And when the brain is treated, it can heal
Medical science now agrees that addiction is a disease, not a “choice” or a character flaw. Unfortunately, society at large is not entirely convinced.
Those who say that addiction is a “choice” argue that addiction cannot be a disease because it is caused by behavior and behavior is a “choice.” The “disease” model argues that the symptoms are not actually a choice, but the result of a biological impairment to the midbrain. Just as a diabetic cannot change his or her blood sugar level at will, an addict cannot stop craving at will. In the diabetic, the body’s inability to produce or effectively utilize insulin is the cause. In the addict, improper functioning of the midbrain is the cause. Both diseases produce symptoms that can cause unwanted behaviors. But to successfully treat an illness, you must address the root cause, not simply the symptoms.
Dr. Kevin McCauley defines addiction as, “The dysregulation of the midbrain dopamine system due to unmanaged stress resulting in symptoms of decreased functioning—specifically loss of control, cravings, and persistent drug use despite negative consequences.” 
Although there are other organs involved in addiction, like the liver, pancreas, and more, the brain is our focus because that is where we will find the root cause. Addiction is first a brain disease and here is why.
The prefrontal cortex is associated with what we call “executive” functions like reasoning, abstract thought, self-control, planning and organization, and emotional meaning such as love, morality, spirituality, ethics, and responsibility. Some consider it the “seat of the self,” where personality and conscious awareness reside.
Interestingly, drugs don’t work in the prefrontal cortex; they work in the midbrain. This was first demonstrated by a series of experiments conducted in the ‘60s called the Olds Experiments, in which a probe of the diameter of a hair was used to determine which area of the brain was affected by drug use (specifically, the drug cocaine).
The Olds Experiments inserted probes into every possible region of the brain of rats, but the areas that resulted in addictive behavior—continual self-administration of additional doses of the drug—were the lateral hypothalamus, the nucleus accumbens, and the ventral tegmental areas (VTA) of the midbrain. Test animals would work continuously—lever-pressing at rates of several thousand responses per hour—for days to obtain direct electrical stimulation of the lateral hypothalamus and related brain regions.. The animals did so to the exclusion of other behaviors, starving themselves for the opportunity to self-stimulate if food and stimulation were concurrently available for only a limited portion of each day. (ibid, Routtenberg and Lindy, 1965) Once experienced with the stimulation, rats would cross electrified grids to gain access to the lever, accepting higher shocks to obtain stimulation than they were willing to accept to obtain food, even when deprived for 24 hours. (What person familiar with addiction doubts this result?)
Subsequent research has demonstrated that not only rats, but monkeys as well, will work similarly compulsively for intravenous stimulants to the midbrain. If given unlimited access, they will self-administer intravenous injections of these drugs to the point of severe weight loss and death. What begins as a tentative response tendency becomes a compulsive habit very quickly.
The drug apparently convinces the midbrain that obtaining more of the drug is more important than anything and everything. The drug becomes tantamount to survival.
That’s because the midbrain is where your survival instinct resides. Your midbrain is unconscious and reacts to sensory information all day, every day. It processes the life or death signaling messages, with the fight-flight-or-freeze mechanism on stand-by. These are the areas where addiction is processed, not the prefrontal cortex. The midbrain is also where reward and pleasure are processed. Addiction causes a defect in the midbrain long before the prefrontal cortex is affected. In fact, when the midbrain is activated to go into survival mode, it shuts down the prefrontal cortex. Brain imaging studies have shown this: when the midbrain is lit up, the prefrontal cortex is dark.
The tendency to label an addict or an alcoholic by the behaviors they exhibit while “under the influence” is understandable. If you have been on the receiving end of that behavior, without having the awareness or restraint to keep from lashing out with labels such as selfish, lying, cheating, stealing, criminal, sociopathic, entitled brat, loser, and “in denial,” then welcome to the human race. Unfortunately, that type of interaction only makes matters worse. Why? Because the addict’s prefrontal cortex has been hijacked by the midbrain. To the non-addicted, those of us with access to the executive functioning of the prefrontal cortex, it’s absolutely clear what addicts need to do: change their behavior. But as a practical medical matter, the only way an addict can successfully use the prefrontal cortex to address his or her addiction is by first addressing the defect in the midbrain. Moreover, I question the therapeutic value of labeling someone an addict or alcoholic when the label carries such negative connotations—generating guilt, shame, insecurity, and self-doubt. These, in turn, spark anxiety, depression, insomnia, and fatigue—increasing the stress that, in the addict’s brain, can only be relieved by drugs. Dopamine gets the credit for relieving stress and the blame when addiction neutralizes the dopamine response, but there are other neurotransmitters like glutamine, serotonin, GABA and some we haven’t yet discovered that may also be involved. Moreover, there is some data to suggest that NAD+ itself may function as a neurotransmitter, implying that if NAD+ levels are low, the addicted patient is further prevented from stress relief. However, this warrants further examination.
