CoQ10-Getting Older? Get it in you!
This is not to say that CoQ10 is going to make you immortal, you may feel that way though. CoQ10 is a component of just about every cell in the body. The Mitochondria uses CoQ10 to increase the production of energy within the cell which, in turn, increases the oxygen content of the Mitochondria(3). What is the Mitochondria?
The Mitochondria is the “power plant” of a cell. It is a sausage shaped structure in the fluid of every living cell. The number of Mitochondrion (plural for Mitochondria) is different for each cell and depends on the energy requirements for that cell. For instance, the muscles of the Heart contain thousands of Mitochondrion per cell. The Heart is a pretty busy muscle. Other cells only have dozens of Mitochondrion. It is very important to support the Mitochondria, keeping it happy and functioning.
Having more energy in our Brain cells isn't a bad idea either. CoQ10 concentrates in the Cerebral Cortex of the Brain. This is the area where most learning occurs. More importantly, the Cerebral Cortex receives the nerve impulses for our sense of sound, smell, sight, and touch. The actions of movement including speech are processed in this area of the Brain. Critical to aging are the aspects of thought, reasoning, memory and the recall of memory are coordinated in the Frontal Lobe of the Cerebral Cortex. CoQ10 is extremely important for graceful aging, not only physically but mentally too.
If you are getting older, you need to get CoQ10. I can hear the questions now; where do I get it, how much do I take, is it expensive, will it work for me? Though I cannot answer the last question for you, I can provide some information and then you can decide.
If you suffer from hypoxia (oxygen starvation) CoQ10 may increase the production of free radicals in your system.
(If you suffer with Candida Albicans (yeast infection, thrush, vaginal candidiasis) your available CoQ10 is consumed by the Candida.
Those on Beta-Blockers, HMG-CoA Reductase Inhibitors [statins], Phenothiazines, and Tricyclic Antidepressants are encouraged to supplement with CoQ10 because the medications interfere with the natural production and function of CoQ10(6,7,8). Taking Red Yeast Rice (RYR) for its cholesterol lowering potential? Supplement with CoQ10 because laboratory tests (in animals) have demonstrated RYR suppresses tissue CoQ10 content(9). Supplementing with CoQ10 has many more benefits besides anti-aging. But that is the topic for another post. Right now let's look at what science says about dosing (how much to take). The evidence and studies support a dose between 30 and 3,000 mg per day. But that probably does not help you much. How about I cite some examples of dosage recommendations? |
|
Dose |
Reference |
Comments |
30 to 60 mg |
Am J Health Syst Pharm. 56(6):519-521, 1999 |
Lower to upper range to prevent deficiency in health young people < 21. At 21 years old, the decline starts. |
90 to 390 mg |
Am J Health Syst Pharm. 56(6):519-521, 1999 |
Range for Breast cancer patients. |
100 to 200 mg |
Am J Health Syst Pharm. 56(6):519-521, 1999 |
Range for people with chronic heart disease. |
100 to 200 mg |
The Directory of Life Extension Supplements. Life Extension Media, Florida, USA. 2000:79 |
Range for people 40 or younger with ailments that may benefit from CoQ10. |
150 mg |
Cephalagia. 22(2):137-141, 2002 |
Dosage used in a clinical trial demonstrating prevention of migraine headaches. |
150 mg |
Nature & Health. 22(2):72-74, 2001 |
Dosage recommended that may treat angina. |
300 mg |
Disease Prevention and Treatment 3rd Edition. Life Extension Media. Florida, USA. 2000:200 |
Dosage recommended for increasing energy in chronic fatigue syndrome patients and for congestive heart failure. |
400 mg |
The Directory of Life Extension Supplements. Life Extension Media, Florida, USA. 2000:79 |
Dosage for people with cadiac disease, cancer or brain disease. |
2,400 mg |
Exp Neurol. 188(2):491-494, 2004. |
Dosage used with 1200 IU per day in a pilot trial of Parkinson's disease patients. |
3,000 mg |
Neurology. 65(11):1834-1836, 2005. |
Dosage trial to determine the safety and tolerability of CoQ10 in ALS patients |
Prices for CoQ10 have gone up radically in the last several years, 2006-2010. But there are many places where you can purchase CoQ10. It comes in tablets and capsules and gelcaps. Scientific methods have indicated that the gelcaps or soft gel capsules are absorbed twice as efficiently as dry powdered forms. When you see Ubiquinol, you are looking at the reduced antioxidant form and Ubiquinone is the oxidized form of CoQ10. Both are present in the body as circulating CoQ10.
