Do Consumers’ Genes Influence Their Behavior? Findings on Novelty Seeking and Compulsive Consumption


Elizabeth C. Hirschman and Barbara B. Stern (2001) ,"Do Consumers’ Genes Influence Their Behavior? Findings on Novelty Seeking and Compulsive Consumption", in NA - Advances in Consumer Research Volume 28, eds. Mary C. Gilly and Joan Meyers-Levy, Valdosta, GA : Association for Consumer Research, Pages: 403-410.

Advances in Consumer Research Volume 28, 2001     Pages 403-410


Elizabeth C. Hirschman, Rutgers University

Barbara B. Stern, Rutgers University


Throughout its history, consumer research has progressed by unpacking a series of "black boxes"; that is, by delving into those aspects of consumption that once had appeared impenetrably complex. The present paper examines one of the last remaining such frontiersCconsumers’ genetic heritage, believed by many researchers in neuropsychology to account for approximately half of the variance in human behavior (see e.g. Bouchard 1994; Bouchard et al 1990a,b; Copeland and Hamer 1998; Kagan 1994; Wright 1998). The debate within the social sciences as to whether nature (i.e., genetics) or nurture (i.e., cultural influences) is the predominant cause of human behavior has recently been reignited by a series of studies indicating the large and direct role genetic heritage plays in the lives of individuals (Wright 1998; Zuckerman 1995).

Our intent is to review critically the burgeoning literature in neuropsychology and relate it to two important aspects of consumer behavior (1) the exploratory activities of novelty seeking, innovativeness and sensation seeking and (2) impulsive and compulsive consumption. As we shall show, these two aspects of consumption appear to be the result of the same underlying genetic structure. Our paper develops a longitudinal model of the development of these two characteristics and shows how they are additionally linked to Attention Deficit Hyperactivity Disorder and High Risk Leisre Consumption.


At the present time, most genetic research on human behavior employs the theory and method of quantitative genetics. Quantitative genetics is capable of identifying genetic influence even when multiple genes and significant environmental effects are present (Plomin 1991). This method determines the sum of hereditable genetic influence on a given human trait, regardless of the genetic interactions or the number of genes influencing the behavior. Several behaviors related to consumption have been found to be substantially shaped by genetics.

For example, studies of twins have found estimated genetic influence to range from .52 for general intelligence (i.e., cognitive ability) to .28 for the personality traits of agreeableness and conscientiousness. Studies have also provided evidence as regards the influence of family socialization on behavior. For example, for the five primary personality traits of extraversion, agreeableness, conscientiousness, neuroticism and openness, genetic hereditabilities were estimated at .36, .28, .28, .31, and .46 respectively, while the common environmental component was found to be .00, .09, .04, .05 and .05 for the same five dimensions (Loehlin 1992). Thus, shared home environment appears to have little effect on most human (and presumably, consumer) behaviors (Bouchard 1994).

Molecular Genetics. Increasingly, genetics researchers are supplementing large-scale quantitative studies of general genetic hereditability with more precise, finely tuned studies aimed at identifying the genes or gene systems responsible for observed genetic differences in behavior.

Genetic linkage studies attempt to identify defects in a single gene which cause particular abnormalities. Disorders such as Huntington’s disease result from just such a single-gene defect and carriers may be identified by testing (Plomin, Owen and McGuffin 1994). Single-gene defects have also been implicated in bipolar disorder (manic-depression), but results are not yet conclusive (Wahlsten 1999). However, many traits relevant to consumer behavior are not linked to a single gene, but rather to several genes, each of which may play a role in the behavior (Plomin, Owen and McGuffin 1994). Indeed, many consumer behavior disorders are now viewed by geneticists as normally distributed traits that most persons will exhibit in moderation, while a few will exhibit at extreme levels. For example, impulse buying and drug addiction are now believed to result from extreme manifestations of normally distributed pleasure seeking traits (McGue and Bouchard 1998). Genes that contribute to the genetic variance in these behavioral traits are termed quantitative trait loci (QTL) [An earlier term for QTL was polygenic, meaning that many genes contributed to the observed traits.] (Wahlsten 1999). QTL studies search for particular versions of a gene (termed alleles) that are differentially associated with a given trait (Wahlsten 1999). For example, certain alleles of two neurotransmitter genes have been found associated with impulse purchasing and drug addiction, along with several other forms of compulsive consumption. This phenomenon is also termed allelic association and linkage disequilibrium (Ball et al 1997; Plomin, Owen, & McGuffin 1994).


