Nutrition and Violent Behavior

Robin B. Kanarek

INTRODUCTION

The concept that nutrition can affect behavior is not new. For thousands of years, people have believed that the food they eat can have powerful effects on their behavior. Some foods have been blamed for physical and mental ills, whereas others have been valued for their curative or magic powers. Within this framework, a variety of ideas about the association between food and antisocial behavior have arisen. For example, many primitive societies believe that an individual takes on the characteristics of the food that he/she consumes. Thus, eating aggressive animals (e.g. lion) is associated with belligerent behavior, whereas eating timid creatures (e.g. rabbit) is identified with less hostile acts.

The belief that certain foods can lead to antisocial or aggressive behavior is not limited to primitive societies. In this country, the idea that food affected behavior was an integral part of the nineteenth century health reform movement. The concept that ''you are what you eat" was fundamental to the movement. Diet was believed to determine not only health and disease, but also spirituality, mental health, intelligence, and temperament. The health reform movement produced persuasive leaders who charmed

Robin Kanarek is at the Department of Psychology, Tuffs University.



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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences Nutrition and Violent Behavior Robin B. Kanarek INTRODUCTION The concept that nutrition can affect behavior is not new. For thousands of years, people have believed that the food they eat can have powerful effects on their behavior. Some foods have been blamed for physical and mental ills, whereas others have been valued for their curative or magic powers. Within this framework, a variety of ideas about the association between food and antisocial behavior have arisen. For example, many primitive societies believe that an individual takes on the characteristics of the food that he/she consumes. Thus, eating aggressive animals (e.g. lion) is associated with belligerent behavior, whereas eating timid creatures (e.g. rabbit) is identified with less hostile acts. The belief that certain foods can lead to antisocial or aggressive behavior is not limited to primitive societies. In this country, the idea that food affected behavior was an integral part of the nineteenth century health reform movement. The concept that ''you are what you eat" was fundamental to the movement. Diet was believed to determine not only health and disease, but also spirituality, mental health, intelligence, and temperament. The health reform movement produced persuasive leaders who charmed Robin Kanarek is at the Department of Psychology, Tuffs University.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences their followers with their oratory and their own brand of proselytism. Two of the most prominent leaders of this movement, Sylvester Graham (remembered best for the development of the graham craker) and John Harvey Kellogg (recognized for the introduction of precooked breakfast cereals), lectured widely throughout this country promoting the use of natural foods and decrying the ingestion of meat, which they believed would lead to the deterioration of mental functioning and the arousal of animal passions (Whorton, 1982). Kellogg further concluded that the breakdown products of meat acted as dangerous toxins that, when absorbed from the colon, produced a variety of symptoms including depression, fatigue, headache, and aggression. Kellogg wrote that "the secret of nine-tenths of all chronic ills from which civilized human beings suffer" including "national inefficiency" and "moral and social maladies" could be traced to the meat eater's sluggish bowels (Kellogg, 1919:87). In keeping with his puritanical background, Kellogg also warned his followers that spicy or rich foods would lead to moral deterioration and acts of violence (Kellogg, 1882:244–245). The foregoing historical information should not be seen as simply humorous background material. Ideas about food and behavior continue to be prevalent. The last decade has witnessed an explosion of interest in the field of nutrition and behavior. The current obsession with health and fitness, as well as the desire to use diet as a panacea, has led to a myriad of dietary "self-help" books. Unfortunately, the consumer's desire for simple answers to complex questions has often led to misinterpretation or even misrepresentation of scientific data. Correlational data have been interpreted as signifying cause and effect relations. With the public spotlight focused so strongly on the area of nutrition and behavior, it is crucial that research in this area be based on proper methodology and careful interpretation of data. This is particularly true for studies examining the relationship between diet and antisocial behavior because policy decisions may be made on the basis of this research. RESEARCH ON DIET AND BEHAVIOR METHODOLOGICAL ISSUES One of the more difficult problems in research on diet and behavior is how to separate nutritional from nonnutritional factors. Because food is so intimately involved with other aspects of our daily lives, it contains much more than its obvious nutritional

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences value. Food is an intrinsic part of social functions, religious observations, and cultural rituals. Because food is a "loaded" variable, both experimenters and subjects may harbor biases about expected research outcomes. To minimize the confounding effects of these biases, double-blind procedures in which neither the experimenter nor the subjects know what treatment is given must be used. In general, research on nutrition and behavior would benefit from the methodological controls used in psychopharmacology (Dews, 1986). Two variables that are important in drug studies are dose and length of treatment. Because consumption of a small amount (dose) of a dietary component may produce behavioral effects that differ from consumption of a larger amount, several doses of a dietary component should be tested whenever feasible. By using different doses, researchers can determine if there is a systematic relationship between the dietary variable and behavior. The lack of a systematic effect should be taken as a danger sign either that the apparent effect is spurious or that the variability is greater than expected. The duration of dietary treatment is also critical. Although short-term (acute) studies permit evaluation of the immediate effects of a dietary treatment, they cannot provide information about long-term (chronic) exposure. Because the behavioral effects of dietary components (e.g., food additives) may only appear with extended exposure, both acute and chronic studies should be used to assess the nutrition-behavior interaction. Diurnal variations in subjects' responses to nutrients should also be considered in diet-behavior studies. For example, it was recently observed that a snack (candy bar or yogurt) significantly improved subjects' ability to pay attention to relevant stimuli when it was eaten in the late afternoon, but not when it was consumed in the late morning (Kanarek and Swinney, 1990). Prior nutritional status also has the potential of influencing the results of acute experiments. The types and amounts of foods previously consumed can affect the metabolism of a test nutrient. Standardizing dietary intake prior to evaluating the behavioral consequences of a test nutrient can eliminate this source of variation. Another challenge in planning nutrition and behavior experiments is choosing appropriate subjects. Differences in nutritional history, socioeconomic background, and other environmental factors create subject heterogeneity that poses a threat to the internal validity of the research. Internal validity concerns the ability

