gear and the heart

[bifda]

will a typical cycle of 500mg a week and dbol for 12 weeks have any ill effects on my heart in the long run, say doing 2 of these cycles a year for a few years?

[CHAP]

Always a chance. Dr says my heart is slightly inlarged,but also says that is perfectly normal for people who have lifted for a long time with alot of intensity

[Reed]

Well there is too many factors to determine the outcome for you.
Your current health

Your family health history

Do you smoke

Do you drink

etc


you see its too hard to get a for sure answer but I will venture out and say NO.

Look into CoQ10 for your heart

[alpmaster]

Look into CoQ10 for your heart

CoQ10 does absolutely nothing at all, it's a huge marketing scam.

But agreed on everything else you said, there are many factors.

[Reed]

CoQ10 does absolutely nothing at all, it's a huge marketing scam.

But agreed on everything else you said, there are many factors.

Hmm care to share your research there big guy. Marketing scam, not all supplements are junk and can provide benefits. Its the ones you don't know about that work wonders.

Department of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, 430060 Wuhan City, China.
Statins and coenzyme Q10 are both used as adjuncts in the treatment of chronic heart failure (CHF) due to their anti-inflammatory and antioxidant effects, respectively. And both have been variously shown to improve cardiac function in patients with CHF. The two agents interact in two ways; statins inhibit coenzyme Q10 synthesis through inhibition of HMG-CoA reductase, the rate limiting step in cholesterol synthesis, also shared by coenzyme Q10. Secondly, they both exhibit their antioxidant effects through activation of the enzyme superoxide dismutase, the rate limiting step in nitric oxide metabolism and main antioxidant mechanism of coenzyme Q10. We hypothesize that the interaction between statins and coenzyme Q10 is more than just a replacement, but a synergistic interaction on superoxide dismutase that could result in better cardiac function, improvement in patient symptoms, shortening of duration of hospital stay and improvement in patient quality of life.


Another:
It is well known that by improving mitochondrial bioenergetics, Coenzyme Q10 improves the systolic function in heart failure. The aim of this study was to see whether it benefits the diastolic dysfunction in hypertrophic cardiomyopathy (HCM) cases since diastolic relaxation also requires energy like the systole. 200 mg/day of CoQ10 was added to the conventional treatment in 46 patients with HCM diagnosed clinically and by echocardiography and by excluding cases of long standing hypertension. A comparable group of 41 age/sex matched cases received only conventional therapy. There was a significant improvement in the parameters like NYHA class > or = 1, in quality of life (QOL) on 6 minutes walk test, in diastolic dysfunction by > or = 1 parameter and in MR > or = 1 grade. Post treatment echocardiogram showed significant reduction in left ventricular outflow tract (LVOT) gradient > or = 15 mm Hg in obstructive cases (12 out of 46) in the treatment group. The mean interventricular septal thickness (IVS) showed a 22.4% reduction (p < 0.005). The mean posterior wall thickness showed a 23.1% reduction (p < 0.005). No patient in the treatment Group had ventricular tachycardia (VT) whereas 4 cases in the control group had VT. In both groups 1 patient was lost due to sudden cardiac death (SCD).

Another:
OBJECTIVES: The aim of this study was to investigate the relationship between plasma coenzyme Q(10) (CoQ(10)) and survival in patients with chronic heart failure (CHF). BACKGROUND: Patients with CHF have low plasma concentrations of CoQ(10), an essential cofactor for mitochondrial electron transport and myocardial energy supply. Additionally, low plasma total cholesterol (TC) concentrations have been associated with higher mortality in heart failure. Plasma CoQ(10) is closely associated with low-density lipoprotein cholesterol (LDL-C), which might contribute to this association. Therefore we tested the hypothesis that plasma CoQ(10) is a predictor of total mortality in CHF and could explain this association. METHODS: Plasma samples from 236 patients admitted to the hospital with CHF, with a median (range) duration of follow-up of 2.69 (0.12 to 5.75) years, were assayed for LDL-C, TC, and total CoQ(10). RESULTS: Median age at admission was 77 years. Median (range) CoQ(10) concentration was 0.68 (0.18 to 1.75) micromol/l. The optimal CoQ(10) concentration for prediction of mortality (established with receiver-operator characteristic [ROC] curves) was 0.73 micromol/l. Multivariable analysis allowing for effects of standard predictors of survival--including age at admission, gender, previous myocardial infarction, N-terminal peptide of B-type natriuretic peptide, and estimated glomerular filtration rate (modification of diet in renal disease)--indicated CoQ(10) was an independent predictor of survival, whether dichotomized at the ROC curve cut-point (hazard ratio [HR]: 2.0; 95% confidence interval [CI]: 1.2 to 3.3) or the median (HR: 1.6; 95% CI: 1.0 to 2.6). CONCLUSIONS: Plasma CoQ(10) concentration was an independent predictor of mortality in this cohort. The CoQ(10) deficiency might be detrimental to the long-term prognosis of CHF, and there is a rationale for controlled intervention studies with CoQ(10).

