AOR CoQ + NADH contains NADH which is the reduced
form of Nicotinamide Adenine Dinucleotide, a critical component of the
Kreb’s Cycle and Co-Enzyme Q10, an antioxidant for the maintenance of
good health.
| Product Code
|
Size
|
Per Capsule
|
Vegetarian
|
| AOR04267
|
30 Vegi-Caps
|
50 mg
|
100% Vegetarian
|
| Supplement Facts
|
| Serving Size: 1 Capsule
|
|
|
|
|
| NADH
|
10 mg
|
| Co-Enzyme Q10 (ubiquinone-10)
|
40 mg
|
|
|
|
Non-medicinal ingredients: Microcrystalline cellulose. Capsule: hypromellose, gellan gum, water.
|
AOR™ guarantees that no
ingredients not listed on the label have been added to the product.
Contains no wheat, gluten, corn, nuts, dairy, eggs, fish, shellfish, or
any animal byproduct.
Suggested Use: Take 1 capsule per day without food, or as directed by a qualified health care practitioner.
Caution: Do not use if
pregnant or nursing. Consult a health care practitioner prior to use if
you are taking blood pressure medication, or for use beyond 6 months.
Source: Cotton, soybean, pharmaceutical synthesis.
Main Applications:
NADH, or nicotinamide adenine dinucleotide, is a
natural substance found in most life forms and is essential for energy
production, as is Co Q10, which is synthesized in nearly every tissue of
the body. There is increasing evidence that NADH plays important roles
in many of the brain’s activities such as neurotransmission, learning
and memory.
Heart Health
NADH has also been studied to determine
its ability to lower blood pressure and positively affect lipids. In
laboratory animals, NADH lowers systolic blood pressure, total
cholesterol, and LDL cholesterol. This has led scientists to call for
more research examining the role of NADH supplementation in addressing
the conditions of cardiovascular disease. CoQ 10 is a well-known
cardiovascular protectant. It has been shown to be an effective adjunct
treatment for hypertension. One meta-analysis found that CoQ10 lowered
systolic blood pressure by 11-16 mmHg and diastolic blood pressure by
8-10 mmHg. As an antioxidant, CoQ 10 protects low-density lipoproteins
(LDLs) from oxidation, which protects the heart and blood vessels from
free-radical insult. In heart patients, lower CoQ10 is an independent
predictor of chronic heart failure (CHF) and mortality. Cardiovascular
disease has now been associated with endothelial dysfunction and
mitochondrial dysfunction. One study found that, in heart patients,
endothelial dysfunction improved due to a reversal in mitochondrial
dysfunction.
Chronic Fatigue Syndrome
Both NADH and CoQ 10 have been studied
for their effects on Chronic Fatigue Syndrome, or CFS. One study, of 26
CFS patients found that 31% of the patients in the NADH group were
judged to have experienced ‘notable improvement', with only 8% of
controls receiving a similar assessment. In another study, a total of 31
CFS patients were randomly assigned to either NADH or a combination of
conventional nutritional supplements and psychological therapy. While
the conventional supplements/psychological therapy group also
experienced improvements, it was not until the second and third
trimesters that its symptom scores were able to match those of the NADH
group. In patients with CFS, CoQ10 levels were found to be
non-detectable in half of the patients, suggesting that CFS patients
might benefit from CoQ10 supplementation, since CoQ10 is essential to
energy production. It is suggested that low CoQ10 levels could be a
factor that puts depressed patients at higher risk for chronic heart
failure (CHF), and CHF patients that also suffer from CFS seem to die
younger than CHF patients without CFS. The CFS patients with very low
CoQ10 levels also had concentration and memory disturbances. This shows
how mitochondrial dysfunction and associated CoQ10 levels are related to
neurological symptoms as well as more severe mental impairments.
