Common Neurobiological Links To Food And Drug Abuse

Kenneth Blum, Ph.D., Doctor of Humane Letters and John Giordano, Doctor of Humane Letters, MAC

Common Neurobiological Links To Food And Drug Abuse

Ah, comfort foods. There is nothing like a good Danish pastry to start the morning off right. Foods that tend to elevate our mood almost always have a high sugar or other carbohydrate content. Over one-hundred years ago, the average American consumed 12 pounds of sugar a year. Today it’s more like 144 pounds! Sugar is in nearly everything you buy at the grocery store. Any guesses as to why we’re experiencing a tidal wave of obesity and type II diabetes?

We know the damage these foods do to our bodies, but just what are they doing to our brains?! What is it about these delectable morsels that drive us to keep coming back for more when we know they’re not good for us?

Scientists have long suspected that sugar/carbohydrates – our bodies turn carbs into sugar (glucose) and by the way alcohol too – was the nexus between food and addiction; but not until recently are we able to prove it with tangible evidence showing the effects on the brain. New studies are confirming earlier suspicions. What they have discovered is that sugar and carbohydrates stimulate the brain the same way as drugs do and in the same regions.

Dopamine is the primary neurotransmitter of reward and pleasure. It’s one of the feel-good chemicals produced in the brain. Sugar, just like alcohol and drugs, spikes dopamine release in the brain’s reward center giving us a false sense of happiness and being at ease. But what goes up also comes down. When dopamine function begins crashing, we tend to feel cravings for sweet foods or sugary drinks just as an addict craves drugs, although less intense.

Does this mean we are or could become addicted to sugar and/or carbohydrates? Absolutely!

Below you’ll find a much more comprehensive scientific explanation to the connection between sugar/carbohydrates and food addiction. It is not an easy read but very factual and you will walk away with a better understanding of the relationship between sugar/carbohydrates and addiction.

The concept that food and drugs have common neurobiological and neurogenetic mechanisms has been pioneered first by Hoebel (1985) over 25 years ago and introduced into the media and mainstream America by Gold and associates (2013) and Avena’s group (Murray, et al. 2015).

It is so important for the treatment and recovery community to understand why allowing candy at treatment centers may indeed be a trigger for the unwanted transfer of one addiction (e.g. alcohol, opiates, cocaine) for another addiction. We now know that at least 20% of people undergoing lap-band surgery will develop full-blown drug addiction post-surgery. This phenomena of replacing food for drugs has been carefully researched in both human and animal models. It is not so surprising if you consider that similar neurogenetic variants occur across the brain reward circuitry resulting in a low dopamine function and enhance craving for both glucose and alcohol. In 1996 one of us (Blum et al 1996) coined the term “Reward Deficiency Syndrome” (RDS) to help explain the genetically induced commonality of all addictive behaviors drug and non–drug.

In this regard, it is well known that glucose, alcohol, heroin, nicotine, gambling, internet gaming, music and sex all release dopamine at the brain reward site leading to a false or pseudo feeling of well-being. This is especially true in individuals having compromised dopaminergic function through either gene polymorphisms (variants) or environment (epigenetic). This is simple to understand if you adhere to the mathematical formula whereby Phenotype=Genetics +Environment [P=G+E]. So if both certain genes coupled with a bad environment lead to low dopamine function the effected individual will do just about anything to feel good by finding ways to boost up their brain dopamine through both food or drugs or sex.

Research has revealed that obesity causes changes in both behaviors, and brain structures quite similar to the changes observed in drug addiction. However, addiction to food is not the cause of all cases of obesity. Can it be assumed that a large group of individuals no longer eat to survive, but rather survive to eat?
In this context we must consider the importance of the brain’s reward system in food intake the “thrifty gene hypothesis” (survival gene related to famine and fat metabolism) and as such the commonality between food and drug addiction (Speakman, 2006; Prentice, et al. 2008).

Certain overlaps in the brain circuitry activated by food and drug intake suggests that different types of reinforces (natural and artificial) activate a number of the same neural systems (Hoebel, 1985; Hernandez and Hoebel, 1990; Kelley, et al.
2002; Le Magnen, 1988; Volkow and Wise, 2005; Wise, et al. 1989). In fact, there are several regions in the brain involved in the reinforcement of both feeding and drug intake (Kalivas, et al. 2005; Koob and Le Moal, 2005; Mogenson and Yang, 1991; Baldo, et al. 2010), and a number of neurotransmitters, as well  as hormones, have been studied in these and related brain areas (Baldo, et al. 2010; Simpson, et al. 2012; Spangler, et al. 2004; Schoffelmeer, et al. 2001; Stein and Belluzzi, 1979).

