI in older twins (mean age of 59 years old) from the registry-based Swedish Adoption/ Twin Study of Aging (SATSA; Pedersen, Friberg, Floderus-

to ascertain. However, excluding Cyril Hurt's reports (Hurt, 1966) because of their uncertain status, five major investiga-

Myrhed, McClearn, & Plomin, 1984). Table 4 lists the available correlations for weight and BMI among MZA pairs. MZA data for skinfolds are not available. Overall, across ages and sexes,

tions of weight in MZA twins have been published (T. J. Bouchard, Lykken, Segal, & Wilcox, 1986; Juel-Nielsen, 1980; MacDonald & Stunkard, 1990; Newman, Freeman, & Holzinger,

three studies that have reported MZA data separately for female and male pairs, female MZA correlations average .42 for

MZA correlations average .72 for weight and .62 for BMI. In the

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524

CARLOS M. GRILO AND MICHAEL F. POGUE-GEILE Table 2 Adoptive Siblings Reared Together: Correlations for Weight and Skin/olds Skinfold Reference Biron, Mongeau, & Bertrand(l977) Tecumseh project*" Gam, Cole, & Bailey (1979) Round I Round 11 C. Bouchard, Savard, Despres, Tremblay, & Leblanc(1985)

Age range

n pairs

Wt

Wt/M

1-21

138

.01

-.03

0-18 5-18

198 293

.31

8-26

80

Tricep

Subscapular

.32

.29

-.06

.19

.04

Note. All studies report interclass correlations. Female and male, same- and opposite-sex pairs included together for all studies. All studies were age and sex corrected. Wt = weight, ht = height. * Tecumseh Round I and Round II are longitudinal data on overlapping samples. b Tecumseh project includes both step and adopted siblings.

weight and .56 for BMI, which is lower than male MZA correlations, which average .89 for weight and .69 for BMI. These sex

BMI. For males, a small difference was found between DZT

differences are almost solely due to the findings from the smaller volunteer samples reported by Shields (1962) and T. J.

and DZA pairs (33 vs. .15), whereas for females these was essentially no difference (27 vs. .25). In summary, these comparisons of reared-together and

Bouchard et al. (1986) and are not found in the larger, more representative, registry-based SATSA sample (Stunkard et al.,

reared-apart twins suggest little effect of shared family experiences, even among younger twins who are likely to currently

1990). Furthermore, studies of MZTs (see Table 3) generally do not report sex differences in twin resemblance for weight.

live together. This conclusion is considerably strengthened by the recent findings from the large-scale registry-based SATSA sample Stunkard et al. (1990) that both answer many of the

These findings raise some doubt regarding the representativeness of the female MZA findings from the volunteer samples. Overall, MZT twins are remarkably similar to MZA twins in correlations for weight (.80 vs. .72, respectively) and BMI (74 vs. .62, respectively), suggesting little additional effect of shared rearing environment over that of shared genes. This remains the case for weight when only MZT twins under 18 years old are compared with MZA twins (.82 vs. .72). These overall findings are particularly true for males, for whom MZT and MZA correlations are quite similar for weight (.80 vs. .89) and BMI (74 vs. .69). However, as was mentioned above, probably because of unrepresentative samples, female MZT twins show higher average correlations than female MZAs for weight (86

vs. .42) and BMI (.68 vs. .56). This overall similarity across studies between MZT and MZA twins holds even more closely in the two studies that allow within-study comparisons between the two twin types (MacDonald & Stunkard, 1990; Price & Gottesman, 1991; Shields, 1962; Stunkard et al., 1990). In particular, the largest and most representative such study to date (Stunkaid et al., 1990) has reported essentially no differences in correlations for BMI between MZT and MZA twins (males, .74 vs. .70 and females .66 vs. .66). Similarly, the data gathered by Shields (1962) and its reanalyses (MacDonald & Stunkard, 1990) show no significant differences between MZT and MZA twins for BMI (.75 vs. .61, respectively; Price & Gottesman, 1991). In a final variation on this theme, one study (Stunkard et al., 1990) has also compared DZT and DZA twin correlations for

criticisms of previous MZA data and confirm earlier findings.

MZ and DZ Twins: An Indirect Estimate of Shared Environment To this point, estimates of the effects of shared rearing environment on weight and fatness have been relatively direct and have relied on few assumptions. However, there exists one other commonly used estimate, based on MZ and DZ twins, that is less direct. Its rationale is as follows: Because MZT twins share both 100% of their genes and their rearing environment and DZT twins share only 50% of their genes on average and their rearing environment, then the difference between MZ and DZ correlations for weight (rMZ — rDZ) reflects the effect of sharing 50% of one^ genes. Given this figure, the effect of a shared rearing environment can be calculated by subtraction. In the case of DZ twins, who share both their rearing environments and 50% of their genes, the difference between the observed DZ twin correlation (/j^) and the estimate of the effect of sharing 50% of one's genes alone (faz - roz) yields an estimate of shared rearing environment [r^ - (rMZ - rDZ) or, more simply, 2rDZ rMZ ]. This estimate assumes no genetic epistasis, genetic dominance, assortative mating, or difference between MZ and DZ twins in the importance of shared environments. Genetic epistasis occurs when the effects of genes at different loci are not simply additives and dominance refers to nonadditive effects among alleles at the same locus. The presence of either epistasis

