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Fish Oils In Cancer

By Michelle Gillis B. H.Sc. (Naturopathy)



Essential fatty acids are one of the most widely researched nutritional interventions in the world. Thousands of studies have demonstrated the numerous different activities that these essential fatty acids possess in the human body, and it can not be denied that we are generally an omega 3 deficient country due to our poor diet and lifestyle choices. As mortality and morbidity rates rise in response to our modern existence, fish oils pose a relatively inexpensive preventative treatment option.


As integrative health professionals, we are very familiar with the amazing medicinal qualities of fish oils and the importance of prescribing premium quality products. Studies show that tissue levels of arachidonic acid – and eicosapentaenoic acid (EPA) derived eicosanoids influence many physiological processes: calcium transport across cell membranes, angiogenesis, apoptosis, cell proliferation and immune cell function. All of these processes are integral to the function of the immune system, and hence the pathogenesis of many chronic immune and autoimmune diseases, as well as cancer. 1


A vast amount of epidemiological evidence illustrates certain groups of people who consume diets rich in omega 3 fatty acids may experience a lower prevalence of some types of cancer, such as prostate, mammary, pancreatic and colorectal.2-5 In addition, a large number of animal and in vitro studies have shown protective effects of omega 3 fats (alpha-linolenic acid, EPA, DHA) while omega 6 fats (linoleic acid, arachidonic acid) have been found to promote some cancers. It appears that the results from human studies are rather equivocal and call for much needed research in the field. One 2004 review, reported at least seven human studies which demonstrated an association between higher ratio of omega 3 to omega 6 fats and reduced risk of breast cancer. 6


To date, much of the research supporting the use of fish oils in cancer stems from what we know about how these essential fatty acids work biochemically. There have been numerous hypothesizes proposed as to the mechanisms that omega 3 fatty acids exert their suppressive effects upon tumour growth 5, 7;


1. Eicosanoid biosynthesis, cell proliferation, apoptosis, metastasis, and angiogenesis.

2. Influences on transcription factor activity, gene expression, and signal transduction which leads to changes in metabolism, cell growth and differentiation.

3. Alteration of oestrogen metabolism which leads to reduced oestrogen-stimulated cell growth.

4. Increased or decreased production of free radicals and reactive oxygen species.

5. Mechanisms involving insulin sensitivity and membrane fluidity.7


Eicosanoid metabolism

One of the more important functions of omega 3 fatty acids is related to their enzymatic conversion into eicosanoids, which are short lived, hormone-like lipids with a wide array of biological activities: modulation of inflammatory and immune responses and playing a critical role in platelet aggregation, cellular growth and cell differentiation. 7 Omega 3 fatty acids – DHA and EPA effectively compete with arachidonic acid for Cyclo-oxygenase (COX) activity, resulting in the production of three-series prostaglandins (PGE-3) and five series leukotrienes and reduced production of prostaglandin-2 (PGE-2). PGE-2 release is believed to play an important role in the initiation and progression of cancer by inhibiting apoptosis, stimulating cell proliferation and promoting tumour angiogenesis. 7, 8 By decreasing the availability of arachidonic acid precursors, the substitution with omega 3 fatty acids suppresses the biosynthesis of arachidonic derived eicosanoids in favour of EPA-derived PGE3 and five-series leukotrienes. 5 , 7 COX-2 inhibitors have been used to suppress the growth of colon cancers 9, demonstrating that suppression of COX-2 may be a useful strategy to slow the growth of metastatic tumours.


Figure 1: Polyunsaturated fatty acid (PUFA) metabolism demonstrating how the essential fatty acids EPA and DHA are required for the production of anti-inflammatory prostaglandins. Also note DGLA’s activity in producing anti-inflammatory prostaglandin-1.


