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In: Case Studies

November 15, 2010

Sleep Deprivation

New York-Presbyterian Hospital-Weill Medical College of Cornell University

ENADAlert® (NADH), A NUTRITIONAL SUPPLEMENT, IMPROVED ASPECTS OF COGNITIVE PERFORMANCE FOLLOWING SLEEP DEPRIVATION

White Plains, N.Y. Researchers in the Sleep-Wake Disorders Center, New York Weill Cornell Medical Center, tested the ability of oral stabilized NADH* (ENADAlert) to improve alertness, mood, and performance on cognitive (thinking) tasks in 25 healthy middle-aged adults after one night of total sleep deprivation. In previously published clinical studies, NADH has been shown to increase energy and alertness in adults with Chronic Fatigue Syndrome1 and to reduce the effects of jet lag on cognitive performance and sleepiness2.

Sleep deprivation is a common problem affecting most people during adulthood. It impacts otherwise healthy individuals who cross time zones, work during evening or nighttime hours, or have infant children, as well as patients with sleep disorders, certain psychiatric disorders, and medical conditions such as those that produce chronic pain. Sleep deprivation can lead to declines in cognitive performance, impacting the quality of waking time and, if severe enough, can lead to vehicle collisions and occupational consequences.

In this double-blind crossover study, subjects performed significantly better on some measures of cognitive performance following one night of total sleep deprivation when they received the NADH supplement compared to placebo. In particular, overall performance efficiency (number of correct answers per minute) measured one hour after consuming 20 mg lozenge NADH was significantly higher than after placebo. In a second analysis, math throughput and visual sequence comparison speed and throughput were themselves significantly better following NADH. Self-reported alertness, sleepiness (both self-reported and objectively quantified), and mood did not differ when the subjects consumed NADH or placebo. Although several subjects reported typical effects of total sleep deprivation, no adverse effects were attributed to NADH.

This study is among the first to rigorously evaluate a non-prescription substance other than stimulants, like caffeine, for alleviating the effects of sleep deprivation. Dr. Margaret Moline, the lead researcher and Director of the Sleep-Wake Disorders Center at the Westchester Division of New York-Presbyterian Hospital in White Plains, states, “NADH is the first non-stimulant, non-herbal product to show signs of improved cognitive performance, despite normally reported increased sleepiness and fatigue following sleep deprivation. These results suggest that NADH may have an important role to play in mitigating some of the effects of unavoidable sleep deprivation.”

References: *Coenzyme; nicotinamide adenine dinucleotide hydrogen

1. Forsyth LM, Preuss HG, MacDowell AL, Chiazze L, B GD, Bellanti JA. Therapeutic effects of oral NADH on the symptoms of patients with chronic fatigue syndrome. Annals of Allergy Asthma & Immunology 1999, 82:185-191.

2. Kay GG, Viirre E, Clark J. Stabilized NADH as a countermeasure for jet lag: Abstract presented and published in the proceedings of the 48th International Congress of Aviation and Space Medicine, September 2000.

This study was sponsored by MENUCO Corporation.

For Release December 18, 2001

Contact:

Jonathan Weil
212 821-0566
jweil@med.cornell.edu

or

Camille Tibaldeo
212 246-6543
camillebuzz@yahoo.com

November 15, 2010

Safety

ON THE SAFETY OF REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE (NADH)

THE MAXIMUM TOLERATED DOSE (MTD) IN DOGS IS 500 MG PER KG*

B J.G.D.1 2 , Nadlinger K.F.R.’

1. Dept. of Research & Development, B Laboratories, Vienna, Austria
2. Dept. of Medical Chemistry, University of Graz, Graz, Austria

Read more:

On the safety of reduced nicotinamide adenine dinucleotide

NADH by James South

Safety of Stabilised NADH – 26 week Chronic Toxicity Study

10mg ENADAlert Quality testing 2003

Stability Test of 10mg ENADAlert

November 15, 2010

Jet Lag Remedy


Current remedies for jet lag (phototherapy, melatonin, stimulant, and sedative medications) are limited in efficacy and practicality. The efficacy of a stabilized, sublingual form of reduced nicotinamide adenine dinucleotide (NADH, ENADAlert®, Menuco Corp.) as a countermeasure for jet lag was examined.

Hypothesis

Because NADH increases cellular production of ATP and facilitates dopamine synthesis, it may counteract the effects of jet lag on cognitive functioning and sleepiness.