Alzheimer’s and Parkinson’s Disease
NADH has the ability to mediate calcium
homeostasis, which is a critical factor in nearly all of the major
processes in the brain. The alteration of calcium homeostasis is a
factor in the aging of the brain and in various brain disorders
including Alzheimer’s disease. There is a school of thought which
believes that supplementing with NADH can stimulate the body's own
production of the neurotransmitter dopamine. This has led to human
studies with Parkinson's disease patients. One open study involved 885
subjects with Parkinson's disease, with 80% showing improvement and most
improvement coming from the younger patients and those with the
shortest duration of Parkinson's. In another open study, 17 patients
with dementia associated with Alzheimer's disease were treated with NADH
for 12 weeks, and researchers reported improvements in all of them.
CoQ10 by itself has also been shown to
prevent neurodegeneration because of its effects on the mitochondria.
Trials have shown that CoQ10 supplementation delays brain atrophy and
the formation of amyloid plaque in aged animals. Previous trials have
also shown that co-administration of CoQ10 with other substances capable
of preventing mitochondrial damage such as alpha lipoic acid or vitamin
E was more effective than administration of CoQ10 by itself. Studies
also show that CoQ10 may be an effective agent for the treatment and
prevention of Alzheimer’s type dementia. Mitochondrial dysfunction
appears to be associated with neurodegenerative diseases such as
Alzheimer’s and Parkinson’s. One study on Alzheimer’s mouse models
showed that CoQ10 decreased amyloid plaque in the brain.
The NAD+/NADH Theory
It is important to note that there is an
increasing body of scientific evidence suggesting that a host of
favourable metabolic conditions are associated with a high ratio of NAD+
to NADH. If this is so, then the question of the very idea of NADH
supplementation being in conflict with the latest research is not an
unfair one. The first answer is simply that NADH supplementation in its
own right is supported by a respectable amount of clinical research,
therefore ensuring a following and a rightful place within the
preventative health community. The second answer is related to the first
in that the pharmacokinetics and mechanism of action for NADH
supplementation are simply not clearly understood at this time. One
proposed explanation that scientists have put forward is that endogenous
NADH converts back into NAD+, which would explain its clinical
credentials in the face of the emerging NAD+/NADH ratio theory.
It’s All About the Mitochondria!
Since both NADH and CoQ10 are essential
components of energy production, and energy drives all function, it is
not surprising that new evidence is finding that mitochondrial
dysfunction is associated with a host of metabolic diseases, ranging
from depression to neurodegenerative to cardiovascular diseases. AOR’s
CoQ + NADH provides these two molecules in one formula in a specialized
capsule form designed to protect it from degradation by stomach acids
and to maximize their potential health benefits.
Comparison of oral nicotinamide adenine dinucleotide (NADH) versus conventional therapy for chronic fatigue syndrome.
P R Health Sci J. 2004 Jun;23(2):89-93.
Santaella ML, Font I, Disdier OM.
OBJECTIVE: To compare
effectiveness of oral therapy with reduced nicotinamide adenine
dinucleotide (NADH) to conventional modalities of treatment in patients
with chronic fatigue syndrome (CFS).
BACKGROUND: CFS is a
potentially disabling condition of unknown etiology. Although its
clinical presentation is associated to a myriad of symptoms, fatigue is a
universal and essential finding for its diagnosis. No therapeutic
regimen has proven effective for this condition.
METHODS: A total of 31
patients fulfilling the Centers for Disease Control criteria for CFS,
were randomly assigned to either NADH or nutritional supplements and
psychological therapy for 24 months. A thorough medical history,
physical examination and completion of a questionnaire on the severity
of fatigue and other symptoms were performed each trimester of therapy.
In addition, all of them underwent evaluation in terms of immunological
parameters and viral antibody titers. Statistical analysis was applied
to the demographic data, as well as to symptoms scores at baseline and
at each trimester of therapy.
RESULTS: The twelve
patients who received NADH had a dramatic and statistically significant
reduction of the mean symptom score in the first trimester (p <
0.001). However, symptom scores in the subsequent trimesters of therapy
were similar in both treatment groups. Elevated IgG and Ig E antibody
levels were found in a significant number of patients.
CONCLUSIONS: Observed
effectiveness of NADH over conventional treatment in the first trimester
of the trial and the trend of improvement of that modality in the
subsequent trimesters should be further assessed in a larger patient
sample.
