Presented by:
Confidential Group Members and Kaitlin Deason

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 First discovered by Prof. Fredrick L. Crane and coworkers in 1957.
 Chemical structure was identified by Dr. Karl
Folkers in 1958.
 Chemical structure of Coenzyme Q10 is similar to vitamin K but it classified as a lipid.
 Coenzyme Q10 known as CoQ10, ubiquinone, ubidecarenone

 In early seventies, CoQ10 was introduced into clinical therapy in Japan.
 In mid eighties CoQ10 was further classified in the group of cardiovascular drugs for metabolic disturbances in Japan.
 CoQ10 was effective used for mild congestive heart failure, symptoms such as edema, lung congestion and swollen liver.

 Coenzyme Q10 (2, 3 dimethoxy-5 methyl -6decaprenyl bezoquinone) is further abbreviated as
CoQ10, where Q is refers to the quinone chemical group and 10 refer to the number of isoprenyl groups associated with the center molecule

 The biosynthesis of CoQ10 involves three steps:
 1. formation of benzoquinone structure.
 2. synthesis of the isoprene side chain.
 3. combining of these two substrates.
 CoenzymeQ10 synthesizes through the mevalonate pathway
 Biosynthesis of CoQ10 begins to decline at the age of twenty and further decreases rapidly after the age of forty

 CoQ10 is found all the tissues in the body
 Concentrations are relatively high in organs with high – energy turnover such as
 Heart
 Liver
 Kidney
 Pancreas

 Red meat products
 Especially organ meats such as liver and heart
 Oily fish such as salmon and tuna
 Whole grain
 Rapeseed oil

 It plays a critical role during cellular respiration and
ATP formation.
 Functions as endogenous antioxidant by accepting electrons from free radicals
 Acts as a proton translocator
 Antioxidant activity of vitamin E also depends on the availability of CoQ10.

 Third most popular dietary supplement in USA is
CoQ10 behind Omega 3’s and Multivitamins
 Coenzyme Q10 is artificially manufactured by fermenting beets and sugar cane with special strains of yeast
Popular Brand names:
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Co-Q-Max
Co-Q-Omega
• Co-Q Max Daily
• Co-Q-Rescue Serum

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• acts as an energy booster acts as an antioxidant strengthens the immune systems counteracts muscle pain improves heart function maximizes oxygen uptake increases exercise performance in cardiac patients.
used to treat gum disease

 CoQ10 supplementation may lower high cholesterol levels compared to healthy individuals of the same age
 Increases sperm motility leading to enhanced fertility
 Improves immune function in individuals with immune deficiencies (HIV/AIDS).

 Tablets (chewable and non chewable).
 Powder-filled capsules.
 Soft gel containing oil suspension.
 Oral spray
 Ingredient for various cosmetic products such as:
 Facial cream
 Skin lotions

 Adults (above 18 years) is 30-100mg/day.
 Therapeutic doses for adults generally range from
100-300mg/day.
 High doses ranging from 1200-3000mg/day have also been used under medical supervision to treat early Parkinson’s disease.

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Nausea
Vomiting
Stomach upset
Heartburn
 Irritability
 Diarrhea
 Skin itching
 Rash

Routes of Administration:
 Enteral route (orally)
 Bio availability CoQ10 is largely determined by the rate of absorption in the gastrointestinal tract.
 Absorption of dietary CoQ10 is slow and limited due to its higher molecular weight and poor water solubility.
 Rate of absorption can be enhanced by interaction with food or food component.
 Parentaral route (topically)

 Plasma peak of CoQ10 can be observed 2-6 hours after the oral administration.
 Elimination half life is about 33 hours.
 Data on metabolism of CoQ10 is limited.
 Major routes of elimination are biliary excretion and fecal excretion.

