Enada NADH (nicotinamide adenine dinucleotide) is the original and only patented, stabilized, and absorbable form of food grade NADH, formulated to provide sustained energy as well as a boost in mental alertness and clarity. Enada is used by thousands of people to help alleviate symptoms of chronic health conditions.
Enada is an enteric coated 5mg tablet of NADH and is the bio-available, anti-oxidant form of Vitamin B-3. It is essential to the production of ATP (cellular energy). ATP, or adenosine triphosphate, is the primary energy carrier of the body. NADH plays a key role in cellular energy production, particularly in the brain and central nervous system. NADH is also involved in basic metabolism, the breakdown of glucose and fats, and supplies energy to the brain, nerves, muscles, heart, and all other organs. Enada helps symptoms of health conditions such as Chronic Fatigue Syndrome (CFS), Fibromyalgia, depression, Alzheimers, Parkinsons, Jet Lag, ADHD (Attention Deficit Hyperactivity Disorder), and provides sustainable energy. It also supports DNA repair, boosts immune system, and helps cell regeneration. What was commonly used to help relieve symptoms of conditions resulting in lack of energy, is now used by athletes, executives, and everyday people to increase energy, improve mental clarity, and improve physical performance. NADH also is a vital part in making the popular supplement CoQ10 effective into an antioxidant.
Many case studies of NADH have been done. Listed below are some of the results.
Attention Deficit Hyperactivity Disorder (ADHD)
Adults and children with ADHD are found to have a deficit in specific vitamins and supplements. Studies have shown that giving a child with ADHD 10mg of NADH will increase brain performance by up to 25%. NADH is a natural supplement that helps increase brain activity, improve focus, and helps relieve symptoms of ADHD.
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).
Oral reduced B-nicotinamide adenine dinucleotide (NADH) affects blood pressure, lipid peroxidation, and lipid profile in hypertensive rats (SHR).7
Chronic Fatigue Syndrome
Sufferers of Chronic Fatigue Syndrome (CFS) can be heartened by the favorable results of clinical trials of the nutritional supplement Enada NADH for use in the treatment of their debilitating disorder. The outcome of the Enada NADH study has recently been published in the respected medical journal Annals of Allergy, Asthma & Immunology. (Vol. 82, pp. 185-191, Feb.1999). Healthwatch and The CFIDS & FM Health Resource published preliminary results of this study, which was conducted at the prestigious Georgetown University Medical Center in Washington, D.C. This trial marks one of the first times the FDA has approved a nutritional supplement for evaluation as a medical treatment.
Benefits Seen in the Double-blind, Placebo-Controlled Study Twenty-six patients who met The Centers for Disease Control and Prevention’s (CDC) criteria for CFS completed the 12-week double-blind, placebo-controlled study. Double-blind is a scientific term meaning neither the investigating doctors nor the patients knew who was given Enada NADH or the placebo. During weeks one through four, patients received either 10 mg of Enada NADH or a placebo, whereas weeks five through eight were a ‘wash-out’ period during which patients received no active treatment. During weeks nine through twelve, patients’ treatment was switched so they received the alternate treatment – either placebo or Enada NADH – relative to their first four weeks. Laboratory tests were completed at the beginning and end of the study, and symptoms were evaluated based on patients’ response to an extensive questionnaire given prior to the study, as well as at the conclusion of weeks four, eight and twelve.
Eight of the patients showed at least a 10% improvement while taking Enada NADH, as opposed to only two of those taking the placebo. The success rate after only four weeks of Enada NADH treatment was 31% versus only 8% for patients given the placebo. Presented statistically, patients receiving Enada NADH were four times more likely than those taking a placebo to experience a reduction in symptoms. A Longer Open Label Study Yields Greater Results The authors of this published study feel there is cause for optimism as to even potentially greater benefits of Enada NADH, a safe, naturally- occurring antioxidant, in the treatment of CFS. These doctors believe that a longer period of treatment may result in a higher percentage of patients responding favorably. To test this theory, doctors enrolled patients in a longer, open label (as opposed to double-blind, placebo) follow-up study. The Annals of Al-lergy, Asthma & Immunology journal article reports that to date 72% of patients in this open study have reported significant improvement of their symptoms and energy levels. However, Matthew Fitzsimmons, the president of Menuco Corporation, which supplied the patented form of Enada NADH used in the study, recently revealed that up to 80% of patients in the longer (ongoing) study have responded favorably.
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. 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).
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 has been known to improve symptoms of Fibromyalgia, among a number of other conditions. Since one of the main symptoms of FMS is lack of energy, NADH will help increase the energy production in the body—naturally. NADH also supports the synthesis of the neurotransmitter dopamine. These brain chemicals affect mood, memory, alertness and concentration. So by increasing the level of NADH in your cells, there is an increase in dopamine production and thus users feel elevated mental clarity, levels of concentration and memory capacity.
Fibromyalgia syndrome (FMS) is a chronic condition that causes extreme pain in the muscles, connective tissues, and joints. It has a number of other symptoms that affect the entire body as well, all revolving around the feeling of hurting all over and feeling tired all the time. This means that it can be very difficult for people who suffer from Fibromyalgia to exert in physical activity, and may have trouble concentrating and remembering facts. It is difficult to detect because of its range of symptoms and is often frequently misunderstood, thus is often misdiagnosed. In fact there is no test to determine whether one has Fibromyalgia, even though it’s known to affect 3 to 6 million people in the US every year. Sometimes it isn’t diagnosed at all, therefore those who suffer from Fibromyalgia suffer from lack of medical care as well.
NADH is a coenzyme that exists naturally in every cell in your body. It actually exists in all living things. It is responsible for the production of ATP in the mitochondria. In non-scientific terms, this means that it is responsible for the production of energy in your body’s cells. Children have a very high level of NADH naturally—hence their high energy levels—but production of NADH tends to dwindle as we age. That’s why NADH supplements are so beneficial to your health.*
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).
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.21-24
Researchers in the Sleep-Wake Disorders Center, New York Weill Cornell Medical Center, tested the ability of oral stabilized NADH 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 Syndrome26 and to reduce the effects of jet lag on cognitive performance and sleepiness27.
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.”
|Serving Size: 1 vegetarian tablet as needed
Servings Per Container: 30
|Amount Per Serving
|NADH (reduced ß-nicotinamide adenine dinucleotide)
|Other Ingredients: D-Mannitol, Sodium Bicarbonate, Microcrystalline Cellulose, Magnesium Stearate, Sodium Ascorbate, Enteric Coating (sodium alginate, stearic acid).
|Guaranteed for Purity, Freshness and Potency. Contains No Caffeine, No Hormones, No Sugar, No Yeast, No Dairy, No Starch, No Preservatives, No Artificial Colors or Flavors
ENADA® NADH are the only stabilized, absorbable form of NADH and is protected by U.S. patents 5,332,727; 5,654,288 and 5,712,259.
Dosage and Use:
- Take one whole Enada® tablet each morning on an empty stomach, 30 minutes before a meal, with water only. Optimal effectiveness shown in four weeks of continuous usage.
Note: Store at room temperature or refrigerate, protect from light, heat and humidity
- If pregnant, nursing, or taking medication, consult your physician before taking this product
- Keep out of reach of children
- Do not exceed recommended dose
26. Forsyth LM, Preuss HG, MacDowell AL, Chiazze L, Birkmayer 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.
27. 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.
* These statements have not been evaluated by the Food and Drug Administration. This Product is not intended to diagnose, treat, cure or prevent any disease.