How many more should I pull from pubmed

You must understand that we do not understand EVERYTHING about our bodies or the drugs we take (even steroids ) yet but studies are coming up showing the benefits of this supplement

[*RAGE*]

Hmm care to share your research there big guy. Marketing scam, not all supplements are junk and can provide benefits. Its the ones you don't know about that work wonders.

Department of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, 430060 Wuhan City, China.
Statins and coenzyme Q10 are both used as adjuncts in the treatment of chronic heart failure (CHF) due to their anti-inflammatory and antioxidant effects, respectively. And both have been variously shown to improve cardiac function in patients with CHF. The two agents interact in two ways; statins inhibit coenzyme Q10 synthesis through inhibition of HMG-CoA reductase, the rate limiting step in cholesterol synthesis, also shared by coenzyme Q10. Secondly, they both exhibit their antioxidant effects through activation of the enzyme superoxide dismutase, the rate limiting step in nitric oxide metabolism and main antioxidant mechanism of coenzyme Q10. We hypothesize that the interaction between statins and coenzyme Q10 is more than just a replacement, but a synergistic interaction on superoxide dismutase that could result in better cardiac function, improvement in patient symptoms, shortening of duration of hospital stay and improvement in patient quality of life.


Another:
It is well known that by improving mitochondrial bioenergetics, Coenzyme Q10 improves the systolic function in heart failure. The aim of this study was to see whether it benefits the diastolic dysfunction in hypertrophic cardiomyopathy (HCM) cases since diastolic relaxation also requires energy like the systole. 200 mg/day of CoQ10 was added to the conventional treatment in 46 patients with HCM diagnosed clinically and by echocardiography and by excluding cases of long standing hypertension. A comparable group of 41 age/sex matched cases received only conventional therapy. There was a significant improvement in the parameters like NYHA class > or = 1, in quality of life (QOL) on 6 minutes walk test, in diastolic dysfunction by > or = 1 parameter and in MR > or = 1 grade. Post treatment echocardiogram showed significant reduction in left ventricular outflow tract (LVOT) gradient > or = 15 mm Hg in obstructive cases (12 out of 46) in the treatment group. The mean interventricular septal thickness (IVS) showed a 22.4% reduction (p < 0.005). The mean posterior wall thickness showed a 23.1% reduction (p < 0.005). No patient in the treatment Group had ventricular tachycardia (VT) whereas 4 cases in the control group had VT. In both groups 1 patient was lost due to sudden cardiac death (SCD).

Another:
OBJECTIVES: The aim of this study was to investigate the relationship between plasma coenzyme Q(10) (CoQ(10)) and survival in patients with chronic heart failure (CHF). BACKGROUND: Patients with CHF have low plasma concentrations of CoQ(10), an essential cofactor for mitochondrial electron transport and myocardial energy supply. Additionally, low plasma total cholesterol (TC) concentrations have been associated with higher mortality in heart failure. Plasma CoQ(10) is closely associated with low-density lipoprotein cholesterol (LDL-C), which might contribute to this association. Therefore we tested the hypothesis that plasma CoQ(10) is a predictor of total mortality in CHF and could explain this association. METHODS: Plasma samples from 236 patients admitted to the hospital with CHF, with a median (range) duration of follow-up of 2.69 (0.12 to 5.75) years, were assayed for LDL-C, TC, and total CoQ(10). RESULTS: Median age at admission was 77 years. Median (range) CoQ(10) concentration was 0.68 (0.18 to 1.75) micromol/l. The optimal CoQ(10) concentration for prediction of mortality (established with receiver-operator characteristic [ROC] curves) was 0.73 micromol/l. Multivariable analysis allowing for effects of standard predictors of survival--including age at admission, gender, previous myocardial infarction, N-terminal peptide of B-type natriuretic peptide, and estimated glomerular filtration rate (modification of diet in renal disease)--indicated CoQ(10) was an independent predictor of survival, whether dichotomized at the ROC curve cut-point (hazard ratio [HR]: 2.0; 95% confidence interval [CI]: 1.2 to 3.3) or the median (HR: 1.6; 95% CI: 1.0 to 2.6). CONCLUSIONS: Plasma CoQ(10) concentration was an independent predictor of mortality in this cohort. The CoQ(10) deficiency might be detrimental to the long-term prognosis of CHF, and there is a rationale for controlled intervention studies with CoQ(10).

