Are Simple Carbohydrates Physiologically Addictive?

Addiction R<,.srank, 19Y7. Vol. 5 ( 2 ) pp.145-160 Reprints available directly froin the publisher Photocopy permitted by license rinly

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ARE SIMPLE CARBOHYDRATES PHYSIOLOGICALLY ADDICTIVE?

RICHARD HAMMERSLEY”* and MARIE REID

Behavioural Sciences Group, University of Gltsgow, Glasgow G I 2 8QQ3 Scotland, UK, Consumer Sciences, Glasgow Culedonian University,

Glasgow G3 GLP, Scotland, U K

Sugar and other carbohydrates are among the things to which it is claimed people can become addicted. A plausible physiological mechanism has been put forward to explain ‘carbohydrate addiction’ and this meshes with the folk psychology of dieting. Review shows evidence for the physiological basis of ‘carbohydrate addiction’ to be weak compared to drug addictions. If ‘carbohydrate addiction’ is a genuine phenomena then it is probably a habitual dependence based on strong reinforcement, like gambling, rather than a substance-based one.

Keywords; Sugar; carbohydrate; carbohydrate-craving; addiction

Dieting, obesity and eating disorders are sometimes considered to belong to the domain of addictive behaviour (e.g., Orford, 1985; Nirenberg & Maisto, 1987). One aspect of eating problems may be the effects of carbohydrates on behaviour and this review will consider the proposal that sugars or other carbohydrates have drug-like effects on human physiology which would largely explain their use, particularly their use despite adverse effects such as obesity. It has been suggested that carbohydrates lead to substance-specific cravings (Wurtman, 1990). Broadly, these include effects on subjective mood and on subsequent eating behaviour which might be regarded as signs of addiction.

It is important to note a key difference from the outset. Life without drugs is feasible, whereas life without carbohydrates is unlikely. Thus, one cannot literally translate definitions of drug or alcohol addiction or dependence to ‘dependence’ on carbohydrates and moderation rather than abstinence will be the goal of treatment or natural recovery. Indeed, this review will avoid providing a precise definition of ‘dependence’ or ‘addiction’ and focus

*Corresponding author. Behavioural Sciences Group, University of Glasgow, Glasgow G12 800 Scotland.

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146 R. HAMMERSLEY and M . REID

instead on the proposal that carbohydrates have drug-like effects on brain physiology which could help to generate some of the key components of dependence, including subjective craving, use of the substance to offset negative mood states, persistent unsuccessful attempts to moderate behaviour, reports of thoughts of carbohydrate consumption when not consuming them, the planning of binges and continued use despite adverse effects.

This review will question the idea that carbohydrates have physiological effects of major psychological importance. In the absence of such effects carbohydrate ‘addiction’ might nonetheless be caused by learned cognitive mechanisms, as is gambling. That is, the taste and the psychological meaning of carbohydrate-rich food may well be reinforcing and thus encourage continued, even dependent, consumption. It would, however, be premature to define pre- cisely what ‘carbohydrate dependence’ might be. Carbohydrates might have physiological effects which trigger dependence, but at the extreme opposite, the psychological conflict over foods which taste nice, but which are ‘fattening’ and have other effects perceived to be undesirable may suffice to explain why some people report being addicted to them (see Orford, 1985).

DEFINING “SIMPLE CARBOHYDRATES”

The effects of carbohydrates depend on the other food constituents present. For example, as little as 4% protein consumed with carbohydrate reduces the latter’s effect on serotonin (Young, 1991). Here, we will use “simple carbohydrates” to refer to the ingestion of food which is high in sugars or simple starches that are rapidly metabolised to glucose. In industrialised societies, the most common causes of high blood concentrations of glucose are highly refined or manufactured foods including sugars and refined flours. These contain simple carbohydrates, various proportions of fat, and little else. Being highly palatable, carbohydrates, particularly carbohydrate- fat mixtures, tend to be eaten in preference to other food. This in itself is not evidence that carbohydrates are addictive, but merely that their orosensory properties are highly reinforcing.