NADH supplementation decreases pinacidil-primed I K ATP in ventricular cardiomyocytes by increasing intracellular ATP.
Br J Pharmacol. 2003 Jun;139(4):749-54.
Pelzmann B, Hallström S, Schaffer P, Lang P, Nadlinger K, Birkmayer GD, Vrecko K, Reibnegger G, Koidl B.
1 The aim of this study
was to investigate the effect of nicotinamide-adenine dinucleotide
(NADH) supplementation on the metabolic condition of isolated guinea-pig
ventricular cardiomyocytes. The pinacidil-primed ATP-dependent
potassium current I(K(ATP)) was used as an indicator of subsarcolemmal
ATP concentration and intracellular adenine nucleotide contents were
measured.
2 Membrane currents
were studied using the patch-clamp technique in the whole-cell recording
mode at 36-37 degrees C. Adenine nucleotides were determined by HPLC.
3 Under physiological
conditions (4.3 mM ATP in the pipette solution, ATP(i)) I(K(ATP)) did
not contribute to basal electrical activity.
4 The ATP-dependent
potassium (K((ATP))) channel opener pinacidil activated I(K(ATP))
dependent on [ATP](i) showing a significantly more pronounced activation
at lower (1 mM) [ATP](i).
5 Supplementation of
cardiomyocytes with 300 micro g ml(-1) NADH (4-6 h) resulted in a
significantly reduced I(K(ATP)) activation by pinacidil compared to
control cells. The current density was 13.8+/-3.78 (n=6) versus
28.9+/-3.38 pA pF(-1) (n=19; P<0.05).
6 Equimolar amounts of the related compounds nicotinamide and NAD(+) did not achieve a similar effect like NADH.
7 Measurement of
adenine nucleotides by HPLC revealed a significant increase in
intracellular ATP (NADH supplementation: 45.6+/-1.88 nmol mg(-1) protein
versus control: 35.4+/-2.57 nmol mg(-1) protein, P<0.000005).
8 These data show that
supplementation of guinea-pig ventricular cardiomyocytes with NADH
results in a decreased activation of I(K(ATP)) by pinacidil compared to
control myocytes, indicating a higher subsarcolemmal ATP concentration.
9 Analysis of intracellular adenine nucleotides by HPLC confirmed the significant increase in ATP.
Stabilized NADH (ENADA) improves jet lag-induced cognitive performance deficit
Wien Med Wochenschr. 2002;152(17-18):450-4.
Pelzmann B, Hallström S, Schaffer P, Lang P, Nadlinger K, Birkmayer GD, Vrecko K, Reibnegger G, Koidl B.
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.
Because NADH increases cellular production of ATP and facilitates
dopamine synthesis, it may counteract the effects of jet lag on
cognitive functioning and sleepiness. 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 received either 20 mg of sublingual stabilized NADH (n = 18)
or identical placebo tablets (n = 17). All participants completed
computer-administered tests (including Cog Screen) to assess changes in
cognitive functioning, mood, and sleepiness in the morning and
afternoon. 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 4 cognitive test
measures (P < or = .05) and reported less sleepiness compared with
those who received placebo. No adverse effects were observed with NADH
treatment. Stabilized NADH significantly reduced jet lag-induced
negative cognitive effects and sleepiness, was easily administered, and
was found to have no side effects.
Therapeutic effects of oral NADH on the symptoms of patients with chronic fatigue syndrome.
Ann Allergy Asthma Immunol. 1999 Feb;82(2):185-91.
Forsyth LM, Preuss HG, MacDowell AL, Chiazze L Jr, Birkmayer GD, Bellanti JA.
BACKGROUND: Chronic
fatigue syndrome (CFS) is a disorder of unknown etiology, consisting of
prolonged, debilitating fatigue, and a multitude of symptoms including
neurocognitive dysfunction, flu-like symptoms, myalgia, weakness,
arthralgia, low-grade fever, sore throat, headache, sleep disturbances,
and swelling and tenderness of lymph nodes. No effective treatment for
CFS is known.