Methods

Thirty-five healthy, employed subjects participated in this double-blind, placebo-controlled study. Training and baseline testing were conducted on the West Coast before subjects flew overnight to the East Coast, where they would experience a 3-hour time difference. Upon arrival, individuals were randomly assigned to receive either 20 mg of sublingual stabilized NADH (n=18) or identical placebo tablets (n=17). All participants completed computer-administered tests (including CogScreen7) to assess changes in cognitive functioning, mood, and sleepiness in the morning and afternoon.

Results

Jet lag resulted in increased sleepiness for over half the participants and deterioration of cognitive functioning for approximately one third. The morning following the flight, subjects experienced lapses of attention in addition to disruptions in working memory, divided attention, and visual perceptual speed. Individuals who received NADH performed significantly better on 5 of 8 cognitive and psychomotor test measures (P<.05) and showed a trend for better performance on the other three measures (P<.10). Subjects also reported less sleepiness compared with those who received placebo. No adverse effects were observed with NADH treatment.

Conclusions

Stabilized NADH significantly reduced jet lag-induced disruptions of cognitive functioning, was easily administered, and was found to have no adverse side effects.

November 15, 2010

Increased Brain Performance

The sensor for blood-flow need with neural activity and exercise is not known. We tested the hypothesis that accumulation of electrons in cytosolic free nicotinamide adenine dinucleotide (NAD) activates redox signaling pathways to augment blood flow. NAD is the primary carrier of electrons from glucose and lactate for ATP synthesis. Because increased glycolysis transfers electrons from glucose to NAD+ faster than they are used for mitochondrial ATP synthesis, electrons accumulate in cytosolic NADH. Because cytosolic NADH and intra- and extracellular lactate/pyruvate (L/P) ratios are all in near-equilibrium, NADH can be increased or decreased by i.v. lactate or pyruvate. Here, we report that elevated plasma LJ`P in non-nal rats increases blood flow in numerous resting tissues and augments blood flow increases in activated somatosensory (barrel) cortex and contracting skeletal muscle. Increased flows are largely prevented by injection of pyruvate (to lower L/P), a superoxide dismutase mimic (to block vascular effects of superoxide), or an inhibitor of nitric oxide synthase (to block *NO vasodilatation). Electrons carried by. NADH, in addition to fueling ATP synthesis, also fuel redox signaling pathways to augment blood flow in resting and working tissues. These novel findings are fundamental to understanding blood-flow physiology and pathology.

Read more:

NADH sensor of blood flow need brain, muscle, and other tissue

Bioavailability of Reduced Nicotinamide-adenin-dinocleotide

Brain Research Prevent Nitration of Tyrosine Hydroxylase

Cornell University Cognitive Performance Study Oct 2001

November 15, 2010

Heart Healthy Diet

The aim of this study was to investigate the effect of NADH-supplementation on the metabolic condition of isolated guinea pig ventricular cardiomyocytes using the pinacidil-primed IK(ATp) as an indicator of subsarcolemmal ATP concentration. Membrane currents were studied using the patch-clamp technique in the whole-cell recording mode at 36-37oC. Under physiological conditions (4.3 mM ATP in the pipette solution, ATPj) IK(ATP) did not contribute to basal electrical activity The K(ATP) channel opener pinacidil activated IK(ATP) dependent on [ATP]i showing a significantly more pronounced activation at lower (1 mM) [ATP]j. Incubation of cardiomyocytes with 300 μg/mI NADH (4-6 h) resulted in a significantly reduced IK(ATp) activation by pinacidil compared to control cells. Equimolar amounts of the related compounds nicotinamide and NAD+ were not able to achieve a similar effect like NADH.

These data show that incubation of guinea pig ventricular cardiomyocytes with NADH results in a decreased activation Of IK(ATp) by pinacidil compared to control myocytes indicating a higher subsarcolemmal ATP concentration due to NADH -supplementation. Measurement of adenine nucleotides by HPLC revealed a significant increase in intracellular ATP (NADH supplementation: 45.59 ± 1,88 nmol/mg protein versus control: 35.35 ± 2.57 nmol/mg protein, P < 0.000005).

Read more:

NADH Supplementation Decreases

November 15, 2010

Energy Charts

NADH Energizes Mental and Physical Performance

Every living cell, from bacteria up to human, contains coenzyme nicotinamide adenine dinucleotide (NADH), a coenzyme critical to cellular energy producfion.1 Cells that use the most energy, such as brain and muscle cells, also hold the highest amounts of NADH. Human heart cells, for instance, contain a whopping 90 mcg of NADH per gram of tissue.