CoQ10 is not just a “health industry” fad; if you are getting older – get it in you!
------- References: -------
1. Monograph: Coenzyme Q10. Alternative Medicine Review. 12(2):159-168, 2007.
CoQ10 levels decline with advancing age, and this decline might contribute in part to some of the manifestations of aging.
2. Kagan, T., et al. Coenzyme Q10 can in some circumstances block apoptosis, and this effect is mediated through mitochondria. Annals of the New York Academy of Sciences USA. 887:31-47, 1999.
The mitochondrial component coenzyme Q10 has been used for many years as a dietary supplement intended to promote good health by trapping free radicals, thus preventing lipid peroxidation and DNA damage. The authors tested its use as a generic anti-apoptotic compound and have found that its ability to protect against apoptosis varies depending on both cell type and mode of cell death induction. This protection may be mediated by its effect on mitochondrial function and viability. The protective effect on mitochondrial membrane potential does not always result in altered mitochondrial enzyme activity and neither does it guarantee survival.
3. Barbiroli, B., et al. Coenzyme Q10 improves mitochondrial respiration in patients with mitochondrial cytopathies. An in vivo study on brain and skeletal muscle by phosphorous magnetic resonance spectroscopy. Cell Molecular Biology. 43(5):741-749, 1997.
With phosphorus magnetic resonance spectroscopy (31P-MRS) the authors studied in vivo the effect of six-month coenzyme Q10 treatment on the efficiency of brain and skeletal muscle mitochondrial respiration in six patients with different mitochondrial cytopathies. Before coenzyme Q 10 the authors found a low creatine phosphate content (average of 25% decrease from controls) in the occipital lobes of all patients. Calculated [ADP] and the relative rate of adenosine triphosphate (ATP) synthesis were high (as an average, 57% and 16% above control group respectively), whereas the cytosolic phosphorylation potential was low (as an average, 60% of control value). 31P-MRS also revealed an average of 29% reduction of the mitochondrial function in the skeletal muscle of patients compared with controls. After a six-month treatment with 150 mg coenzyme Q10 per day all brain variables were remarkably improved in all patients, returning within the control range in all cases. Treatment with coenzyme Q10 also improved the muscle mitochondrial functionality enough to reduce the average deficit to 56% of the control group. These in vivo findings show the beneficial effect of coenzyme Q10 in patients with mitochondrial cytopathies, and are consistent with the view that increased coenzyme Q10 concentration in the mitochondrial membrane increases the efficiency of oxidative phosphorylation independently of enzyme deficit.
4. Kent, S. The multiple health benefits of coenzyme Q10. Life Extension. 2(2), 1996.
Approximately 50% of the body’s total coenzyme Q10 is located in mitochondrion. It performs three functions in the mitochondria: 1) assisting enzymes present in the mitochondria to convert dietary nutrients into adenosine triphosphate; 2) to exert antioxidant effects against free radicals generated during the energy-producing process; and, 3) protecting the structural integrity of the mitochondrial membrane.
5. Porter, D. A., et al. The effect of oral coenzyme Q10 on the exercise tolerance of middle-aged, untrained men. International Journal of Sports Medicine. 16(7):421-427, 1995.
