Friday  – Saturday   •   November 20 – 21, 2020   •   Virtual Summit

 This program schedule will be updated periodically

Friday, November 20
9:00 - 9:15Welcome and Introduction
9:15 - 10:00Keynote speaker: DAN SCHNEIDER, PharmD, The Pharmacist

Addiction Neurobio and Treatments

Dr. Podesta will briefly review the neurobiology and traditional treatments and outcomes, and also review complementary evidenced based treatments.
10:45 - 11:00Break
11:00 - 11:45SUSAN BROOM GIBSON, PhD

Intravenous Administration of Nicotinamide Adenine Dinucleotide Significantly Improves Withdrawal Symptoms Associated with Chronic Opioid Exposure

I will discuss the neuro-mechanisms associated with the positively and negatively reinforcing effects of chronic opioid exposure and emphasize the importance of developing treatment protocols that provide therapeutic benefits while minimizing abuse liability. Research findings to date suggest that BR+NAD is safe and effective in treating acute withdrawal symptoms associated with opioid use disorders.
11:45 - 12:30JAMES P. WATSON, MD

Theories of How NAD+ works: The Adenosine Hypothesis

NAD+ is a key molecule in over 50 different intracellular functions or pathways. Although the most well-known role for NAD+ is that of a carrier for high energy electrons (NAD+ to NADH, and NADH to NAD+), NAD+ is not consumed or destroyed in this role. However in many other enzymatic reactions, NAD+ is hydrolyzed by NAD+ consuming enzymes. Most of the attention on these NAD+ consuming enzymes has been focused on intracellular enzymes such as Sirtuins, PARPs, MARTs, and other enzymes found within the cytoplasm, mitochondria, and cell nucleus. However there is an increasing level of awareness that enzymes found outside the cell rapidly hydrolyze the dinucleotide (NAD+) into mono nucleotides, including nicotinamide, NMN, AMP, and adenosine. Adenosine is a well-known neurotransmitter in the brain and outside the brain. The role of adenosine in alcohol addiction and alcohol withdrawal is well-known and extensively published. This lecture summarizes the many roles of NAD+ inside and outside the cell, explains how NAD+ is converted into adenosine outside the cell, and why the adenosine disappears shortly after NAD+ is broken down. This lecture then outlines an unproven hypothesis of how adenosine could explain the side effects of IV NAD+ infusion, mimicking adenosine-based cardiac stress testing.
12:30 - 1:00Lunch Break
1:00 - 1:45DAVID J. LEFER, PhD

NAD, Hydrogen Sulfide, and Nitric Oxide

Magnetic resonance-based NAD imaging for preclinical and human brain applications at ultrahigh field

Nicotinamide adenine dinucleotide (NAD) exists in oxidized (NAD+) or reduced (NADH) form in all living cells. The NAD+/NADH redox state mediates ATP energy production. NAD+ also modulates metabolic signaling via regulating the activities of NAD+-dependent enzymes; thus, participates in many important cellular processes including aging, neurodegeneration and cell death. Recently, we have developed a novel 31P magnetic resonance spectroscopy (MRS)-based in vivo NAD assay that is capable of noninvasively measuring NAD+ and NADH contents and the NAD+/NADH redox ratio in animal and human brains across a broad range of magnetic field strength from 4 to 16.4 Tesla. Our results provide first-hand information on the cellular NAD concentrations and redox state in the brains of healthy volunteers. In addition, an age-dependent increase in intracellular NADH and age-dependent reductions in NAD+, total NAD contents and NAD+/NADH redox potential were found in healthy human brains. The overall findings not only provide direct evidence of declined mitochondrial functions and altered NAD homeostasis that accompanies the normal aging process but also elucidates the merits and potentials of this new NAD assay for noninvasively studying the intracellular NAD metabolism, NAD redox state and mitochondrial functionality in the normal and diseased brain in situ.
2:30 - 2:45Break
2:45 - 3:30JAMES P. WATSON, MD

The Role of NAD+ in Defense from Viruses, Such as SARS-CoV-2

Inside the cell, NAD+ plays an indispensable role in the recognition of DNA damage as a cofactor needed for Poly-ADP-ribose Polymerases (PARPs). Recently, it has been discovered that both PARPs and mono-ADP-ribose transferases (MARTs) play an intracellular role in preventing viral replication. Outside the cell, NAD+ also appears to play a role in activating NK cells in response to viral infections, via the membrane-bound NAD+-consuming enzyme, CD38. This lecture outlines what is known about the intracellular role of NAD+ and the extracellular role of NAD+ in the defense against viruses. Special mention will be made of recent research showing a possible link between SARS-CoV and SARS-CoV-2 viral defense and the role of NAD+ for these two similar RNA viruses.
3:30 - 4:30Panel Discussion with Susan Broom Gibson, PhD; James P. Watson, MD; Wei Chen, PhD; Xiao-Hong Zhu, PhD; David and J. Lefer, PhD
Saturday, November 21

The Dos and Don’ts of NAD Treatment

As the “buzz” about NAD has intensified, more and more practitioners claim to be offering “NAD treatment.” Unfortunately, those who are untrained in proper NAD administration, or who use an inferior product, or who don’t even mean “nicotinamide adenine dinucleotide” by the letters “NAD” do both their patients and NAD’s therapeutic reputation a huge disservice. This presentation will highlight the dos and don’ts of proper intravenous NAD treatment delivery, which we have honed over 20 years of experience treating patients with substance use disorders, depression, anxiety, post-traumatic stress, and neurodegenerative diseases include Alzheimer’s, CTE, and Parkinson’s.
9:45 - 10:30HENRY LIANG, DO

NAD+ and Ketamine Combination Therapy Case Presentations

An overview of NAD and ketamine combination therapy with case presentations and discussion
10:30 -10:45Break

NAD and your genome: Where do they Interact?

