Susan Broom Gibson, PhD, is an associate professor of psychology, School of Natural and Behavioral Sciences, William Carey University, in Hattiesburg, MS, a research consultant for Springfield Wellness Center, and co-chairs the advisory board of NAD Research, Inc. She received her PhD in experimental psychology from the University of Mississippi in 2002 and completed research associate/fellowship positions at Boston University School of Medicine and Tulane University School of Medicine. Her areas of specialty include: the neuro-mechanisms of drug abuse and withdrawal, animal models of drug abuse and stress, and alternative treatment for substance use disorders.
Over the past 15 years she has conducted research in the therapeutic potential of IV administration of NAD for the treatment of acute withdrawal symptoms associated with substance use disorders and Parkinson’s, and in the therapeutic potential of intranasal (sphenocatheter) administration of NAD for migraines and the maintenance of symptoms associated with Parkinson’s Disease. She spoke with us via Zoom in March 2023.
NAD Research: How did you become interested in NAD?
Broom Gibson: My interest in NAD grew out of my previous experience in drug research. Beginning as an undergrad at Ole Miss (University of Mississippi), I worked as a research assistant for Dr. Kenneth Sufka, whose lab was primarily interested in chronic inflammatory pain and in animal screening models for anti-inflammatory and anti-anxiety
medications. Many experiments involved screening novel compounds developed by the pharmaceutical industry aimed at treating clinical conditions such as chronic pain and anxiety. That experience taught me a lot about screening potential pharmaceuticals, not only for the therapeutic benefits, but also the avoidance of negative side effects, including abuse liability.
When I got into graduate school, also at Ole Miss, we had a new faculty member, Dr. Karen Sabol, whose lab was measuring the neurotoxicity of methamphetamine and also studying its behavioral effects in rodents. Working as a graduate research assistant, I also got a good background in how to measure changes in extracellular neurotransmitters in vivo. At the same time, I was also working
for the National Center for Natural Products Research at Ole Miss, which focused on developing the pharmacokinetic profile of various botanical extracts and then study them in animal models for therapeutic potential.
In summary, the research I now conduct using NAD+ complements my previous work involving development of non-pharmaceutical alternatives that possess high therapeutic potential while minimizing negative side effects.
I then completed two internships. I worked with Dr. Brian
Yamamoto at Boston University Medical School in the Laboratory of
Neurochemistry between 2002 and 2004 performing research funded by the National Institute on Drug Abuse (NIDA) investigating the neurotoxic effects of high-dose methamphetamine-exposed, or amphetamine- or cocaine-exposed rodents. In addition to high-dose amphetamine exposure, our research also showed significant effects of chronic stress on mesolimbic dopamine function. It is also noteworthy that the neurotoxic effects of amphetamines related to basal ganglia circuitry are often used in the study of Parkinson’s Disease.
My second internship was at Tulane Medical School in the
Department of Structural and Cellular Biology, from 2004 until Hurricane Katrina wiped everything out. Prior to Katrina, I was working with Dr. Richard Harlan on research to understand different patterns of opioid self-administration behavior, which is a very commonly used animal paradigm to look at the establishment and maintenance of substance abuse patterns. He was particularly interested in sex differences in self-administration of opioids. That was one of the reasons I wanted to work with him, because intravenous self-administration (by pressing a lever connected to a syringe that will pump a dose of morphine via catheter) was a behavioral model I was familiar with, but had not directly set up. In addition to behavioral analysis, we planned to conduct additional research on associated neurochemical changes that might explain observed sex differences in opioid self-administration.
After Katrina, however, I moved to William Carey University and started teaching. I wasn’t really involved in research until I met Dr. Mestayer at a holiday dinner. We got to talking and my involvement grew from there.
At the time we met, we didn’t yet know that the molecule we
were interested in was NAD. We were still thinking it was amino acids, which is what Dr. Hitt (from the Hitt Clinic in Mexico) called his formula. Over these past 15-plus years, we’ve gone from utilizing intravenous NAD to address cravings associated with substance use disorders to now addressing all of these other clinical conditions: depression, post-traumatic stress, Alzheimer’s, Parkinson’s, migraines, traumatic brain injury, and even CTE. It’s pretty amazing. There’s so much potential here. It’s such an exciting time. I was just telling my new research students, “Get ready. There is just so much to do.”
NAD Research: That is so true. Which is why it’s so frustrating that the lack of funding is constantly limiting the amount we can get done.
Please tell us about the investigations into NAD that you’ve
conducted to date.
