Is it possible to be “addicted” to food, much like an addiction to substances (e.g., alcohol, cocaine, opiates) or behaviors (gambling, shopping, Facebook)? An extensive and growing literature uses this terminology in the context of the “obesity epidemic”, and looks for the root genetic and neurobiological causes (Carlier et al., 2015; Volkow & Bailer, 2015).
Fig. 1 (Meule, 2015). Number of scientific publications on food addiction (1990-2014). Web of Science search term “food addiction”.
Figure 1 might lead you to believe that the term “food addiction” was invented in the late 2000s by NIDA. But this term is not new at all, as Adrian Meule (2015) explained in his historical overview, Back by Popular Demand: A Narrative Review on the History of Food Addiction Research. Dr. Theron G. Randolph wrote about food addiction in 1956 (he also wrote about food allergies).
Fig. 2 (Meule, 2015). History of food addiction research.
Thus, the concept of food addiction predates the documented rise in obesity in the US, which really took off in the late 80s to late 90s (as shown below).1
Prevalence of Obesity in the United States, 1960-2012
Sources: Flegal et al. 1998, 2002, 2010; Ogden et al. 2014
One problem with the “food addiction” construct is that you can live without alcohol and gambling, but you'll die if you don't eat. Complete abstinence is not an option.2
Another problem is that most obese people simply don't show signs of addiction (Hebebrand, 2015):
...irrespective of whether scientific evidence will justify use of the term food and/or eating addiction, most obese individuals have neither a food nor an eating addiction.3 Obesity frequently develops slowly over many years; only a slight energy surplus is required to in the longer term develop overweight. Genetic, neuroendocrine, physiological and environmental research has taught us that obesity is a complex disorder with many risk factors, each of which have small individual effects and interact in a complex manner. The notion of addiction as a major cause of obesity potentially entails endless and fruitless debates, when it is clearly not relevant to the great majority of cases of overweight and obesity.
Still not convinced? Surely, differences in the brains' of obese individuals point to an addiction. The dopamine system is altered, right, so this must mean they're addicted to food? Well think again, because the evidence for this is inconsistent (Volkow et al., 2013; Ziauddeen & Fletcher, 2013).
An important new paper by a Finnish research group has shown that D2 dopamine receptor binding in obese women is not different from that in lean participants (Karlsson et al., 2015). Conversely, μ-opioid receptor (MOR) binding is reduced, consistent with lowered hedonic processing. After the women had bariatric surgery (resulting in mean weight loss of 26.1 kg, or 57.5 lbs), MOR returned to control values, while the unaltered D2 receptors stayed the same.
In the study, 16 obese women (mean BMI=40.4, age 42.8) had PET scans before and six months after undergoing the standard Gastric Bypass procedure (Roux-en-Y Gastric Bypass) or the Sleeve Gastrectomy. A comparison group of non-obese women (BMI=22.7, age 44.9) was also scanned. The radiotracer [11C]carfentanil measured MOR availability and [11C]raclopride measured D2R availability in two separate sessions. The opioid and dopamine systems are famous for their roles in neural circuits for “liking” (pleasurable consumption) and “wanting” (incentive/motivation), respectively (Castro & Berridge, 2014).
The pre-operative PET scans in the obese women showed that MOR binding was significantly lower in a number of reward-related regions, including ventral striatum, dorsal caudate, putamen, insula, amygdala, thalamus, orbitofrontal cortex and posterior cingulate cortex. Six months after surgery, there was an overall 23% increase in MOR availability, which was no longer different from controls.
Fig. 1 (modified from Karlsson et al., 2015). Top: μ-opioid receptors are reduced in obese participants pre-operatively (middle), but after bariatrc surgery (right) they recover to control levels (left). Bottom: D2 receptors are unaffected in the obese participants.
Karlsson et al. (2015) suggest that:
The MOR system promotes hedonic [pleasurable] aspects of feeding, and this can make obese individuals susceptible to overeating in order to gain the desired hedonic response from food consumption, which may further promote pathological eating. We propose that at the initial stages of weight gain, excessive eating may cause perpetual overstimulation of the MOR system, leading to subsequent MOR downregulation. ... However, bariatric surgery-induced weight loss and decreased food intake may reverse this process.
The unchanging striatal dopamine D2 receptor densities in the obese participants are in stark contrast to what is seen in individuals who are addicted to stimulant drugs, such as cocaine and methamphetamine (Volkow et al., 2001). Drugs of abuse are consistently associated with decreases in D2 receptors.
Fig. 1 (modified from Volkow et al., 2001). Ratio of the Distribution Volume of [11C]Raclopride in the Striatum (Normalized to the Distribution Volume in the Cerebellum) in a Non-Drug-Abusing Comparison Subject and a Methamphetamine Abuser.
So the next time you see a stupid ass headline like, “Cheese really is crack. Study reveals cheese is as addictive as drugs”, you'll know the writer is on crack.
Further Reading - The Scicurious Collection on Obesity
Overeating and Obesity: Should we really call it food addiction?
No, cheese is not just like crack
Dopamine and Obesity: The D2 Receptor
Dopamine and Obesity: The Food Addiction?
Cheesecake-eating rats and food addiction, a commentary
1 Not surprisingly, papers on the so-called obesity epidemic lagged behind the late 80s-mid 90s rise in prevalence.
2 Notice in Fig. 2 that anorexia is considered the opposite: an addiction to starving.
3 Binge eating disorder (BED) might be another story, and I'll refer you to an informative post by Scicurious for discussion of that issue. You do not have to be obese (or even overweight) to have BED.
Carlier N, Marshe VS, Cmorejova J, Davis C, Müller DJ. (2015). Genetic Similarities between Compulsive Overeating and Addiction Phenotypes: A Case for "Food Addiction"? Curr Psychiatry Rep. 17(12):96.
Castro, D., & Berridge, K. (2014). Advances in the neurobiological bases for food ‘liking’ versus ‘wanting’ Physiology & Behavior, 136, 22-30 DOI: 10.1016/j.physbeh.2014.05.022
Karlsson, H., Tuulari, J., Tuominen, L., Hirvonen, J., Honka, H., Parkkola, R., Helin, S., Salminen, P., Nuutila, P., & Nummenmaa, L. (2015). Weight loss after bariatric surgery normalizes brain opioid receptors in morbid obesity Molecular Psychiatry DOI: 10.1038/mp.2015.153
Meule A (2015). Back by Popular Demand: A Narrative Review on the History of Food Addiction Research. The Yale journal of biology and medicine, 88 (3), 295-302 PMID: 26339213
Volkow ND, Baler RD. (2015). NOW vs LATER brain circuits: implications for obesity and addiction. Trends Neurosci. 38(6):345-52.
Volkow ND, Wang GJ, Tomasi D, Baler RD. (2013). Obesity and addiction: neurobiological overlaps. Obes Rev. 14(1):2-18.
Ziauddeen H, Fletcher PC. (2013). Is food addiction a valid and useful concept? Obes Rev. 14(1):19-28.
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