In order to determine the effect of oral Coenzyme Q10 (CoQ10) dosing on exercise capacity, 15 middle-aged men (44.7 +/- 2.0 years) received either CoQ10 (150 mg/day x 2 months-Q10 GRP) or placebo (2 months-CON GRP). Blood CoQ10 levels increased (p < 0.05) during the treatment in the Q10 GRP (Pre = 0.72 +/- 0.06, 2 months = 1.08 +/- 0.14 micrograms/ml) and were unchanged in the CON GRP (Pre = 0.91 +/- 0.05, 2 month = 0.69 +/- 0.05 microgram/ml). Similarly, the subjective perception of vigor (visual analog scale 1-10 where, 10 = very energetic, and 0 = very, very unenergetic) increased (p < 0.05) in the Q10 GRP (Pre = 5.73 +/- 0.35, 2 month = 6.64 +/- 0.45). However, maximal oxygen consumption (VO2max Pre = 2.97 +/- 0.18, 2 month = 3.05 +/- 0.15 l/min) and lactate threshold (LT Pre = 2.04 +/- 0.12, 2 month = 2.08 +/- 0.12 l/min), as measured on the cycle ergometer, were unchanged as a result of the CoQ10 treatment. Neither forearm oxygen uptake, nor forearm blood flow was found to be affected by the CoQ10. Although lactate release during hand-grip testing tended to decrease in the Q10 GRP (Pre = 227 +/- 49, 2 month = 168.3 +/- 40 mumole/min) this was not significant (p > 0.05). It can be concluded that short-term (2 months) oral dosing with CoQ10 increases circulating blood levels of CoQ10 and the subjective perceived level of vigor in middle-aged men. However, short-term dosing does not improve aerobic capacity or firearm exercise metabolism as measured in this investigation.
6. Gaby, A. R. The role of coenzyme Q10 in clinical medicine. Part II. Cardiovascular disease, hypertension, diabetes mellitus and infertility. Alternative Medical Review . 1(3):168-175, 1996.
This review discusses the role of coenzyme Q10 (CoQ10) in cardiovascular disease, hypertension, diabetes mellitus, and infertility. Deficiencies of CoQ10 have been documented in patients with heart disease. Administration of CoQ10 has been shown to prolong survival and improve quality of life in patients with cardiomyopathy. In patients with congestive heart failure, CoQ10 ameliorated symptoms, reduced the number of hospitalizations and appeared to increase the survival rate. CoQ10 has been shown to prevent adriamycin cardiotoxicity and to reduce the incidence of postoperative cardiac dysfunction in patients undergoing heart surgery This nutrient may be of value for patients with diabetes mellitus or male infertility, but additional studies are needed in these areas. CoQ10 status may be adversely affected by treatment with certain cholesterol-lowering drugs, beta blockers, tricyclic antidepressants, and phenothiazines
7. Rundek, T., et al. Atorvastatin decreases the coenzyme Q10 level in the blood of patients at risk for cardiovascular disease and stroke. Archives of Neurology. 61(6):889-892, 2004. Department of Neurology, Columbia University College of Physicians & Surgeons, New York, NY, USA.
Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) are widely used for the treatment of hypercholesterolemia and coronary heart disease and for the prevention of stroke. There have been various adverse effects, most commonly affecting muscle and ranging from myalgia to rhabdomyolysis. These adverse effects may be due to a coenzyme Q(10) (CoQ(10)) deficiency because inhibition of cholesterol biosynthesis also inhibits the synthesis of CoQ(10). The objective of this study was to measure CoQ(10) levels in blood from hypercholesterolemic subjects before and after exposure to atorvastatin calcium, 80 mg/d, for 14 and 30 days. This was a prospective blinded study of the effects of short-term exposure to atorvastatin on blood levels of CoQ(10). The setting was a stroke center at an academic tertiary care hospital. The authors examined a cohort of 34 subjects eligible for statin treatment according to National Cholesterol Education Program: Adult Treatment Panel III criteria. The mean +/- SD blood concentration of CoQ(10) was 1.26 +/- 0.47 micro g/mL at baseline, and decreased to 0.62 +/- 0.39 micro g/mL after 30 days of atorvastatin therapy (P<.001). A significant decrease was already detectable after 14 days of treatment (P<.001). Even brief exposure to atorvastatin causes a marked decrease in blood CoQ(10) concentration. Widespread inhibition of CoQ(10) synthesis could explain the most commonly reported adverse effects of statins, especially exercise intolerance, myalgia, and myoglobinuria.
