Nutritional Supplements



Nutritional Supplements






NAME: L-arginine


Common Names:

Arginine


Description and Source:

Semi-essential amino acid


Biologic Activity



  • Substrate necessary for nitric oxide synthesis and maintenance of activity


  • Nitric oxide acts as a vasodilator, reduces platelet aggregation, reduces monocyte/vessel wall interactions, and reduces smooth muscle cell proliferation (Boger & Ron, 2005). It also stimulates release of growth hormone, insulinlike growth factor 1, insulin, and prolactin and researchers are attempting to discover whether arginine via NO may actually promote or inhibit tumor growth (Lind, 2004).


  • Improves blood flow and reduces total and very-low-density lipoproteins (Maxwell & Anderson, 1999)


  • Carrier of nitrogen, which is important for ammonia detoxification


Nutritional Sources:

Peanuts and peanut butter, brown rice, cashews, pecans, almonds, chocolate, sunflower seeds. Synthesized by the body from glutamine.


Current Use



  • Improves coronary blood flow and endothelial function in persons with atherosclerosis (Yin et al., 2005) and MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke) (Koga et al., 2006) and in women with type II diabetes used along with vitamins C and E (Regensteiner et al., 2003)


  • Improves walking distance in persons with intermittent claudication (Maxwell et al., 1999)


  • Improves endothelium-dependent diabetes with significant hypercholesterolemia (7 g three times a day) (Clarkson et al., 1996; Yin et al., 2005). It also reduces LDL oxidation but may increase total cholesterol levels (Kumar et al., 2005).


  • Improves blood flow and reduces chest pain in patients with nonobstructive coronary artery disease (Lerman et al., 1998). It did not benefit patients who had suffered an acute myocardial infarction (Schulman et al., 2006).



  • May enhance penile engorgement in men and sexual function in women


  • In a small study, L-arginine prolonged pregnancy and improved neonatal outcomes in women with pre-eclampsia (Rytlewski et al., 2006).


  • Arginine alpha-ketoglutarate (AAKG) was given to athletically trained men, and it enhanced their exercise performance (Campbell et al., 2006).


  • Patients with pressure ulcers received arginine, vitamin C, and zinc, which healed much quicker than in those taking a placebo (Desneves et al., 2005).


  • May improve senile dementia (Ohtsuka & Nakaya, 2000)


Available Forms, Dosage, and Administration Guidelines:

Dosages found to be effective for the treatment of cardiovascular disease range from 6 to 9 g a day. Sustainedrelease products maintain steadier blood levels.


Pharmacokinetics—If Available (form or route when known):

Not known


Toxicity:

None known


Contraindications:

Persons susceptible to herpes: arginine activates herpesvirus replication


Side Effects:

GI upset, may exacerbate GERD. It may also increase total cholesterol levels.


Long-Term Safety:

Not known


Use in Pregnancy/Lactation/Children:

Not known


Drug/Herb Interactions and Rationale (if known):

Not known


Special Notes:

Current studies are very short (6 months or less); long-term studies are necessary.



BIBLIOGRAPHY

Boger RH, Ron ES. (2005). L-arginine improves vascular function by overcoming deletevious effects of ADMA, a novel cardiovascular risk factor. Alternative Medicine Review. Nov;10(1):14-23.

Campbell B, et al. (2006). Pharmacokinetics, safety and effects on exercise performance of L-arginine alpha-ketoglutarate in trained adult men. Nutrition. Sep;22(9):872-881.


Clarkson P, et al. (1996). Oral L-arginine improves endothelium-dependent dilation in hypercholesterolemic young adults. Journal of Clinical Investigation. 97(8):1989-1994.

Desneves KJ, et al. (2005). Treatment with supplementary arginine, vitamin c, and zinc in patients with pressure ulcers: A randomised controlled trial. Clinical Nutrition. Dec;24(6):979-987.

Koga Y, et al. (2006). Endothelial dysfunction in MELAS improved by L-arginine supplementation. Neurology. Jun 13;66(11):1766-1769.

Kumar P, et al. (2005). L-arginine supplementation increases serum cholesterol level. Indian Journal of Pharmacology. 37:183.

Lerman A, et al. (1998). Long-term L-arginine supplementation improves small-vessel coronary endothelial function in humans. Circulation. 97(21):2123-2128.

Lind DS. (2004). Arginine and cancer. Journal of Nutrition. Oct;134[10 Suppl.]:2837S-2841S; discussion 2853S.