 Certain cholesterol-lowering drugs or statins such as atorvastatin, cerivastatin and lovastatin tend to decrease the natural levels of CoQ10 in the body by decreasing the bio-synthesis.
 CoQ10 has been shown to decrease the anticoagulant effect of Warferin (Coumadin), resulting in higher dosage requirements for Warferin.

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CoQ10 may enhance the effectiveness of certain blood pressure medications.
CoQ10 supplementation allows individuals to take lower doses of blood pressure medications such as
Diltiazem (Cardizem), Metoprolol (Lopressor), and Enalapril (Vasotec). This should only be done under the observation of a medical doctor.
Coenzyme Q10 supplements may potentiate the effects of diuretic herbs such as licorice and horsetail by lowering blood pressure

Coenzyme Q10 in the treatment of hypertension: a meta analysis of the clinical trials, Rosenfeldt, F.L., has,
S.J., Krum, H., Hadj, A., Ng,K.,
Leong,J.Y., Watts, G.F. (2007), Journal
Human hypertensions, 21(4), 297-306.

Purpose :
 To determine the effects of CoQ10 on hypertension by looking at several previously published clinical trials.
Method :
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Carried out a Meta analysis by reviewing and pooling the data of all the published clinical trials of CoQ10 for hypertension
Assessed the overall efficacy and consistency of therapeutic action and reported side effects.

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Methods con’t
– Twelve clinical studies, including three randomized controlled trials, one crossover study, and eight open label trials were used for this study.
Results:
– After pooling the all published data authors concluded that CoQ10 decrease systolic blood pressure by up to 17mmHg, and diastolic blood pressure by up to 10mmHg without any significant side effects.

Antifatigue effects of coenzyme Q10 during physical fatigue, Mizuno, K.,
Tanaka, M., Nozaki, S., Mizuma, H.,
Ataka, S., Tahara, T., Sugino, T., Shirai,
T., kajimoto, Y., kuratsune, H., kajimoto,
O., Watanabe, Y. (2008), Nutrition, 24,
293-299.

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Purpose:
– to investigate antifatigue effects of coenzyme Q10 during physical fatigue.
Method:
– Seventeen healthy volunteers participated in a double blind, placebo controlled, triple crossover study.
– Subjects were randomly administered oral CoQ10
(100 or 300mg/d) or placebo for eight days.

 Results:
 Suggest that CoQ10, enhances the exercise performance
 A decrease in the subjective fatigue sensation was observed compared to the placebo group

Effects of acute and 14 day coenzyme Q10 supplementation on exercise performance in both trained and untrained individuals, Cooke, M., Iosia,
M., Buford,T., Shelmadine, B., Hudson,G.,Kerkisick,
C., Rasmussen, C., Greenwood,M., Leutholtz, B.,
Willoughby, D., Kreider,R. (2008), Journal of the
International society of sports nutrition,5:8, 251-258

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Purpose:
 To investigate the effects of acute and 14-day coenzyme Q10 supplementation on exercise performance in both trained and untrained individuals.
Method :
 Twenty-two trained and nineteen untrained male and female subjects participated in a
 randomized, double blind, placebo controlled study.
Subjects were randomly administered either
100mg of a dextrose placebo or a fast melt CoQ10 supplement twice a day for 14 days

 Results:
 Chronic and acute CoQ10 supplementation resulted in higher muscle concentration of
CoQ10.
 Both types of supplementation decreased oxidative stress
 Tendency to increase the time to exhaustion of muscles during exercise was observed

Improvement of the oral bioavailability of coenzymeQ10 by emulsification with fats and emulsifiers used in the food industry,
Tanatukorn,P., Kawai, K., Hayanakawa,
M., Hayashi, M., Kajiwara, K.(2009),
Food Science & Technology,42,385-390.

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 To investigate the effect of emulsification of
CoenzymeQ10 on oral bioavailability by using five commercially available fats and four types of emulsifiers.
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 Five healthy volunteers participated in this experiment and administered a model emulsified
CoQ10 (100mg) product and commercially available product (100mg).

