The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 19 No. 6 • July 2016


by Sandy Shaw

Reward deficiency syndrome is the actual name of a psychiatric disorder, in which people do not have as much dopaminergic activity in the brain’s reward circuitry as most other people do. A reduced number of DRD2 dopamine receptors is a way that this can happen.

Some of those who appear to suffer from “reward deficiency syndrome” could be classed as “losers.” Yet, some “losers” are in fact quite successful in material terms, but are simply unable to FEEL good about their material or other successes. A good example could be Ray Charles, who surely must have earned an immense amount of money in his life, yet sung (and possibly wrote) many songs with the theme of being a loser; his “BORN TO LOSE” is a particularly apt example.

The reward deficiency syndrome is characterized by behavior that you can see in many people around you and which now seems to have spread throughout the population of young adults, particularly among men. The most notable features of reward deficiency syndrome can include risk-seeking, novelty seeking, a high risk for addictive, impulsive, and compulsive behavioral propensities such as compulsive shopping, pathological gambling, sexual infidelity and promiscuity, as well as drug addiction, smoking, and often suffering from attention-deficit hyperactivity disorder. (See, for example, Blum, 2008)

The key mechanism behind the reward deficiency syndrome is explained: In individuals possessing an abnormality in the DRD2 dopamine receptor gene, the brain lacks sufficient numbers of dopamine receptor sites to use the normal amount of dopamine in reward centers. (Blum, 2008) What this means is that individuals with this form of the DRD2 gene (and it is far from uncommon, judging from the features of the reward deficiency syndrome as noted in the paragraph above) are driven to “engage in activities that will increase brain dopamine function...” because it is “...the DRD2 gene that makes it difficult for neurons to respond to dopamine, the neurotransmitter that is involved in feelings of pleasure and the regulation of attention.” (Blum, 2008)

Obese individuals have fewer D2 dopamine receptors than lean individuals do. Eating causes a release of dopamine in the dorsal striatum and the amount of dopamine released is correlated with the pleasure of eating. “It has therefore been postulated that obese individuals have hypofunctioning reward circuitry, which leads them to overeat to compensate for a hypofunctioning dopamine reward system.” (Stice, 2008) In order to study striatal dopamine activity, the authors (Stice, 2008) used blood oxygen level-dependent (BOLD) fMRI to identify the areas of the brain activated when the subjects ate either a chocolate milk shake or a “tasteless solution” placebo (water). The results were consistent with the hypothesis that “the dorsal striatum is less responsive to food reward in obese, relative to lean, individuals, potentially because the former have reduced D2 receptor density and compromised dopamine signaling, which may prompt them to overeat in an effort to compensate for this reward deficit.” (Stice, 2008)


Stice et al. Relation between obesity and blunted striatal response to food is moderated by Taq1A allele. Science. 322:449-52 (2008).

Blum et al. Attention-deficit-hyperactivity disorder and reward deficiency syndrome. Neuropsychiatr Dis Treat. 4(5):893-917 (2008).

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