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences to conclude that a causal relationship exists between an independent and a dependent variable. Because of subject heterogeneity, alternative explanations may exist for the observed experimental effects, which lowers internal validity. For example, research on the dietary treatment of hyperactive children has shown that the home environment can affect the results of a study. Children from an unsupportive home environment show much less improvement with dietary treatment than children from a more supportive home environment (Rumsey and Rapoport, 1983). Finally, the external validity of experimental findings must be considered. For example, the behavioral effects of a nutritional variable, observed in male college students, and tested in a laboratory during a single test session, may have little to do with the behavior of the general public in its everyday lives. Researchers face a dilemma in trying to choose between a controlled but artificial laboratory setting and a "real" or naturalistic setting that may be full of confounding factors. "Quasi-natural" studies, which could capture the advantages of both the laboratory and the real world, should be considered (Kanarek and Orthen-Gambill, 1986). EXPERIMENTAL STRATEGIES Three primary strategies have been used in research on diet and behavior. Correlational studies have been employed for generating hypotheses about diet-behavior relationships. The major objective of these studies is to define a link between dietary intake and behavior, with the specific expectation that statistical associations will be derived between the two variables. This type of research can provide important insights for experimental evaluation of the diet-behavior relation. There are, however, several conditions that must be met before the validity of a correlational study can be accepted. First, reliable and valid measures of dietary intake must be made. One of the most widely used approaches for assessing dietary intake is the 24-hour recall in which subjects are asked to record everything that they have consumed during the preceding day. However, because there are wide day-to-day variations in an individual's food intake, a 24-hour record may not provide an accurate determination of average food intake. As a result, it has been suggested that a minimum of seven 24-hour recalls be used (Anderson and Hrboticky, 1986). Second, proper subject sampling techniques must be used. In general, the larger the number of subjects, the better. If the number

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences of subjects is too small, the probability of observing a significant relation between a dietary variable and behavior is reduced, and a false negative association may be assumed. On the other hand, correlation studies using large numbers of subjects risk the possibility of false positive associations. For example, when correlations are made between several dietary variables and behavior, the chance of achieving statistically significant results increases with the number of subjects and with the number of correlations made. In addition, when large numbers of subjects are used, small correlations can become statistically significant, making it necessary for the researcher to decide on the clinical importance of such results (Anderson and Hrboticky, 1986). A common method of subject selection used in studies of diet and behavior involves the placement of media advertisements. Although this method is convenient, such sampling increases the probability of including self-selected members of the general population. For example, if a researcher wants to test the hypothesis that sugar influences hyperactivity in children and advertises the study as such, the subjects may be derived predominantly from families in which parents believe such an association exists. Finally, cause and effect relations cannot be established from correlational data. For example, positive correlations have been reported between sugar intake and hyperactive behavior in children. These results have been interpreted by some (especially in the popular media) as demonstrating that sugar causes hyperactivity. However, it is just as possible that high levels of activity increase sugar intake or that a third unidentified variable influences both sugar intake and hyperactivity. In contrast to correlational studies, experimental studies have the potential of identifying causal links between diet and behavior. The manipulation of a specific dietary component (the independent variable) may alter the occurrence of a behavioral measure or cognitive function (the dependent variable). Two major paradigms have been used in these studies. In dietary replacement studies, the behavioral effects of two diets, one containing the food component of interest (e.g. food additives) and the other not containing that food component, are compared over some period of time (e.g. two to three weeks). One obvious advantage of this method is that chronic dietary effects can be assessed. However, because making two diets equivalent in all factors except the food component being studied is difficult, it may be impossible to use appropriate double-blind techniques. Another limitation

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences is that it is not feasible to test more than one dose of the dietary variable. There is also evidence that the order of diet presentation can influence the results of replacement studies. Finally, replacement studies are expensive with respect to both time and money. Dietary challenge studies are used to evaluate the acute effects of dietary components. In these studies, behavior is usually rated for several hours after an individual has consumed the food component of interest or a placebo. Double-blind procedures are relatively easy to institute. The food component and the placebo can be packaged so that neither the subjects nor the experimenters can detect which is being presented. A crossover procedure in which the subjects are given the food component on one day and the placebo on another, with the order of presentation varied among the subjects, can also be employed. In addition, although not often done, more than one dose of the dietary variable can easily be tested in challenge studies. The obvious disadvantage of challenge studies is that they do not provide information on the possible cumulative effects of a food component. SUGAR AND BEHAVIOR Of the many components in our diets, none has been condemned as frequently and as vehemently as sugar. Studies reviewed by the federal government indicate that sugar is the food people most consistently want to avoid and the one they look for most often on a food label's list of ingredients (Lecos, 1980). The use of sugar in our food has become a controversial issue involving scientists, dietitians, physicians, government officials, and private citizens. The public strongly believes that sugar has negative effects on behavior. This belief has been fostered by popular reports blaming sugar for a variety of adverse behavioral outcomes including hyperactivity, depression, mental confusion, irritability, drug and alcohol addiction, and antisocial behavior (e.g. Dufty, 1975; Ketcham and Mueller, 1983; Schoenthaler, 1985). One of the most celebrated examples of our negative views of sugar is the case of San Francisco City Supervisor Dan White who shot and killed the city's mayor and another city supervisor. White's lawyers argued that their client acted irrationally and suffered from "diminished mental capacity" as a result of his overconsumption of sugar-containing "junk" foods. On the basis of this argument, which