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 Concentration levels of CoQ10 and cholesterol in plasma were determined using High Performance Liquid
Chromatographic system
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 The results suggest that the oral bio availability of the model emulsified product was slightly greater than that of commercially available product.

 CoQ10 supplements can be used to increase the
CoQ10 levels in various tissues in the body, although there is no adequate scientific evidence to prove the effectiveness of replacing of CoQ10 with supplements
 As a dietitian it is important to be aware that there is not enough scientific evidence to prove the effectiveness CoQ10. However, if the body is deficient in CoQ10, it may be beneficial to bring up these levels. Other uses are not proven and are just claims.

http://a.abcnews.com/images/GMA/redyeastrice_090615_mn.jpg

– Can be used to improve health
– Treatment in mild gastric disturbance
– Blood circulation
– Improve spleen and stomach health

 Today, the growth of consumer spending on red yeast products for health use escalated nearly 80% in the United States from 2005 to 2008 reaching estimated sales of $20 million in 2008.

Red Yeast Rice is fermented rice
 Fermented by a red colored yeast called
Monascus purpureus.
 It gives its distinct appearance
 It is still found in some Asian foods and used as a dietary supplement for health purposes.
Picture: http://a.abcnews.com/images/GMA/redyeastrice_090615_mn.jpg

 RYR is made of monacolins, isoflavonoids, monounsaturated fats, and sterols.
 RYR has a “natural statin” similar to lovastatin called monacolin K
 Monacolin K inhibits endogenous cholesterol synthesis by inhibiting enzyme 5-hydroxy-3methylglutaryl-coenzyme reductase (HMGCR).
 HMGCR enzyme is the rate limiting step for cholesterol synthesis.

Monacolin K or
X
X http://www6.ufrgs.br/favet/imunovet/molecular_immunology/cholesterol_synthesis.gif

Scientifically proven
 Lowers cholesterol in hyperlipidemia patients claims
 Helps blood circulation
 Treatment of dyslipidemia in HIV patients
 Indigestion.
 Diarrhea.
 Improving blood circulation.
 Spleen and stomach problems.
 Other conditions.

Generic Names
 Chinese Red Yeast Rice
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Zhi Tai
Xuezhikang
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XZK
Angkak
Monascus Purpureus
Went
Red Yeast
Brand Names
 Red Rice Yeast
 Cholestin
 Chol-Reg

Red yeast rice is available in United States
 In capsule and tablet form
 Teas and tinctures (extract)
 Each capsule or tablet usually contains 600 mg of
RYR and may contain 5-10 mg of monacolin K
• The recommended dosage for adults is 1200mg to
2400 mg once or twice daily
 It is not recommended for children

 Little is known at this time
 It is theorized monacolin K may have similar absorption, metabolism and excretion as lovastatin.
 Lovastatin is absorbed in intestines and metabolized by CYP3A4 in the liver and excreted in bile and urine.
 Research is needed for the official pharmacokinetics of RYR.

Minor Side Effects
 Upset stomach, Heartburn, Gas, Bloating,
 Headache, Dizziness and others.
Severe Side Effects
 Myalgia (muscle pain)
 Rhabdomyolysis (muscle fiber breakdown)
 Hepatoxicity (liver toxicity)
 Kidney problems http://www.alcis.com/images/muscle_pain.jpg

May cause hepatoxicity when combined with:
 Acetaminophen (pain reliever)
 Carbamazepine (anti-seizure)
 Phenytoin (anti-seizure)
 Isoniazid (treatment of TB)
 Methotrexate (antimetabolite-tx of cancer)
 Fluconazole (antifungal tx)
 Erythromycin (antibiotic)
 Other Statins

May cause muscle problems when combined with:
 Cyclosporine (immunosuppressant)
 Niacin (reduce cholesterol and TG)
 Gemfibrozil (lower lipid levels)
 Other Statins

 RYR is also known to lower coenzyme Q-10 levels.
 St. John’s Wort can lower serum levels of statin drugs and so it may reduce the effects of red yeast rice.