Maxwell AJ, Anderson BA. (1999). A nutritional product designed to enhance nitric oxide activity restores endothelium-dependent function in hypercholesterolemia. Journal of the American College of Cardiology. 33:282A.

Maxwell AJ, et al. (1999). Improvement in walking distance and quality of life in peripheral arterial disease by a nutritional product designed to enhance nitric oxide activity. Journal of the American College of Cardiology. 33:277A.

Ohtsuka Y, Nakaya J. (2000). Effect of oral administration of L-arginine on senile dementia. American Journal of Medicine. Apr 1;108(5):439.

Regensteiner JG, et al. (2003). Oral L-arginine and vitamins E and C improve endothelial function in women with type 2 diabetes. Vascular Medicine. 8(3):169-175.

Rytlewski K, et al. (2006). Effects of L-arginine on the foetal condition and neonatal outcome in pre-eclampsia: A preliminary report. Basic and Clinical Pharmacology and Toxicology. Aug;99(2):146-152.

Schulman SP, et al. (2006). L-arginine therapy in acute myocardial infarction: the Vascular Interaction With Age in Myocardial Infarction (VINTAGE MI) randomized clinical trial. Journal of the American Medical Association. Jan 4;295(1):58-64.

Swanson B, Keithly JK. (2002). A pilot study of the safety and efficacy of supplemental arginine to enhance immune function in persons with HIV/AIDS. Nutrition. Jul-Aug;18(708):688-690.

Yin WH, et al. (2005). L-arginine improves endothelial function and reduces LDL oxidation in patients with stable coronary artery disease. Clinical Nutrition. Dec;24(6):988-997.



NAME: L-carnitine


Common Names:

L-carnitine (LC), acetyl-L-carnitine (ALC), l-propionylcarnitine (PLC)


Description and Source



  • LC is an essential amino acid that is necessary for the conversion of fatty acids into energy for muscle activity. It is primarily stored in the muscles, including the heart.


  • Three forms of carnitine are available



    • LC: the most common form; it has the most research and costs less than the other forms


    • ALC: effects are primarily directed toward cerebral function and memory


    • PLC: may have the most profound effect on the heart and its function


  • Do not substitute one form of carnitine for another. D-carnitine competes with other forms of carnitine and can cause deficiency.


Biologic Activity



  • Necessary for production of acetylcholine


  • Antioxidant and O2 free radical scavenger


  • Facilitates transport of long chain fatty acids across cell membranes to be used in ATP production (Sinatra, 2005)


  • ALC stimulates message transmission in brain cells, retards loss of receptors in brain cells (rats) (Castorina & Ferraros, 1994), and increases cerebral blood flow and enzyme activity in the brain.


  • ALC is therapeutically active in hyperlipidemia, lowering LDL and very-low-density lipoprotein cholesterol and triglyceride levels (25%) and elevating HDL (63%). It is also indicated for preventing and treating atherosclerosis. LC has shown benefits for ischemic heart disease, CHF, angina pectoris, and mild arrhythmias (Stanley et al., 2005).


  • Levels of LC may be low in patients with CFIDS; more research is necessary (Sinatra, 2005; Werbach, 2000).


  • LC may play a role in reversing insulin resistance (Kelly, 2000).


Nutritional Sources:

Red meats, and to a lesser degree poultry, fish, and dairy products



Current Use



  • ALC may improve mental functioning in patients with mild Alzheimer’s disease, senile dementia, chronic alcoholism, and Down syndrome (more research is necessary) (Pettegrew et al., 1995; Sano et al., 1992).


  • ALC enhances behavioral performance and results on memory tests (Cucinotta et al., 1988; Salvioli & Neri, 1994).


  • ALC can be used to prevent and treat ischemic heart disease (Singh et al., 1996; Sinatva, 2005).


  • ALC has been shown to be a well-tolerated and effective treatment for paclitaxel, cisplatin, and antiretroviral-induced neuropathies (Maestri et al., 2005; Osio et al., 2006).


  • ALC was effective in reversing and preventing symptoms of hyperthyroidism, and it showed benefit for enhancing bone density (Benvenga et al., 2001).


  • ALC was more effective and safer than tamoxifen for treating acute and early Peyronie’s disease (Biagiotti & Cavallini, 2001).


  • Improves symptoms of neuropathy in diabetics (Fontana et al., 2006)


  • Protects the heart from adriamycin toxicity (Pauly & Pepine, 2003)


  • ALC is being given to AIDS patients (6 g a day) to reduce the toxicity of AZT on the muscle cells, thus reducing muscle fatigue and pain.