How many more should I pull from pubmed

You must understand that we do not understand EVERYTHING about our bodies or the drugs we take (even steroids) yet but studies are coming up showing the benefits of this supplement

Oh no he didnt

OWNED

with a back like that how could you be wrong

[*RAGE*]

I would say the same look how long it has been around and how many times they use it and how many are still here....I am not saying that it will not affect you because I dont know you...

[Reed]

Don't worry I have been wrong before. Just seen the research in all kinds of places with this supplement.

Its all good we learn something new everyday. I work with Nark now and get owned on a regular basis

[bifda]

thanks reed, ive got some Q10 just never really took it regular.

how much is a normal(if there is one) dose, ive got 75 mg caps.

[Reed]

thanks reed, ive got some Q10 just never really took it regular.

how much is a normal(if there is one) dose, ive got 75 mg caps.

I say the upper range doses are showing real benefits. I read MD alot as they put in tons of research articles and if I remember correctly they had a article on a study that said 200-400mg is showing amazing benefits such as adding years to peoples lives. Thats what I remember, don't quote me. But as you can see there is benefit to it

It is found in membranes of many organelles and its primary function in cells is generating energy with the highest concentrations found in the mitochondrion. I also think that the highest concentration in tissue samples was found in the heart compared to other parts

I think 200mg would do

[spywizard]

Don't worry I have been wrong before. Just seen the research in all kinds of places with this supplement.

Its all good we learn something new everyday. I work with Nark now and get owned on a regular basis

well, that's not hard to do.. nor is it something to be ashamed about..

[Reed]

well, that's not hard to do.. nor is it something to be ashamed about..

You are right. I worry to much about being wrong and getting looked down on by my peers or losing "status" if I get proven wrong. When I need to take the opportunity to learn and progress.

It just seems that sometimes we all, myself included, get some type of pleasure out of proving one another wrong or flaming someones lack of knowledge when the fact is none of us were born with this knowledge even the guru's that we believe are "gods". We are human and we are falliable

[alpmaster]

I have seen many studies showing supplemented CoQ10 to have very low bio-availability and generally not effective as a miracle cure for the many things it is supposed to be. A good professor of mine, Dr. Beau Greer (Here is his bio and many certifications and degrees) has showed me the many studies showing it's just plain inneffective orally. Also, I too can pull up a host of well documented studies showing the contrary to Reed's :

The effect of coenzyme Q10 in patients with congestive heart failure.

Ann Intern Med 2000 Apr 18;132(8):636-40

Khatta M, Alexander BS, Krichten CM, Fisher ML, Freudenberger R, Robinson SW, Gottlieb SS.

University of Maryland School of Medicine and Veterans Affairs Medical Center, Baltimore 21201, USA.

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.
PMID: 10766682 [PubMed - indexed for MEDLINE]


Nutritional and exercise-based therapies in the treatment of mitochondrial disease.

Curr Opin Clin Nutr Metab Care 2002 Nov;5(6):619-29

Mahoney DJ, Parise G, Tarnopolsky MA.

Departments of Medical Sciences, Kinesiology, and Medicine (Division of Neurology), McMaster University, Hamilton, Ontario, Canada.

PURPOSE OF REVIEW This review will critically summarize the nutritional and exercise-based interventions that have been used to treat mitochondrial disease, with a focus on the biochemical or molecular rationale for their use as well as recent advances in the field.RECENT FINDINGS Many nutritional-based treatment strategies have been used in an attempt to target energy impairment and its sequelae. Recently, coenzyme Q10, idebenone and triacylglycerol have been shown to bypass defective respiratory enzymes or scavenge free radicals, whereas creatine monohydrate has provided an alternative energy source. Thiamine has been used to decrease lactate levels and increase flux through aerobic metabolism, and riboflavin has been used as a precursor to complexes I and II. Several therapies employing various antioxidants in combination with other supplements have been effective at targeting several of the final common pathways of mitochondrial disease. Miscellaneous supplements, such as L-arginine and uridine, have also had recent success. However, although positive responses have been reported with these agents, many reports have shown no benefit, and there is widespread disparity in the literature. An alternative approach to treatment is exercise training. Both resistance and endurance exercise training have had positive outcomes in patients with mitochondrial disease, although several questions remain to be answered.SUMMARY There is no currently recognized treatment for mitochondrial disease. Future clinical trials are needed, as well as research into the potential for in-vitro screening of various compounds within affected cells from patients. Until this time, an accurate diagnosis will facilitate treatment on a case-by-case basis.