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences has become known as the "Twinkie defense," White was convicted of manslaughter rather than first-degree murder. Is there a scientific basis for our attitudes about sugar? Before this question can be answered, the term sugar must be defined. Although many different types of sugar are found in our foods, most people use the word sugar to describe the simple carbohydrate sucrose. Sucrose, the sugar on our tables and typically used in cooking, is a disaccharide composed of the monosaccharides fructose and glucose. Sucrose is broken down into its monosaccharide components in the digestive tract and absorbed across the small intestine. After absorption, glucose and fructose are carried by the blood to the liver and other tissues. Because fructose is rapidly metabolized to glucose in the intestinal mucosa and the liver, any discussion of carbohydrate metabolism is essentially a discussion of glucose. Glucose is the metabolic fuel for most cells in the body and the primary energy source for cells in the central nervous system. The critical role of glucose in the normal functioning of the central nervous system has helped to foster the belief that sugar can affect behavior. SUGAR, HYPOGLYCEMIA, AND BEHAVIOR Sugar intake has been condemned as the cause of a large number of psychological problems, including alterations in mood, irritability, aggression, and violent behavior. One "physiological" explanation for sugar's adverse effects is hypoglycemia or "low blood sugar." Unfortunately, the term hypoglycemia has frequently been misused. Many doctors, as well as patients, are confused about the condition (Yager and Young, 1974; Nelson, 1985). Clinically, hypoglycemia is defined by (1) low circulating blood glucose levels—50 milligrams per deciliter (mg/dl) or less; (2) symptoms including sweating, tremors, anxiety, headaches, weakness and hunger; and (3) amelioration of symptoms when blood glucose is restored to normal levels by food intake (Nelson, 1985; McFarland et al., 1987). Hypoglycemia can occur in diabetics after the administration of insulin. Additionally, other drugs such as antibiotics, anti-inflammatory agents, and antidepressants; insulin-secreting tumors; and renal disease can lead to hypoglycemia. It has been suggested that sugar consumption is a causal factor in hypoglycemia. The rationale for this idea begins with the assumption that simple sugars are more rapidly digested and absorbed than complex carbohydrates and thus cause a greater increase in blood glucose levels. This rapid rise in blood glucose

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences levels stimulates insulin secretion, which has the effect of decreasing blood glucose levels. This regulatory effect has been called reactive or functional hypoglycemia. There are several problems, however, with the idea that sugar intake can cause reactive hypoglycemia. First, recent studies have shown that a simple distinction cannot be made between sugars and more complex carbohydrates with respect to blood glucose and insulin responses (Crapo, 1985). Foods high in sugar can actually lead to smaller increases in blood glucose levels than foods containing complex carbohydrates. Thus, the assumption that sugar-containing foods uniformly lead to wide fluctuations in blood glucose values must be viewed with caution. Another related problem is that low blood glucose levels are not consistently associated with clinical signs of hypoglycemia. Additionally, symptoms of hypoglycemia are frequently reported in the absence of low blood glucose levels (McFarland et al., 1987). In many cases, a diagnosis of hypoglycemia is made on the basis of symptoms without appropriate laboratory evidence (Nelson, 1985; McFarland et al., 1987). To make a diagnosis of hypoglycemia, a relationship between low blood glucose levels and the symptoms of the disease must exist. The most common ways of doing this are to conduct an oral glucose tolerance test (OGTT) or to measure blood glucose levels after a normal meal. In either case, for a diagnosis of hypoglycemia, clinical symptoms must be associated with blood glucose levels of less than 50 mg/dl. This association is rarely observed. Patients who have glucose levels lower than 50 mg/dl are infrequent (Yager and Young, 1974; Nelson, 1985; McFarland et al., 1987). Given the relative rarity of functional hypoglycemia, why has the disease become so popular? For individuals with psychological complaints, a diagnosis of hypoglycemia may have certain benefits. First, the disease is socially acceptable. Rather than endure a "psychological" or otherwise stigmatizing condition, the patient can suffer from a respectable metabolic illness. Second, hypoglycemia gives individuals a way of easily and actively dealing with their complaints. By following certain dietary prescriptions, the patient believes that his symptoms can effectively be eliminated. In many cases, the act of attributing psychological problems to hypoglycemia and altering one's diet in response to this condition may provide some relief. Finally, hypoglycemia may be preferable to facing the possibility of a more serious condition.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences SUGAR AND VIOLENT BEHAVIOR During the past decade, theories relating sugar intake to violent behavior have received increasing attention. Once relegated to articles and books directed at food faddists, such theories are now discussed at meetings of criminologists, and are found in books and articles aimed at personnel in the correction and criminal justice systems. Moreover, on the basis of these theories, correctional facilities in several states have revised their dietary policies in an effort to reduce sugar intake and control violent behavior (Gray, 1986). Interest in the relationship between sugar and violent behavior was sparked by studies by Virkkunen and colleagues suggesting that hypoglycemia was common in criminals and delinquents displaying habitually violent behavior (Virkkunen and Huttunen, 1982; Virkkunen, 1982, 1983a, 1986a,b; Roy et al., 1986; Linnoila et al., 1990). These studies compared glucose and insulin levels during an OGTT between violent male offenders and male controls matched for age and relative body weight. In comparison to controls, men diagnosed as having either antisocial personality disorder or intermittent explosive disorder (American Psychiatric Association, 1987) initially displayed greater increases in blood glucose concentrations during the OGTT, followed by rapid declines in glucose values to levels indicative of reactive hypoglycemia. Comparisons between the two groups of offenders revealed that individuals with intermittent explosive disorder displayed a more rapid decline of glucose levels following the initial hyperglycemia, as well as a more rapid return from hypoglycemic levels to the original baseline values, than individuals with antisocial personality disorder. Men with antisocial personality disorder also demonstrated enhanced insulin secretion compared to controls. This increase in insulin secretion could act to augment glucose uptake by the cells and thus contribute to hypoglycemia. In contrast to men with antisocial personality disorder, men with intermittent explosive disorder did not have significantly elevated insulin values compared to controls. Subsequent correlational analyses suggested that a positive relationship existed between the duration of hypoglycemia during the OGTT and behavioral or sleeping problems, truancy, stealing, number of crimes against property, and multiple prison sentences (Virkkunen, 1982; Virkkunen and Huttunen, 1982; Virkkunen, 1986a,b; Roy et al., 1986). One explanation hypothesized for the relationship between hypoglycemia and aggression is that a functional deficit in serotonergic