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ENVIRONMENTAL INFLUENCES ON WEIGHT AND OBESITY

525

Table 3 MZT Twin Pair Correlations for Weight and Obesity Measures Skinfolds Reference Newman, Freeman, & Holzinger (1937) Shields (1962) MacDonald & Stunkard (1990)' Brook, Huntley, & Slack (1975)

Total Louisville twin studyb Wilson (1976)

Sex M, F

F M F M F F M M F M M, F

M,F M,F M, F

M,F Wilson (1979) Wilson (1986) Feinleibetal. (1977) Fischbein (1977)11

M, F

M,F M,F M F

F F F F F F M M M M M M M M M C. Bouchard, Savard, Despres, Tremblay, &Leblanc(1985) Stunkard, Foch, & Hrubec (1986)" Slattery et al. (1988) Abdel-Rahim, Nagoshi, & Vandenberg (1990) Stunkard, Harris, Pedersen, & McClearn (1990)

M, F

M M M M,F

Age bands

3-15 3-15 3-15

Birth 1 2 3 5 8 15 42-56 10 11 12 13 14 15 16 10 11 12 13 14 15 16 17 18 8-26

M, F M, F

F M F M F M

1-59 1-66 9-80+ 13-80+ 3-15 3-15

M, M, M, M,

F F F F

M,F

By sex

NA 9-59 13-53 13-53 9-59 13-53 3-10 11-15 3-10 11-15

15-28 40-53 22-66 12-19 21-80+ 21-80+ 1-66 1-80+ 3-26 18

M Totals"

Age range

Age/sex corrected

Wt

50 29 15

N N N

.92 .81 .79

25 14 24 16 20 18 40 38 78

N N Y Y Y Y Y Y Y

159 146 143 137 NA NA 86

N N N N N N N

.61 .87 .89 .89 .85 .88 .87

250 17

N Y

.79 .93

41 43 43 41 37 22 18 42 44 44 44 44 42 37 26 87

Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y

.92 .92 .92 .92 .88 .89 .76 .82 .84 .86 .86 .86 .86 .88 .92

1,974 1,974

.85 .74

77

N N Y

36 88

N Y

.84

66

Y N N Y N Y N N N N N N Y Y

« pairs

2,561 2,244

165 207 78 2,224 2,205 64 2,273 113 2,131

40 38

BMI

Tricep

Subscap

.55 .95 .48 .87

.61 .86 .84 .95

.80 .65 .72

.79 .89 .83

.77

.78

Obesity concordance

.76 .68

.81 .67

57% 60%

.76 .66 .74 .80 .74 .75

.80

.72

.83

.80 .65

.79 .89

.82 .74 .67 .86 .80 -.68

.74

Note. Correlations are based on available monozygotic twins reared together studies, except small case reports, Hurt's (1966) data, and studies not reporting data in terms of intraclass correlations (e.g, Bakwin, 1973; Borjeson, 1976; Liljefors, 1970; Medlund, Cederlof, Floderus-Myrhed, Friberg, & Sorensen, 1976). Wt = weight, BMI = body mass index, Y = yes, N = no. M, F denotes that male and female data are not reported separately. M and F denote male and female pairs, respectively " Reanalysis of Shields (1962) data. b Denotes longitudinal study. c Overall total denotes the average correlation across studies weighted by sample size. In the special case of longitudinal studies, an average correlation was calculated across ages for each study. This figure was then weighted by the average sample size (across ages) for each study. As a consequence of this procedure, some derived sample sizes and correlations may not total.

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526

CARLOS M. GRILO AND MICHAEL F. POGUE-GEILE Table 4 MZA Twin Inlraclass Correlations for Weight and Obesity Measures

Reference Newman, Freeman, & Holzinger(1937) Shields (1962)' MacDonald & Stunkard (1990)" Price & Gottesman (1991)b Juel-Nielsen (1980) T. J. Bouchard, Lykken, Segal, & Wilcox (1986) Stunkard, Harris, Pedersen, & McClearn (1990) Overall totals0 By sex

n pairs

Age range

F M F M

19 29 15 24 14

M, F

Sex

corrected

Weight

11-59 8-59 14-52 16-59 16-52

N N N N N

.89 .37 .87

34

16-59

Y

.63

M, F

12

22-77

N

.66

F M

23 17

NA NA

N N

.49 .91

F M

44 49

21-80+ 21-80+

Y Y

M, F M, F

105 131

11-77 8-80+

N N

.72

F M F M

52 32 68 63

11-77 11-77 8-80+ 8-80+

N N N N

.42 .89

M, F

BMI

.39 .64 .61

.66 .70 .62

.56 .69

Note. M, F denotes male and female pair data not reported separately. MZA = monozygotic twins reared apart, BMI = body mass index, N = no, Y = yes. • Shields's (1962) report includes several pairs of twins with physical problems. b Reanalyses using the BMI data of Shields's (1962) study. c Overall total denotes the average correlation across studies weighted by sample size.

