FOOD ADDICTION
v Introduction
This is a brief review of the concept of food
addiction in humans. Most of the evidence for or against addiction (now called
dependency in the Diagnostic and Statistical Manual of Mental Disorders)
focuses on similarities and differences between food craving and drug craving.
If food is addictive then other questions arise such as: “Is food then bad for
us? Is palatable food particularly bad for us? Should we then outlaw extremely
palatable food? Will the obesity epidemic go away if we all stick to gruel?” Drug
addicts crave, but do not enjoy, a drug (1). In such discussions, the terms
liking, wanting, and reward are frequently used. Yet there tends to be a great
deal of confusion over the definitions of and the relations among these terms.
Liking is defined as the hedonic response to a stimulus. Liking is synonymous
with pleasantness or the evaluative response to a stimulus.
(2). Hunger has traditionally been the focus of
studies on obesity. So, many question the practical value of understanding
desire for a specific food, or craving. However, evidence has recently been
building that craving and related phenomena do predict intake. Binge
eating/bulimia have long been associated with food craving (3). Cravings are
associated with more snacking and less compliance with dietary restrictions (4)
and also predict higher BMI (5). In 1954, Olds and Milner (6) reported on brain
sites that, when electrically stimulated, were extremely rewarding and led to
very high rates of bar pressing in rats. So these were clearly reward
“centers,” but the assumption that wanting and liking were one and the same was
so strong that they were frequently called “pleasure centers.” In the 1960s a
handful of patients with intractable brain diseases were implanted with such
electrodes. The assumption was that the stimulation must be pleasurable,
because the patients reported that they felt compelled to continue pressing the
button for stimulation (7). Yet their self-reports were that the stimulation
felt strange, not pleasant.
The most commonly cited example of the
wanting/liking distinction is that drug addicts report that they continue to
crave their drug long after they have stopped enjoying it .Although craved
foods are generally also liked, there are some examples of a wanting/liking
distinction for food as well . The purpose of the study was to determine
whether nutritional deprivation was necessary to produce food craving. The
experimental manipulation was to place subjects on a nutritionally adequate but
boring and restrictive diet, a vanilla-flavor dietary supplement beverage, for
5 d. By the end of the monotony phase of the study, subjects reported that they
did not find the beverage to be particularly palatable and there was, indeed, a
large increase in frequency of food cravings during this period. So nutritional
deprivation is not necessary to produce food cravings. An unexpected outcome of
the study was that a few of the subjects reported craving the beverage during
the week in which they returned to baseline eating even though they did not
like it.
v Neurochemistry
A study of the neurochemistry of reward provides
a great deal of evidence for similarity between food and drug cravings. Two of
the major players in the reward circuit are dopamine and the endogenous
opiates. Cocaine use causes release of striatal dopamine [see (9) for a recent
review] and in a raclopride binding study, Small et al. (10) demonstrated that
the same is true for food. Drug abuse is associated with decreased sensitivity of
the dopamine-reward system (9). The same is true in obese individuals (11).
Wang et al. (11) used raclopride binding to measure density of D2 receptors and
found an inverse relationship between D2 receptor density and BMI. Of course
the direction of causality for these differences in sensitivity to dopamine is
not known. Is it a result of repeated overstimulation of the system? Or is it a
preexisting risk factor for obesity or drug abuse? Although dopamine is
rewarding, its depletion or blockade doesn't diminish pleasurable responses to
palatable foods in animals or humans (12). So dopamine may play a more
important role in wanting than in liking.
Endogenous opioids also play a role in the reward
circuit. Release of these transmitters leads to higher levels of striatal
dopamine, that is, to what we think is rewarding. And indeed, the rewarding
properties of alcoholic beverages (13) and of sweet (or palatable) foods (14)
are thought to be mediated by this pathway. However, opioids also play a role
in pleasure. Naltrexone, an opioid blocker, reduces short-term food intake, but
more importantly, this effect may be limited to palatable foods. Naltrexone
treatment does lead to reduced pleasantness ratings for foods, but it does not
appear to affect hunger [see (15) for a review].
v Neuroanatomy
Anatomy is another point of comparison between
food and drug cravings. Although there have been numerous brain imaging
studies on subjects who were thinking about food (16), few of them have
made an attempt to limit the images to craving. In an fMRI study by Pelchat et
al. (2), great care was taken to isolate craving-related activation from
activation related to hunger or liking. Two groups of subjects were studied.
One was on a nutritionally adequate however monotonous diet for one.5 d before
imaging and therefore the alternative cluster consumed Associate in Nursing
unrestricted diet with sampling of the monotonous diet thus that they would
become familiar with it
v Learning
Food and drug cravings may also be learned in similar ways. Conditioning
effects have been used to explain the once puzzling compulsion to use drugs
long after withdrawal (19). The classic example is that a highly motivated
individual goes through withdrawal and finishes rehab with flying colors. He sets
forth into the outside world with no intention of relapsing. Yet, when he
returns to the old neighborhood and old friends, he finds himself craving and
using drugs even though he is no longer experiencing withdrawal symptoms.
v Conclusion
There are many parallels between food and drug cravings in humans and in
animals (see other articles in this session). Do these parallels demonstrate
that food is addictive? Of course, that depends on the definition of
“addictive.” Two of the criteria mentioned in the Diagnostic and Statistical
Manual of Mental Disorders are tolerance and withdrawal and there is evidence
for food withdrawal and tolerance in animals (23,24). However, many of the
clinical criteria for addiction/dependence focus on the consequences of continued
use or on failure to discontinue use. If there are no negative consequences of
eating food and there are no failed attempts to discontinue eating large
amounts or certain types of food, there is no diagnosis of addiction. On this
basis, most healthy, normal-weight people would not be diagnosed as food
addicts and food would not be considered an addictive substance, because, for
the most part, it produces positive rather than negative consequences. Drugs of
abuse are different from food. The shared neural substrates for food and drug
cravings probably evolved to encourage healthy behaviors such as eating and
reproduction (25). Drugs of abuse are undesirable because they are able to take
over these substrates and to divert efforts away from healthier goals.
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