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences neurons in the central nervous system may lead to abnormalities in glucose metabolism that can be conducive to violent behavior (Roy et al., 1988; Linnoila et al., 1990). Unfortunately, the details of this hypothesis remain to be elucidated. Although individuals with a history of violent behavior had a greater tendency toward hypoglycemia than controls, this finding cannot be viewed as unequivocal evidence of an association between hypoglycemia and aggression. First, no determination of nutritional status was made in any of the studies examining this association. However, in several papers, the authors noted that habitually violent men generally had poor appetites and may not have consumed food for many hours prior to an act of violence. It is possible that the nutritional status of these men was not adequate. This seems particularly likely because all of the violent offenders in the studies by Virkkunen and colleagues had a history of alcohol abuse. Chronic alcoholics frequently substitute alcohol for much of their normal food intake, and therefore often consume insufficient amounts of protein and essential vitamins and minerals (Shaw and Lieber, 1988). Inadequate nutrition can lead to abnormal glucose responses. Thus, it may not be that hypoglycemia results in violent behavior, but rather that a lifestyle that encompasses alcohol abuse and other behaviors that contribute to inadequate nutrition results in hypoglycemia. A second problem is that in some studies, violent offenders were given their normal diet for three days preceding the OGTT (e.g. Virkkunen, 1983a), and in others, a hospital diet containing a minimum of 48–55 percent calories as carbohydrate (e.g. Virkkunen, 1986a). The diet of control subjects was not manipulated in any of the studies. It is thus conceivable that differences in dietary intake immediately preceding the OGTT contributed to the differences in blood glucose and insulin responses observed between violent offenders and normal controls. Future research exploring hypoglycemia and aggressive behavior should include assessments of nutrient intake for all subjects. Another difficulty with this research is that recent work has indicated that the OGTT may not be a good indicator of the changes in blood glucose levels that occur after a normal meal (Crapo, 1985). Thus, the finding that individuals with a history of violent behavior have lower glucose levels during an OGTT does not imply that this occurs under normal feeding conditions. Measurements of glucose and insulin levels in subjects following standard meals would be useful for determining the relationship between hypoglycemia and violent behavior.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences An additional problem is that although positive associations were reported between the duration of hypoglycemic responses during the OGTT and a number of measures indicative of behavioral problems, there is no evidence that violent behavior actually occurred when insulin secretion was enhanced or low blood sugar levels were experienced. Examination of mood changes and other experimental behavioral indices of aggressive impulses during the OGTT could help to resolve this problem. Finally, as previously mentioned, all of the violent offenders studied by Virkkunen and colleagues had a history of alcohol abuse. Although, as pointed out by these investigators, alcohol may enhance insulin secretion and thus lead to a reduction in blood glucose levels, it has a variety of other effects on the central nervous system. These other actions certainly play a role in alcohol's effects on aggressive behavior (see Miczek, Haney, et al., in this volume). In a series of studies employing a dietary replacement strategy, Schoenthaler (1982, 1983a-c, 1985) investigated the effects of reducing sugar consumption on the behavior of inmates in juvenile detention facilities. A similar experimental approach was used in all studies. At a specific point in time, the institution modified its food policy in an effort to reduce sugar intake. Typical changes in the diet included substituting honey for table sugar; molasses for white sugar in cooking; fruit juice for Kool-aid; unsweetened cereal for presweetened cereal; and fresh fruit, peanuts, coconut, popcorn, or cheese for high-sugar desserts. The dependent variable in all of these studies was the number of disciplinary actions recorded by staff members before and during the change in food policy. On the basis of these studies, Schoenthaler (1982, 1983a-c, 1985) claimed that antisocial behavior in juvenile offenders could be decreased by 21 to 54 percent if sugar intake was reduced. Because this claim has important policy implications, it warrants careful scrutiny. The first problem posed by Schoenthaler's work is identification of the independent variable. Sugar intake is reported to be the independent variable. However, one does not have to be a nutritionist to appreciate that the dietary manipulations used were of dubious value in limiting sugar intake. Many of the dietary changes merely replaced one sugar for another (e.g. honey for sucrose). Moreover, no measurements of actual sugar intake were made in any of these studies. Thus, it is impossible to determine if the dietary alterations actually led to a reduction in sugar consumption. Intake data are essential to establish if dietary manipulations

