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Stabilisiertes NADH (ENADAR) verbessert die durch Jetlag reduzierte Hirnleistung
Abstract
Zusammenfassung: Jetlag ist ein Zustand, der eintritt, wenn man mehrere Zeitzonen, insbesondere gegen die Uhr, überfliegt. Die Symptome sind generelle Müdigkeit, Abgeschlagenheit, gestörter Schlafrhythmus und reduzierte Hirnleistung. Mittel gegen Jetlag wie Melatonin, Koffein, Sedativa oder Phototherapie sind von begrenzter Wirksamkeit oder Praktikabilität. Die Wirksamkeit der stabilisierten sublingualen Form von reduziertem Nikotinamid-Adenin-Dinukleotid (NADH, ENADAlert®, Menuco Corp.) wurde als Gegenmittel für Jetlag-Symptome in einer doppelblinden, placebokontrollierten wissenschaftlichen Studie geprüft. 35 gesunde Personen wurden von der Westküste der USA über Nacht an die Ostküste geflogen, was zu einem Zeitunterschied von drei Stunden führt. Am Abend vor dem Abflug und in der Früh nach der Landung wurden alle Probanden einem Hirnleistungstest unterzogen. Eine Gruppe erhielt 20 mg ENADAlert®, die andere Gruppe identische Placebotabletten. Alle Teilnehmer der Studie beendeten die computergesteuerten Hirnleistungstests (Cog Screen), die die Hirnfunktion, die Stimmung, den Schläfrigkeitsgrad am Morgen und zu Mittag nach dem Flug messen. Jetlag führte zu einer erhöhten Schläfrigkeit bei mehr als der Hälfte der Teilnehmer und zu einer Verschlechterung der Hirnleistungsfunktionen. Am Morgen nach dem Nachtflug kam es zu Fehlern im Aufmerksamkeitstest sowie zu Störungen im Arbeitsgedächtnis, der geteilten Aufmerksamkeit und der Geschwindigkeit der visuellen Perzeption. Probanden, die NADH erhielten, hatten in vier Hirnleistungstests signifikant bessere Ergebnisse (P ≤ .05) und berichteten eine geringere Schläfrigkeit im Vergleich zu den Probanden, die Placebo einnahmen. Die Gruppe, die NADH-Tabletten bekam, hat keine Nebenwirkungen beobachtet. Zusammenfassend kann gesagt werden, daß stabilisiertes sublingual absorbierbares NADH (ENADAlert®) die durch Jetlag induzierten negativen Wirkungen auf die Hirnleistung und die Schläfrigkeit signifikant verbessert.
... At present, oral or i.v. NADH have been reported to reduce anxiety (Alegre et al., 2010), attenuate sleep disturbances (Santaella et al., 2004;Forsyth et al., 1999), improve cognitive performance (Birkmayer, 1996), lower the number and duration of headaches (Forsyth et al., 1999), and ameliorate symptoms of jet lag (Birkmayer et al., 2002). Treatment with NADH has also been shown to slow down the progression of dementia, and improve outcomes in verbal fluency and visual-constructional ability (Demarin et al., 2004). ...