In contrast, many addictive substances including tobacco, opiates, cocaine and alcohol have sensory properties which are not unequivocally reinforcing: For example, novice smokers or opiate users are often nauseated. Part of the addiction process appears to be to learn to ignore or minimise the negative aspects of substance use and to emphasise the positive. However, the following

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ADDICTIVE CARBOHYDRATES? I47

effects of eating simple carbohydrates have also been proposed. If there was evidence for some of these effects then perhaps it would not be stretching the idea of “addiction” or “dependence” too far to include simple carbohydrates.

1. They generally increase subsequent eating (Geiselman & Novin, 1982a). 2. They increase subsequent appetite, or specifically induce craving for more

simple carbohydrates (Geiselman & Novin, 1982b; Novin er al., 1973). 3. They affect mood in ways which may in turn encourage the habitual,

repeated ingestion of simple carbohydrates (Wurtman, 1990). As with drugs (see Hammersley, Lavelle & Forsyth, 1992 for review), it has been suggested that people seek out simple carbohydrates to self-medicate against undesired mood states (Wurtman, 1990).

4. Restrained eating, or obesity, or both, may lead to or be associated with physiological abnormalities which make restrained eaters (dieters) or the obese particularly susceptible to the effects of simple carbohydrates (Wurtman & Wurtman, 1984; Xenakis et al, 1981; Wurtman er al., 198 1). It has also been suggested that there is a specific disorder of ‘carbohydrate craving obesity’ (Wurtman, 1990).

5. Nutritional deficits, hormonal imbalances or neurotransmitter levels are corrected by substances in certain food substances such as carbohydrate- rich foods, e.g. affective disorders, specifically premenstrual tension and seasonal affective disorder, may be associated with carbohydrate craving in some people (Wurtman et al., 1989; Wurtman, 1990).

While some have proposed that the physiological basis of drug addiction has been overstated (e.g., Davies, 1992), most authors see the specific physiological effects of a drug as critical in determining addiction to it. Putting this cautiously, physiological action probably makes it easier to become addicted to some drugs rather than to others. While non-chemical addictions, notably to gambling, are documented, the claims made about carbohydrates have largely been based on their physiological action and it is this line of thinking that will be reviewed here.

THE SEROTONIN MECHANISM

There is a plausible physiological explanation for the effects of carbohydrates on behaviour. Animal studies initially established a connection between serotonin metabolism and sleep, when sleep latency was significantly curtailed

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148 R. HAMMERSLEY and M. REID

after animals received tryptophan, which affects serotonin synthesis. Human studies have also shown that tryptophan administration increases rated sleepi- ness, sleep latency and rated drowsiness (Hartmann, 1983; Liberman et al., 1982/83; Greenwood et al., 1975). Since glucose increases brain tryptophan, affecting serotonin (Fenstrom, 1985), a clear model exists of how cxbohy- drates could reduce arousal.

Subsequent human studies using serotonin re-uptake inhibitors found effects upon appetite regulation and mood. The discovery that there was a relation between certain affective disorders and eating behaviour (Rosenthal et ul., 1992) resulted in a more extensive theory connecting appetite and mood (O’Rourke et al. 1992). It has been proposed that disorder of serotoninergic function in which low levels of brain serotonin leads to a negative mood is implicated in the etiology of Seasonal Affective Disorder, Carbohydrate Craving Obesity and Pre-menstrual tension. According to this theory, low or depressed mood associated with these disorders could be ameliorated by frequent carbohydrate rich snacks consumed particularly during the afternoon or evening.

However, one should be cautious in invoking serotonin deficiency as a specific cause of such disorders, especially since serotonin mechanisms have been implicated in numerous behaviours including appetite regulation, pain, sleep, other depression and drug abuse. Another problem is that only large quantities of pure carbohydrate have been shown to affect serotonin. The foods eaten to improve mood are rarely of this kind. According to Booth (1 994) “carbohydrate addiction” may not be mediated by mood changes and have no specific physiological basis.

Furthermore, questionnaires used to define these syndromes and to evalu- ate disturbances of appetite associated with them have not always been adequately validated and experimental results are not well substantiated (Fernstrom, 1988). Also, the doses of tryptophan administered in some of the earlier work exceed that which could be generated during natural eating (Young, 1991), which raises the question of whether carbohydrates have the same effect (Reid & Hammersley, 1995). Nonetheless, Wurtman and colleagues (Wurtman & Wurtman, 1984; Wurtman et d, 1981; Wurtman, 1990) have explicitly proposed that there is a functional relationship between carbohydrate preference, serotonin and mood. If this hypothesis were sus- tained then carbohydrate might indeed have addictive drug-like effects.