Stress? We ALL have stress!
Although we all have stress, not all of us can handle the stress we’re facing, in part because stress changes the physiology of the midbrain. We each experience stress differently depending on our coping mechanisms, some of which are hereditable—the genetic and epigenetic ones. However, above a certain threshold that is unique to each individual, the midbrain processes stress as a threat to survival, commanding the body to remain in constant “fight-flight-or-freeze” mode until dopamine, the body’s stress-reliever, is released, which enables it to relax. An addict has learned to get that dopamine release from a drug. That strategy makes sense because an addicted brain’s dopamine-production ability has been shut down—by the drug.
For those addicted to opiates or other painkillers, the same dynamic functions with endorphins, the body’s natural painkiller. The brain’s production capacity has been replaced by the drug, leaving a single pathway to pain relief: the narcotic. (A secondary reason for an addict to seek a drug is to get relief from excruciating withdrawals.)
The truth is that being under the influence of a substance is not limited only to the state of intoxication. A person is still under the influence of the drug even after they sober up because their brain is still impaired. The midbrain continues to insist that survival is at stake, and only a dopamine release will change that. At this point, addicts are no longer seeking to get “high,” but to relieve the agony produced by stress and the cortisol-releasing factor (CRF) in the midbrain. In fact, the limited success of most drug treatment programs is based on substituting one (legal) drug for the illegal one that has caused the addiction in the first place. Whether the replacement drug is methadone, Suboxone, caffeine, nicotine, or sugar, its biochemical role is the same: to quiet the midbrain with a dopamine release. Twelve-step programs like AA and NA attempt to augment biochemical coping strategies with social and emotional support—because these, too, reduce anxiety. But none of them do what intravenous NAD appears to do: reset the brain to its pre-addicted state.
As the American Addiction Foundation reports, NAD “binds to opioid receptors and reduces withdrawal symptoms. It replaces the vitamins and minerals which have been depleted from substance abuse. It improves brain function and acts as an antidepressant. It greatly helps to repair and restore your body from the damage caused by addiction and also helps counter the depression and mood swings associated with post-acute withdrawal syndrome. It reduces cravings and eases the pain of withdrawal.”
Further, the Summary Report on Nicotinamide Adenine Dinucleotide prepared by the University of Maryland for the FDA, reported that: “NAD was nominated for use in the management of fatigue, Alzheimer’s disease, and detox and withdrawal relating to addiction via 20-250 mg/mL and 250- 1200 mg intravenous (IV) and subcutaneous injections and oral products. Nominators provided references from published peer-reviewed literature to describe the pharmacology and support the clinical use of NAD.
“Reasons provided for nomination [of NAD] to the 503B Bulks List included:
- There are no FDA-approved formulations of NAD.
- Existing FDA-approved drugs have greater side effects, have more interactions when taken with other drugs, and may be less effective.
- Methadone is a long-term substitute for addictive drugs and becomes a replacement drug because it does not alleviate the root cause of the addictive behavior – the craving for drugs or alcohol.
- Compounded NAD may be the only product to effectively treat the indication for which it is intended.”
These third-party investigators confirm what our clinical experience has taught us: Addiction is a brain disease, and when the brain is treated, it can heal. Intravenous NAD is the most effective substance yet identified to help restore the brain. That’s why we call our treatment “BR+NAD+.” The BR is for Brain Restoration.
 Olds 1958b, Annau et al. 1974 http://www.cell.com/neuron/pdf/S0896-6273(02)00965-0.pdf
 Wise, Roy A. Brain Reward Circuitry: Review Insights from Unsensed Incentives, Neuron, Vol. 36, 229–240, October 10, 2002, Cell Press. http://www.cell.com/neuron/pdf/S0896-6273(02)00965-0.pdf
Originally published in Addiction: Dark Night of the Soul; NAD+: The Light of Hope, Balboa Press, 2019, by our founder, Paula Norris Mestayer. Reprinted with permission.
For more information on how NAD affects the brain, see: NAD in the News (Part 1) | NAD Treatment in Louisiana (springfieldwellnesscenter.com).