 Taken with food increases absorption
 Grapefruit juice decreases metabolism of RYR
 Alcohol may cause liver damage

 In 2001, a RYR product called Cholestin, manufactured by a company called Pharmanex, was found to contain the drug lovastatins.
 Because it contained lovastatin, it cannot be sold without a prescription.
 In 2007, the FDA released a safety warning against three products: (1) Red yeast rice from Nature’s
Value Inc. and (2) Red Yeast Rice/ Policosanol
Complex from Kabco Inc., and (3) Cholestrix sold by Sunburst Biorganic.
 May cause kidney or muscle problems

 Citrinin
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Byproduct and contaminant of RYR fermentation
Nephrotoxin -may cause kidney failure
 Variability of monacolin K in RYR
 An analysis of 9 proprietary brands of RYR determined that different amount of monacolin K found in RYR products despite label information
(0.15-3.37 mg MK /capsule).
 Seven out of nine brands contained citrinin

 Women who are pregnant or breastfeeding
 People with asthma
 Kidney disease
 Recent surgery
 Organ transplant
 People who >2 alcohol beverages per day
 People with liver disease

Venero, C.V., Venero, J.V., Wortham,
D.C., & Thompson, P.D. (2010). Lipidlowering efficacy of red yeast rice in a population intolerant to statins. The
American Journal of Cardiology, 105(5),
664-666.

Purpose
 Observational study evaluated the lipid-lowering efficacy of RYR in patients intolerant to statins.
Methods
 They reviewed 1,400 medical charts and assessed
25 patients with hyperlipidemia who were on RYR for >4 weeks.
 They assessed the lipid levels before and after treatment with 1200 mg daily of RYR
Venero, Venero, Wortham & Thompson (2010).

Results
 Treatment took place over a 74+39 day period
 Average total cholesterol decreased by 15%
 LDL cholesterol decreased by 21%
 Triglycerides decreased by 6%, and
 HDL decreased by 0.5%
Conclusion
 92% tolerance for RYR, it may be a reliable alternative for the treatment of hyperlipidemia when patients are intolerant to statin drugs.
Venero, C.V., Venero, J.V., Wortham, D.C., & Thompson, P.D. (2010). Lipid-lowering efficacy of red yeast rice in a population intolerant to statins. The American Journal of Cardiology, 105(5), 664-
666 .

Halbert , S. C., French, B., Gordon, R. Y., Farrar, J. T.,
Schmitz, K., Morris, P. B., Thompson, P. D., Rader,
D.J., & Becker, D.J. (2010). Tolerability of red yeast rice (2,400 mg twice daily) versus Pravastatin (20 mg twice daily) in patients with previous statin intolerance. The American Journal of Cardiology,
105(2), 198-204.

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Halbert et al., (2010).

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Both treatments showed a low rate of recurrent myalgia, and significantly lowered the amount of LDL, total cholesterol, triglycerides and slightly lowered
HDL.
There were some dropouts in both groups but was not considered statistically significant (p=0.99).
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The low rate of side effects for RYR treatment may be related to the natural low dose of MK (<10 mg/day).
The other components of RYR lowered cholesterol to a greater degree than expected.
Halbert et al., (2010).

Li, J. J., Lu, Z. L., Kou, W. R., Chen, Z., Wu, Y. F., Yu, X. H., &
Zhao, Y. C. (2009). Beneficial impact of Xuezhikang on cardiovascular events and mortality in elderly hypertensive patients with previous myocardial infarction from the China Coronary Secondary Prevention Study
(CCSPS). Journal of Clinical Pharmacology, 49(8), 947-956.