From a consumer behavior standpoint, probably the most important site of genetic influence is in the brain. The human brain is a highly complex organ composed of approximately 100 billion neurons, a specialized class of cells anatomically and chemically designed for intercellular communication (Barondes 1993; Carlson 1995). Neurons come in diverse shapes and sizes, making possible numerous patterns of interaction. The basic shapes and branching patterns of neurons and the slection of the partners with which they form synapses are largely determined by the genes that control nervous system structure (Cooper, Bloom and Roth 1991). This is the mechanism by which genetics influences consumer behavior (see e.g., Kolb and Whishaw 1995, 1998).


The complexity of interneuronal transmission is increased dramatically by the existence of many different neurotransmitters, each having distinctive chemical properties. Several are amino acids, including glutamate, the primary excitatory neurotransmitter, and glycine and GABA, the major inhibitory (i.e., retarding) neurotransmitters. Others are monoamine derivatives of amino acids, including dopamine, norepinephrine, and epinephrine, collectively called the catecholamines, which originate from the protein tyrosine. A fourth neurotransmitter, serotonin, is derived from tryptophan. These four monoamines are of great importance to consumer behavior as they are believed to influence one’s emotional state, as well as experiences of fear and pleasure (see e.g. Carlson 1995). Another group of substances involved in synaptic communication is the neuropeptides. Among the most significant of these for consumer behavior are the endorphins, which play a role in pain perception. Their actions are mimicked by some widely abused drugs, such as morphine and heroin (see Carlson 1995).

When neurotransmitters are released into the synaptic cleft, they create their effects by binding to receptors on the postsynaptic neuron. To stop this action, the neurotransmitter must be removed from the receptors, either by chemical degradation (decomposition) of the neurotransmitters or by pumping the neurotransmitter molecules back to the neuronal terminal that released them. The catecholamines and serotonin are removed by the latter process, which is termed reuptake (see e.g. Barondes 1993). Several recent anti-depressant drugs (e.g., Prozac, Zoloft) inhibit this reuptake process in order to elevate the mood of depressed persons (see e.g., Zuckerman 1994,1995).

Brain Plasticity and Gene Expression

Brain structure can adapt as a result of experience over the consumer’s lifetime (Kolb and Whishaw 1995). It is believed that experience leads to the observed brain structural differences by altering gene expression; this is the degree to which a given gene is able to act upon the physical aspects of the individual. As Kolb and Whishaw (1998) observe, "there is ample evidence that the expression of genes in the mature brain is influenced by environmental and behavioral events...Gene expression thus provides a mechanism whereby [neuronal] cells can synthesize new proteins needed to form more synapses...[Neuronal] activity initiated by experience or behavior could therefore increase the activity of genetic mechanisms responsible for dendritic and synaptic growth and, ultimately, behavioral change (p. 60)."

Although each of us is born with a full set of genes, not all are operative at any one time (Tully 1997). Some genes are activated only at specific stages of the life span, while others may became inactivated over time (Pederson et al 1992). Environmental influences, such as those studied by consumer researchers [For example, the relationship between conformist tendencies and dysfunctional consumer behaviors such as alcohol consumption and drug addiction (Rose, Bearden, and Teel 1992) has been studied primarily among young people-high school and college students. Although this relationship was found to be robust across adolescence and young adulthood, the absence of longitudinal studies does not allow for possible developmental variations in comorbidity.] vary throughout the life span. If only a single set of genes operates throughout one’s development, while environmental effects are accumulated over time, we would expect to see a decrease in the hereditability of behavioral traits over one’s life. However, contrary to this "accumulated environment" thesis, many significant behaviors have been found to exhibit increased hereditabilty (i.e., genetic influence) as one ages, up to at least mid-life (see e.g. Pederson et al 1992). For example, general cognitive ability has been found to be 80% genetically determined at age 65, while it is about 50% genetically determined in adolescence (Pederson et al 1992).