  • ALC should be considered in treating hyperlipidemia and atherosclerosis.


  • ALC has shown benefits in reducing muscle pain and fatigue associated with CFS/fibromyalgia (Plioplys & Plioplys, 1997). It also improved muscle tone and exercise endurance in thalassemic patients (El-Beshlawy et al., 2007).


  • Increases sperm motility in men who are infertile (Isidori et al., 2006)


Available Forms, Dosage, and Administration Guidelines:

1 to 3 g a day, divided into two or three doses


Pharmacokinetics—If Available (form or route when known):

Eliminated in urine: PLC—½ to 1½ hours; LC—½ to 15 hours


Toxicity:

None known



Contraindications:

Seizure activity, bipolar disorders, liver or kidney disease


Side Effects:

Diarrhea, nausea, vomiting with 4 g or more a day; fishy body odor


Long-Term Safety:

Unknown; additional research needed


Drug/Herb Interactions and Rationale (if known):

Co-Q10 seems to enhance ALC’s effects but may increase anticoagulation effects. Do not take when on dialysis or in hypothyroidism. Monitor carefully with antiseizure medications.



BIBLIOGRAPHY

Benvenga S, et al. (2001). Usefulness of L-carnitine, a naturally occurring peripheral antagonist of thyroid hormone action, in iatrogenic hyperthyroidism: A randomized, double-blind, placebo-controlled clinical trial. Journal of Clinical Endocrinology and Metabolism. Aug;86(8):3579-3594.

Biagiotti G, Cavallini G. (2001). Acetyl- L-carnitine vs. tamoxifen in the oral therapy of Peyronie’s disease: A preliminary report. BJU International. Jul;88(1):63-67.

Castorina M, Ferraros L. (1994). Acetyl- L-carnitine affects aged brain receptorial system in rodents. Life Science. 54:1205-1214.

El-Beshlawy A, et al. (2007). Effect of L-carnitine on the physical fitness of thalassemic patients. Annals of Hematology. Jan;86(1):31-34.

Ferrari R, et al. (2004). Therapeutic effects of L-carnitine and propionyl- L-carnitine on cardiovascular diseases: A review. Annals of the New York Academy of Sciences. Nov;1033:79-91.

Fontana G, et al. (2006). Nitrogenous compounds of interest in clinical nutrition. Nurtrición Hospitalaria. May;21(Suppl. 2):14-27;15-29.

Isidori AM, et al. (2006). Medical treatment to improve sperm quality. Reproductive Biomedicine Online. Jun;12(6):704-714.

Kelly GS. (1998). L-carnitine: Therapeutic applications of a conditionally essential amino acid. Alternative Medicine Review. 3(5):345-360.

Maestri A, et al. (2005). A pilot study on the effect of acetyl-L-carnitine in paclitaxel- and cisplatin-induced peripheral neuropathy. Tumori. Mar-Apr;91(2):135-138.


Osio M, et al. (2006). Acetyl-L-carnitine in the treatment of painful antiretroviral toxic neuropathy in human immunodeficiency virus patients: An open label study. Journal of the Peripheral Nervous System. Mar;11(1):72-76.

Pauly DF, Pepine CJ. (2003). The role of carnitine in myocardial dysfunction. American Journal of Kidney Disease. Apr;41[4 Suppl. 4]:S35-S43.

Pettegrew JW, et al. (1995). Clinical and neurochemical effects of acetyl-L-carnitine in Alzheimer’s disease. Neurobiology of Aging. 16:1-4.

Plioplys AV, Plioplys S. (1997). Amantadine and L-carnitine treatment of chronic fatigue syndrome. Neuropsychology. 35(1):16-23.

Salvioli G, Neri M. (1994). L-acetyl-carnitine treatment of mental decline in the elderly. Drugs: Experimental and Clinical Research. 20:169-176.

Sano M, et al. (1992). Double-blind parallel design pilot study of acetyl levo-carnitine in patients with Alzheimer’s disease. Archives of Neurology. 49:1137-1141.

Sinatra ST, et al. (2005). The Sinatra Solution: Metabolic Cardiology. New Jersey: Basic Health Publications.

Singh RB, et al. (1996). A randomized, double-blind, placebo-controlled trial of L-carnitine in suspected acute myocardial infarction. Postgraduate Medicine. 72:45-50.