Broom Gibson: I started around 2008 doing retrospective analyses on the treatment’s effect on opioid and alcohol cravings. This was data the clinic had already collected using a self-assessment questionnaire. We’ve been building on that Excel worksheet since 2008, when we presented the data as a poster at the Society for Neuroscience gathering in Washington, DC. Then, in 2014, we made another poster
presentation on cravings outcomes in opioid and alcohol patients, now that we knew the active ingredient was NAD.
NAD Research: Yes. However, the treatment was essentially the same; we just hadn’t identified the active ingredient.
Broom Gibson: That’s right. In addition to the retrospective
studies, we were interested in looking at case report research designs in order to begin setting up larger scale (i.e., more expensive) experiments to establish safety and efficacy of IV NAD+.
Our first case involved a 77-year-old male patient with a 10-year
history of Parkinson’s Disease and no known history of mental disorder or substance abuse. The patient was intravenously supplemented with NAD+ at Springfield Wellness Center for a period of eight treatment days, with two non-treatment days in between.
Before arrival, the patient suffered from severe head and bilateral hand tremors, inability to perform activities of daily living, peripheral hallucinations, and decreased social interactions due to PD.
In his prior treatment of PD, the patient was utilizing Carvedilol, Vytorin,
Pramipexole, and Olmesartan as medications.
Before beginning day one of treatment, the patient experienced severe bilateral hand tremors. Two hours into receiving his first NAD+ treatment, his tremors stopped, both at rest and while holding an object. By later that evening, his hand tremors had returned somewhat, yet he was able to hold utensils and sign his name—two activities he’d been unable to do when he arrived. By day two of treatment, some hand tremors were present, yet were significantly improved, with an additional newly marked absence of visual hallucinations. By day three of treatment, the patient experienced some hand tremors only, but their severity had subsided dramatically. By the following day of non-treatment, the patient had slight hand tremors, similar to the prior
day, yet the severity remained at a constant, diminished rate. Likewise, by the next day of non-treatment, slight hand tremors were reported, which increased as the day progressed.
Beginning day four of treatment, the patient’s tremors had subsided at rest in the early afternoon, and by late evening all visible tremors were absent. On day five of treatment, no visible shaking was noticed,
and his handwriting was legible. On day six of treatment, although he reported slight tremors in both thumbs upon awakening, the patient displayed no visible tremors at the clinic throughout the day and into the evening. On day seven of treatment, there likewise were no visible tremors. On day eight of treatment, the patient had no visible tremors, and although he had experienced peripheral hallucinations upon awakening before treatment, his hallucinations had fully
subsided after the day’s intravenous treatment.
By the end of his intravenous NAD+ treatment, the patient
had received a total of 6,250mg of NAD+. For PD maintenance, the patient continues to receive regular intravenous NAD boosters, approximately every 4-6 weeks, in addition to symptom maintenance treatment with a 300mg-ml nasal spray (0.1ml. per spray), twice daily. This regimen has continued to keep his tremors to a minimum, and the patient has managed to discontinue all PD-related medications, with no adverse effects.
In the fall of 2019, we presented a 2nd case report involving a patient seeking treatment for tremors associated with Parkinson’s. In fact, this patient actually created an app on his watch to measure his tremors. The patient was a 58-year-old male, who had been diagnosed with PD five years prior to treatment. He reported taking PD medications in the class of dopamine agonists and had received only minimal alleviation of symptoms.
Our treatment consisted of IV infusions of NAD as well as oral supplementation of Vitamin C, Balance D and electrolytes. The patient received IV NAD+ (two days of 1,500mg followed by four days of 750mg) for a total of six days. Tremor measurements were recorded (dominant right hand) beginning on Day 2, using the patient’s cell phone gyroscope and accelerometer (Toozon Tremor) to empirically measure tremors (Hz) on Vertical, Horizontal and Anterior-Posterior axes. We used an assessment tool called Luminosity to assess cognitive performance (Memory, Attention, Problem Solving) on Day 1 (Baseline) and Day 5. Following day 6, the patient received sublingual NAD+ tablets (300mg 2Xday) and recorded his mean tremors for 14 days.
The study, which was originally presented at the Society for Neuroscience Conference in 2019, was later published in the HSOA
Journal of Gerontology and Geriatric Medicine, showed that IV BR+NAD effectively reduces tremors and improves cognitive performance in a subset of Parkinson’s Disease patients. We also demonstrated the longevity and endurance of the initial IV NAD+ followed by sublingual tablets (300mg 2x/day) in maintaining
the alleviation of PD symptoms.
Our next project was with Dr. Ross Grant, who led a pharmacokinetic
pilot study to measure increases in NAD+ levels in plasma and urine
following an infusion. My role was to conduct the participants’ cognitive performance tests, which are secondary measures of intravenous NAD effectiveness. I identified an assessment tool called MicroCog, which I administered to the subjects. Dr. Grant has published his section on the pharmacokinetics in Frontiers in Aging
Neuroscience (September 12, 2019), and I am scheduled to follow up with the cognitive performance data, which we have presented at the Mississippi Academy of Sciences and also at the American Congress of Rehabilitative Medicine. The results showed that IV NAD appears to improve measures of cognitive performance over and above “practice” effects.