Intranasal NAD: A New Way to Go

My presentation will discuss the original proposal of how the BR+NAD intranasal trial came about, based upon the theory that the administration of intranasal BR+NAD is safe and efficacious, making it available to cross the blood-brain barrier and offering potential excellent benefits to the patient. I will talk about conditions the trial team has treated including addiction, anxiety, depression, TBI, brain optimization, and neurological and autoimmune diseases. I will offer results that the trial team has seen up to this point, and limitations and side effects of the use of intranasal NAD compared to other ways of administering NAD including IV, sublingual, topical, subcutaneous, nasal spray and the patch. Future steps in the trial will be reviewed.
12:15 - 12:45Lunch

Alpha Waves Effects on Neurotransmitters
1:30 - 2:15TOM UBL

Kidney Restoration Plus (KR+ NAD), an emerging network and NAD+ fellowship opportunity.

Tom Ubl, founder of Bell Eve Treatment Center, is developing a treatment protocol that is restoring hope to people with Chronic Kidney Disease (CKD) and facing dialysis as their only treatment option, short of transplantation. KR+NAD is an alternative CKD treatment that, in the limited applications that have been conducted, have enabled 100% of recipients to postpone dialysis. The protocol utilizes NAD+ with complementary treatments such as heavy metal chelation to achieve and maintain stable kidney function, producing dramatic improvements in GFR (glomerular filtration rate) results. The protocols are evolving under the direction of Dr. Daniel Woodard, NASA MD and Institutional Review Board (IRB) participant, towards the goal of funding a larger IRB-approved study.
2:15 – 2:30Break
2:30 - 3:15ROSS GRANT, PhD

Testing blood NAD+ levels; why and how?

We all accept that maintaining adequate NAD+ levels in the body is important for optimal health and that increasing NAD+ synthesis or availability can/may be beneficial for a range of clinical conditions including drug addiction recovery, mitochondrialopathies, degenerative neurological conditions and more. However, as with many biological systems, it is rarely the case that when a little is good, more is always better: So how do we know when we have reached the ‘sweet spot’? Are there potential adverse effects of having too much NAD+? This presentation will give a brief overview of why NAD+ testing is important before discussing the challenges and limitations of currently available methodologies.
3:15 - 4:30ROSS GRANT, PhD

NAD+, homocysteine & CVD risk: Associations, possible predictive power & potential mechanisms

Homocysteine (Hcy) mediates the development of cardiovascular disease (CVD) through multiple mechanisms. However despite known biochemical linkages between Hcy and NAD+ metabolic pathways, associations between CVD risk, Hcy and the NAD+ metabolome have (to the best of our knowledge) not yet been explored in humans.

To address this gap in the literature we interrogated data collected as part of a cross-sectional study involving one hundred non diabetic, generally healthy, middle aged (40-75 years) participants. Fasting plasma levels of NAD+ and its metabolites were measured by LC/MS/MS. The percentage of red blood cell saturated fatty acids (RBC SFA) was quantitated using GC-FID. Routine techniques were employed to measure standard pathology markers, including plasma homocysteine and blood pressure.

As anticipated, plasma [Hcy] was positively associated with an increase in the 10 year Framingham Risk Score (10yrFRS)(p=0.011), an estimation of CVD risk. A positive association between [Hcy] and the inflammatory indicator; albumin to globulin ratio (Alb:Glob) (p=0.001), was also found. The Alb:Glob ratio was also positively associated with an increase in red blood cell (RBC) saturated fatty acid (SFA) levels (p=0.001).

Importantly an inverse association was found between NAD+ levels and cardiac risk (i.e. a higher 10yrFRS (p=0.013)). In fact, plasma NAD+ concentrations were found to be as good a predictor of the 10yrFRS as homocysteine [Hcy] (R2=0.262 vs. R2=0.206). A novel inverse association between plasma Hcy levels and both [NAD+] (p=0.025) and the NAD+ precursor nicotinic acid [Na] (p=0.040) was observed. We also observed that Increased RBC SFA were associated with reduced plasma [NAD+](p=0.044). Consistent with this RBC SFAs were also positively associated with plasma NADH (p=0.042), 2PY (p=0.026), NAM (p=0.026) and methyl-NAM (p=0.025).

Although more research is required this data suggests that plasma NAD+ levels may be an effective indicator of CVD risk. We postulate that this is likely mediated through its sensitivity to methylation alterations and/or inflammatory activity.
4:30- 5:30Panel Discussion with Paula Norris Mestayer, M.Ed, LPC, FAPA; Henry Liang, DO; Sharon Hausman-Cohen, MD, ABIHM; Patty DiBlasio, MD, MPH; Krishna Doniparthi, MD; Tom Ubl; Ross Grant, PhD