PMID: 12394637 [PubMed - in process]

Alberta Stroke Program, Department of Clinical Neurosciences, Foothills Hospital, University of Calgary, Calgary, Alberta, Canada

b Professor of Stroke Research, Rm 1162, Foothills Hospital, 1403–29th St. NW, Calgary, Alberta T2N 2T9 Canada

Objective: Release of oxygen free radicals occurs following cerebral ischemia. Studies show that oxygen free radicals mediate ischemic brain injury. CoQ10 is a potent free radical scavenger and may offset brain injury associated with reperfusion. We tested exogeneous CoQ10 as a neuroprotectant in rats following both global and focal ischemic insults. Methods: Rats were subjected to either 4-vessel occlusion ischemia (4-VO, 10 min occlusion, 7-day survival) or middle cerebral artery occlusion (MCAO, 120 min-occlusion, 22.5 h survival). Regional cerebral blood flows (rCBF) and physiological variables such as blood pressure, pO2, pCO2, plasma glucose and hematocrit were monitored and measured in focal ischemia. The animals were randomized to receive treatments of either phosphate buffered saline (PBS) vehicle or CoQ10 following global or focal ischemia. Injection times were at the end of ischemia and 3 h later for both models of ischemia. Histological outcomes are expressed as a percentage of hippocampal CA1 cell injury in global ischemia or percentage of cortical infarct over that of non-ischemic hemisphere in focal ischemia. Results: In global ischemia, animals treated with PBS vehicle and CoQ10 had 86±5% (n=8) and 83±10% (n=8), respectively, of hippocampal CA1 cell injury (P>0.05). The percentage of infarct volumes in animals following focal ischemia were 23±9% (control, n=10) and 25±9% (CoQ10, n=10). There were no temperature or physiological differences between the two treatment groups. Conclusion: Acute treatment with CoQ10 via intraperitoneal injection does not prevent neuronal injuries following global and focal ischemia.



According to the free radical and mitochondrial theories of aging, oxidative damage of cell structures by reactive oxygen species (ROS) plays an important role in the functional declines that accompany aging (22). ROS are generated by mitochondria as a byproduct of ATP production. If not neutralized by antioxidants, ROS may damage mitochondria over time, causing them to function less efficiently and to generate more damaging ROS in a self-perpetuating cycle. Coenzyme Q10 plays an important role in mitochondrial ATP synthesis and functions as an antioxidant in mitochondrial membranes. Moreover, tissue levels of coenzyme Q10 have been reported to decline with age (21). One of the hallmarks of aging is a decline in energy metabolism in many tissues, especially liver, heart, and skeletal muscle. It has been proposed that age-associated declines in tissue coenzyme Q10 levels may play a role in this decline (23). In recent studies, lifelong dietary supplementation with coenzyme Q10 did not increase the life spans of rats or mice (15, 24); however, one study showed that coenzyme Q10 supplementation attenuates the age-related increase in DNA damage (25).] Presently, there is no scientific evidence that coenzyme Q10 supplementation prolongs life or prevents age-related functional declines in humans.


To date, only one clinical trial has examined whether coenzyme Q10 might be efficacious in human patients with Huntington's disease. A 30-month randomized placebo-controlled trial of coenzyme Q10 (600 mg/d), remacemide, or both in 347 patients with early Huntington's disease found that neither coenzyme Q10 nor remacemide significantly altered the decline in total functional capacity, although coenzyme Q10 supplementation (with or without remacemide) resulted in a nonsignificant 13% decrease in the decline (65). Currently, there is insufficient evidence to recommend coenzyme Q10 supplements to Huntington's disease patients.



I am also always looking forward to new information, and my original statement was made because I had already seen many studies shown that supplementation of CoQ10 to be ineffective by a very qualified professor and doctor. This is a billion dollar industry, and any claims made by the results for these supplements are often very over exagerated. My findings in this whole grand blindfold of the supplement industry is: if it works, you can't get it without a prescription, and this has stayed true for about 99.99% of all these miracle products.

I read your postings and have done my research too, I think we can go back and fourth all day posting studies showing the contrary to eachother. I guess we'll have to agree to disagree, but I will state that there is a possible future for effective CoQ10 supplementation, there just haven't been enough clinical studies so far (not to mention, a lot of these experiments have private funding ) to prove all of it's miracle claims. I guess time will tell.

[The Deuce]

So would you say CoQ10 is a good addition to everyone's life who live a VERY ACTIVE HEAVY WEIGHT TRAINING AAS using lifestyle??

