Hi,
     I've never heard that CoQ is a blood thinner. Do you have any
references?  As to the safety, trials have been running a year or two
without any reports of bleeding AFAIK. Below, I post the trials I have
notice my comment at the top.

Thomas

Human trials
Results show inconsistency at low doses, great benefits at hi doses.

Am J Cardiol. 2004 Nov 15;94(10):1306-10. Related Articles, Links
Effect of atorvastatin on left ventricular diastolic function and
ability of coenzyme Q10 to reverse that dysfunction.
Silver MA, Langsjoen PH, Szabo S, Patil H, Zelinger A.
Heart Failure Institute, Department of Medicine, Advocate Christ
Medical Center, University of Illinois/Christ Cardiovascular Disease
Fellowship Program, Oak Lawn, Illinois 60453, USA.
marc.silver@advocatehealth.com <marc.silver@advocatehealth.com>
     This study evaluated left ventricular diastolic function with
Doppler echocardiography before and after statin therapy. Statin
therapy worsened diastolic parameters in most patients; coenzyme Q(10)
supplementation in patients with worsening diastolic function with
statin therapy improved parameters of diastolic function.
PMID: 15541254

2: Biofactors. 2003;18(1-4):91-100. Related Articles, Links
Systematic review of effect of coenzyme Q10 in physical exercise,
hypertension and heart failure.
Rosenfeldt F, Hilton D, Pepe S, Krum H.
Cardiac Surgical Research Unit, Alfred Hospital and Baker Institute,
Melbourne, Victoria, Australia. f.rosenfeldt@alfred.org.au
           COENZYME Q10 IN PHYSICAL EXERCISE. We identified eleven
studies in which CoQ10 was tested for an effect on exercise capacity,
six showed a modest improvement in exercise capacity with CoQ10
supplementation but five showed no effect. CoQ10 IN HYPERTENSION. We
identified eight published trials of CoQ10 in hypertension. Altogether
in the eight studies the mean decrease in systolic blood pressure was
16 mm Hg and in diastolic blood pressure, 10 mm Hg. Being devoid of
significant side effects CoQ10 may have a role as an adjunct or
alternative to conventional agents in the treatment of hypertension.
CoQ10 IN HEART FAILURE. We performed a randomised double blind
placebo-controlled pilot trial of CoQ10 therapy in 35 patients with
heart failure. Over 3 months, in the CoQ10 patients but not in the
placebo patients there were significant improvements in symptom class
and a trend towards improvements in exercise time. META-ANALYSIS OF
RANDOMISED TRIALS OF COENZYME Q10 IN HEART FAILURE. In nine randomised
trials of CoQ10 in heart failure published up to 2003 there were
non-significant trends towards increased ejection fraction and reduced
mortality. There were insufficient numbers of patients for meaningful
results. To make more definitive conclusions regarding the effect of
CoQ10 in cardiac failure we recommend a prospective, randomised trial
with 200-300 patients per study group. Further trials of CoQ10 in
physical exercise and in hypertension are recommended. PMID: 14695924
    Notable in this paper is a good reduction in pulse pressure, mega
studies usually show muted results due to the inclusion of some trials
with flaws such as low dosage, or short duration, and the fact that
recent neuro studies have suggested increased efficacy at upto 2400
mg/day. Beta blockers weaken the beating of the heart to reduce blood
pressure, coQ10 strengthens it and yet gives good results. The
mechanisms of action for coQ suggest better results over long term
usage, yet only short term, low dose trials have been completed. These
considerations suggest much more efficacy than is currently
contemplated.

