Evidence-Based Addiction Medicine (EBAM), Are We There Yet?

In the August issue (2015) of Lancet Psychiatry Hall, et al make a case that the brain disease model of addiction (BDMA) is not supported by the evidence and has not delivered on its promises [1]. They assert this partly by using the example of the spontaneous recovery of many heroin-addicted US veterans of the Vietnam War when they returned stateside [2]. But their argument is predicated on their mistaking recreational drug use with the disease of addiction. Simple recreational use of drugs is not addiction. The ability of an individual to spontaneously extinguish recreational drug use cannot be used to support their position that addiction is not a brain disease. The accepted diagnostic criteria of the process of addiction include a compulsion to use the chemical, loss of control over the quantity consumed, and continued use despite the harm caused by the substance. The disease of addiction often has a relapsing-remitting course with predictable, devastating consequences. Additionally, in the same issue of Lancet Psychiatry, Volkow and Koob put forth a correct counterpoint that clinical studies have consistently delineated specific molecular and functional neuroplastic changes at the synaptic circuitry level that are triggered by repeated drug exposure. They go on to say that these findings, along with ongoing research, are helping us to understand the neurobiological processes associated with the loss of control, compulsive drug-taking, inflexible behavior, and negative emotional states associated with addiction [3]. Additionally, there is ample evidence suggesting addiction is a biological disease of the human reward system. The neurochemical basis of the reward is the release of dopamine in the nucleus accumbens (NAc), and it is intimately connected to the ventral tegmental area, amygdala, hippocampus, orbitofrontal cortex, and prefrontal cortex. Repeated use of substances of abuse results in this system being hijacked and a phenomenon of tolerance developing. It has been demonstrated in animals that such tolerance develops with the release of transcription factors such as cyclic-AMP response element binding protein (CREB) and subsequently deltaFosB, which in turn causes organisms to get sensitized to the effects of drugs of abuse, and compulsive drug-taking takes place. Eventually, there is the release of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) that causes changes in the dendritic structures in or near the NAc [4,5,6,7]. As well as being supported by animal studies, it is also backed by neuroimaging studies in humans. In patients who have the diagnosis of addiction, it appears that it is a clear-cut brain disease implicating the reward system. This disease appears to have about a fifty percent contribution of genetics [8].