Purpose:
 To analyze the impact of Xuezhikang on cardiovascular events and mortality in elderly hypertensive patients with previous myocardial infarction (MI).
Method:
 Randomized, double blind, placebo controlled, parallel-group clinical trial.
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The Xuezhikang group had 772 participants who received 0.6 g twice daily
The placebo group had 758 participants.
 Xuezhikang contained 2.5-3.2 mg/capsule of MK, a small amount of LV hydroxyl acid, ergosterol and some other elements.
Li, Lu, Kou, Chen, Wu, Yu, & Zhao (2009).

Results
 After an average of 4.5 years in the intervention, the results showed that participants who were treated with RYR had less cardiovascular events than the placebo group.
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Xuezhikang therapy significantly reduced risk of nonfatal MI by 53.4% and coronary death by 29.2% compared to placebo.
RYR therapy significantly reduced the total number of strokes, cancer death, and total cancer compared to placebo.
Conclusion
 Xuezhikang may effectively reduce cardiovascular events and other morbidities in Chinese elderly hypertensive patients with previous MI.
Li et al., (2009).

Hong, M. Y., Seeram, N. P., Zhang, Y., & Heber, D.
(2008) Anticancer effects of Chinese red yeast rice versus monacolin K alone on colon cancer cells. Journal of Nutritional Biochemistry, 19(7),
448-458.

Purpose:
 To examine the effects of RYR on two types of colon cancer cells, HCT-116 and HT-29, related to cell proliferation.
 Also to evaluate the colon cancer cells’ apoptosis, and transcription levels of HMGCR and sterol response element binding protein-2 (SREBP-2) with RYR.
Hong, Seeram, Zhang, & Heber (2008)

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Methods
They examined lovastatin, RYR, MK-free RYR, pigment-rich fraction RYR (PF-RYR), monacolinrich fraction RYR (MF-RYR) on colon cancer cell proliferation in vitro.
Apoptosis was assessed by Cell Death Detection
ELISA.
RNA was extracted, reverse transcription was determined.
Gene expression of HMGCR and SREBP-2 were determined quantitatively with a detector.
Hong, Seeram, Zhang, & Heber (2008)

Results:
 RYR and PF-RYR demonstrated the most antiproliferation and pro-apoptosis activity in both cancer cells compared to other types of RYR and lovastatin.
 RYR did not elevate the gene expression of
HMGCR or SREBP-2 unlike lovastatin.
Hong, Seeram, Zhang, & Heber (2008)

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Conclusion:
Anti-proliferation and pro-apoptosis activity may be related to monacolin K and pigment compounds found in RYR.
 Further investigation is needed in animal models and ultimately human subjects to determine if
RYR will in fact act as a possible treatment for colon cancer.
Hong, Seeram, Zhang, & Heber (2008)

 RYR is prescribed for statin-intolerant patients may be well tolerated.
 RYR may lower the chance of cardiovascular events in elderly with previous MI.
 Inhibition of cancer cell proliferation and gene expression by RYR are still in its early stages of research.

 Red yeast rice may be sought out more for treatment of hyperlipidemia.
 Red yeast rice recommendations should be used with caution.
 It is important to inform patients of possible side effects, efficacy and safety with RYR use.

http://planning.up.nic.in/innovations/inno3/fi/chitosan.htm

 Chitin and chitosan were discovered in 1982 during a project sponsored by The Ministry of Agriculture and Fisheries, in Japan.
 Deacetylated form of chitin- isolated from mushrooms and the shells of crustaceans, including crabs, lobsters, and shrimp
 Aside from cellulose, chitosan is the most abundant natural polymer
 There are no significant dietary sources
(http://www.chitopia.co.kr/e-book004.html)

 Water purification
 Soil enrichment
 Antioxidant properties to prolong shelf-life
 Serves as a functional food
 Controlled drug release
 Antitumor and wound healing
 Used much less as a supplement that for its other uses

 Lowers cholesterol
 Reduces fat absorption  reduces weight
 Reduces dental plaque formation