Influence on transcription factor activity, gene expression and signal transduction

It is theorized that some PUFAs and their metabolites may exert some of their anti-tumour effects by affecting gene expression or the activities of signal transduction molecules involved in the control of cell growth, differentiation apoptosis, angiogenesis and metastasis. 7 One proposed mechanism by which omega 3 fatty acids may demonstrate anti-tumour activity is via inhibiting nuclear factor-kB (NF-kB). Constitutive activation of NF-kB in cancers appears to play a role in tumour growth and cancer cell survival. NF-kB is the transcription factor that induces the expression of inflammatory response cytokines, including interleukins-1 and -6, COX-2 and tumour necrosis factor α and of growth factors such as interleukin-2 and granulocyte colony stimulating factor. 5, 10, 11 Other mechanisms proposed to influence transcription factor activity, gene expression and signal transduction are via regulating peroxisome proliferator-activated receptor-alpha, ras and protein kinase C, ornithine decarboxylase, 3-hydroxy-3-methylglutaryl coenzyme A reductase and nitric oxide. 7


Alteration of oestrogen metabolism

The proliferation of some cancers such as oestrogen-sensitive breast cancer by oestrogen, are very well known. Other cancers such as prostate and colon cancers may also exhibit oestrogen receptors and consequently the growth of these cancers can also be promoted by oestrogen. PGE2 activates P450 aromatase which converts 19-carbon steroids to oestrogens. 7 PGE3 on the other hand (an EPA derived product) does not activate P450 aromatase and thus a decrease in PGE2 and increase in PGE3 would be expected to result in a decreased production of oestrogen and thus reduction in oestrogen stimulant cell growth. 5


Which fish oil is best?

When providing your patient with any nutritional product, particularly fish oil, it is desirable to offer the best tasting, freshest, most pure and premium quality supplement available on the market. Nordic Naturals ProEFA Liquid is a great tasting balanced blend of omega 3, omega 6 and omega 9 by combining fish oil with borage oil. GLA which is derived from borage oil is an excellent complement to fish oil as together they help to reduce the synthesis of pro-inflammatory prostaglandins which have been implicated in cancer initiation and progression. GLA itself has shown promise in the treatment of cancer, both as a cytotoxic agent and as an adjunct to chemotherapy. In one human study, 38 women with breast cancer were randomized and given either 2.8g GLA and 20mg of Tamoxifen or Tamoxifen alone daily. The combination of GLA and Tamoxifen was found to enhance the efficacy of Tamoxifen and increase the response rate which was evident by the sixth week. There was greater reduction in oestrogen receptor expression in the combination group than the Tamoxifen only group. 12


1 MacLean CH, et al., Effects of Omega-3 Fatty Acids on Cancer Risk. JAMA, 2006. 295(4): p. 403-416.


2 Kato I, et al., Prospective study of diet and female colorectal cancer: the New York University Woman's Health Study. Nutr Cancer, 1997. 28: p. 276-281.


3 Takezaki T, et al., Diet and lung cancer risk from a 14-year population based prospective study in Japan: With special reference to fish consumption. Nutr Cancer, 2003. 45(2): p. 160-167.


4 Schuurman AG, et al., Association of energy and fat intake with prostate carcinoma risk: results from the Netherlands Cohort Study. Cancer, 1999. 86: p. 1019-1027.


5 Hardman EW, Omega 3 fatty acids to augment cancer therapy. Journal of Nutrition, 2002. 132: p. 3508-3512.


6 Donaldson MS, Nutrition and cancer: a review of the evidence for an anti-cancer diet. Nutrtion Journal, 2004. 3: p. 19-40.


7 Larsson SC, et al., Dietary long-chain n-3 fatty acids for the prevention of cancer: a review of potential mechanisms. Journal of Clinical Nutrition, 2004. 79: p. 935-945.


8 Gogos CA, et al., Dietary omega-3 polyunsaturated fatty acids plus vitamin E restore immunodeficiency and prolong survival for severely ill patients with generalized malignancy. Cancer, 1998. 82: p. 395-402.


9 Rao CV, et al., Chemoprevention of colon carcinogenesis by Sulindac, a non-steroidal antiinflammatory agent. Cancer Research, 1995. 55: p. 1464-1472.


10 Schwartz SA, Hernandez A, and Evers BM, The role of NF-kB/IkB proteins in cancer; implications for novel treatment strategies. Surg Oncol, 1999. 8: p. 143-153.


11 Karin M and Greten FR, NF-kB: linking inflammation and immunity to cancer development and progression. Nature Reviews, 2005. 5: p. 749-759.