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences reactivity. Again, no significant differences were observed as a function of sugar intake. Taken together, the results of dietary challenge studies do not support the idea that sugar plays a major role in ADHD. In studies using hyperactive and normal children of varying ages and employing a range of experimental situations, sugar intake had no effects on behavior. However, although experimental evidence is weak, parents or teachers continue to supply anecdotal reports of the deleterious consequences of sugar. How do we reconcile these differences? Several factors could contribute to the differing views of scientists and parents or teachers. One limitation of dietary challenge studies is that in most, only a single dose of sucrose was used. The amount of sucrose used in these studies may have been too small relative to the children's normal daily intake. Larger amounts might have produced negative reactions. Similarly, challenge studies can be criticized because they do not allow for the assessment of chronic sugar intake. Cumulative sugar intake may produce behavioral effects not detectable in single challenge tests. To help solve these problems, precise dietary histories and dose-response determinations of sucrose's effects on behavior are required. Another difficulty with challenge studies is the choice of an appropriate placebo. In most studies, either aspartame or saccharin has been used as the placebo. Although this procedure successfully blinds the subjects to the item they are consuming, it does not control for the fact that the challenge food not only contains sugar, but also provides substantial calories. This presents the possibility that any changes in behavior could be attributed to calories rather than to sugar. Additionally, it has recently been proposed that aspartame may have negative effects on behavior. Time parameters may also be important in determining sugar's effect on behavior. Most experiments have limited behavioral observations to one time after sugar intake and may have missed the critical period for its effects on behavior. To overcome the objections raised about dietary challenges studies, and to further investigate the hypothesis that sugar intake has negative behavioral consequences, Wolraich and his colleagues (1994) evaluated hyperactive behavior and performance on cognitive tests of school-age and preschool children placed on diets high in sucrose, aspartame, or saccharin. To ensure that the subjects ate only the specified diets, all food was removed from the children's

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences home prior to the study, and experimental diets were provided to the subjects and their families on a weekly basis by the research team. The children were fed each of the diets for three weeks with the order of diet presentation varied among the children. Results of the study were resoundingly negative. For the school-age children, all of whom were reported by their parents to be sensitive to sugar, none of the 39 behavioral or cognitive variables measured differed as a function of dietary conditions. For the normal preschool children, 4 of 31 variables did differ significantly among dietary conditions. However, there was no consistent pattern as a function of diet in the differences that were observed. Parents and teachers may be misperceiving a relation between sugar and behavior. Hyperactive children have difficulties in altering their behavior to changing environmental demands. Thus, in school these children have trouble changing their behavior from the relatively unstructured nature of a snack or party period to the highly structured demands of class work. Because many of the foods children consume at snack time contain sugar, it may be that the association teachers report between sugar and behavior represents these children's difficulties in getting back on task following an unstructured activity. Similarly, parents often note behavioral deterioration after their child has consumed sugar in a party situation. Hyperactive children are known to have more difficulty in groups, and the effects parents observe may be more a function of the situation than of the consumption of sugar-containing foods. Finally, if parents believe that sugar intake has negative consequences, they may be more sensitive to their child's behavior after the child has consumed a sugar-containing food. FOOD ADDITIVES AND ATTENTION DEFICIT DISORDER WITH HYPERACTIVITY In the early 1970s, Dr. Benjamin Feingold, a pediatrician and allergist, called attention to the fact that more than 2,000 additives are part of our food supply and hypothesized that these additives played a causal role in childhood hyperactivity (Feingold, 1973, 1975). To test this hypothesis, Feingold began treating children with ADHD with a diet free of food additives. Additionally, as a result of a presumed cross-reactivity of yellow food dye with acetylsalicylic acid (aspirin), Feingold also advocated the removal of foods containing natural salicylates (e.g. almonds, apples, all berries, oranges, raisins, tomatoes, and green peppers) from the

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences diet of hyperactive children. On the basis of his clinical work, Feingold claimed that a diet free of food additives and natural salicylates led to dramatic improvements, with 50 to 70 percent of the hyperactive children placed on this diet displaying complete remission. To obtain success, Feingold insisted that adherence to the diet was mandatory: any infringement could lead to a return of symptoms. He also proposed that successful treatment required the entire family to be on the diet and that an individual sensitive to food additives must avoid them for life. Feingold's ideas were widely publicized and rapidly gained popularity among the public (Lipton et al., 1979; Conners, 1984). Open clinical trials, in which parents or physicians placed children on an additive-free diet supported Feingold's claims. However, carefully controlled double-blind studies have generally yielded more negative results (e.g. Conners et al., 1976; Harley et al., 1978; Goyette et al., 1978; Weiss et al., 1980). Using a dietary replacement paradigm, Harley and colleagues (1978) compared the behavioral effects of Feingold's diet with an ordinary diet containing additives. Food for families in the study was provided by the experimenters, and neither the researchers nor the family knew which diet was being consumed at any particular time; diet phases were alternated so that all families ate both diets. No significant improvements in behavior were noted by teachers or objective raters in the 36 school-aged hyperactive boys in the study. However, some parents reported improvement on the Feingold diet, but this occurred only when the diet was given after the control diet. When 10 preschool children were tested in the same situation, all of their mothers and most of their fathers rated the children as more improved on the additive-free than on the control diet. Harley and colleagues (1978:827) concluded, ''While we feel confident that the cause-effect relationship asserted by Feingold is seriously overstated with respect to school-age children, we are not in a position to refute his claims regarding the possible causative effect played by artificial food colors on preschool children." The effects of food additives on hyperactive behavior have also been examined by using dietary challenges. In these studies, children reported by their parents to respond positively to the Feingold diet were blindly "challenged" by the addition of food additives to the diet. Although some challenge studies have demonstrated a decrement in behavior when children are given food additives (Conners, 1980; Swanson and Kinsbourne, 1980), others revealed no detrimental effects of food additives (Conners, 1980; Weiss et al., 1980; Mattes and Gittelman, 1981). Several factors