There have been many studies in the scientific literature that unequivocally support these commonality theories as proposed by Avena et al. (2013) and by Blum et al. (1996). In clinical situations, treatment of both food and drug addiction typically appear to present with reciprocal comorbidity and this common comorbidity deserves intensive investigation.

While overeating may have important neurochemical links to drug abuse, less is known about other eating disorders like bulimia
(Mann, et al. 2014) and anorexia (Jordan, et al. 2003). However, there is increasing evidence that the same gene polymorphisms that can predict both food and drug abuse, the Dopamine D2 receptor A1 form, can also predict eating disorders like anorexia and bulimia and even binge eating disorder.

Many articles have examined research developments and current treatments for obesity, including diet and exercise, psychotherapy, surgical interventions, and pharmacotherapies (Volkow and Baler, 2015; Michaelides, et al. 2012; Blum, et al. 2011). There are, however, some clinical issues that merit attention and provide information that sheds light on the commonality concept of food and drug co-morbidity. For example, after several years of effective bariatric surgeries used to treat obese patients, clinicians now report that some patients are substituting compulsive overeating with other compulsive behaviors. These behaviors involve decreased dopamine (DA) type 2 receptors (DRD2) and include alcoholism, gambling, drugs, compulsive shopping, and exercise (Cuellar Barboza, et
al. 2015; Dunn, et al. 2010). Potentially because of neurochemical similarities, overeating and obesity may act protectively by decreasing drug reward (Hodgkins, et al. 2007). Similar to the process of opiate withdrawal, in animal sugar addiction withdrawal models, imbalances occur in neurotransmitters such as acetylcholine and DA (Avena, et al. 2015; Gold and Avena, 2013). Additionally, several human neuroimaging studies have reinforced the link between food craving and drug craving (Avena, 2010).

The authors suggested that these findings show that cocaine cues activate similar, though not identical, pathways to those activated by food cues and that striatal D2/D3 receptors modulate these responses, suggesting that chronic cocaine exposure might influence brain sensitivity not just to drugs but also to food cues
(Tomasi, et al. 2015).

The term Reward Deficiency Syndrome (RDS) was coined to describe the genetic determinants that predict addiction. The predictive value of being a carrier of the DRD2 Taq A1 allele, which may cause future RDS behaviors, was 74% (Blum, et al. 1995). People with the DRD2 Taq A1 allele, carry a reduced number of D2 receptors and, therefore, have reduced DA function. Additionally, RDS is polygenetic, involves a cascade of reward genes. The deficiency concept of DA may not be the only way to gain weight there is also evidence for a DA surfeit theory (Yokum, et al. 2014). However, DA function disruptions, in particular, may predispose people to obesity and other addictive disorders. A family history of alcoholism is considered to be a substantial obesity risk factor (Pach, et al. 2014). Thus, we hypothesize that RDS is the cause of replacing food addiction with other addictive behaviors and may describe this recent phenomenon of addiction transfer that is common following bariatric surgery.

Research into the neuroscience of glucose and cocaine treatments have shown that both food and drug abuse treatment should include DA agonist therapy inducing dopamine release as opposed to present Antagonistic DA therapy (Adler, et al. 2000).

Several molecular and metabolic processes involved in the interaction of dopaminergic system and glucose may provide possible common therapeutic targets for both food and drug abuse. They include:

  •  In the mesolimbic structure, the enkephalinergic neurons are found close to the vicinity of glucose receptors;
  • Highly concentrated glucose triggers the calcium channel to activate DA P12 cell release;
  • A significant connection between blood glucose and cerebrospinal fluid levels of homovanillic acid the DA metabolite;
  • In pharmacological doses, the glucose analog, 2-deoxyglucose (2DG), is related to improved DA yields and produces acute glucoprivation.

Dopamine function deregulation is a significant cause of addictive behaviors, like drug abuse and alcohol, and food addiction. Dopamine and other reward neurotransmitters are also part of a largely dispersed neural network responsible for regulation of eating behavior, affecting both homeostatic and hedonic mechanisms (Berridge and Kringelbach, 2015; Li, et al. 2015). Considering this, the dopaminergic and opioidergic mechanisms are especially involved in palatable food modulation, and opioid antagonists weaken drug cravings and palatable food appetite.