12 Kenny FS, et al., Gamma linolenic acid with tamoxifen as primary therapy in breast cancer. Int J Cancer, 2000. 85: p. 643-648.

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Dietary antioxidants and cancer protective nutrients

By Samantha Coulson B.HSc (Compl. Med), Adv Dip Nat


Dietary epidemiologic studies have provided initial leads for the identification of numerous naturally occurring chemopreventive agents, and laboratory studies have identified many potential agents that suppress carcinogenesis in animal models. Chemopreventive agents that have been researched include micronutrients (e.g. vitamins A, C, and E, pancreatin, bromelain, fibre, betacarotene, molybdenum, calcium, selenium), and phytochemicals (e.g. indoles, polyphenols, isothiocyanates, flavonoids, monoterpenes, organosulfides).


Vitamin A

Vitamin A modulates cell to cell interaction by being a catalyst in the synthesis of cell membrane glycoproteins. These glycoproteins act as communicator beacons between cells and are very important in maintaining contact inhibition between cells. Vitamin A also enhances immune competence. Retinoids also play a possible role in inducing apoptosis in ovarian cancer. 1, 2


Vitamin C (ascorbic acid)

Vitamin C is a potent antioxidant. It protects against nitrite and benzo-pyrene ingestion. It reduces abnormal rates of cell division in human breast cancer tissue exposed to tobacco smoke. It increases the intercellular ground substance resistance to hydrolysis by hyaluronidase, the enzyme that potentiates the spread, or dissemination of cancer cells.3 It also reduces platelet aggregation and increases fibrolytic activity thereby reducing the possibility of the cancer cell being masked from the immune defense system.4,5 Vitamin C may possibly modify the rate of tumour growth and regression through its immune stimulating effects. Vitamin C administration inhibits DNA, RNA and protein synthesis in neoplastic blood cells and squamous cells. It also decreases bladder, cervical, colorectal, oesophageal, lung, prostatic and, stomach cancers, leukaemia and non-Hodgkin’s lymphoma, and salivary gland cancer risk.3


Vitamin E (D-alpha tocopherol succinate)

This nutrient protects the cell membrane from oxidative damage and particularly against chemical plant toxins such as quinones and hydrazides. Vitamin E levels are extremely low in the lungs of smokers. Gamma tocopherol is a potential anti-cancer agent and should be taken every time alpha-tocopherol is used. Tocopheryl succinate is the most effective form of vitamin E that induces apoptosis in many cancer cell lines (e.g. prostate, breast) by increasing the activity of FAS and FAS ligand expression.6, 7


Tocopheryl succinate also inhibits vascular endothelial growth factor gene expression thus inhibiting tumour angiogenesis.8 During the malignant progression, tumour cells become insensitive to the growth inhibiting effects of Transforming Growth Factor-ß (TGF-ß). Vitamin E succinate improves TGF-ß signaling and helps normalize growth. 9, 10


Flavonoids (Quercetin)

Flavonoids are potent antioxidants and anti-inflammatory agents. Some flavonoids such as quercetin have demonstrated modulation of microsome-mediated activation of aflatoxin B and other mutagens thus reducing resultant DNA damage. Quercetin, rutin and kaempferol have demonstrated anti-promoter activity. Due to their anti-inflammatory activity they reduce the spread of cancer i.e. metastasis. 11,12 Quercetin is also a powerful modulator of COX 1&2 and lipoxygenase activity. Quercetin blocks the G0/G1 phase of the cell division cycle. It binds oestrogen beta-receptors thus reducing the effects of sex hormones on cancer growth.13 It has shown some promise against ovarian cancer, prostate, melanoma, oestrogen receptor negative breast cancer and leukaemia.14,15,16



Dietary selenium significantly inhibits the induction of skin, prostate, liver, colon, and mammary tumours.35 Selenium is a cofactor to the enzyme glutathione peroxidase, which is essential for destroying lipid hydroperoxides, and endogenous hydrogen peroxides, thus reducing, or preventing oxygen radical-induced fat rancidity.34 Sodium selenite is effective in colon cancer by suppressing the transcription factor NFkB and AP-1.32,39 Selenomethionine induces apoptosis in prostatic, melanoma, lung and colon cancer cell lines. 33,35,36,37,38 Selenomethionine depletes cellular levels of polyamine levels. This depletion of polyamines leads to the induction of apoptosis and perturbation in the cell cycle.38


Tumour cells demonstrate a differential sensitivity to selenomethionine which is approximately 1000 times more than normal diploid cells to the inhibitory effects of selenium.37 Selenium deficiency is associated with adenocarcinoma of the bowel.