How does this contrary result come about? As Plomin and Bergeman (1991, p. 373) state, "In the traditional stimulus-response model, the environment is independent of the organism. It is something imposed on the organism from the outside...This view allows no role for DNA, because the organism has [no control over] the environment that impinges on it." What this simple S¦R model overlooks, Plomin and Bergeman note, is that an organismBguided by its geneticsBcan actively manipulate its environment, making the environment more compatible with its inborn traits and tendencies (Scarr 1992, 1997). Thus, over time the environment surrounding the organism becomes more genetically determined, rather than the organism becoming more environmentally determined (Scarr and McCartney 1983; McGue et al 1993).

Researchers have identified three distinct types of interactions that can occur between an individual’s genetic structure and the environment:

(1) Passive interaction occurs when children inherit from their parents a family environment that is linked to their familial genetic propensities. (For example, intelligent parents may provide more books for their intelligent child). Thus, high cognitive ability in the parents and child is not caused by the presence of books, rather the presence of books is caused by genetically high cognitive ability in the parents and child.

(2) Reactive interaction refers to the experiences of children resulting from others’ reactions to their genetic propensities. For example, a child whose anti-social behavior is caused by hereditary factors may cause others (e.g., parents, teachers) to treat him/her negatively, thus further exacerbating the anti-social trait.

(3) Active interaction occurs when people select, modify or create experiences as a result of their hereditary traits (Plomin 1995). For example, a novelty-seeking consumer may surround him/her self with new, interesting products.

With this background, we now turn to two consumer behavior applications: novelty seeking and impulsive/compulsive consumption. As we shall see, these two disparate areas of consumption are not only genetically influenced, but also integrally linked.


Although novelty seeking (Hirschman 1981), sensation seeking (Raju 1980, Zuckerman 1983, 1994, 1995) and innovativeness (Rogers 1995) have long been topics of interest to consumer researchers, it is only within the past few years that a possible genetic and neuropsychological basis for this behavioral pattern has been discovered. All three of these consumer behavior traits are characterized by high levels of exploratory behavior (i.e., venturesomeness) in hopes of finding potentially rewarding stimuli (Cloninger 1987; Zuckerman 1983, 1994, 1995). Cloninger et al (1993, 1996) proposed that individual variations in innovativeness, sensation seeking and novelty seeking are mediated by genetic variability in the transmission of the neurotranmitter, dopamine.

Thus, it was empirically encouraging when a 1996 study, (Ebstein et al) reported that high scores on the Cloninger Novelty Seeking Scale [Individuals who score higher on Cloninger=s TPQ Novelty Seeking scale are impulsive, exploratory, excitable, quick-tempered and extravagant, whereas those who score lower are characterized by being cautious, rigid, stoic, slow-tempered, and frugal (Cloninger 1987, et al 1996, 1993; Plomin et al 1994).] "are significantly associated with...the 7-repeat allele in the locus for the D4 dopamine receptor gene (D4DR)" (p. 78), a finding that "provides the first replicated association between a pecific genetic locus involved in neurotransmission and a normal personality trait (p. 78)." [Not all studies have replicated this finding, see e.g., Chang et al 1997.] Insofar as the 7-repeat allele has a longer string of proteins that can serve as binding sites for the dopamine neurotransmitter, consumers carrying this allele exhibit a different pattern of dopamine reception than do other consumers. This variation in dopamine utilization causes them to exhibit novelty seeking behavior, likely as a means to generate additional internal production of dopamine, which serves as a chemical #reward’ by stimulating pleasure-responding areas of the brain. Indeed, novelty seekers experience "exhilaration or excitement in response to novel stimuli" (Benjamin et al 1996); thus, the discovery of a novel product would stimulate a pleasurable response in a novelty seeking/innovative consumer. The broad hereditability of novelty seeking has been found to be 41% in twin studies, hence there is ample room for genetic causation.

In addition to the D4DR allele already discussed, a second dopamine receptor gene has also been found related to innovativeness, novelty seeking and sensation seeking. The A-1 allele of the DRD2 dopamine receptor gene has also been linked to these exploratory traits (McGue and Bouchard 1998). This allele causes fewer than normal dopamine receptor sites to be present in the brain. In order to stimulate additional dopamine production, the individual seeks out new and exciting experiences, which then create a sense of pleasure due to the enhanced levels of dopamine. Thus, consumer innovators are stimulated, in part, by their genes to seek out new products.

Research on the dopamine receptor genes has opened up an additional avenue of research with direct relevance to consumer behaviorBthat of the origins of compulsive consumption.