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences may account for these discrepancies. First, the types of food additives used in these studies have varied substantially. Second, a wide ranges of doses have been used. It has been argued that the dose of food additives used in some experiments was too low to produce adverse behavioral effects. However, it should be noted that the results of studies using larger doses have been both positive and negative. Finally, age may alter sensitivity to food additives. In general, younger children have been found to be more sensitive to food additives than older children (Harley et al., 1978; Conners, 1980; Weiss et al., 1980). The preceding data allow several inferences to be drawn about the effects of food additives on hyperactive behavior. First, Feingold's claims and those from other open trials have been overstated. At best, only a small percentage of hyperactive children may be adversely affected by food additives. Second, younger children may be more sensitive to food additives than older children. Third, there may be a dose-response curve for food additives, just as there is for any toxic substance, but this has yet to be demonstrated. In conclusion, the data on food additives and behavior are such to preclude any major legislative or administrative action to remove food additives or severely limit their use. Further studies of those few children who appear to respond negatively to food additives seem warranted. Additionally, research with experimental animals examining whether food additives have any biological activity in the central nervous system is recommended. RELATIONSHIP BETWEEN BLOOD CHOLESTEROL AND VIOLENT BEHAVIOR Over the past 10 years, the results of several types of experiments have suggested that an inverse relationship may exist between blood cholesterol concentration and violent behavior (Virkkunen, 1983b; Virkkunen and Penttinen, 1984; Kaplan and Manuck, 1990; Muldoon et al., 1990). For example, Virkkunen and colleagues (Virkkunen, 1983b; Virkkunen and Penttinen, 1984) measured fasting serum cholesterol levels in male homicidal offenders and found that those with antisocial personality disorder or intermittent explosive disorder with habitually violent tendencies had lower cholesterol levels than other offenders. This difference was particularly pronounced in men under the age of 30. It was hypothesized that the lower cholesterol levels in the violent offenders may be a consequence of enhanced insulin secretion.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences Although the proposed relation between cholesterol levels and violent behavior is provocative, it suffers from the same problems as the proposed association between hypoglycemia and violence. No information on dietary history is provided in any of the studies by Virkkunen and colleagues. Additionally, the role of alcohol in influencing both cholesterol level and violent behavior is not addressed. Moreover, other differences between the violent offenders and other offenders (e.g. activity levels) are never explored. To further investigate the relation between cholesterol level and aggressive behavior, Muldoon and colleagues (1990) compared the causes of mortality for subjects in intervention groups and control groups in six large primary prevention trials for reducing cholesterol levels. Cholesterol reduction in the intervention groups was accomplished in two studies by nutritional manipulations aimed at reducing dietary cholesterol and saturated fat intake and in the remaining four studies by pharmacological treatment. Causes of mortality were divided into three categories: coronary heart disease, cancer, and causes not related to illness, which included deaths due to accident, suicide, or homicide. In all studies, the treatments led to significant reductions in cholesterol levels. Compared to controls, the average cholesterol concentration of participants in the intervention groups was reduced by approximately 10 percent. This reduction in cholesterol was not associated with a significant decline in total mortality. However, cholesterol reduction was associated with a lower mortality rate from coronary heart disease and, in some studies, with a slightly higher mortality rate from cancer. With regard to mortality not related to illness, the chance of dying from suicide or violence was approximately twice as great in the intervention groups than in the control groups. The association between lower cholesterol levels and increased mortality from causes other than illness was found regardless of whether lipid lowering was based on dietary or pharmacological treatment. Although the results of a number of studies have suggested an inverse relation between cholesterol levels and deaths due to accidents or violence, this association has not been universally observed. For example, Pekkanen et al. (1989) found little evidence of an inverse association between serum cholesterol values and increased mortality due to accidents and deaths in their 25 year follow-up of 1,580 Finnish men. Additional epidemiological investigations and experimental research are clearly required to assess the relationship between blood cholesterol level and violent behavior.