8. Kelly, P. Coenzyme Q10 Improves myopathic pain in statin-treated patients. Abstract 1001-1117. American College of Cardiology 54th Annual Scientific Session. Orlando, Florida, USA. March 6, 2005. University Hospital Medial Center, Stony Brook, New York, USA.
Patients with significant myopathy who are taking statin therapy have a significant decrease in myopathic pain after 30 days of supplementation with coenzyme Q10. The author randomized in a double-blind design 41 statin-treated patients with myopathic pain to 30 days of supplementation with 400 IU of vitamin E or 100 mg of coenzyme Q10 per day. However, the reported side effects of statin treatment include myopathy, muscle damage associated with increased levels of creatinine phosphokinase, and abnormalities of liver function. The researchers conducted the present trial to determine if coenzyme Q10 supplementation would improve muscle related adverse effects in patients on statins. If coenzyme Q10 supplementation were effective in reducing the symptoms of myopathy associated with statin use, it would be possible for patients to retain the beneficial effects of cholesterol lowering while reducing significant side effects. The two treatment groups were similar with respect to demographic and clinical parameters. Pre- and post- vitamin E, pain remained unchanged (3.9 versus 4.4, P = NS). Pre- and post coenzyme Q10, pain improved significantly (6.2 1.7 versus 3.1, P <.001). Pain improved in three of 20 vitamin E patients and 18 of 21 coenzyme Q10 patients (P <.001). There was no significant change in creatinine phosphokinase with treatment in either group nor did these levels correlate with pain severity. Coenzyme Q10 did not have any effect on lipid levels and was safe and well tolerated. This study provides encouraging evidence for the use of coenzyme Q10 in alleviating myopathic pain in patients taking statins.
9. Yang, H. T., et al. Acute administration of red yeast rice (Monascus purpureus) depletes tissue coenzyme Q10 levels in ICR mice. British Journal of Nutrition. 93(1):131-135, 2005. School of Pharmaceutical Science, Taipei Medical University, Taipei, Taiwan.
In this study, the authors attempted to evaluate the effect of administration of a high quantity of red yeast rice on coenzyme Q10 (CoQ10) synthesis in the tissues of ICR mice. Eighty-eight adult male ICR mice were housed and divided into control and experimental groups for red yeast rice treatment. Animals were gavaged [force-fed through a tube] with a low (1 g/kg body weight) or a high dose (5 g/kg body weight, approximately five times the typical recommended human dose) of red yeast rice dissolved in soyabean oil. After gavagement, animals of the control group were immediately killed; mice of the experimental groups (eight for each subgroup) were killed at different time intervals of 0.5, 1, 1.5, 4 and 24 h. The liver, heart and kidney were taken for analysis of monacolin K (liver only) and CoQ10 analysis. Liver and heart CoQ10 levels declined dramatically in both groups administered red yeast rice, especially in the high-dose group, within 30 min. After 24 h, the levels of hepatic and cardiac CoQ10 were still reduced. A similar trend was also observed in the heart, but the inhibitory effect began after 90 min. The higher dose of red yeast rice presented a greater suppressive effect than did the lower dose on tissue CoQ10 levels. In conclusion, acute red yeast rice gavage suppressed hepatic and cardiac CoQ10 levels in rodents; furthermore, the inhibitory effect was responsive to the doses administered.
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