As will be reviewed, whatever the underlying physiology, the basic effects of carbohydrate on behaviour are yet to be convincingly established.

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ADDICTIVE CARBOHYDRATES? 149

A basic methodological problem is that control “placebo” food is often not feasible and thus behaviour changes observed after eating may often be due to palatability and/or expectancy effects, rather than to physiological changes per se. To an unknown extent people may behave after eating according to how they expect the food to affect them. Some studies have reported their results as evidence for physiological changes without consid- ering the role of cognitive, psychological effects.

INCREASED EATING?

In normal subjects, high-carbohydrate, low protein meals may reduce satiety less effectively than meals higher in protein (Hill & Blundell, 1986; Booth et al., 1970). But several other studies have failed to find this effect (e.g., Geliebter et a/., 1979, see Reid 1994 for full review) and other studies have found that high-carbohydrate foods decreased eating, although not as milch as foods rich in protein (Booth et al., 1982: Rolls et al., 1988). Using a blind procedure, with orosensory factors well-controlled, we have found that sucrose delays subsequent eating compared to saccharin (Reid & Hammersley, 1994; 1995). Simple carbohydrate foods may not be as satiating as some others, but they nonetheless decrease subsequent appetite. However a few studies have found that subjects do not subsequently eat sufficiently less to compensate fully for the energy content of a carbohydrate preload (Rolls et a/ . , 1988; Teff, et a/., 1989; Spitzer & Rodin, 1987-see Reid, 1994, for full review). This literature suggests that carbohydrates satiate rather than actively stimulating appetite, but that satiation is somewhat inaccurate. A review by Blundell et al. ( 1994) on carbohydrates and appetite reports that carbohydrates such as glucose, sucrose, fructose inaltodextrins and polysaccharides will decrease subsequent food intake. According to Blundell et al. (1994) most carbohydrates will . . “Suppress later intake by an amount roughly equiv- alent to their energy value, although the time course of the suppressive action may vary according to the rate at which the carbohydrates are metabolized.”

In some circumstances the consumption of high carbohydrate food may herald the onset of a period of unrestrained eating (and this may apply to both normal and restrained eaters). But this does not imply that high carbohydrate food has simple physiological effects on appetite

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unmediated by psychological factors. Often, the choice of high carbohydrate food may be influenced by the meaning of the social situation and the latter factor may also determine subsequent eating behaviour. People do not, for example, generally enter the cinema clutching a green salad. Having popcorn in the cinema may well lead on to having ice cream too, but this is learned behaviour. A related example would be the abstinence violation effect when restrained eaters “go off the diet”. A similar explanation has recently been offered for the alleged but unsubstantiated relationship between sugar consumption and child hyperactivity (Wolraich et nl., 1994).

So far we have discussed eating, rather than hunger or craving. In prac- tice, defining craving for a nutrient is even more difficult than in the study of drug problems (Weingarten & Elston, 1990). Most studies have failed to distinguish between general hunger, craving and actual eating, so there is currently little clarity about which, if any, of these two phenomenological states and one behaviour are affected by carbohydrate.

In summary, consumption of simple carbohydrates satiates, although inaccurately. When it appears to trigger increased eating then this is probably due to learned, cognitive factors.

INCREASED APPETITE FOR SIMPLE CARBOHYDRATES?

An actual increase in eating might be caused by insulin induced hypo- glycemia, leading to a need for rich sources of glucose (Karlan & Cohn, 1946; Johnson et d., 1980). However, choice of foodstuff in humans appears to primarily be governed by non-physiological factors including their palatability (Blundell & Hill, 1985), people’s beliefs about the food (Wooley, 1972; 1976; Schacter, 1967), the time of day (Schacter & Koch, 1968) and what food is available (Nisbett, 1968b; Weingarten, 1985). Studies which purport to show increased appetite caused by physiological mechanisms have generally failed to control for more psychological factors. The two most common problems are first that the initial priming carbohydrate is not given blind, allowing expectations to influence behaviour. Second, that subsequent consumption is measured in a situation where subjects have free access to palatable food in a laboratory with little opportu- nity for other activity, encouraging eating as the only available alternative to boredom. Again, when carbohydrate-rich food “triggers” further con-

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ADDICTIVE CARBOHYDRATES? 151

sumption of such food this seems to be caused by the high palatability of the food (Rogers, 1993) as well as its meaning as a “forbidden” stuff (Rozin, 1986). For example people may binge on chocolate, but not because its ingestion has triggered off some simple physiological “need” for more chocolate (Rogers, 1993).