Thomas

23: Mol Cell Biochem. 2003 Apr;246(1-2):75-82. Related Articles, Links

Effect of coenzyme Q10 on risk of atherosclerosis in patients with
recent myocardial infarction.
Singh RB, Neki NS, Kartikey K, Pella D, Kumar A, Niaz MA, Thakur AS.
Medical Hospital and Research Centre, Moradabad, India.
icn@mickyonline.com
            In a randomized, double-blind, controlled trial, the
effects of oral treatment with coenzyme Q10 (CoQ10, 120 mg/day), a
bioenergetic and antioxidant cytoprotective agent, were compared for 1
year, on the risk factors of atherosclerosis, in 73 (CoQ, group A) and
71 (B vitamin group B) patients after acute myocardial infarction
(AMI). After 1 year, total cardiac events (24.6 vs. 45.0%, p < 0.02)
including non-fatal infarction (13.7 vs. 25.3%, p < 0.05) and cardiac
deaths were significantly lower in the intervention group compared to
control group. The extent of cardiac disease, elevation in cardiac
enzymes, left ventricular enlargement, previous coronary artery disease
and elapsed time from symptom onset to infarction at entry to study
showed no significant differences between the two groups. Plasma level
of vitamin E (32.4 +/- 4.3 vs. 22.1 +/- 3.6 umol/L) and high density
lipoprotein cholesterol (1.26 +/- 0.43 vs. 1.12 +/- 0.32 mmol/L) showed
significant (p < 0.05) increase whereas thiobarbituric acid reactive
substances, malondialdehyde (1.9 + 0.31 vs. 3.1 + 0.32 pmol/L) and
diene conjugates showed significant reduction respectively in the CoQ
group compared to control group. Approximately half of the patients in
each group (n = 36 vs. 31) were receiving lovastatin (10 mg/day) and
both groups had a significant reduction in total and low density
lipoprotein cholesterol compared to baseline levels. It is possible
that treatment with CoQ10 in patients with recent MI may be beneficial
in patients with high risk of atherothrombosis, despite optimal lipid
lowering therapy during a follow-up of 1 year. Adverse effect of
treatments showed that fatigue (40.8 vs. 6.8%, p < 0.01) was more
common in the control group than CoQ group.PMID: 12841346    The
apparent lack of benefit for B vitamins is no surprise in a one year
study. There's no mention of any synergism between coQ and statins
which has been hypothesized on theoretical grounds.
XXXX

The effect of coenzyme Q10 in patients with congestive heart failure.
Khatta M, Alexander BS, Krichten CM, et al. Ann Intern Med
2000;132:636-640.
BACKGROUND: Coenzyme Q10 is commonly used to treat congestive heart
failure on the basis of data from several unblinded, subjective
studies. Few randomized, blinded, controlled studies have evaluated
objective measures of cardiac performance. OBJECTIVE: To determine the
effect of coenzyme Q10 on peak oxygen consumption, exercise duration,
and ejection fraction. DESIGN: Randomized, double-blind, controlled
trial. SETTING: University and Veterans Affairs hospitals. PATIENTS: 55
patients who had congestive heart failure with New York Heart
Association class III and IV symptoms, ejection fraction less than 40%,
and peak oxygen consumption less than 17.0 mL/kg per minute (or <50% of
predicted) during standard therapy were randomly assigned. Forty-six
patients completed the study. INTERVENTION: Coenzyme Q10, 200 mg/d, or
placebo. MEASUREMENTS: Left ventricular ejection fraction (measured by
radionuclide ventriculography) and peak oxygen consumption and exercise
duration (measured by a graded exercise evaluation using the Naughton
protocol) with continuous metabolic monitoring. RESULTS: Although the
mean (+/-SD) serum concentration of ~coenzyme Q10 increased from
0.95+/-0.62 microg/mL to 2.2+/-1.2 microg/mL in patients who received
active treatment, ejection fraction, peak oxygen consumption, and
exercise duration remained unchanged in both the coenzyme Q10 and
placebo groups. CONCLUSION: Coenzyme Q10 does not affect ejection
fraction, peak oxygen consumption, or exercise duration in patients
with congestive heart failure receiving standard medical therapy.
(low dose and probably short term)