Impulsive Consumption. Since Rook’s work in the mid-1980’s (Rook 1987), impulsive consumption has been of interest to consumer researchers. Impulse purchasing appears to be a widespread phenomenon in America, with an average of 38 percent of adults in national surveys conducted between 1975 and 1992 responding affirmatively to the statement, "I am an impulse buyer" (DDB Needham Annual Lifestyle Survey,1974-1993). In recent research, impulse buying has been defined as "a consumer’s tendency to buy spontaneously, unreflectively, immediately and kinetically...their thinking is likely to be relatively unreflective, prompted by physical proximity to a desired product, dominated by emotional attraction to it, and absorbed by the promise of immediate gratification (Rook and Fisher 1995 p. 306)". This response pattern bears much in common with Cloninger’s definition of novelty seeking. And there is yet another related behavioral pattern, as well. Ratey and Johnson (1997) suggest that a large proportion of impulse purchasing is due to mild to moderate adult levels of Attention Deficit Hyperactivity Disorder (ADHD), which is highly hereditary (60%), (McGue and Bouchard 1998). As adults, persons exhibiting Attention Deficit Hyperactivity Disorder are impulsive in their behavior and easily distractible by external stimuli. ADHD is caused by slower than average metabolism in the frontal lobes of the brain, the region responsible for controlling attention and motor behaviors, as well as impulses. Persons with ADHD metabolize glucose at a rate 10 to 12 percent below average; this low rate of metabolism makes it difficult for them to control their behavioral impulses and easily distractable by nearby stimuli, such as a varied array of products (Cook et al 1995).

The below average frontal lobe activity in ADHD accounts for the ability of stimulant medications such as Ritalin and Dexedrine to reduce impulsivity. Once metabolism is increased to normal levels via stimulants, the frontal lobes are able to exert control over behavior. Significantly, the chemical mechanism throughwhich this is accomplished is an increase in the levels of the neurotransmitters dopamine and norepinephrine (Ratey and Johnson 1997).

Consumers with ADHD also exhibit a strong tendency to utilize cocaine, caffeine and nicotine (i.e., cigarettes), because these stimulant drugs act to increase dopamine and norepinephrine levels (Volkow et al 1993). Ratey and Johnson (1997) point out that "Adults with frank cases of ADHD are notorious risk-takers; they are attracted to any situation that shocks the brain (p. 196)". Thus, it is likely that at least a portion of the high-risk leisure consumption described by Celsi, Rose and Leigh (1993)Bas well as novelty seeking, sensation seeking and innovativenessCis attributable to ADHD. If this reasoning is correct, we would anticipate a positive correlation among ingestion of central nervous system stimulants (cocaine, tobacco, caffeine), impulsive purchasing, novelty seeking, and high-risk leisure consumption, as all are linked to consumers’ efforts to increase frontal lobe activation by enhancing dopamine and norepinephrine levels. And indeed, in recent genetic linkage studies this connection has been found (Battaglia et al 1996).

This constellation appears to be traceable, in part, to the neurological effects of the designated alleles in the D4DR and D2DR dopamine receptor genes. Alleles of these genes, which result in reduced numbers of dopamine receptors in the consumer’s brain, leave him/her in a reward deficient state (Blum et al 1995, 1996); to compensate for this, these consumers may engage in stimulating, high risk activities, seek out new and different products, purchase on impulse and ingest legal and/or illegal stimulants (e.g. cocaine, caffeine, nicotine, chocolate).

These genetically dopamine-deficient consumers also typically experience feelings of anger, aggressiveness, hyperactivity, irritability or defiant behavior when/if their dopamine levels fall. To remedy these unpleasant feelings, they usually seek out stimulation and/or ingest substances which will alleviate their emotional distress. Thus, Blum and his colleagues (Blum et al 1996; Blum, Briggs and Trachtenberg 1989; Blum and Kozlowski 1990; Blum and Noble 1994; Blum et al 1990) proposed that genetic dopamine deficiencies are responsible, in part, for a host of compulsive consumption disorders, ranging from drug abuse to obesity to compulsive purchasing. The next section discusses the empirical evidence supporting their proposal.

Compulsive Consumption.