Studies to date have not controlled psychological factors sufficiently to test properly the hypothesis that carbohydrates physiologically trigger craving, but this hypothesis is unlikely on the basis of existing research.

GENERAL EFFECTS ON MOOD?

In normal subjects the most commonly reported effect is that ingesting simple carbohydrates leads to a drowsy, unaroused mood (Pivonka & Grunewald, 1990; Spring, 1983). But, if such effects exist at all, then they are small and readily eliminated by changes in experimental procedure such as time of day (Craig, 1986) and the duration of prior fasting (see Read & Hammersley, 199.5). Amongst other explanations it is possible that the effects of carbohydrate on mood are actually reversals of the effects of fasting, rather than deviations from normal, although if both food and food deprivation affect mood, the choice of baseline ‘normal mood’ becomes problematic.

Duffy (1 97.5) reported that simple carbohydrates increased arousal rather than lowering it. Benton & Owens (1993) demonstrated positive effects of simple carbohydrate on mood, but to do so they had to use 354 subjects. They concluded that any such effects were “subtle.” In other words the effects are unlikely to have much noticeable influence on an individual’s mood state. However, the effects may be more marked for some clinical groups, reviewed below, for whom carbohydrate appears to increase rather than reduce arousal.

If simple carbohydrates do not noticeably change mood then why should people consume them to this end? In other studies Benton (1990) has demonstrated that increased blood glucose increases performance on cognitive tasks. This suggests that people could use simple carbohydrates rather as they use caffeine, to enhance performance. It has not, however, been demonstrated that people actually do use them in this fashion, although the marketing of some carbohydrate snacks, such as “Boost”, suggests some awareness of this.

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I52 R. HAMMEKSLEY and M . REID

It has also been suggested that ingesting simple carbohydrates initially increases arousal (and hence performance) followed by a drowsy, unaroused state (Thayer, 1987). If this were true then the obvious specula- tion is that people might take more simple carbohydrates to offset this latter state (Wurtman, 1990), much as people may smoke more crack cocaine to offset the dysphoria which occurs after the initial elation. For normal subjects, the only established component of this theory is that when simple carbohydrates elevate blood sugar (this itself being a varied process modulated by many factors) then performance improves. Thus, an increase in energy and concentration might be the kind of effects expected or sought from drinkshacks high in carbohydrate in particular circumstances such as the workplace, or a sports centre. Such expectancies will influence how people use carbohydrates and in what quantities. Someone who has a glucose drink to increase energy might have come to like the drink for what they ‘expect’ i t to achieve for them, even if it often fails to do so. Further research is required in this area.

Learned factors may also be important for mood in everyday life. Being rewarded with sweets or ice cream may well elevate mood, but not merely via the specific physiological effects of simple carbohydrates. Carbo- hydrate metabolism may have some effects on mood, but at this time it seems unlikely that these effects are substantial enough generally to rein- force carbohydrate consumption. Nonetheless, the hypothesis that simple carbohydrates are sometimes consumed to boost cognitive performance requires further investigation.

DIETING, RESTRAINT AND OBESITY

Carbohydrate consumption has been linked to obesity via the concealed calories it can provide (Wooley rt al., 1975; Yudkin, 1973; Yenakis et al., 1981), although fat may well be more of a problem (Kraner & Gold, 1980). This explanation turns on the idea that the obese are relatively poor at balancing their energy intake. Although in the long term people are capable of balancing their dietary intake to compensate for what they have previously consumed, this physiological adjustment is not accurate and is readily over- ridden by cognitive, temporal and orosensory factors, especially in the short-term (Wooley, 1976; Roger? & Schutz, 1992). In particular people are poor at adjusting for concealed calories, which are most common in the

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ADDICTIVE CARBOHYDRATES’? 1 s3

form of simple sugars and/or fat contained in food. There is some evidence that the obese are more likely to eat on the basis of cognitive and orosensory factors, but this effect is probably not sufficient to explain their obesity (Rodin, 1981) and it is far from clear that the non-obese differ qualitatively in their control of eating (Prentice et ul., 1989).