XXXXXXXXXXXXXXXXXXXXXXXXXXXXXXX

Cerebral effects

Arch Neurol. 2002 Oct;59(10):1541-50. Related Articles, Links
Comment in:
Arch Neurol. 2002 Oct;59(10):1523.
Arch Neurol. 2003 Aug;60(8):1170-2; author reply 1172-3.
Arch Neurol. 2003 Aug;60(8):1170; author reply 1172-3.
 Effects of coenzyme Q10 in early @Parkinson disease: evidence of
slowing of the functional decline.
Shults CW, Oakes D, Kieburtz K, Beal MF, Haas R, Plumb S, Juncos JL,
Nutt J, Shoulson I, Carter J, Kompoliti K, Perlmutter JS, Reich S,
Stern M, Watts RL, Kurlan R, Molho E, Harrison M, Lew M; Parkinson
Study Group.
Department of Neurosciences, Mail Code 0662, University of
California-San Diego, 9500 Gilman Dr, La Jolla, CA 92093-0662, USA.
cshults@ucsd.edu
            BACKGROUND: Parkinson disease (PD) is a degenerative
neurological
disorder for which no treatment has been shown to slow the
progression. OBJECTIVE: To determine whether a range of dosages of
coenzyme Q10 is safe and well tolerated and could slow the functional
decline in PD. DESIGN: Multicenter, randomized, parallel-group,
placebo-controlled, double-blind, dosage-ranging trial. SETTING:
Academic movement disorders clinics. PATIENTS: Eighty subjects with
early PD who did not require treatment for their disability.
INTERVENTIONS: Random assignment to placebo or coenzyme Q10 at dosages
of 300, 600, or 1200 mg/d. MAIN OUTCOME MEASURE: The subjects
underwent evaluation with the Unified Parkinson Disease Rating Scale
(UPDRS) at the screening, baseline, and 1-, 4-, 8-, 12-, and 16-month
visits. They were followed up for 16 months or until disability
requiring treatment with levodopa had developed. The primary response
variable was the change in the total score on the UPDRS from baseline
to the last visit. RESULTS: The adjusted mean total UPDRS changes were
+11.99 for the placebo group, +8.81 for the 300-mg/d group, +10.82 for
the 600-mg/d group, and +6.69 for the 1200-mg/d group. The P value for
the primary analysis, a test for a linear trend between the dosage and
the mean change in the total UPDRS score, was.09, which met our
prespecified criteria for a positive trend for the trial. A
prespecified, secondary analysis was the comparison of each treatment
group with the placebo group, and the difference between the 1200-mg/d
and placebo groups was significant (P =.04). CONCLUSIONS: Coenzyme Q10
was safe and well tolerated at dosages of up to 1200 mg/d. Less
disability developed in subjects assigned to coenzyme Q10 than in
those assigned to placebo, and the benefit was greatest in subjects
receiving the highest dosage. Coenzyme Q10 appears to slow the
progressive deterioration of function in PD, but these results need to
be confirmed in a larger study.PMID: 12374491.........................
Exp Neurol. 2004 Aug;188(2):491-4. Related Articles, Links
Pilot trial of high dosages of coenzyme Q10 in patients with
Parkinson's disease.
Shults CW, Flint Beal M, Song D, Fontaine D.
Department of Neurosciences, University of California, San Diego, La
Jolla 92093-0662, USA. cshults@ucsd.edu
           The safety and tolerability of high dosages of coenzyme Q10
were studied in 17 patients with Parkinson's disease (PD) in an open
label study. The subjects received an escalating dosage of coenzyme
Q10--1200, 1800, 2400, and 3000 mg/day with a stable dosage of vitamin
E (alpha-tocopherol) 1200 IU/day. The plasma level of coenzyme Q10 was
measured at each dosage. Thirteen of the subjects achieved the maximal
dosage, and adverse events were typically considered to be unrelated to
coenzyme Q10. The plasma level reached a plateau at the 2400 mg/day
dosage and did not increase further at the 3000 mg/day dosage. Our data
suggest that in future studies of coenzyme Q10 in PD, a dosage of 2400
mg/day (with vitamin E/alpha-tocopherol 1200 IU/day) is an appropriate
highest dosage to be studied.
PMID: 15246848    (Two yrs after a very successful pilot trial they do
a small phase I dose evaluation trial??)
J Neurol Sci. 2004 May 15;220(1-2):41-8. Related Articles, Links
Effect of coenzyme Q10 on the mitochondrial function of skin