 Available in 500 mg capsules
 Recommended dosage usually around 1500 mg to
1.5 g per day
 Generic names: chitosan, chitin, and kitosan,
 Brand names: Chitosan Plus™, Fat Absorb™, and
Fat Blocker™ http://www.womenbeautycare.com/2010/12/overweightwomen-develop-osteoporosis.html

 May cause gas, constipation and nausea
 Should not be taken by:
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People with shellfish allergies (because derived from shellfish)
Pregnant or breast feeding women
Children
 Those with malabsorptive disorders

 Functions like fiber by trapping and eliminating fat and cholesterol
 Chitosan gains a positively charged, free amino acid group allowing it to attach to negatively charged compounds
 Chitosan binds to fatty acids, bile acids or salts, cholesterol, and other molecules causing decreased absorption and excretion of these compounds

 Little information is known
 Similar in structure to cellulose and seems to function like this
 Not absorbed by the intestines and is primarily eliminated through the feces

 May decrease absorption of fat soluble vitamins
 May slow gastric emptying leading to delayed absorption of nutrients and drugs
 May interact with absorption and metabolism of some drugs
 May alter activity of CYP 450

Gades, M. D. & Stern, J. S. (2005).
Chitosan supplementation and fat absorption in men and women. Journal
of the American Dietetic Association,
105(1), 72-77.

 Purpose:
 To determine the effect of chitosan on fecal fat excretion
 Methods:
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12 men and 12 women completed 12-day trial
Cross-over design
5 meals per day were provided. Ea. contained at least 15g fat for men and 10g fat for women
Supplemented 6 days with 2.5 g chitosan. 500mg per meal
Gades & Stern (2005).

 Results:
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 non-clinically significant increase in fecal fat excretion in men but no change in women no benefit from chitosan supplementation
 Conclusion:
 Study is limited by short duration and small sample size
 Chitosan is not an effective way to prevent fat absorption and does not aid in weight loss
Gades & Stern (2005).

Nadai, M., Tajiri, C., Yoshizumu, H., Suzuki,
Y., Zhao, Y. L., Kimura, M., Tsunekawa, Y.,
Hasegawa, T. (2006). Effect of chitosan on gastrointestinal absorption of waterinsoluble drugs following oral administration in rats. Biological and
Pharmaceutical Bulletin, 29(9), 1941-1946.

 Purpose:
 to determine how chitosan effects GI absorption of the drugs indomethacin, griseofulvin, acetaminophen, and cephalexin, in rats
 Background:
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Indomethacin and griseofulvin are water-insoluble
Acetaminophen and cephalexin are water-soluble drugs
Nadai et al., (2006).

 Methods:
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Eight to nine week old rats were pre-treated with either 5 mg/kg of chitosan, 25 mg/kg of chitosan, or a control
 After 15 minutes, one of the four drugs was administered. C max
, T max
, and AUC were measured
Results:
No effect on absorption of water-soluble drugs
 Pre-treatment with 25 mg/kg of chitosan significantly delayed T max for the water-insoluble drugs. C max
AUC were unchanged compared to the control and
Nadai et al., (2006).

 Conclusion:
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The results indicate that chitosan may alter
(decrease) absorption of water-insoluble drugs but the mechanisms of action are still unknown
Effect in human model is yet to be determined, but this study provides good evidence that human studies are needed
Nadai et al., (2006).

Tapola, N. S., Lyyra, M. L.,
Kelehamainen, R. M., Sarkkinen, E. S.,
& Schauss, A. G. (2008). Safety aspects and cholesterol-lowering efficacy of chitosan tablets. Journal of the
American College of Nutrition, 27(1),
22-30.