An alternative is that the issue is one of restraint rather than body weight. Perhaps “restrained eaters”-people who are dieting and or exercising to attempt to control their weight-differ from non restrained eaters. Again, this is far from established (Ruderman, 1986). Furthermore, the overeating behaviour of restrained eaters when they abandon restraint has sometimes been explained in terms of the physiological mechanisms already reviewed above and found inconclusive.

It is worth pointing out that whatever homeostatic mechanisms to regu- late food intake humans possess probably evolved under conditions where deprivation and malnutrition were the norm, as they still are today in many parts of the world. For this reason, a mechanism which accurately prevented long term over-eating would have served little evolutionary purpose. Optimum survival behaviour under conditions of deprivation is to eat as much as possible when food is available and to seek out energy-dense food- stuffs when ever possible. Modern conditions in developed countries mean that many people have access to a surfeit of food and modern manufactur- ing techniques mean that much of this food is relatively high in carbohydrates and fat and low in dietary fibre. Furthermore, more people have longer life-spans within which to gain weight. A very modest weight gain of less than 1 kg per year would suffice to make someone seriously obese over 20 years, but nonetheless is compatible with a good, although not exact, physiological control mechanism. It may once have been unlikely that there would only be times of plenty allowing a modest annual gain to accumulate.

If this evolutionary account is broadly correct then the any initial physiological difference between the obese and non-obese may be quite small. Schacter’s influential specific proposal that non-restrained, non-obese individuals are better at utilising internal signals of satiety (Schacter, 1967) has not been unequivocally supported (Wooley, et al., 1972; Rodin, 1975). Both lean and obese people seem poor at regulating short-term intake on the basis of internal signals alone (Sylvestre et al., 1989; Rolls et al., 1986; Spiegel, 1973). Another possibility is that the unrestrained lean utilise different cognitive mechanisms from the obese or the restrained.

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For example, perhaps for lean people food generally has fewer psychological connotations. Gourmet or aesthete, perhaps the lean rarely eat because they are anxious, or feel they want a reward, or to please other people, or for the other reasons which can arise from the psychological meaning of food rather than from its purely nutritional or aesthetic value. This is only one possibility. In fact, the parameters of normal eating habits have yet to be mapped in sufficient detail to permit accurate claims about abnormality.

Despite this, studies of the obese or the restrained eater have tended to make untested assumptions about the nature of normal eating; essentially that it is normal to eat according to a daily routine, with one or more iden- tifiable meals occurring at set times each day. Yet, for example, people on low incomes today often have to fast on the last day or two before their next income is due. Some people routinely fast for religious reasons. Many people probably have quite different eating patterns during the week and at the weekend. Most people eat differently during festivals and holidays.

In this context, it cannot for example be taken for granted that eating five thousand or more calories a couple of days a week and eating little on the other days is entirely abnormal. Indeed some studies have found that binge- ing behaviour occurs among a large minority of women (Palmer, 1987). This is normally interpreted to mean that bulemia is a very common problem, but as with drug use (in contrast to drug dependence), it could also mean that eating norms do not entirely follow a set three-meals-a-day pat- tern. Until such issues have been adequately examined, it is premature to hypothesise that the restrained or the obese are compelled addictively to eat as they do.

SPECIAL GROUPS

Both seasonal affective disorder (KrCuchi & Wirz-Justice, 1988) and premenstrual syndrome (Wurtman et al., 1989) have been linked to increased carbohydrate consumption with subsequent improvement in mood. Furthermore, the administration of d-fenfluramine improves mood and decreases carbohydrate consumption among these groups (Wurtman et al., 1981; 1987). The Wurtmans and colleagues interpret these findings as indi- cating that carbohydrate consumption improves mood by increasing serotonin levels (Wurtman, 1988; 1990). However, it is possible that low mood

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ADDICTIVE CARBOHYDRATES‘? 155

in these disorders is associated with low serotonin levels and that d- 1 fenfluramine and 1 -tryptophan treatments can improve mood by increasing serotonin levels, but that the mechanism of action of carbohydrates is different. Carbohydrates might influence mood cognitively, serving as a rein- forcer which improves mood, rather than a direct chemical intervention. When mood is not low, then the frequency of this kind of eating decreases. This possibility is made more plausible by the observation that the high carbohydrate foods consumed in the preceding studies tended to be highly- palatable carbohydrate-fat snacks of the kind which would generally be regarded as ‘treats’ (Drenowski, 1987).