OBJECTIVE: The purpose
of the study was to evaluate the efficacy of the reduced form of
nicotinamide adenine dinucleotide (NADH) i.e., ENADA the stabilized oral
absorbable form, in a randomized, double-blind, placebo-controlled
crossover study in patients with CFS. Nicotinamide adenine dinucleotide
is known to trigger energy production through ATP generation which may
form the basis of its potential effects.
METHODS: Twenty-six
eligible patients who fulfilled the Center for Disease Control and
Prevention criteria for CFS completed the study. Medical history,
physical examination, laboratory studies, and questionnaire were
obtained at baseline, 4, 8, and 12 weeks. Subjects were randomly
assigned to receive either 10 mg of NADH or placebo for a 4-week period.
Following a 4-week washout period, subjects were crossed to the
alternate regimen for a final 4-week period.
RESULTS: No severe
adverse effects were observed related to the study drug. Within this
cohort of 26 patients, 8 of 26 (31%) responded favorably to NADH in
contrast to 2 of 26 (8%) to placebo. Based upon these encouraging
results we have decided to conduct an open-label study in a larger
cohort of patients.
CONCLUSION:
Collectively, the results of this pilot study indicate that NADH may be a
valuable adjunctive therapy in the management of the chronic fatigue
syndrome and suggest that further clinical trials be performed to
establish its efficacy in this clinically perplexing disorder.
Oral reduced B-nicotinamide
adenine dinucleotide (NADH) affects blood pressure, lipid peroxidation,
and lipid profile in hypertensive rats (SHR).
Geriatr Nephrol Urol. 1998;8(2):95-100.
Bushehri N, Jarrell ST, Lieberman S, Mirdamadi-Zonozi N, Birkmayer G, Preuss HG.
A gradual increase in blood pressure
(BP), often attaining hypertensive levels, is common during
aging--"age-related hypertension." Therefore, means to prevent or
ameliorate this elevated BP safely are important. Although oral
B-nicotinamide adenine dinucleotide (NADH), a natural coenzyme, is used
principally to treat various neurologic disorders, we wished to
investigate whether this agent had the same potential to lower BP and
benefit the cardiovascular system as does coenzyme Q10, a similar-type
agent. As a first approximation, spontaneously hypertensive rats (SHR)
were used to determine effects of oral NADH. In a blinded,
placebo-controlled study, ten rats received placebo; and ten, NADH for
ten weeks. Systolic BP was measured by tail plethysmography. Blood was
collected terminally, and chemistries were performed by routine
methodologies. Thiobarbituric acid reactive species (TBARS) (an estimate
of lipid peroxidation/free radical formation) was measured in renal and
hepatic tissues. The following was noted: water and food intake were
comparable, and the steady weight gain of young SHR were similar in the
placebo and NADH groups. Although systolic BP did not differ between the
two groups over the first month, it decreased and stayed markedly lower
for the remainder of study in SHR receiving oral NADH. At the end of 60
days, SBP in NADH-treated SHR was 184 mm Hg +/- 2.8 (SEM) compared to
201 mm Hg +/- 2.1 (SEM) in control SHR (p < 0.001). No significant
differences were seen in blood levels of glucose, insulin, triglyceride,
and HDL levels but NADH intake lowered total cholesterol (p < 0.002)
and LDL (p < 0.02). Renal TBARS were also significantly lower in SHR
receiving NADH (P < 0.001). Accordingly, supplementation with the
natural coenzyme NADH theoretically could prove to be useful in
preventing age-related increases in BP and, thus, various cardiovascular
maladies.
Nicotinamidadenindinucleotide (NADH): the new approach in the therapy of Parkinson's disease.
Ann Clin Lab Sci. 1989 Jan-Feb;19(1):38-43.
Birkmayer W, Birkmayer GJ.