Stanley WC, et al. (2005). Metabolic therapies for heart disease: Fish for prevention and treatment of cardiac failure? Cardiovascular Research. Nov 1;68(2):175-177.

Tamamogullari N, et al. (1999). L-carnitine deficiency in diabetes mellitus complications. Journal of Diabetes Complications. 13(5-6):251-253.

Werbach MR. (2000). Nutritional strategies for treating chronic fatigue syndrome. Alternative Medicine Review. 5(2):93-108.


NAME: Chondroitin


Common Names:

Chondroitin sulfate


Description and Source



  • A high-viscosity mucopolysaccharide (glycosaminoglycan)


  • Can be extracted from natural sources (bovine, porcine, avian) or synthesized in the laboratory


  • Is a flexible connecting matrix between proteins and filaments in cartilage



  • May replace proteoglycans, a substance that forms cartilage (Morreale et al., 1996)


Biologic Activity



  • Helps and attracts essential fluid into proteoglycan molecules, “water magnets” that act as shock absorbers, and moves nutrients into cartilage (Lamari et al., 2006)


  • Stimulates chondrocyte activity. Chondrocytes must get their nutrition from the synovial fluid because there is no vasculature to nourish them. During inflammation, chondrocyte activity is disturbed (Volpi, 2006).


  • May inhibit human leukocyte elastase and hyaluronidase, which are found in high concentrations in persons with rheumatoid disease


  • Chondroitin sulfate B inhibits venous thrombosis; antithrombolytic and may decrease heparin requirements


Nutritional Sources:

None


Current Use



Available Forms, Dosage, and Administration Guidelines:

Follow manufacturer directions. Usually combined with glucosamine sulfate. Dosage is based on weight.

<120 lb: 800 mg

120 to 200 lb: 1,200 mg

>200 lb: 1,600 mg

Divide into two to four smaller doses and take with food


Pharmacokinetics—If Available (form or route when known):

Absorption, 0% to 13%; very large molecule size


Toxicity:

None known; long-term clinical trials needed


Contraindications:

Bleeding disorders



Side Effects:

GI upset (dyspepsia, nausea), headache


Long-Term Safety:

Unknown


Use in Pregnancy/Lactation/Children:

Unknown; do not use


Drug/Herb Interactions and Rationale (if known):

Do not take with anticoagulants: may potentiate bleeding.


Special Notes:

In clinical practice, the effects of chondroitin seem marginal, especially compared with those of glucosamine sulfate. Purity is a problem with chondroitin. There is a significant variability with different products.



BIBLIOGRAPHY

Lamari FN, et al. (2006). Metabolism and biochemical/physiological roles of chondroitin sulfates: Analysis of endogenous and supplemental chondroitin sulfates in blood circulation. Biomedical Chromatography. Jun;20(607):539-540.

McCarty MF, et al. (2000). Sulfated glycosaminoglycans and glucosamine may synergize in promoting synovial hyaluronic acid synthesis. Medical Hypotheses. 54(5):798-802.

Morreale P, et al. (1996). Comparison of the anti-inflammatory efficacy of chondroitin sulfate and diclofenac sodium in patients with knee osteoarthritis. Journal of Rheumatology. 23:1385-1391.

Rovetta G, et al. (2004). A two-year study of chondroitin sulfate in erosive osteoarthritis of the hands: Behavior of erosions, osteophytes, pain and hand dysfunction. Drugs Under Experimental and Clinical Research. 30(10):11-16.

Uebelhart D, et al. (2004). Intermittent treatment of knee osteoarthritis with oral chondroitin sulfate: A one-year, randomized, double-blind, multicenter study versus placebo. Osteoarthritis and Cartilage. Apr;12(4):269-276.

Verges J, et al. (2005). Clinical and histopathological improvement of psoriasis with oral chondroitin sulfate: A serendipitous finding. Dermatology Online Journal. Mar 1;11(1):31.

Volpi N. (2006). Advances in chondroitin sulfate analysis: Application in physiological and pathological states of connective tissue and during pharmacological treatment of osteoarthritis. Current Pharmaceutical Design. 12(5):639-658.



NAME: Chromium


Common Names:

None


Description and Source



  • Naturally occurring trace element


  • The organic form found in natural foods appears to be absorbed better than the inorganic form.


Biologic Activity



Nutritional Sources:

Brewer’s yeast, liver, lean meats, whole grains, and cheese. Cooking with stainless-steel cookware increases the chromium content of foods (Integrative Medicine Access, 2000).