 Purpose:
 To determine how fat-soluble vitamins and cholesterol concentrations are effected by chitosan supplementation
 Methods:
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56 individuals not previously taking cholesterol lowering drugs participated in 8 week study
Subjects were randomly assigned to receive 4.5 g of chitosan (n=15), 6.75 g of chitosan (n=12), glocomannan, an active control (n=15), or a placebo (n=14)
Participants were instructed to take 6 tablets, 3x per day,
15 minutes before breakfast, lunch and dinner. No changes were made to the diet.
Tapola, Lyyra, Kelehamainen, Sarkkinen, & Schauss (2008).

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Methods con’t:
 Baseline weight, blood pressure, and blood samples were collected and compared with weight, blood pressure, and blood samples collected at the conclusion of the trial.
Results:
 No significant changes in fat-soluble vitamin levels, total cholesterol levels, LDL cholesterol levels, body weight, or blood pressure in either chitosan treatment group
 There were no serious adverse events reported, and while some experienced nausea, constipation, and heartburn, these side effects were not statistically significant
Tapola, et al., (2008).

 Conclusion:
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The weaknesses of this study- the small sample size, short duration, and the variability in participant diets. In addition, the actual amount of chitosan being consumed before each meal may not have been the same because some of the pills were placebos
The main findings indicate that chitosan supplementation is a safe supplement, but it is not effective in lowering cholesterol
Tapola, et al., (2008).

Yao, H., Lii, C., Chou, R., Lin, J., Yang, H.,
& Chiang, M. (2010). Effect of chitosan on hepatic drug-metabolizing enzymes and oxidative stress in rats fed low- and highfat diets. Journal of Agricultural and Food
Chemistry, 58(8), 5187-5193.

 Purpose:
 To determine the effect of chitosan on the enzymes
CYP P450, GST, UGT, and oxidative stress in rats
 Background:
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CYP 450 is a catalyst for phase I biotransformation of drugs
GST and UGT are catalysts for phase II biotransformation
Each of the enzymes play an important role in drug metabolism, and without them oxidative stress increases
Yao, Lii, Chou, Lin, Yang, & Chiang (2010).

 Methods:
 6 week old Wistar rats were randomly assigned to recieve one of four diets.
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 a low fat (LF) diet with either chitosan or a control (cellulose) a high fat (HF) diet with either chitosan or a control
Feeding occurred for 4 weeks and then the rats were killed after a 12-hour fast.
Blood samples were taken to determine oxidative stress and the effect on the drug metabolizing enzymes. Several CYP enzymes were examined for expression and activity.
Yao et al., (2010).

 Results:
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Chitosan decreased the expression of total CYP, and this was most prominent in the rats fed a HF diet
The activity of CYP 3A and CYP 1A1 were significantly decreased by chitosan, but no effect was seen on other CYP enzymes. In addition, chitosan with either diet significantly decrease activity of GST but not
UGT
Chitosan increased oxidative stress, which is to be expected because there is less of an effect from the phase I and phase II enzymes resulting in more free radicals
Yao et al., (2010).

 Conclusion:
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Overall, this study provides important evidence that chitosan may decrease drug metabolism, and people taking chitosan need to be advised about this possible drug interaction in order to prevent toxicity or further adverse effects.
However, studies in human models are needed to confirm the results of this study.
Yao et al., (2010).

 Studies indicate little effect from supplementation
 Evidence that chitosan may interact with some drugs and nutrients by altering their absorption and/or metabolism
 Chitosan is currently considered a safe, natural, nontoxic product
 There is no regulation of this supplement by the
Food and Drug Administration
 There are no long-term studies regarding safety

 No real benefit from chitosan
 Possible drug/nutrient interactions should be conveyed to patients
 Should not be recommended until further research is conducted. Especially because of study results from animal studies
 It is important to stay up to date on new information regarding safety

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Bhagavan, H.N., & Chopra, R.K. (2006). CoenzymeQ10: absorption, tissue uptake, metabolism and pharmacokinetics, 40(5), 445-453.
Cooke, M., Iosia, M., Buford, T., Shelmadine, B., Hudson, G., Kerkisick, C., & Rasmussen, C.,
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