Then, last year (2022), we presented a poster on Intranasal administration of nicotinamide adenine dinucleotide alleviates headaches associated with migraine pain: A case report with my undergraduate research student, Abby Thompson, at the Mississippi Academy of Sciences. That case report, conducted by Dr. Patty DiBlasio, was with an 87-year-old woman with a 50-year history of migraines, who received NAD/lidocaine at 100 mg/mL, 0.5% per protocol of 0.5 mL, intranasally into each nostril via sphenocatheter. For follow-up, the patient was prescribed Real NAD+ (150mg/day) sublingual lozenges over a three-month period, with follow-up interviews conducted at one week, six weeks, three months, and one year. The patient reported no adverse effects and has not had a single recurring migraine since.
Also in 2022, we presented a poster at the Society for Neuroscience Conference in San Diego, California. Jake White, another former
student, worked with Dr. Arwen Podesta on Intranasal Administration of Nicotinamide Adenine Dinucleotide Alleviates Headaches Associated with Migraine Pain and Reduces Adverse Effects of Anxiety Disorders: A Case Report. That patient was a 55-year-old male with
debilitating panic attacks, migraines that had been poorly controlled by
medications (quetiapine, oxcarbapezine, sumatiptan, and oxygen), anxiety and agoraphobia, as well as attempted suicide. The patient was treated with .375 ml of 100 mg/ml NAD+ and .25 ml of 20 mg/ml lidocaine into each nostril via sphenocatheter. The treatment was repeated at one and four weeks, and then interrupted by the Covid pandemic. However, follow-up measures of the patient’s well-being were conducted at two months, eight months, one-year, and two-year
time points, utilizing the Warwick-Edinburg Mental Well-being Scale (WEMWBS).
The results can be seen on the poster at the NAD Research website, but to summarize, NAD+ dramatically reduced the patient’s migraine symptoms and improved his WEMWBS score in less than four days. Moreover, despite an interrupted treatment schedule, the improvements were maintained to a lesser extent for two years.
Our most recent poster presentation is one that another undergraduate student Zalee King completed with data from three of Dr. Tyson Olds’ Parkinson’s patients at Springfield Wellness Center. That particular treatment design was novel in that the patients initially received
intravenous NAD, with follow-up maintenance doses of NAD administered using the sphenocath. The study demonstrated that for those three patients, the sphenocath was an effective way of maintaining suppression of Parkinson’s symptoms. One of the patients also had pain, which might have diminished his response to treatment, as we pointed out in the presentation.
NAD Research: Can you tell us a little bit more about the sphenocath procedure? How well do most patients tolerate it?
Broom Gibson: I’m not hearing anything adverse. I looked at Dr. Olds’ patient consent sheet, which listed some possible side effects, such as stinging and burning, but the NAD is usually administered with lidocaine, so any stinging is eliminated pretty quickly.
Personally, I think the sphenocatheter is amazing because it
delivers an effect comparable to the IV in a much shorter amount of time, which of course makes it easier for providers to administer and for patients to afford.
I’ve had the sphenocath twice. I was Dr. Podesta’s “test patient” when Dr. Dave Workman came to train our team. It’s a very straightforward procedure. You’re seated in a reclining chair, they insert the catheter into each nostril, administering the NAD/lidocaine directly into your
sphenopalatine ganglia (over the course of about a minute or two) and you stay in a reclining position for about 15 minutes. That’s it. You can feel the effects immediately, or within an hour at most. On the initial insertion, it felt a little bit like when you get water up your nose, but Dr. Olds has since modified the catheter, so this effect doesn’t seem as uncomfortable as before. And because there’s lidocaine in the solution, you’ll feel a numbness on either side of your nose, which is how they know it’s been delivered to the right place. Again, that’s temporary. The numbness doesn’t last very long. In both cases, I experienced relaxation of the muscles in my neck and shoulders for at least 12 hrs. The benefits definitely outweigh the risks.
NAD Research: What are your thoughts about why NAD is effective at treating these various conditions—from addiction to Parkinson’s to migraines?
Broom Gibson: For starters, NAD is the livelihood of the cell. It produces the energy the cell needs to function. When you see that these clinical conditions are all strongly associated with declines in NAD levels, it’s easy to see why intravenous or intranasal NAD supplementation would help to alleviate them. And the more we
study NAD, the more we identify additional roles it plays in maintaining
health—in DNA repair, as a signaling molecule, and in epigenetics and brain function. It appears that NAD plays a different vital role in the viability of different types of cells.
