Many perspectives try to explain addiction. One such perspective views addiction as fundamentally an impulse control disorder. While a bit of an oversimplification, the view argues that there comes a moment, usually as a craving climaxes, that someone decides whether or not to use, whether to drink or to abstain.
The perspective contends that long-term abstinence boils down to self-control, and the ability to inhibit an urge to drink, to snort, to smoke, and so froth. According to the position, the difference to between addiction and recovery is an ability to respond to a craving, instead of acting it out.
Research from neuroscience links the function of impulse control to the hippocampus. To borrow a computer analogy, the hippocampus functions as a central processing chip, as it helps direct new information to the appropriate areas of the brain, while it also helps to coordinate the recall of stored bits of information, memories, etc. The hippocampus is a vitally important area of the brain that, if damaged, can result in a global slow down in brain functioning. As an example, damage to the entrohinal cortex – as the conduit to the hippocampus – represents the epicenter of Alzheimer’s Disease, and precipitates the pervasive loss of cognitive functioning associated with the disease. Alzheimer’s cruel effects highlight the central role of the hippocampus in our neurocognitive experience.
Research has also demonstrated that many people with moderate to severe addictions will evidence diminished volumes in the hippocampal area. Anti-depressant medications can potentially speed up the neurocognitive recovery that typically demands months to years after someone finally sobers up. A handful of studies* evidence how anti-depressants stimulate the brain’s plasticity and activate neuronal growth in the hippocampus. That is, anti-depressant medications can help recoup the hippocampal matter that shrank over the course of an addiction. In turn, a more robust hippocampus will enhance impulse control, along with processing speed and memory skills. More broadly, a healthy hippocampus can greatly aid in integrating the program that people develop in the early stages of change maintenance.
Anti-depressants can assist addiction treatment in other ways as well. Most people who check into residential treatment will generally be depleted of the neurotransmitters responsible for 1) elevating mood, 2) sparking motivation, and 3) priming the experience of pleasure. Anti-depressants can augment the availability of those neurotransmitters, and minimize the type of dysphoria (i.e., emptiness) commonly complained of in the earliest stages of change maintenance. It’s dysphoria that is often identified as the trigger to slips in the weeks and months after rehab. Potentially, then, anti-depressants can help to prevent slips in the first few months after treatment.
If you check into AToN or another residential center, be open regarding your concerns or hesitations in taking an anti-depressant. More times than not, a physician only expects to prescribe medications like Prozac or Wellbutrin in the short-term, over the course of months, to help stabilize someone so he or she can more actively engage in change maintenance.
Admissions into facilities like AToN are always voluntary. So, you will always possess the right to discontinue a medication if it simply does not agree with you during a trial run. The benefits – reduced risk of relapse, enhanced cognitive functioning, elevated mood – typically outweigh the risks or common side effects as associated with anti-depressant medications.
Dr. Kevin Murphy, Psy.D.
AToN Center 888-535-1516
*References:
- Miller, BR & Hen, R. (2015). The current state of the neurogenic theory of depression and anxiety. Curr Opin Neurobiology, 30:51–58
- Duman RS. Role of neurotrophic factors in the etiology and treatment of mood disorders. Neuromolecular Med 2004; 5: 11–25.
- Wang JW, David DJ, Monckton JE, Battaglia F, Hen R. Chronic fluoxetine stimulates maturation and synaptic plasticity of adult- born hippocampal granule cells. J Neurosci 2008; 28: 1374–1384.
- Malberg JE, Eisch AJ, Nestler EJ, Duman RS. Chronic anti-depressant treatment increases neurogenesis in adult rat hippocampus. J Neurosci 2000; 20: 9104–9110.
- Boldrini M, Underwood MD, Hen R, Rosoklija GB, Dwork AJ, John Mann J et al. Antidepressants increase neural progenitor cells in the human hippocampus. Neuropsychopharmacology 2009; 34: 2376–2389.
- Jacobs BL, van Praag H, Gage FH. Adult brain neurogenesis and psychiatry: a novel theory of depression. Mol Psychiatry 2000; 5: 262–269.
