A number of mechanisms have been advanced to explain the physiological and pathological changes in behavior that lead to food cravings and a loss of control over eating. The latter, of course, is a major concern with obesity and a number of eating disorders.
Researchers have employed functional magnetic resonance imaging (fMRI) to explore the neural basis of cravings. The imaging data suggest that components of the amygdala, anterior cingulate, orbital frontal cortex, insula, hippocampus, caudate, and dorsolateral prefrontal cortex are activated during periods of pining for food. It appears that there may be a network of neural regions that is involved with the emotion, memory, and chemosensory stimuli of food craving.
Eating is generally a pleasurable social experience. Using chocolate consumption as an example, it follows that there may be constituents in chocolate that influence satiation or alter our acceptance of the treat, including psychoactive or mood-altering endogenous compounds such as phenylethylamine, tyramine, serotonin, tryptophan, and magnesium. It is important to note, however, that many other foods, including dairy products, also contain these compounds at higher concentrations. Yet, these foods tend to have somewhat lesser emotional appeal than chocolate.
Chocolate craving, especially among women, may result from a sense of deprivation, in reaction to stress, perimenstrual hormonal fluctuation, and modulation of neuropeptide concentrations. Regardless of the factor or factors that initiate chocolate cravings in women, the apparent physiological explanations are inconsistently expressed in a diversity of cultures, especially among those that consume large amounts of chocolate. Spanish women, for example, eat relatively large quantities of chocolate and exhibit limited chocolate craving. This is in contrast to many American women, who consume a similar level of chocolate per capita yet present a stronger chocolate craving. Clearly, the relationship between food preferences, mood, and the menstrual cycle is complex.
Some investigators have proposed that carbohydrate craving (with resulting consumption) attenuates depression. This theory results from some observations that diet can modulate the serotonergic system in the brain, which is linked to mood. Research shows that administration of naloxone, an opiate antagonist, appears to reduce food intake and provides additional evidence for a nutrition–neurological interaction. This effect appears to inhibit mainly the consumption of sweet, high-fat foods such as chocolate.
Studies of cannabinoids and antagonism of cannabinoid receptors have shed more light on the complex neurochemistry of selective appetite. In addition, research on satiety or appetite-control mechanisms residing in the gastrointestinal tract has led to the identification of an entire spectrum of gut neuropeptides with elaborate central nervous system feedback.
After acknowledging the complexity of the influences on appetite and the mechanisms of “normal” appetite and craving, it is important to review what we know about pathology. For example, pagophagia is frequently observed in children, pregnant women, and young adults. This behavior can both signal and lead to severe iron deficiency anemia. Geophagia, such as eating termite hills in Africa, is a practice in many cultures. This eating disorder can result in a host of bacterial and parasitic infections as well as various poisonings and life-threatening toxicities.
Several mechanisms have been proposed to assist our understanding of food cravings and pica, the desire to consume nonfood items. Nutrient deficiencies may result from these abnormal behaviors; however, the scientific literature does not support a causal relationship with food cravings or pica. “Cravings” undoubtedly represent a true bio-psycho-social paradigm in which sociocultural factors, stressful environments, and hormonal fluctuation participate in a complex drama performed on a neurological stage. The result has varied and as yet incompletely understood implications for nutrition and health.
Rogers, P.J. and Smit, H.J. 2000. Food craving and food “addiction”: A critical review of the evidence from a biopsychosocial perspective. Pharm. Biochem. Behav. 66: 3-14.
by Roger Clemens, Dr.P.H.,
Director, Analytical Research,
Professor, Molecular Pharmacology & Toxicology,
USC School of Pharmacy,Los Angeles, Calif.
by Peter Pressman, M.D.,
Attending Staff, Internal Medicine,
Cedars-Sinai Medical Center, Los Angeles, Calif.