NAD Research: When you say that these conditions—addictions, Parkinson’s, and migraines—are associated with declining NAD levels, are we talking about intracellular NAD? Or extracellular? I was fascinated by Michael Payne’s reference to free-circulating
mitochondria—which may be where intravenous NAD is having such an immediate effect.
Broom Gibson: The research shows that NAD levels decline with age in all kinds of tissues—including the cells of the liver, skeletal muscle, adipose tissue, heart, brain, kidney, pancreas, lungs, spleen, and skin, as well as in extracellular fluids. A condition can be the result of more than one thing happening: NAD levels naturally decline with age, and also with age you tend to have accumulated more inflammation, or “inflammaging,” which can cause disease. My
experience with Drs. Sabol and Yamamoto involved measuring extracellular fluids—what’s floating around in the extracellular space between two neurons—which was done through in vivo micro dialysis. But I would be really interested in looking more closely at NAD on the intracellular level.
NAD Research: Is NAD deficient also in migraine sufferers—who may or may not be old?
Broom Gibson: It’s possible. With migraines, it might be more about NAD’s role in certain anti-inflammatory processes. I’m not an expert on migraine headache, but based on my experience with chronic arthritic-type pain, I would say that NAD plays a role in repairing the damage caused by inflammation, whether chronic and low-grade or acute.
I have a really good friend in her early 40s who has severe migraines and also Lyme disease and other medical problems that date back to
her teenage years. I think I finally have convinced her to go see Dr. Olds and let him treat her with NAD. She can be another case report because I’m convinced it will work for her, based on the other patients that we’ve seen.
NAD Research: Okay. Last question. What are your aspirations for future NAD research?
Broom Gibson: I want to keep doing what we’re doing. I want to move it forward, with more researchers on board because there’s just so much potential here, and I personally don’t have enough hours in the day to get to everything that needs to be done.
I’ll also say that I have a soft spot for the substance use disorder population. I think it’s really important that we help these individuals, the ones addicted to opioids, because right now the alternative is
to treat them with another narcotic. That’s not a solution. We shouldn’t be doing that, and we don’t have to. With NAD, we’re showing great, positive outcomes without any abuse liability. I think that’s the direction we need to go.
NAD Research: Can you give us a short list of your high-priority projects—so readers can understand why we need funding?
Broom Gibson: The number one priority for me right now is moving forward with our long-term outcomes project. This is the study that follows our substance use disorder patients long-term and tracks their cravings and any relapses. Eventually we’ll expand it to cover long-term outcomes for all patients at Springfield Wellness Center—addiction patients, Parkinson’s, Alzheimer’s, CTE, migraines, all of
We’re hoping to get an app developed so that every patient
will be able to report back on their long-term wellbeing—including cognitive performance assessment. Dr. Mestayer and Dr. LeBon are particularly interested in cognitive performance recovery in individuals who have traumatic brain injury. There’s an area of the frontal cortex called the orbital frontal lobe that is severely damaged in TBI and also from repeated concussions and such.
Research also shows that the frontal cortex is damaged by
substance use disorder, so part of the process of keeping individuals sober is going to be rehabilitating that particular area of the brain that we need for executive functioning for impulse control.
Also, Dr. Arwen Podesta’s group has recently reached out to
us regarding the Pennington group, which has suggested that we develop a grant application to look at using NAD in the treatment of autism disorders. That’s a whole other avenue of investigation. The potential for getting grant funding for that would be extremely beneficial. Michael Payne has treated autism patients with NAD, so we could publish at least one case report on NAD and autism.
Finally—and this is actually perhaps the most important—we
need to publish results that further establish the safety and efficacy of IV NAD for addiction detox, as well as for the previously mentioned case reports that provide important direction in setting up larger scale experimental research designs. Intravenous delivery really produces the most robust effects. It stops the cravings associated with withdrawal from opioids, alcohol, stimulants and polydrug
groups, and the tremors in Parkinson’s almost immediately. It’s incredible.
I think the substance use disorder population probably presents the biggest opportunity because, one, we are currently in an opioid
crisis, which was further exacerbated by the COVID-19 pandemic and the increased availability of synthetic opioids such as fentanyl. Second, traditional/covered detox treatments involving “medically assisted therapy” are using a drug to replace a drug, period. They don’t work, as evidenced by the increasing rates of overdoses and deaths associated with relapse. We’re not doing that. Plus, we have the longest history of data collection on that population, so we’re in a really good place to get an even bigger picture of why NAD+ should be the standard of care for these at-risk populations. So, we’ve got a lot of work to do. The data are there; we just need time and resources to