Current Use



  • Low chromium levels may contribute to hypoglycemia, cardiovascular disease, glaucoma, and osteoporosis.


  • Chromium promotes a normal insulin activity in persons with diabetes (enhances insulin use) (Yang et al., 2005). A combination of chromium picolinate (600 mg) and biotin (2 mg) improved glucose control and triglycerides in patients taking oral antihyperglycemic medication (Singer & Geohas, 2006).


  • May benefit insulin resistance (metabolic syndrome)


Available Forms, Dosage, and Administration Guidelines


Preparations:

Capsules, tablets. Several forms of chromium are available in the marketplace, including chromium polynicotinate and chromium picolinate (the best forms to use), chromium-enriched yeast, and chromium chloride.



Typical Dosage:

50 to 500 mcg a day; diabetics: 500 mcg BID; hypoglycemia: 200 mcg a day


Pharmacokinetics—If Available (form or route when known):

Eliminated through the kidney


Toxicity:

Irritation of GI tract (nausea, vomiting, ulcers) at high doses. Hexavalent (industrial) chromium is a heavy metal and causes kidney, liver, and lung damage.


Contraindications:

Not known


Side Effects:

Rare, but headache, irritability, and insomnia have been reported


Long-Term Safety:

Safe


Use in Pregnancy/Lactation/Children:

Safe


Drug/Herb Interactions and Rationale (if known):

Calcium carbonate and antacids reduce chromium absorption.


Special Notes



  • Adequate intake of chromium



    • Males (14-50): 35 mcg a day


    • Females (19-50): 30 mcg a day


    • Pregnancy: 30 mcg a day


  • Although rare, chromium deficiency (e.g., peripheral neuropathy or encephalopathy, increased glucose use during pregnancy) may play a role in the development of adult diabetes.


  • Chromium deficiency leads to impaired lipid and glucose metabolism and may put the person at risk for cardiovascular disease (Keszthelyi et al., 2004).


  • Several studies have not found a correlation between chromium levels and diabetes (Gunton et al., 2005; Komorowski & Juturu, 2005).



BIBLIOGRAPHY


Aghdassi E, et al. (2006). Is chromium an important element in HIV-positive patients with metabolic abnormalities? An hypothesis generating pilot study. Journal of the American College of Nutrition. Feb;25(1):56-63.

Cerulli J, et al. (1998). Chromium picolinate toxicity. Annals of Pharmacotherapy. 32:428-431.

Gunton JE, et al. (2005). Chromium supplementation does not improve glucose tolerance, insulin sensitivity, or lipid profile: A randomized, placebo-controlled, double-blind trial of supplementation in subjects with impaired glucose tolerance. Diabetes Care. Mar;28(3):712-e.

Integrative Medicine Access. (2000). Chromium. Newton, MA: Integrative Medicine Communications.

Keszthelyi Z, et al. (2004). The central effect of chromium on glucose metabolism. Pharmacopsychiatry. Sep;37(5):242.

Komorowski J, Juturu V. (2005). Chromium supplementation does not improve glucose tolerance, insulin sensitivity, or lipid profile: A randomized, placebo controlled, double-blind trial of supplementation in subjects with impaired glucose tolerance. Response to Gunton et al. Diabetes Care. Jul;28(7):1841-1842, author reply 1842-1843.

Mita Y, et al. (2005). Supplementation with chromium picolinate recovers renal Cr centration and improves carbohydrate metabolism and renal function in type 2 diabetic mice. Biological Trace Element Research. Summer;105(1-3):229-248.

Rabinovitz H, et al. (2004). Effect of chromium supplementation on blood glucose and lipid levels in type 2 diabetes mellitus elderly patients. International Journal for Vitamin and Nutrition Research. May;74(3):178-182.

Shara M, et al. (2005). Safety and toxicological evaluation of a novel niacin-bound chromium (III) complex. Journal of Inorganic Biochemistry. Nov;99(11):2161-2183.

Singer GM, Geohas J. (2006). The effect of chromium picolinate and biotin supplementation on glycemic control in poorly controlled patients with type 2 diabetes mellitus: A placebo-controlled, double-blinded, randomized trial. Diabetes Technology and Therapeutics. Dec;8(6):636-643.

Yang X, et al. (2005). A newly synthetic chromium complexchromium (phenylalanine)3 improves insulin responsiveness and reduces whole body glucose tolerance. FEBS Letters. Feb 28;579(6):1458-1464.