Research from the late 1980’s and early 1990’s has suggested that the phenomenon of compulsive consumption is generalized across several domains, including drug abuse (Hirschman 1992), compulsive purchasing (O’Guinn and Faber 1989), binge eating (Braun, Sunday and Halmi 1994; Castonguay, Eldredge and Agras 1995; Faber, Christenson, Zwaan and Mitchell 1995), alcoholism (Blum and Noble 1994), kleptomania (Marlatt et al 1988), and bulimia (Krahn 1991). For a given consumer, various forms of compulsive consumption may occur simultaneously or may be manifest in a serial fashion.

Since 1970 a series of studies (Blum, Briggs and Trachtenberg 1989; Blum and Noble 1994; Blum et al 1996; Comings et al 1991; Lawford et al 1995; Noble et al 1991) has confirmed that a very high proportion of severe alcoholics carry the A-1 allele of the D2DR gene. This allele is relatively common, appearing in 20% to 25% of the general population (Ratey and Johnson 1997). However, genetic linkage research has found that this same allele is disproportionately present in persons having a variety of compulsive consumer behaviors. For example, it is found in 51% of cocaine addicts and in 80% of persons addicted to cocaine who also exhibit other forms of substance abuse (Comings et al 1994). Further, among compulsive eaters, the allele is found 50 percent of the time, (Bouchard 1995) and rises to 87% when the compulsive eater is also a substance abuser (Blum et al 1996). Among pathological gamblers, the allele’s presence is 51%; among those pathologicl gamblers who are also substance abusers, the rate rises to 80% (Blaszczynski, Wilson and McGonaghy 1986). In general, the more severe the addictive behavior, the greater the likelihood that the consumer carries the A-1 D2DR allele (Comings et al 1996a, b, c).

Additional research (Copeland and Hamer 1998) revealed that this same allele was often present in persons exhibiting Obsessive-Compulsive Disorder (OCD). This was a theoretically satisfying finding, because addictive behaviors share an underlying compulsive quality (see O’Guinn and Faber 1989). Further, recent research has indicated that the D4DR allele found associated with novelty seeking is also present in some alcohol and heroin dependency (Sander et al 1997; Muramtsu et al 1996; Li et al 1997). Recall that this allele, like D2DR, is believed to be a genetic source of lowered dopamine synthesis in the brain.

These findings are of great importance to consumer behavior because staggering numbers of consumers are estimated to use illicit drugs on a monthly basis, likely in an effort to alter their deficient dopamine levels. According to Nash (1997), in a given month 200,000 consumers use heroin, 800,000 use amphetamines, 1.5 million use crack/cocaine, 10 million use marijuana, 11 million will become drunk on alcohol, 61 million acquire nicotine via cigarettes, over 130 million consume caffeine, and millions more overeat [Some obese consumers eat large quantities of carbohydrates (termed >carbohydrate craving=) in order to boost their dopamine levels. In the digestive system, carbohydrates are transformed to glucose, which stimulates dopamine production.] buy compulsively or engage in pathological levels of gambling. The empirical data suggest that these consumers are bound together by a common genetic bondCpossession of the D2DR and/or the D4DR allele, as well as others as yet unidentified, in a QTL system (see e.g., Black 1996, Black et al 1998).

Thus, the research conducted within neuropsychology leads us to reformulate our views of both innovativeness/novelty seeking and compulsive consumption. At a biological level, these two distinct forms of consumer behavior appear to be integrally related. Both appear genetically tied to below normal levels of dopamine which lead to higher levels of environmental scanning for stimulation, above average environmental distractibility (due to lowered ability to remain internally focused, i.e., ADHD) and a lack of impulse control.

Copeland and Hamer (1998, pp 30-32) describe aspects of this systematic linkage in their description of Novelty Seeking behavior:

High novelty seekers find pleasure in varied, new, and intense experiences. They are not necessarily fond of risk, but they are willing to take risks for the reward of the new sensation...

Although novelty seeking is a single temperamental trait, it can be expressed in many different ways. Physical thrill seeking includes the desire to participate in dangerous sports such as mountain climbing, surfing, or skydiving. Experience seeking [refers to the fact that] novel stimuli can be mental or social. New sensations can be found through the mind and senses, such as through avant-garde music and art, exotic travel, or counter-culture experiences. High scorers get excited about new ideas; they are unconventional or innovative.

Disinhibition and impulsiveness are the final dimensions of novelty seeking and are the most important to the real-life problems of drinking, drug use, risky sex, and gambling. [Novelty Seekers] cannot control their impulses. [They] live at the edge.