Nicotinamide adenine dinucleotide (NAD+) is an essential pyridine nucleotide that is present in all living cells. NAD+ acts as an important cofactor and substrate for a multitude of biological processes including energy production, DNA repair, gene expression, calcium-dependent secondary messenger signalling and immunoregulatory roles. The de novo synthesis of NAD+ is primarily dependent on the kynurenine pathway (KP), although NAD+ can also be recycled from nicotinic acid (NA), nicotinamide (NAM) and nicotinamide riboside (NR). NAD+ levels have been reported to decline during ageing and age-related diseases. Recent studies have shown that raising intracellular NAD+ levels represents a promising therapeutic strategy for age-associated degenerative diseases in general and to extend lifespan in small animal models. A systematic review of the literature available on Medline, Embase and Pubmed was undertaken to evaluate the potential health and/or longevity benefits due to increasing NAD+ levels. A total of 1545 articles were identified and 147 articles (113 preclinical and 34 clinical) met criteria for inclusion. Most studies indicated that the NAD+ precursors NAM, NR, nicotinamide mononucleotide (NMN), and to a lesser extent NAD+ and NADH had a favourable outcome on several age-related disorders associated with the accumulation of chronic oxidative stress, inflammation and impaired mitochondrial function. While these compounds presented with a limited acute toxicity profile, evidence is still quite limited and long-term human clinical trials are still nascent in the current literature. Potential risks in raising NAD+ levels in various clinical disorders using NAD+ precursors include the accumulation of putative toxic metabolites, tumorigenesis and promotion of cellular senescence. Therefore, NAD+ metabolism represents a promising target and further studies are needed to recapitulate the preclinical benefits in human clinical trials.
The existence of biological clocks that control many of our daily activities and physiological functions has always been part of tacit knowledge. Biological clocks tuned to the earth's 24‐h light/dark cycles are a fundamental property of all life on earth. We now understand that essentially every cell in our body has a free‐running molecular clock with an intrinsic periodicity of ∼24 h. These peripheral clocks are synchronized by a central timekeeper in the brain whose periodicity is determined by the amount of light entering the eyes. The central pacemaker coordinates peripheral clocks with the earth's rotation cycle. Social activities, occupations, and environmental exposures (e.g., light pollution, working at night, stress, conflict, illness, social pressures, chemical exposures, noise, and lifestyle) that disrupt biological clocks affect the quality of our sleep, our sense of well‐being, as well as our ability to function, perform tasks and learn. More importantly, chronic circadian disruption negatively impacts our health and susceptibility to chronic diseases and aging. An estimated 20–30% of the modern workforce is employed in jobs that require working night shifts associated with circadian disruption, putting a significant fraction of the workforce at increased risk of poor performance, errors, accidents, and decreased quality of life and health. To address this increasing public health issue, toxicologists, industrial hygienists, and occupational health clinicians must understand mechanisms by which exposures disrupt biological clocks, and use this knowledge to develop and implement targeted preventive, interventions, and mitigation strategies to reduce risks.
Cyclic voltammetric and Raman and UV-vis spectroscopic measurements were performed on thin films of non-peripherally substituted bis[1,4,8,11,15,18,22,25-octakis(octyl)phthalocyaninato] lutetium(III) (R16LuPc2). Voltammograms exhibit one-electron quasi-reversible redox processes in 1.5M LiClO4 aqueous solutions. The red-shift of the Q-band of R16LuPc2 in the UV-visible absorption spectra upon oxidation is attributed to the shortening of the inter-ring distance between the two phthalocyanine moieties. This observation is also consistent with the shift in the redox-sensitive vibrational modes in the Raman spectra due to the localization of the positive charge on phthalocyanine moieties. Neutralization of the oxidized R16LuPc2+ film by dihydronicotinamide adenine dinucleotide (NADH) using different concentrations varying from 0.05 mM to 3 mM has been studied by UV-vis absorption and Raman spectroscopies. The reduction processes for a three month old film were found to be slower than those for freshly prepared films and showed a dependence upon NADH concentration. The data provide a basis for application of R16LuPc2 as a sensor for NADH.
Er is in de literatuur geen beleid te vinden voor de bedrijfsgeneeskundige begeleiding van de frequente (dienst- of zaken)reiziger. Navraag bij grote internationale bedrijven bevestigt deze lacune. In dit beschrijvende, explorerende onderzoek is gekeken naar de risico’s die de frequente reizigers lopen om tot een beleid te komen die het effect van deze risico’s zoveel mogelijk beperkt of hiervoor adequate nazorg biedt.