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences LEAD TOXICITY AND ANTISOCIAL BEHAVIOR It has recently been found that lead poisoning during childhood can have long-term detrimental effects on behavior (Needleman, 1989, 1990). Exposure to lead, which most frequently occurs when young children consume lead-based paints, has been associated with ADHD. As previously mentioned, ADHD is a well-established risk factor for later antisocial behavior. The rate of later delinquency in children who display ADHD and conduct disorder has been estimated to be 0.58. The attributable risk for hyperactivity in children with elevated levels of lead is 0.55. Multiplying the lower 95 percent confidence limits for these two proportions produces a joint probability of .2 for delinquency, given excess exposure to lead. The relation between lead exposure and delinquency has not yet been systematically studied, but clues suggest that this relationship should be given serious consideration (Needleman, 1989). CONCLUSIONS The study of the relationship between diet and behavior is still in its infancy. Within this growing field, a number of hypotheses have been developed about the role of dietary variables in determining violent behavior. Although experimental studies have been initiated to test these hypotheses, it is too early to draw definitive conclusions from this research. Better-controlled experiments employing appropriate research methodology are required. Additionally, it is important to remember that diet is but one of the many factors that could contribute to violent behavior. Research conducted thus far suggests that it may make a relatively minor contribution. REFERENCES American Psychiatric Association 1987 Diagnostic and Statistical Manual of Mental Disorders, Third Edition—Revised. Washington, D.C.: American Psychiatric Association. Anderson, G.H., and N. Hrboticky 1986 Approaches to assessing the dietary component of the diet behavior connection. Nutrition Reviews 44(suppl.):42-51. Behar, D., J.L. Rapoport, A.A. Adams, C.J. Berg, and M. Cornblath 1984 Sugar challenge testing with children considered behaviorally "sugar reactive." Nutrition and Behavior 1:277–288.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences Conners, C.K. 1980 Food Additives and Hyperactive Children. New York: Plenum Press. 1984 Nutritional therapy in children. Pp. 159–192 in J. Galler, ed., Nutrition and Behavior. New York: Plenum Press. Conners, C.K., C.H. Goyette, D.A. Southwick, J.M. Lees, and P.A. Andrulonis 1976 Food additives and hyperkinesis: A controlled double-blind experiment. Pediatrics 58:154–166. Crapo, P.A. 1985 Simple versus complex carbohydrates in the diabetic diet. Annual Review of Nutrition 5:95–114. Dews, P.B. 1986 Dietary pharmacology. Nutrition Reviews 44(Suppl.):246–251. Dufty, W. 1975 Sugar Blues. New York: Warner Books. Feingold, B.F. 1973 Introduction to Clinical Allergy. Springfield, Ill.: Charles C. Thomas. 1975 Hyperkinesis and learning disabilities linked to artificial food flavors and colors. American Journal of Nursing 75:797–803. Ferguson, H.B., C. Stoddart, and J.G. Simeon 1986 Double-blind challenge studies of behavioral and cognitive effects of sucrose-aspartame ingestion in normal children. Nutrition Reviews 44(Suppl.):144–150. Goyette, C.H., C.K. Conners, and T.A. Petti 1978 Effects of artificial colors on hyperkinetic children: A double-blind challenge study. Psychopharmacology Bulletin 14:39–40. Gray, G.E. 1986 Diet, crime and delinquency: A critique. Nutrition Reviews 44(suppl.): 89–94. Harley, J.P., R.S. Ray, L. Tomasi, P.L. Eichman, C.G. Matthews, R. Chun, C.S. Cleeland, and E. Traisman 1978 Hyperkinesis and food additives: Testing the Feingold hypothesis. Pediatrics 61:818–828. Hirsch, E. 1987 Sweetness and performance. Pp. 205–223 in J. Dobbing, ed., Sweetness . New York: Springer-Verlag. Kanarek, R.B., and N. Orthen-Gambill 1986 Complex interactions affecting nutrition-behavior research. Nutrition Reviews 44(suppl.):172–175. Kanarek, R.B., and D. Swinney 1990 Effects of food snacks on cognitive performance in male college students. Appetite 14:15–27. Kaplan, H.K., F.S. Wamboldt, and M. Barnhart 1986 Behavioral effects of dietary sucrose in disturbed children. American Journal of Psychiatry 143:944–945.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences Kaplan, J.R., and S.B. Manuck 1990 The effects of fat and cholesterol on aggressive behavior in monkeys. Psychosomatic Medicine 52:226–227. Kellogg, J.H. 1882 Plain Facts for Old and Young. Burlington, Iowa. 1919 The Itinerary of Breakfast. New York: Funk & Wagnalls. Ketcham, K., and L.A. Mueller. 