I personally take 3 supplements year round regardless of what I am ON or Not ON for compounds...

RED YEAST RICE- Cholesterol Benny's
MILK THISTLE - Liver Benny's
O m e g a 3- Heart Benny's


oh and TRT (250mgs/200mgs EW) but that doesn't count...


Not to mention I try to take some sort of MULTI V also Year round... but sometimes I just don't....



BASICALLY WOULD IT BE A BAD THING TO ADD COQ10 TO MY LINEUP OF SUPPS???

Thanks Reed...

[Reed]

Yes I feel it would be a good addition to any supp program. Thats my opinion and I am no expert. I still have alot of learning to do

The only thing I would take out of the three you take is milk thistle. It has yet to be proven effective, or I think you have to run a extremely high dose for a long period of time to see any benefit which makes it not worth the money.

If looking for liver care more on to liv-52, but I only take it after a oral cycle to aid in helping the liver regenerate itself. This product has tons of research to back itself up and its helpfulness with the liver.

[G-Force]

The only thing I would take out of the three you take is milk thistle. It has yet to be proven effective, .

this is news to me

i take milk thistle all year round
and get my blood tested about 3 times a year as i i like to use orals every cycle and i like a GOOD drink now and again

my liver enzymes are ALWAYS in the normal range

could be a co-incidence i guess but i think i will continue to take it

[The Deuce]

Nice !! I will remove it starting tomorrow !! ... reason being.. I AM ALL OUT AND WAS GOING TO GO BUY MORE TOMORROW !!LOL...

Already have the LIV-52... Just wouldnt use it until I finished a course of Orals.. Like you said... and well I havent recently finished any course of orals.. so it's un-needed at this time.

But instead of picking up the Milk Thistle... I am going to grab this COQ10 instead...

THANKS REED !!!

[Reed]

Your studies you posted do not relate to any of what I posted about CHF. Actually read what you put.

The first study talks about increasing exercise duration and peak oxygen duration. Same can be said about the effectiveness from a ton of supplements we take from BCAAs to glutamine and I never had a study or said it was effective in increasing either of these

The second is about mitochondrial disease and its effectiveness with that, you only highlight a certain part that makes it seem to be ineffective to what we are talking about but the statement is directed to other supplements like L-arginine and uridine, they are not talking CHF or particulars on Coq10. There is no known effective treatment for this disease.

The third is about ischemia which is a restriction of blood supply caused by factors IN the blood vessel and again has nothing to do with the heart or CHF

The fourth is the only thing worth anything with what we are talking about BUT I sure there are studies to contradict this finding.

The fifth study is about Huntington's disease which is a neurodegenerative disorder that can cause changes in personality,cognition, or physical skills. This disease does not deal with the heart or CHF


Nice try but the studies do not deal with the issues at hand or anything I stated. You picked up studies that were not related to the heart or CHF. How many studies could I find on one particular product that works well with one thing but not on another

And I guessing you take no supplements as you state "if its works, you can't get it without a prescription," Well you're missing out on major benefit thats for sure. My supp and diet regiment that my trainer tweaked for me did incredible things to my body in a weeks time, hell even within two days I saw a difference. But it was the combo of the two and like I said its the supps that no one thinks about or knows much about that can work wonders. The supps that I take now are not BCAAs, creatine, NO, glutamine or any other popular supplement. I'm not taking any of the listed above.

But these are all merely yours and mine opinion and you do not have to believe anything that is posted. We can agree to disagree

[The Deuce]

Regardless.... lets not bicker about this...


REED... what is the average dose one should take daily of CoQ10???

[CJ.]

Regardless.... lets not bicker about this...


REED... what is the average dose one should take daily of CoQ10???

Reed posts, "200mgs will do". I myself will buy CoQ10 tomorrow. Is liv-52 OTC or do you need a script? If so do docs write it out easily. I also heard essential forte' is good for the liver. I do not know if this is a OTC or not.

[Reed]

^^^ It is OTC. You'll probably have to order it online though but its perfectly legal. Use it AFTER the oral to aid in the regeneration process that the liver is already doing. You guys gotta remember the liver scare is WAY over played.


Hepatoxicty: Hepatoxicty: Fact or Fiction?

A excellent read w/ great info and a good laugh if you actually take the time to read it

[Zookl]

CoQ10 is not a bunk supplement. Infact, besides the studies online, it had proven to help many situations dealing with health. The University of Wisconsin has done many studies on the enzyme. It is very beneficial, and in my opinion, should be added to everyones daily vitamin.

[Immortal Soldier]

As the old saying goes: Who needs a heart?