CBD and NAD+ – a very potent combination for fighting inflammation
Current research shows the powerful role that inflammation plays as an underlying cause in most pervasive chronic conditions.
Ultimately, the main issue with higher levels of inflammation that manifests as damage to tissue is the fact that when inflammation has been turned on, it increases the production of damaging free radicals, a situation we call oxidative stress. When oxidative stress is running rampant, damage occurs to our proteins, and fat, and even our DNA.
Reducing dietary sugar and carbohydrates, while at the same time increasing dietary consumption of good fats, goes a long way towards reducing inflammation.
Emerging research now demonstrates that both CBD and NAD+ have significant potential in terms of limiting inflammation.
Both CBD and NAD+ have been touted for a wide variety of health issues, with strong scientific evidence for effectiveness in treating some of the cruelest childhood epilepsy syndromes, such as Dravet syndrome and Lennox-Gastaut syndrome (LGS), which typically don’t respond to antiseizure medications.
CBD is commonly used to address anxiety, and for patients who suffer through the misery of insomnia, studies suggest that CBD may help with both falling asleep and staying asleep.
CBD demonstrates neuroinflammatory effects in mice with significant decrease of Il-6 and TNF markers of inflammation.
Dr. Nady Braidy presented at conference, NAD+ was shown to decrease IL-2, IL-6, and CRP markers of inflammation in humans.
Research on NAD+
Extracellularly applied NAD(+) prevents astrocyte death caused by excessive activation of poly(ADP-ribose) polymerase-1, In this study, we examined whether the intact form of NAD(+) is incorporated into astrocytes. A large portion of extracellularly added NAD(+) was degraded into metabolites such as AMP and adenosine in the extracellular space. The uptake of adenine ring-labeled [(14)C]NAD(+), but not nicotinamide moiety-labeled [(3)H]NAD(+), Taken together, these results indicate that exogenous NAD(+) is degraded by ectonucleotidases and that adenosine, as its metabolite, is taken up into astrocytes via the P2X7R-associated channel/pore.
The mechanisms of neuronal death in protein misfolding neurodegenerative diseases such as Parkinson’s and prion diseases are poorly understood. We used a highly toxic misfolded prion protein (TPrP) model to understand neurotoxicity induced by prion protein misfolding. We show that abnormal autophagy activation and neuronal demise is due to severe, neuron-specific, nicotinamide adenine dinucleotide (NAD+) depletion. Toxic prion protein-exposed neuronal cells exhibit dramatic reductions of intracellular NAD+ followed by decreased ATP production, and are completely rescued by treatment with NAD+ or its precursor nicotinamide because of restoration of physiological NAD+ levels. Toxic prion protein-induced NAD+ depletion results from PARP1-independent excessive protein ADP-ribosylations. In vivo, toxic prion protein-induced degeneration of hippocampal neurons is prevented dose-dependently by intracerebral injection of NAD+. Intranasal NAD+ treatment of prion-infected sick mice significantly improves activity and delays motor impairment. Our study reveals NAD+ starvation as a novel mechanism of autophagy activation and neurodegeneration induced by a misfolded amyloidogenic protein. We propose the development of NAD+ replenishment strategies for neuroprotection.
We discovered that TPrP induces neuronal death via a profound depletion of intracellular nicotinamide adenine dinucleotide (NAD+) levels causing metabolic failure. Neuronal death can be rescued in vitro and in vivo by NAD+ replenishment.
our data demonstrate for the first time that a failure of NAD+ metabolism is the cause of neuronal ailing
Moreover, our TPrP toxicity model reveals a new mechanism of NAD+ depletion independent of PARP1.
Misfolded amyloidogenic protein can induce neuronal death by genuine NAD+ starvation and that ailing neurons can be completely rescued by NAD+ treatment
Our study shows that neuronal death induced by NAD+ depletion is reversible and that NAD+ replenishment mitigates neurodegeneration.
In previous trials NADH has been shown to improve cognitive functioning in patients with Parkinson’s disease, depression and AD.
The present trial was a randomized, placebo-controlled, matched-pairs, double-blind, 6-month clinical study. Patients with probable AD (n = 26) were randomized to receive either stabilized oral NADH (10 mg/day) or placebo.
After 6 months of treatment, subjects treated with NADH showed no evidence of progressive cognitive deterioration and had significantly higher total scores on the MDRS compared with subjects treated with placebo (p < 0.05). Analysis of MDRS subscales revealed significantly better performance by NADH subjects on measures of verbal fluency (p = 0.019), visual-constructional ability (p = 0.038) and a trend (p = 0.08) to better performance on a measure of abstract verbal reasoning.
Consistent with earlier studies, the present findings support NADH as a treatment for AD.
Research on CBD
In research published in Free Radical Biology and Medicine, scientists at the University of Mississippi medical center describe the potential benefits of using CBD, which has been demonstrated to be specifically effective in dealing with various types of pain. This activity is also thought to represent a manifestation of CBD working as an anti-inflammatory.
Further, many of the health-related issues associated with obesity are a consequence of increased inflammation. CBD is being explored extensively in relation to obesity in hopes of reducing some of these important health consequences.
According to the authors:
Inflammation and oxidative stress are intimately involved in the genesis of many human diseases. Unraveling that relationship therapeutically has proven challenging, in part because inflammation and oxidative stress “feed off” each other. However, CBD would seem to be a promising starting point for further drug development given its anti-oxidant (although relatively modest) and anti-inflammatory actions on immune cells…
The research in terms of medical application of CBD is expanding dramatically, and with good reason. As a natural, plant derived anti-inflammatory, CBD joins other familiar players in this arena like turmeric which is derived from curcumin, as well as ginger and many others.
Below are some other recent research studies on CBD for pain management and inflammation. Quotes are taken directly from the studies.
Our findings obviously demonstrate that CBD has multi-functional protective assets to improve cardiac injuries; preliminary through scavenging of free radicals, and reduction of oxidative stress, apoptosis, and inflammation.
Cannabinoids are known to have analgesic properties.
The mean reduction in pain intensity scores (primary outcome measure) was greater in patients receiving sativex than placebo (mea adjusted scores1.48 points vs.0.52 points on a 0–10 Numerical Rating Scale (p= 0.004; 95% CI:1.59,0.32). Improvements in Neuropathic Pain Scale composite score (p= 0.007), sleep NRS (p= 0.001), dynamic allodynia (p= 0.042), punctate allodynia(p= 0.021), Pain Disability Index (p= 0.003) and Patient’s Global Impression of Change (p< 0.001) were similarly greater on sativex vs. placebo.
An open-label extension study showed that the initial pain relief was maintained without dose escalation or toxicity for 52 weeks.