Herstelbehoefte van 1 à 2 dagen na een reis met jetlag komt duidelijk naar voren. Oudere werknemers hebben hier meer last van dan jongere. In hoeverre dit gevolgen heeft op het cognitieve functioneren is nog onvoldoende onderzocht. Bedrijven zouden zich moeten beraden over de vraag of het wenselijk is om mensen belangrijke zaken te laten regelen als ze nog last hebben van jetlag. Compliance aan malariaprofylaxe is slechter gebleken dan in de literatuur gerapporteerd. De gevolgen hiervan zijn vooralsnog onvoldoende gedocumenteerd.
Screening op tuberculose is een zinvolle interventie. De frequentie van de screening zal echter sterk afhangen van de inschatting van het gelopen risico.
Since NADH has been implicated in medication for some symptoms and as a possible supplement for health, we characterized the metabolic fate of NADH orally given to mice by comparing with those of nicotinamide (Nam), NAD+ and NADH intraperitoneally or orally administered. Mice were individually housed in metabolic cages, and divided into two sets of four groups. Within each set, one group was intraperitoneally or orally administered saline and the other three groups received intraperitoneal or oral administration of a pharmacological dose of Nam, NAD+ or NADH (5 micromol/mouse). Twenty-four hour urine samples for the day before and days 1 to 4 after administration were collected and analyzed for Nam and its metabolites. When mice were administered saline alone, urinary excretion of Nam and its metabolites, such as nicotinamide N-oxide (Nam N-oxide), N1-methylnicotinamide (MNA), N1-methyl-2-pyridone-5-carboxamide (2-Py), and N1-methyl-4-pyridone-3-carboxamide (4-Py), was unchanged from day 0 to day 4. Intraperitoneal injection of Nam, NAD+ and NADH produced significant increases in urinary excretion of Nam and its metabolites. Similar results were obtained when Nam and NAD+ were given orally. On the other hand, oral administration of NADH did not bring about an increase in urinary excretion of Nam and its metabolites, suggesting that NADH in digestive organs has been decomposed to a compound(s) that cannot yield Nam. In fact, incubation of NADH at acidic pH to mimic the stomach resulted in rapid conversion of NADH to an unknown compound. Better understanding of the fate of oral NADH is needed for its therapeutic and supplemental use.
To determine the safety and efficacy of memantine in treating Age-Associated Memory Impairment (AAMI).
Sixty adults between 50-79 years of age meeting diagnostic requirements for AAMI were randomly assigned to either memantine (titrated to 20 mg) or a matched placebo and treated for 90 days. An extensive battery of computerized cognitive tests was administered at screening, baseline and, thereafter, at monthly intervals.
Study results suggest that the primary cognitive effects of memantine in this population are on attention and information processing speed, rather than on memory. There were no differences in adverse events between memantine and placebo.
Nicotinamide adenine dinucleotide (NADH) may be utilized for the synthesis and regeneration of tetrahydrobiopterin (BH(4)), which in turn is an essential cofactor for tyrosine hydroxylase, the rate-limiting enzyme in the synthesis of dopamine (DA). NADH has been reported to relieve some of the symptoms of Parkinson's disease, presumably by altering dopaminergic function. The present study examines the efficacy of NADH in influencing DA activity in the rat striatum. In striatal slices, NADH (350 microM) significantly increased basal DA and DOPAC efflux and caused a 2-fold increase in the DA overflow evoked by high KCl (25 mM). Tissue levels of BH(4), basal BH(4) efflux, and KCl-evoked BH(4) overflow were unaffected by NADH, as was [(3)H]DA uptake into striatal synaptosomes. In contrast to the effects of NADH on DA function in vitro, no effects were observed when NADH was administered systemically. NADH (10 or 100 mg/kg, s.c.) did not influence the tissue content of DA, 5-HT, or their metabolites in the midbrain or striatum, nor did it alter DA extracellular concentrations. These results indicate that NADH can increase DA release from striatal slices, although we are as yet unable to detect this effect in vivo.