Therefore, palatable food cravings could be contemplated as a type of DA-opioid-related addiction. Though there are at least five dopaminergic receptors, the D1 and D2 have been most associated with reward according to research (Li, et al. 2015).

Interestingly, McCutcheon (2015) suggested that post-ingestive mechanisms occurring from nutrients in the gut could impact food consumption and behavioral conditioning. The physiological processes essential to these mechanisms are multifaceted and are thought to join in mesolimbic DA signaling to translate post-ingestive sensing of nutrients that have a reinforcement reward value.

Presently, there are three chief families of opioid receptors (μ, κ, and δ), of which the μ-receptors are most involved in reward. The cases that show common phenotypy between food and drug addiction suggest a common therapeutic target (Karlsson, et al. 2015). They found that low Mu opiate receptor (MOR) availability results in increased feeding behavior. Similarly, dopaminergic agonists reduce appetite (Frank, 2014) while DA antagonists, especially at D2 loci, increase ingestive behavior (Liu, et al. 2012). Have we hatched the common phenotype egg and should we consider common treatment for these two seemingly diverse substances?

Obese versus lean humans have less striatal D2 receptors and show fewer striatal reactions to palatable food intake (Stice, et
al. 2010). These findings align with the idea that those who have hypo-functioning reward circuitry are inclined to overeat, to satisfy a reward deficit. Also, decreases in striatal response to food intake, forecasts weight gain in the future for those at genetic risk for lowered signaling of DA-based reward circuitry, particularly
in adolescents (Stice, et al. 2010). There is also the alternate possibility that a surfeit of DA may also cause weight gain as well (Stice and Yokum, 2014).

However, animal studies specify that palatable food intake causes down-regulation of D2 receptors, decreased D2 sensitivity, and reduced reward sensitivity, suggesting that overeating may denote diminished striatal responsivity.

Stice et al. (2010; 2014) examined whether or not overeating causes decreased striatal responsivity to palatable food intake in humans utilizing repeated-measures of functional magnetic resonance imaging (fMRI). Outcomes specified that females who gained weight during a 6-month period showed a decline in striatal response to palatable food ingestion compared to females who had stable weight. Together, these results imply that low sensitivity to reward heightens the risk for overeating and additionally overeating may diminish the responsivity of reward circuitry in a feed-forward manner, specifically in DRD2 A1 allele carriers (Carpenter, et al. 2013).

Elevated stress levels, along with dopaminergic gene polymorphisms and additional neurotransmitter genetic variants, may have an aggregate effect on the susceptibility to both food and drug addiction involving epigenetic effects (Wright, et al. 2015). Recently Badgaiyan et al. (2015) clearly showed that dopaminergic tone at rest is reduced in RDS. This work suggests that subjects presenting with co-morbid abarant seeking behavior may have a common rubric displaying a hypodopmainergic trait /state.

Finally, Schulte et al. (2015) reported that processed foods, high in fat and glucose, were most frequently associated with addictive-like eating behaviors. Moreover, processing was a large, positive predictor for whether a food was associated with problematic, addictive-like eating behaviors. In a separate model, fat and glucose were large, positive predictors of problematic food ratings. This underscores the need to restrict these foods during recovery from both food and drug addiction. So common treatment must include ways whereby brain dopamine is regulated in a “homeostatic” fashion through a whole body approach.

John Giordano is a thirty-year veteran of clinical addiction treatment. Mr. Giordano is the founder and former owner of G & G Holistic Addiction Treatment Center, a 62 bed JCAHO accredited facility located in North Miami Beach, Fl.; and has contributed by Research Gate to be one of the top researchers in the country. For the latest development in cutting-edge treatment check out his website:

Kenneth Blum is a researcher on neuropsychopharmacology and
aka/the addiction gene, the alcoholic gene. He is one of the world’s foremost experts on addiction and its treatment. Dr. Blum retired as a full professor in the Department of Pharmacology, University of Texas, where he was also chief of the Division of Addictive Diseases, chief of the Division of Substance and Alcohol Misuse, and director of the Laboratory of Pharmacogenetics at the University of Texas Health Science Center (San Antonio, Texas) Dr. Blum is also a retired adjunct professor at UFL, University of Vermont and Keck Medical School Departments of Psychiatry and Behavioral Sciences. He books.