The coenzyme
Nicotinamidadenindinucleotide (NADH) has been used as novel medication
in 34 Parkinson patients in an open label trial. In all patients, a
beneficial clinical effect was observed. Twenty-one patients (61.7
percent) showed a very good (better than 30 percent) improvement of
disability and 13 patients (38.3 percent) a moderate (up to 30 percent)
improvement. The effect of NADH was dependent on the dosage and the
severity of the case. The best therapeutic dose was in the range of 25
to 50 mg per day. The clinical improvement was more pronounced after
i.v. and less after i.m. administration. Concomitant with improvement of
the disability, the urine level of homovanillinic acid (HVA) increased
significantly in all patients (in some patients by more than a 100
percent), indicating a stimulation of the endogenous L-DOPA
biosynthesis. The daily "on phases" of the patients could be increased
from two up to nine hours in the individual patients by NADH
administration
Lower plasma Coenzyme Q10 in
depression: a marker for treatment resistance and chronic fatigue in
depression and a risk factor to cardiovascular disorder in that illness.
Neuro Endocrinol Lett. 2009;30(4):462-9.
Maes M, Mihaylova I, Kubera M, Uytterhoeven M, Vrydags N, Bosmans E.
INTRODUCTION: There is
now evidence that major depression is accompanied by an induction of
inflammatory and oxidative and nitrosative stress (IO&NS) pathways
and by a lowered antioxidant status. Coenzyme Q10 (CoQ10) is a strong
antioxidant that has anti-inflammatory effects.
METHODS: This paper
examines the plasma concentrations of CoQ10 in 35 depressed patients and
22 normal volunteers and the relationships between plasma CoQ10 and
treatment resistant depression (TRD), the severity of illness as
measured by means of the Hamilton Depression Rating Scale (HDRS) and the
presence of chronic fatigue syndrome (CFS).
RESULTS: We found that
plasma CoQ10 was significantly (p=0.0002) lower in depressed patients
than in normal controls. 51.4% of the depressed patients had plasma
CoQ10 values that were lower than the lowest plasma CoQ10 value detected
in the controls. Plasma CoQ10 was significantly lower in patients with
TRD and with CFS than in the other depressed patients. There were no
significant correlations between plasma CoQ10 and the HDRS.
DISCUSSION: The results
show that lower CoQ10 plays a role in the pathophysiology of depression
and in particular in TRD and CFS accompanying depression. It is
suggested that depressed patients may benefit from CoQ10
supplementation. The findings that lower CoQ10 is a risk factor to
coronary artery disease and chronic heart failure (CHF) and mortality
due to CHF suggest that low CoQ10 is another factor explaining the risk
to cardiovascular disorder in depression. Since statins significantly
lower plasma CoQ10, depressed patients and in particular those with TRD
and CFS represent populations at risk to statin treatment.
Coenzyme Q10 deficiency in
myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is related
to fatigue, autonomic and neurocognitive symptoms and is another risk
factor explaining the early mortality in ME/CFS due to cardiovascular
disorder.
Neuro Endocrinol Lett. 2009;30(4):470-6.
Maes M, Mihaylova I, Kubera M, Uytterhoeven M, Vrydags N, Bosmans E.
INTRODUCTION: Myalgic
encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a medical illness
characterized by disorders in inflammatory and oxidative and
nitrosative (IO&NS) pathways.
METHODS: This paper
examines the role of Coenzyme Q10 (CoQ10), a mitochondrial nutrient
which acts as an essential cofactor for the production of ATP in
mitochondria and which displays significant antioxidant activities.
Plasma CoQ10 has been assayed in 58 patients with ME/CFS and in 22
normal controls; the relationships between CoQ10 and the severity of
ME/CFS as measured by means of the FibroFatigue (FF) scale were
measured.
RESULTS: Plasma CoQ10
was significantly (p=0.00001) lower in ME/CFS patients than in normal
controls. Up to 44.8% of patients with ME/CFS had values beneath the
lowest plasma CoQ10 value detected in the normal controls, i.e. 490
microg/L. In ME/CFS, there were significant and inverse relationships
between CoQ10 and the total score on the FF scale, fatigue and autonomic
symptoms. Patients with very low CoQ10 (<390 microg/L) suffered
significantly more from concentration and memory disturbances.