1983 Eating Right to Live Sober. New York: Signet. Kruesi, M.J.P., J.L. Rapoport, M. Cummings, C.J. Berg, D.R. Ismond, M. Flament, M. Yarrow, and C. Zahr-Waxler 1987 Effects of sugar and aspartame on aggression and activity in children. American Journal of Psychiatry 144:1487–1490. Lecos, C.W. 1980 Food labels and the sugar recognition factor. FDA Consumer April:3–5. Linnoila, M., M. Virkkunen, A. Roy, and W.Z. Potter 1990 Monoamines, glucose metabolism and impulse control. Pp. 218–241 in H.M. Van Praag, R. Plutchik, and A. Apter, eds., Violence and Suicidality: Perspectives in Clinical and Psychobiological Research . New York: Brunner/Mazel. Lipton, M.A., C.B. Nemeroff, and R.B. Mailman 1979 Hyperkinesis and food additives. Pp. 1–27 in R.J. Wurtman and J.J. Wurtman, eds., Nutrition and the Brain, Vol. 4. New York: Raven Press. Mahan, L.K., M. Chase, C.T. Furukawa, S. Sulzbacher, G.G. Shapiro, W.E. Pierson, and C.W. Bierman 1988 Sugar "allergy" and children's behavior. Annals of Allergy 61:453–458. Mattes, J.A., and R. Gittelman 1981 Effects of artificial food colorings in children with hyperactive symptoms. Archives of General Psychiatry 38:714. McFarland, K.F., C. Baker and S.D. Ferguson 1987 Demystifying hypoglycemia. Postgraduate Medicine 82:54–65. McLoughlin, J.A., and M. Nall 1988 Teacher opinion of the role of food allergy on school behavior and achievement. Annals of Allergy 61:89–91. Milich, R., and W.E. Pelham 1986 Effects of sugar ingestion on the classroom and playgroup behavior of attention deficit disordered boys. Journal of Consulting and Clinical Psychology 54:714–718. Muldoon, M.F., S.B. Manuck, and K.A. Matthews 1990 Lowering cholesterol concentrations and mortality: A quantitative review of primary prevention trials. British Medical Journal 301:309–314. Needleman, H.L. 1989 The persistent threat of lead: A singular opportunity. American Journal of Public Health 79:643–645.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences 1990 The long-term effects of exposure to low doses of lead in childhood. New England Journal of Medicine 322:83–88. Nelson, R.L. 1985 Hypoglycemia: Fact or fiction. Mayo Clinic Proceedings 60:844–850. Pease, S.E., and C.T. Love 1986 Optimal methods and issues in nutrition research in the correctional setting. Nutrition Reviews 44(suppl.):122–132. Pekkanen, J., A. Nissinen, S. Punsar, and M.J. Karvonen 1989 Serum cholesterol and risk of accidental or violent death in a 25 year follow-up. Archives of Internal Medicine 149:1589–1591. Prinz, R.J., W.A. Roberts, and E. Hantman 1980 Dietary correlates of hyperactive behavior in children. Journal of Consulting and Clinical Psychology 48:760–769. Roy, A., M. Virkkunen, S. Guthrie, R. Poland, and M. Linnoila 1986 Monoamines, glucose metabolism, suicidal and aggressive behavior. Psychopharmacology Bulletin 22:661–665. Roy, A., M. Virkkunen, and M. Linnoila 1988 Monoamines, glucose metabolism, aggression towards self and others. International Journal of Neuroscience 41:261–264. Rumsey, J.M., and J.L. Rapoport 1983 Assessing behavioral and cognitive effects of diet in pediatric populations. Pp. 101–162 in R.J. Wurtman and J.J. Wurtman, eds., Nutrition and the Brain, Vol. 6. New York: Raven Press. Schoenthaler, S.J. 1982 The effect of sugar on the treatment and control of anti-social behavior: A double-blind study of an incarcerated juvenile population. International Journal of Biosocial Research 3:1–9. 1983a Diet and crime: An empirical examination of the value of nutrition in the control and treatment of incarcerated juvenile offenders. International Journal of Biosocial Research 4:25–39. 1983b Diet and delinquency: A multi-state replication. International Journal of Biosocial Research 5:70–78. 1983c The Los Angeles probation department diet-behavior program: An empirical analysis of six institutional settings. International Journal of Biosocial Research 5:88–98. 1985 Nutritional policies and institutional anti-social behavior. Nutrition Today 20:16–25. Shaw, S., and C.S. Lieber 1988 Nutrition and diet in alcoholism. Pp. 1423–1449 in M.E. Shils and V.R. Young, eds., Nutrition in Health and Disease. Philadelphia: Lea & Febiger. Swanson, J.M., and Kinsbourne 1980 Food dyes impair performance of hyperactive children on a laboratory learning test. Science 207:1485–1486.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences Virkkunen, M. 1982 Reactive hypoglycemia tendency among habitually violent offenders. Neuropsychobiology 8:35–40. 1983a Insulin secretion during the glucose tolerance test in antisocial personality. British Journal of Psychiatry 142:598–604. 1983b Serum cholesterol levels in homicidal offenders. Neuropsychobiology 10:65–69. 1986a Insulin secretion during the glucose tolerance test among habitually violent and impulsive offenders. Aggressive Behavior 12:303–310. 1986b Reactive hypoglycemic tendency among habitually violent offenders. Nutrition Reviews 44(Suppl.):94–103. Virkkunen, M., and M.O. Huttunen 1982 Evidence for abnormal glucose tolerance test among violent offenders. Neuropsychobiology 8:30–34. Virkkunen, M., and H. Penttinen 1984 Serum cholesterol in aggressive conduct disorder: A preliminary study. Biological Psychiatry 19:435–439. Weiss, B., J.H. Williams, S. Margen, B. Abrams, B. Caan, L.J. Citron, C. Cox, J. McKibben, D. Ogar, and S. Schultz 1980 Behavioral response to artificial food colors. Science 207:1487–1488. Whorton, J.C. 1982 Crusaders for Fitness: The History of the American Health Reforms . Princeton, N.J.: Princeton University Press. Wolraich, M., R. Milich, P. Stumbo, and F. Schultz 1985 Effects of sucrose ingestion on the behavior of hyperactive boys. Journal of Pediatrics 106:675–682. Wolraich, M.L., S.D. Lindgren, P.J. Stumbo, L.D. Stegink, M.I. Appelbaum, and M.C. Kiritsy 1994 Effects of diets high in sucrose or aspartame on the behavior and cognitive performance of children. New England Journal of Medicine 330:301–307. Yager, J., and R.T. Young 1974 Non-hypoglycemia is an epidemic condition. New England Journal of Medicine 291:907–908.

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