The research reviewed can be summarized by the relationships depicted in Figure 1. A complex QTL system of interrelating genes is the origin of novelty seeking behavior. Thus far, two members of this QTL system, specific D2DR and D4DR alleles, have been identified, but many more are likely operant. These are currently being searched for using genetic linkage techniques (see eg. Gelernter et al 1997; Kidd 1996). During early childhood, and continuing into adulthood, consumers carrying this Novelty Seeking QTL system will exhibit not only heightened levels of exploratory behavior (i.e., novelty seeking, sensation seeking, innovativeness, variety seeking, etc.), but wil also typically be characterized by Attention Deficit/Hyperactivity Disorder.

By adolescence, these consumers will be engaging in various forms of compulsive consumption (likely mediated by social norms, Rook and Fisher 1995), as well as impulse purchasing, innovativeness and #high risk’ leisure consumption activities. As adults these same consumers will migrate into relatively stable patterns of impulsive, compulsive, innovative and excitatory consumption, consistent with their genetic heritage. (Recall the extensive findings that genetic influence increases through mid-life). Thus, genetics research provides us with an answer to a question we have never been able to satisfy before regarding innovativeness, impulse purchasing and compulsive consumption: Why do some, but not all, consumers manifest these behaviors excessively? The answer suggested by the present empirical evidence is that the consumers who do exhibit these behaviors in an extreme fashion are those whose genetic structure impels them to do so.

Some Consumer Welfare Issues

The fact that consumption phenomena such as impulsive purchasing, substance abuse, novelty seeking, and high risk leisure activities are genetically influenced confronts us with the need to rethink our notions regarding free will and consumer behavior. Virtually all consumer behavior models have been premised upon the assumption of free will; that is, that persons are born into the world with the primary responsibility for their consumption decisions, and that they possess the ability to reason and to choose in a rational fashion. Indeed, perhaps the most influential theory of consumer behavior, Bettman’s information processing model (1979), assumed the primacy of rational cognitive processes controlling consumer choice. Although this framework has been substantially modified in recent years to accommodate emotional factors (Bettman, Luce and Payne 1998), the discovery of specific alleles associated with novelty seeking and compulsive consumptionBas well as the documented hereditability of general cognitive ability and common disorders such as ADHD and obesityCchallenge the notion that all consumers are able to control their actions and choices. Clearly, we do not all start at the same genetic base-line for consumer behavior, do not all have the same cognitive or emotional structures to guide our decisions, and do not all have the same predispositions for constructing preferences and comparing alternatives.

Given that our heredity will affect our behaviors within and upon the consumption environment, how are we to deal with those whose genotypic endowment encourages impulsive or compulsive behaviors? Should those consumers bearing, say, D2DR A-1 alleles be freed from the responsibility for their impulsive actions if they go on a shopping binge? Schwartz and his colleagues (Schwartz et al 1996; 1997) have recently presented very encouraging results in their work with persons having obsessive-compulsive disorder (OCD), which is associated with the same genetic pattern underlying novelty seeking and impulsive purchasing. OCD responds not only to medication (Prozac), but also to cognitive treatment as well. Schwartz has found that once OCD patients are made aware of the genetic/structural anomolies associated with their condition, they often can utilize behavior modification therapy to overcome or at least control the disorder. Most significantly, the treatment, which consists of both cognitive and behavioral exercises, has been shown to alter metabolic activity in the key brain structures believed responsible for the disorder. In essence, as Schwartz et al (1997) note, consumers can use their minds to change their brains. Thus, consumers are not hopelessly bound by their genetic traits.

Yet, as Schwartz et al (1996; 1997) also found, not all OCD sufferers were able to fully eradicate their compulsions. It appears that while the mind can help the brain deal with its predispositions, it cannot always overcome them. This confronts consumers with the responsibility for leaning as much as possible about their inborn tendencies. This need not involve direct biological testing, as reliable survey instruments are available (Bucholz et al 1994). Knowledge of one’s innate behavioral predispositions can be used auspiciously to help guide one’s life. With such awareness each of us can best develop our strengths and best control our weaknesses, as consumers and as human beings.






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Elizabeth C. Hirschman, Rutgers University
Barbara B. Stern, Rutgers University


NA - Advances in Consumer Research Volume 28 | 2001

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