The Wurtmans have also proposed the existence of a specific carbohydrate-craving obesity, where overeating is driven by the need to increase serotonin levels (Wurtman, et al., 1987). As with SAD and PMS patients, self-selected carbohydrate cravers indeed ate less carbohydrate after d- 1 fenfluramine or 1 -tryptophan treatment, but this does not prove that carbohydrate directly affected serotonin levels. Other studies have found evidence which suggest that cognitive mechanisms rather than serotonin depletion determine carbohydrate craving and consumption (Schlundt et al., 1993; Hill, Weaver & Blundell, 1991). This contention is supported by the Wurtmans’ own findings cited above, for they do not find that carbohydrates (or carbohydrate-fat snacks) clearly raise arousal, but rather than they lead to a calm, relaxed state-a state of low arousal, but with positive emotional tone. One would expect changes in serotonin levels to affect arousal, but not necessarily to affect emotionality, which is generally considered to be the product of cognitive evaluation of one’s internal and external state rather than something which can be directly altered by physiological changes alone (e.g., Oatley, 1992). A caution is that i t is not clear how this sort of psychological model can explain how anti-depressant drugs improve mood in the depressed, but are not psychoactive in the non- depressed.

At the moment, while there is evidence that serotonin depletion is implicated in some kinds of depression, the evidence that carbohydrate consumption chemically reverses serotonin depletion is not convincing. Low mood can apparently cause carbohydrate consumption, but any improvement in mood may be cognitive rather than physiological in origin. As men- tioned above, the question also remains of whether the quantities of carbohydrate consumed by depressed people would suffice to elevate serotonin levels.

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DISCUSSION

All five hypotheses reviewed have been proposed at times with great confi- dence and have worked their way into the folklore of eating and dieting. They fit well with people’s, particularly dieters, everyday experiences which are, of course, saturated with their beliefs about the effects of food. Nonetheless, there is little clear or convincing evidence that any of the hypotheses are correct. In the short term when people do not know what they are eating, carbohydrates appear to decrease rather than increase appetite and not to stimulate directly further carbohydrate consumption. Some people with low mood appear selectively to consume carbohydrates, particularly carbohydrate-fat mixtures, but this might be self-reinforcement rather than self-medication. Carbohydrate metabolism will certainly figure in a comprehensive future theory of eating behaviour, but probably not as the main component.

Carbohydrate consumption is probably initiated and maintained because carbohydrates often taste good, particularly mixed with fat. Weight gain may occur partly because it is d cult to judge the energy content of some simple carbohydrate foods (such as snacks with hidden sugars) and people are inaccurate at compensating. The addictive-type conflict over simple carbohydrate consumption is probably due in part to this potential for weight gain and in part to the image of some simple carbohydrate (or carbohydrate- fat) foods as fattening luxury treats with the potential both to induce guilt and anxiety and to serve as reinforcers, perhaps improving mood.

From the evidence to date there is no need to additionaIly postulate that carbohydrate metabolism directly triggers appetite or mood effects. Such effects can only be demonstrated in studies where simple carbohydrate foods are administered blind to subjects. In such conditions, simple carbohydrates satiate and have at most very small effects on mood. It remains feasible that carbohydrate-fat mixtures have different effects, but this has not yet been demonstrated.

To the extent that addictive and eating behaviours are both learned, they obviously have much in common and it is feasible that any appetitive behaviour can become compulsive (see Orford, 1985). Nonetheless, the difference remains that the specific physiological aspects of drug addiction do not appear to have any analogue in the consumption of carbohydrates. At this time, there is no convincing evidence that patient or client complaints of being addicted to sugar or chocolate have a simple neurochemical basis and

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the metabolism of carbohydrates is unlikely to be a main causal explanation of obesity or restrained eating patterns. This leaves psychological and behavioural factors as the keys to understanding carbohydrate “addiction”.

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