or dominance leads to underestimates of shared environmental effects in the classical twin design. Similarly, if MZ twins shared more similar trait-relevant environments than DZ twins, this design would also tend to underestimate effects of shared environment. In contrast, homogamous assortative mating, in which similar-weight persons selectively mate, would tend to overestimate shared environmental effects. For more details on these issues, see Plomin, DeFries, and McClearn (1990).

tasis. Overall, these results are generally quite consistent with the more direct estimates reviewed above.

Spouses: Living Apart and Living Together Analysis of resemblance between spouses represents an additional design in which environmental experience is shared but genes are not. Spouses obviously share a different form of envi-

Table 5 contains the DZ twin results from the major twin

ronmental experience and at a later age than the experiences

studies. Overall, same-sex DZ twins reared together are correlated .43 for weight, .33 for BMI, .43 for tricep, and .32 for

shared, for example, by reared-together siblings and twins re-

subscapular skinfolds. There are no consistent differences in these figures for female and male same-sex pairs. Furthermore,

ing obviously complicates interpretation of such data as direct

there are no obvious differences in resemblance between twins who are under or over 18 years old.

viewed earlier. Furthermore, the possibility of assortative matevidence for the importance of shared environmental experience because any observed spouse resemblance may be due to

Based on these overall figures and those for MZT twins pre-

the fact that individuals marry others who resemble them in weight, rather than to any potential environmental effects of

sented in Table 3, the indirect estimates (2rDZ - /MZ) of the importance of shared rearing environment are .06 for weight, -.08 for BMI,. 11 for tricep, and -. 16 for subscapular skinfoids.

living together. Designs that evaluate duration of cohabitation are necessary to distinguish these two possibilities. First, let us examine the literature on the resemblance of

Similar estimates that are based only on twins under 18 years old, who are likely to be currently living together, are .34 for

couples who have not yet cohabitated. Any similarity observed in these studies can only be attributed to homogamous assorta-

weight, .26 for tricep, and —. 15 for subscapular skinfolds. Overall, these estimates, although mixed for the younger twins, are

tive mating (like marrying like), and not shared environmental experience. This estimate of assortative mating in newly formed couples therefore represents a benchmark for interpreting other

close to zero and suggest little importance for weight and fatness of sharing one's rearing environment. The occurrence of negative estimates may be due to sampling variations or violation of assumptions that would tend to underestimate shared environmental influences, such as genetic dominance or epis-

studies of cohabitating couples. Spuhler (1968), in a review of investigations of assortative mating, cited seven reports of mating with respect to weight. Overall, across those seven studies, the weighted average correlation for engaged couples (who were

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527

ENVIRONMENTAL INFLUENCES ON WEIGHT AND OBESITY

Table 5 Same-Sex DZ Twin Pair Correlations for Weight and Obesity Measures Skinfolds Reference Newman, Freeman, & Holzinger (1937) Shields (1962) Brook, Huntley, & Slack (1975)

Total

n pairs

NA 12-62 3-10 11-15 3-10 11-15 3-15 3-15 3-15

50 25 48 29 37 30 77 67 144

N N Y Y Y Y Y Y Y

.63 .56

F M

Birth 1 2 3 5 8 15 15

107 96 95 96 NA NA 26 30

N N N N N N N N

.70 .55 .55 .52 .48 .49 .33 .62

M F F F F F F F M M M M M M M M M

42-56 10 11 12 13 14 15 16 10 11 12 13 14 15 16 17 18

264 17 63 64 63 61 56 35 20 62 65 67 67 66 61 53 39

N Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y

.51 .66 .74 .69 .60 .46 .44 .23 .68 .69 .68 .71 .68 .61 .54 .62 .57

69 2,097 2,097 88 24 119 89 2,590 2,393 213 130 144 2,361 102 2,447 119 89 77 67

Y N N Y N Y Y N N Y N Y N N N Y Y Y Y

Sex M,F F F F M M F M M, F

Louisville Twin Study' Wilson (1976)

Wilson (1979)

M, F M, F

M,F M,F M,F M, F

Wilson (1986) Feinleib et al. (1977) Fischbein(1977)'

C. Bouchard, Savard, Despres, Tremblay, & Leblanc(1985) Stunkard, Foch, & Hrubec (1986)"

M, F

Slattery et al. (1988) Abdel-Rahim, Nagoshi, & Vandenberg (1990) Stunkard, Harris, Pedersen, & McCleam (1990)

M, F

Overall totals" Age bands By sex

Age/sex corrected

Age range

M M M F M M,F M, M, M, M, M,

F F F F F

F M F M F M

8-26 15-28 42-56 22-66 12-19 21-80+ 21-80+ 1-66 1-56 3-26

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