Like Co-Q10, NADH is involved in the synthesis of adenosine triphosphate (ATP), the body’s primary intracellular energy source.2 When NADH is oxidized in cellular energy-producing organelles called mitochondria, and it forms water and energy. This energy is preserved as ATP. Every energy-consuming reaction requires ATP, so the more NADH a cell has available, the more energy it can produce. To keep up with the cellular demand for energy, the body continuously synthesizes NADH (a process that involves niacin, a B-complex vitamin).3

Although NADH occurs naturally in all plant and animal cells, its most plentiful sources are red meat, poultry and yeast. Vegetables are not as rich in NADH as animal tissues, because food processing, cooking and stomach acids can destroy the NADH present in most foods, sprinkling yeast and meals is a good way to increase NADH consumption.

NADH Energizes Mental and Physical Performance January 1998

Extracellular metabolism of NADH by blood cells correlates

NADH – Biological Rocket Fuel

NADH supplementation decreases pinacidil-primed l k(ATP)

November 15, 2010

CoQ10

Coenzyme Q10, or CoQ10, is not an antioxidant although it is characterized as such in all of the commercial available products. Coenzyme Q10 is the oxidized form of this substance and an oxidant can never ever be an antioxidant. However, when Co Q10 is absorbed into the organism it is reduced by NADH and thus, becomes an antioxidant. In other words, NADH makes Coenzyme Q-10 in the body into an antioxidant; hence, CoQ10 needs NADH to become effective. Additionally, Co Q10 concentrations may be increased with NADH supplements . If you take commercially available coenzyme Q10 without an equivalent dose of NADH, you may deplete the cell from NADH and thereby make the cell energy deficient and prone to degeneration.

This fact implies two consequences: the intake of commercially available CoQ10 is not very meaningful unless the organism has sufficient ammounts of cellular NADH available to reduce Co Q10 and make it an antioxidant.

November 15, 2010

Blood Pressure

Oral reduced B-nicotinamide adenine dinucleotide (NADH) affects blood pressure, lipid peroxidation, and lipid profile in hypertensive rats (SHR).

Read more:

Oral reduced B-nicotinamide adenine dinucleotide (NADH)

November 15, 2010

Antioxidant

Nadh is strong reducing agent and has been suggested to act indirectly as an antioxidant. One such possibility is via the reduction of GSSG to GSH. Only recently the activity of NADH as a directly action antioxidant in mitochondria.

Read more:

In Vitro Antioxidative Properties of Reduced Nicotinamide ad

NAD(P) H, a Directly Operating Antioxidant 2001

The Antioxidative Capacity of ENADA-NADH in Humans Oct 2002

November 15, 2010

Anti-Aging

The aim of this study was to investigate the effect of NADH-supplementation on the metabolic condition of isolated guinea pig ventricular cardiomyocytes using the pinacidil-primed IK(ATp) as an indicator of subsarcolemmal ATP concentration. Membrane currents were studied using the patch-clamp technique in the whole-cell recording mode at 36-37oC. Under physiological conditions (4.3 mM ATP in the pipette solution, ATPj) IK(ATP) did not contribute to basal electrical activity The K(ATP) channel opener pinacidil activated IK(ATP) dependent on [ATP]i showing a significantly more pronounced activation at lower (1 mM) [ATP]j. Incubation of cardiomyocytes with 300 μg/mI NADH (4-6 h) resulted in a significantly reduced IK(ATp) activation by pinacidil compared to control cells. Equimolar amounts of the related compounds nicotinamide and NAD+ were not able to achieve a similar effect like NADH. These data show that incubation of guinea pig ventricular cardiomyocytes with NADH results in a decreased activation Of IK(ATp) by pinacidil compared to control myocytes indicating a higher subsarcolemmal ATP concentration due to NADH -supplementation. Measurement of adenine nucleotides by HPLC revealed a significant increase in intracellular ATP (NADH supplementation: 45.59 ± 1,88 nmol/mg protein versus control: 35.35 ± 2.57 nmol/mg protein, P < 0.000005).

Read more:

NADH supplementation decreases pinacidil-primed l k(ATP)

Publication NADH supplementation decreases pinacidil-primed