Yang X, et al. (2006). Insulin-sensitizing and cholestrol-lowering effects of chromium (d-phenylalanine) (3). Journal of Organic Biochemistry. Jul;100(7):1187-1193.



NAME: Coenzyme Q10


Common Names:

Vitamin Q, ubiquinone, Co-Q10


Description and Source:

Naturally occurring antioxidant. Lipid-soluble benzoquinones, similar in structure to vitamin K. They are found in almost all aerobic organisms in the mitochondria. The Q10 structure is unique to humans.


Biologic Activity



  • Powerful lipophilic antioxidant present in all tissue (Kontush et al., 1997)


  • Membrane-stabilizing properties (Britt, 2005)


  • Improves stroke volume and cardiac output in patients with CHF (Soja & Mortensen, 1997)


  • Improves ejection fraction (Sinatra, 2005)


  • Inhibits platelet vitronectin receptor to reduce thrombotic complications (Serebruany et al., 1997)


  • Works with other enzymes to bring about its effects (Sinatra, 2005)


  • Precursor to energy production in mitochondria (adenosine triphosphate)


  • Oxygen free radical scavenger


  • Regenerates vitamin E from its oxidized form (Ernster et al., 1995)


Nutritional Sources:

Small amounts in meat and seafood


Current Use



  • Improves CHF. Research suggests that patients with New York Hospital Association class III and IV disease with Co-Q10 deficiencies can become class I and II with treatment (Morisco et al., 1993). Co-Q10 improved systolic function in patients with chronic heart failure, but treatment with ACE inhibitors seems to reduce its benefits (Sander et al., 2006). Twenty-seven patients awaiting heart transplants were given Co-Q10. While their echocardiograms did not change, there was improvement in functional status, clinical symptoms, and quality of life (Berman et al., 2004).


  • Benefits cardiomyopathies caused by ischemia and toxins: angina, cardiotoxicity caused by doxorubicin (adriamycin)



  • Slows progression of breast cancer (Lockwood et al., 1994) and enhances immune response


  • Improves tissue health and healing in gingivitis (Integrative Medicine Access, 2000)


  • May improve survival after MI if administered within 3 days (120 mg a day) (Singh et al., 1998; Singh & Niaz, 1999)


  • Decreases blood pressure (Singh et al., 1999): 39% of patients with hypertension have a Co-Q10 deficiency. Four to 12 weeks of supplementation showed benefit (Integrative Medicine Access, 2000).


  • Improves tissue reperfusion after cross clamping during cardiac bypass surgery (Chillo et al., 1996; Nibori et al., 1998)


  • May improve mitral valve prolapse (use with hawthorn), arrhythmias, diabetes, migraines, asthenozoospermia, and age-related macular degeneration


  • Patients with bronchial asthma were able to reduce dosage of corticosteroids when taking Co-Q10 and vitamins E and C (Gvozdjakova et al., 2005).


  • Neuroprotective, Co-Q10 slows the degeneration of neurons in patients with Frederick’s ataxia and Parkinson’s disease (Littarru & Tiano, 2005; Shults, 2005).


  • A combination of Co-Q10, omega 3 fatty acids, and acetyl-L-carnitine prevented further degeneration in patients with early age-related macular degeneration (Feher et al., 2005).


  • Reduces migraines by 50% (Modi & Lowder, 2006).


Available Forms, Dosage, and Administration Guidelines:

Varies with condition; take 50 mg a day as baseline. Use oil-based soft gel for better absorption. Take with food. Take with piperine (Bioperine) (black pepper) for increased absorption (by 30%). Doses over 100 mg a day should be divided. For patients with Parkinson’s disease, take 300 to 1200 mg a day. For hypertension, take 100 to 150 mg a day. For HIV/AIDS, take 200 mg a day. Avoid suddenly stopping taking Co-Q10, as symptoms of heart disease or Parkinson’s may worsen (Bhagavan & Chopra, 2006).


Pharmacokinetics—If Available (form or route when known):

Not known


Toxicity:

None known



Contraindications:

None known


Side Effects:

Loss of appetite (rare), nausea, diarrhea (rare)


Long-Term Safety:

Not known


Use in Pregnancy/Lactation/Children:

Unknown; do not use


Drug/Herb Interactions and Rationale (if known)


Oct 20, 2016 | Posted by in PHARMACY | Comments Off on Nutritional Supplements

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