Addiction is a multifactorial disorder that involves a disruption of normal social, behavioral and physiologic processes. Although definitions vary, most experts agree that "addiction" implies a risk of harm to the addicted individual and a need to discontinue the use of an abused substance, even if the addict does not understand the consequences of substance abuse or agree to abstain. Addicts who choose to enter recovery must contend with alterations in neurotransmitter pathways that result from substance abuse.
Neurotransmitters are chemical messenger molecules, such as dopamine or serotonin, which your brain uses to relay impulses throughout your nervous system. Neurotransmitters are released at the end of one nerve cell, or neuron, and are picked up by receptors on the surface of the next neuron in line. This propagates the impulse from one neuron to the next. Most substances that cause addictive behavior either deplete neurotransmitters in vital brain centers or upset the balance between neurotransmitters and their receptors.
Dopamine is synthesized from the amino acid L-tyrosine at several sites in your body, including your brain. The nearly ubiquitous presence of dopamine receptors in a variety of organs and tissues attests to the importance of this neurotransmitter. Because dopamine plays a vital role in the pleasure centers of your brain, substances that evoke pleasure or euphoria, such as cocaine or methamphetamine, typically cause derangements in dopamine pathways. Dopamine's actions also influence your moods, emotional responses, sleep cycles, ability to sense pain and motor function, or movement.
Disruption of normal sleep cycles is common in addiction, and much of this disturbance is driven by changes in neurotransmitter levels or in the receptors that respond to them. A 2001 article in "The Journal of Neuroscience" outlines dopamine's role in the maintenance of normal sleep cycles and the regulation of various levels of sleep. Aside from its direct effects on sleep architecture, stimulation of dopamine receptors appears to affect alertness, focusing ability and motivation.
Depression and other mood disturbances are frequently experienced by addicted individuals. Such disorders are often the direct result of substance abuse, rather than being a part of the addict's underlying personality. In fact, a diagnosis of depression cannot be made until an addict has been "clean" for some time. Several studies have investigated dopamine's under-appreciated role in depression, including a 2007 review, published in the German journal "Der Nervenarzt."
Recovering addicts must discover ways to overcome the cravings that can thwart their therapeutic efforts. A 2008 study published in "Neuron" demonstrated that some substances, such as methamphetamine, can alter dopamine dynamics in the brain for many months, particularly in brain centers that control cravings and habituation. Replenishing dopamine in these centers and reestablishing normal receptor activity could help to alleviate cravings in recovering addicts.
L-tyrosine is an amino acid that serves as a precursor for dopamine and other catecholamine neurotransmitters, such as norepinephrine and epinephrine. Theoretically, increasing L-tyrosine levels in vital brain centers would amplify the synthesis of dopamine and mitigate some of the symptoms of addiction. Indeed, recovering addicts commonly supplement with L-tyrosine as part of their treatment protocol. However, L-tyrosine has not been scientifically proven to be of benefit in addiction recovery, so individuals interested in trying L-tyrosine should check with their doctors.
- "The Merck Manual of Diagnosis and Therapy, 18th Edition: Drug Use and Dependence"; Mark H. Beers, M.D., Editor-In-Chief; 2006
- "The Journal of Neuroscience"; Dopaminergic Role in Stimulant-Induced Wakefulness; Wisor J, et al.; 2001
- "Der Nervenarzt"; Antidepressant effects of dopamine agonists. Experimental and clinical findings; Lemke M; 2007
- "Neuron"; Repeated exposure to methamphetamine causes long-lasting presynaptic corticostriatal depression that is renormalized with drug readministration; Bamford N, et al.; 2008