fibroblasts from Parkinson patients.
Winkler-Stuck K, Wiedemann FR, Wallesch CW, Kunz WS.
Klinik fur Neurologie der Otto-von-Guericke-Universitat Magdeburg,
Leipziger Strasse 44, 39120 Magdeburg, Germany.
               Several lines of evidence suggest an impairment of
mitochondrial function in the brain of patients with Parkinson's
disease (PD). However, the presence of a detectable mitochondrial
defect in extracerebral tissue of these patients remains a matter of
dispute. Therefore, we investigated mitochondrial function in
fibroblasts of 18 PD patients applying biochemical micromethods.
Putative beneficial effects of coenzyme Q(10) (CoQ(10)), a potent
antioxidant, on the mitochondrial function of skin fibroblast cultures
were evaluated. Applying inhibitor titrations of the mitochondrial
respiration to calculate flux control coefficients of respiratory chain
complexes I and IV, we observed deficiencies of both complexes in
cultivated skin fibroblasts of PD patients. Cultivation of fibroblasts
in the presence of 5 microM CoQ(10) restored the activity of impaired
respiratory chain complexes in the fibroblast cultures of 9 out of 18
PD patients. Our data support the presence of a generalised
mitochondrial defect in at least a subgroup of patients with PD that
can be partially ameliorated in vitro by coenzyme Q(10) treatment.PMID:
15140604..............................
J Neuropathol Exp Neurol. 2002 Jul;61(7):634-9. Related Articles,
Links
Mitochondrial DNA deletions/rearrangements in @parkinson disease and
related neurodegenerative disorders.
Gu G, Reyes PE, Golden GT, Woltjer RL, Hulette C, Montine TJ, Zhang J.
Department of Pathology, Vanderbilt University Medical Center,
Nashville, Tennessee 37232-2561, USA.
Inhibition of mitochondrial respiratory chain function may contribute
to dopaminergic neurodegeneration in the substantia nigra (SN) of
patients with Parkinson disease (PD). Since large-scale structural
changes (e.g. deletions and rearrangements in mitochondrial DNA
[mtDNA]) have been associated with mitochondrial dysfunction, we
tested the hypothesis that increased total mtDNA
deletions/rearrangements are associated with neurodegeneration in PD.
This study employed a well-established technique, long-extension
polymerase chain reaction (LX-PCR), to detect the multiple mtDNA
deletions/rearrangements in the SN of patients with PD, multiple
system atrophy (MSA), dementia with Lewy bodies (DLB), Alzheimer
disease (AD), and age-matched controls. We also compared the total
mtDNA deletions/rearrangements in different brain regions of PD
patients. The results demonstrated that both the number and variety of
mtDNA deletions/rearrangements were selectively increased in the SN of
PD patients compared to patients with other movement disorders as well
as patients with AD and age-matched controls. In addition, increased
mtDNA deletions/rearrangements were observed in other brain regions in
PD patients, indicating that mitochondrial dysfunction is not just
limited to the SN of PD patients. These data suggest that accumulation
of total mtDNA deletions/rearrangements is a relatively specific
characteristic of PD and may be one of the contributing factors
leading to mitochondrial dysfunction and neurodegeneration in PD.
PMID: 12125742
XXXXXXXXXXXXXXXXXXXXXXXXXXXXX

All the advice is greatly appreciated. Lowering the dose would be the
obvious choice, I am just not sure if I want to buy another bottle of
smaller dose just to adjust. Just had another restless night, and
that's after taking 600mg of standartized kava, fell asleep fast enough
but awoke early. I haven't awaken early without the need for it in
YEARS, I also haven't suffered any insomnia in years. If the insomnia
continues much longer, I will simply stop the use of this supplement.
To reply to some previous posts, I am currently working on remodeling
my house and the energy required for that is immense. I literally put
in 12 hour days redoing my floors, painting etc. So I am actually more
tired than usual. Also, I paid less than 14$ for a 120, 50mg softgels
at Sam's Club. Seemed like a really good deal.