DISCUSSION: The results
show that lowered levels of CoQ10 play a role in the pathophysiology of
ME/CFS and that symptoms, such as fatigue, and autonomic and
neurocognitive symptoms may be caused by CoQ10 depletion. Our results
suggest that patients with ME/CFS would benefit from CoQ10
supplementation in order to normalize the low CoQ10 syndrome and the
IO&NS disorders. The findings that lower CoQ10 is an independent
predictor of chronic heart failure (CHF) and mortality due to CHF may
explain previous reports that the mean age of ME/CFS patients dying from
CHF is 25 years younger than the age of those dying from CHF in the
general population. Since statins significantly decrease plasma CoQ10,
ME/CFS should be regarded as a relative contraindication for treatment
with statins without CoQ10 supplementation.
Reversal of mitochondrial
dysfunction by coenzyme Q10 supplement improves endothelial function in
patients with ischaemic left ventricular systolic dysfunction: a
randomized controlled trial.
Atherosclerosis. 2011 Jun;216(2):395-401.
Dai YL, Luk TH, Yiu KH, Wang M, Yip PM, Lee SW, Li SW, Tam S, Fong B, Lau CP, Siu CW, Tse HF.
AIMS: Coronary artery
disease (CAD) is associated with endothelial dysfunction and
mitochondrial dysfunction (MD). The aim of this study was to investigate
whether co-enzyme Q10 (CoQ) supplementation, which is an obligatory
coenzyme in the mitochondrial respiratory transport chain, can reverse
MD and improve endothelial function in patients with ischaemic left
ventricular systolic dysfunction (LVSD).
METHODS AND RESULTS: We
performed a randomized, double-blind, placebo-controlled trial to
determine the effects of CoQ supplement (300 mg/day, n=28) vs. placebo
(controls, n=28) for 8 weeks on brachial flow-mediated dilation (FMD) in
patients with ischaemic LVSD(left ventricular ejection fraction
<45%). Mitochondrial function was determined by plasma
lactate/pyruvate ratio (LP ratio). After 8 weeks, CoQ-treated patients
had significant increases in plasma CoQ concentration (treatment effect
2.20 μg/mL, P<0.001) and FMD (treatment effect 1.51%, P=0.03); and
decrease in LP ratio (treatment effect -2.46, P=0.03) compared with
controls. However, CoQ treatment did not alter nitroglycerin-mediated
dilation, blood pressure, blood levels of fasting glucose, haemoglobin
A1c, lipid profile, high-sensitivity C-reactive protein and oxidative
stress as determined by serum superoxide dismutase and 8-isoprostane
(all P>0.05). Furthermore, the reduction in LP ratio significantly
correlated with improvement in FMD (r=-0.29, P=0.047).
CONCLUSION: In patients
with ischaemic LVSD, 8 weeks supplement of CoQ improved mitochondrial
function and FMD; and the improvement of FMD correlated with the change
in mitochondrial function, suggesting that CoQ improved endothelial
function via reversal of mitochondrial dysfunction in patients with
ischaemic LVSD.
Application of coenzyme Q(10) in combination therapy of arterial hypertension.
Kardiologiia. 2011;51(6):26-31.
Mikhin VP, Kharchenko AV, Rosliakova EA, Cherniatina MA.
We studied effect of coenzyme Q(10) on
24-hour blood pressure profile and function of vascular endothelium in
patients with essential hypertension. Coenzyme Q(10) was used as a
component of combination therapy comprising angiotensin converting
enzyme inhibitor enalapril. Administration of coenzyme Q(10) in
combination with traditional antihypertensive therapy promoted
normalization of vascular endothelial function and more effective
correction of 24-hour blood pressure profile. These findings allow to
consider the use of coenzyme Q(10) as promising component of combination
therapy of arterial hypertension.
Coenzyme Q10 in the treatment of hypertension: a meta-analysis of the clinical trials.
J Hum Hypertens. 2007 Apr;21(4):297-306.
Rosenfeldt FL, Haas SJ, Krum H, Hadj A, Ng K, Leong JY, Watts GF.
Our objective was to review all
published trials of coenzyme Q10 for hypertension, assess overall
efficacy and consistency of therapeutic action and side effect
incidence. Meta-analysis was performed in 12 clinical trials (362
patients) comprising three randomized controlled trials, one crossover
study and eight open label studies. In the randomized controlled trials
(n=120), systolic blood pressure in the treatment group was 167.7 (95%
confidence interval, CI: 163.7-171.1) mm Hg before, and 151.1
(147.1-155.1) mm Hg after treatment, a decrease of 16.6 (12.6-20.6,
P<0.001) mm Hg, with no significant change in the placebo group.
Diastolic blood pressure in the treatment group was 103 (101-105) mm Hg
before, and 94.8 (92.8-96.8) mm Hg after treatment, a decrease of 8.2
(6.2-10.2, P<0.001) mm Hg, with no significant change in the placebo
group. In the crossover study (n=18), systolic blood pressure decreased
by 11 mm Hg and diastolic blood pressure by 8 mm Hg (P<0.001) with no
significant change with placebo. In the open label studies (n=214),
mean systolic blood pressure was 162 (158.4-165.7) mm Hg before, and
148.6 (145-152.2) mm Hg after treatment, a decrease of 13.5 (9.8-17.1,
P<0.001) mm Hg. Mean diastolic blood pressure was 97.1 (95.2-99.1) mm
Hg before, and 86.8 (84.9-88.8) mm Hg after treatment, a decrease of
10.3 (8.4-12.3, P<0.001) mm Hg. We conclude that coenzyme Q10 has the
potential in hypertensive patients to lower systolic blood pressure by
up to 17 mm Hg and diastolic blood pressure by up to 10 mm Hg without
significant side effects.
Coenzyme Q10 effects in neurodegenerative disease.
Neuropsychiatr Dis Treat. 2009;5:597-610.
Spindler M, Beal MF, Henchcliffe C.
Coenzyme Q10 (CoQ10) is an essential
cofactor in the mitochondrial respiratory chain, and as a dietary
supplement it has recently gained attention for its potential role in
the treatment of neurodegenerative disease. Evidence for mitochondrial
dysfunction in neurodegenerative disorders derives from animal models,
studies of mitochondria from patients, identification of genetic defects
in patients with neurodegenerative disease, and measurements of markers
of oxidative stress. Studies of in vitro models of neuronal toxicity
and animal models of neurodegenerative disorders have demonstrated
potential neuroprotective effects of CoQ10. With this data in mind,
several clinical trials of CoQ10 have been performed in Parkinson's
disease and atypical Parkinson's syndromes, Huntington's disease,
Alzheimer disease, Friedreich's ataxia, and amyotrophic lateral
sclerosis, with equivocal findings. CoQ10 is widely available in
multiple formulations and is very well tolerated with minimal adverse
effects, making it an attractive potential therapy. Phase III trials of
high-dose CoQ10 in large sample sizes are needed to further ascertain
the effects of CoQ10 in neurodegenerative diseases.
Coenzyme Q10 reduces beta-amyloid plaque in an APP/PS1 transgenic mouse model of Alzheimer's disease. J Mol Neurosci. 2010 May;41(1):110-3.
Yang X, Dai G, Li G, Yang ES.
We previously reported that coenzyme Q10
(CoQ10) could reduce intracellular deposition in an aged transgenic
mouse model. Here, we further tested the effect of CoQ10 on amyloid
plaque in an amyloid precursor protein/presenilin 1 transgenic mouse
model of Alzheimer's disease (AD). By using immunohistochemistry and
magnetic resonance imaging to determine the burden of amyloid plaque, we
found that oral administration of CoQ10 can efficiently reduce the
burden of the plaques in this mouse model. These data demonstrate that
in addition to reducing intracellular deposition of Abeta, CoQ10 can
also reduce plaque pathology. Our study further supports the use of
CoQ10 as a therapeutic candidate for AD.