Zinc is involved in over eighty different enzyme systems in the body, and is particularly effective in promoting the strength of the immune system. It can reduce heavy metal toxicity particularly of lead and copper.30 It is a cofactor in DNA repair. Zinc in high doses induces necrosis as well as apoptosis in thyroid cancer cell lines.17, 18 Zinc deficiency promotes cancer. Under the influence of Th1 immune cells, zinc inhibits the growth of tumours by activating the endogenous tumour suppressor Endostatin, which inhibits angiogenesis.31


Bromelain, Pancreatic Enzymes and Papain

Therapy with oral proteolytic enzymes containing bromelain, papain and pancreatin as well as trypsin and chymotrypsin has been shown to improve survival of cancer patients by decreased metastasis and improved cellular immunity against tumours.19 - 22, 25, 29 These enzymes also reduce the side effects of radiation and chemotherapy. 25 - 28


Bromelain has been shown to:

• Interfere with the growth of malignant cells

• Inhibit platelet aggregation

• Increase fibrolytic activity

• Regulate inflammatory reactions

• Improve cellular immunity in an immune suppressed cancer patient


These biological functions of bromelain have therapeutic value in modulating tumour growth, angiogenesis, blood coagulation, radiation and inflammatory changes.20, 23, 24





1 Zhang D, Holmes WF, et al. Retinoids and ovarian cancer. J cell Physiol. 2000 Oct;185(1):1-20.


2 Kerr PE, DiGiovanna JJ. From vitamin to Vesanoid: systemic retinoids for the new millennium. Med Health R I. 2001 Jul;84(7):228-31.


3 Head K. Ascorbic acid in the prevention and treatment of cancer. Altern Med Rev 1998;3(3):174-186.


4 Bordia AK. Acute effect of ascorbic acid on fibrinolytic activity. Atherosclerosis 1978;30:351.


5 Cordova C, Musca A, Violi F et al. Influence of ascorbic acid on platelet aggregation in vitro and in vivo. Atherosclerosis 1982;41:15.


6 Israel K, Yu W et al. Vitamin E succinate induces apoptosis in human prostate cancer cells: role for Fas in vitamin E succinate-triggered apoptosis. Nutr Cancer. 2000;36(1):90-100.


7 Neuzil J, Weber T, et al. Selective cancer cell killing by alpha-tocopheryl succinate. Br J Cancer. 2001 Jan 5;84(1):87-9.


8 Malafa MP, Neitzel LT. Vitamin E succinate promotes breast cancer tumour dormancy. J Surg Res. 2000 Sep;93(1):163-70.


9 [No authors listed]. American Institute for Cancer Research 10th annual research conference. The role of nutrition in preventing and treating breast cancer and prostate cancer. Washington, DC, USA. August 31-september 1, 2000. Abstracts. J Nutr. 2001 Jan;131(1):151S-203S.


10 Jha MN, Bedford JS et al. Vitamin E (d-alpha Tocopheryl succinate) decreases mitotic accumulation in gamma-irradiated human tumour, but not in normal cells. Nutr Cancer. 1999;35(2):189-94.


11 Hayashi A, Gillen AC, Lott JR. Effects of daily oral administration of quercetin chalcones and modified citrus pectin. Altern Med Rev. 2000 Dec;5(6):546-52.


12 Yanoshita R, Chang HW et al. Inhibition of lysoPAF acetyltransferase activity by flavonoids. INflamm Res. 1996 Nov;45(11):546-9.


13 Scambia G, Ranelletti FO et al. Quercetin potentiates the effect of Adriamycin in a multidrug-resistant MCF-7 human breast-cancer cell line: P-glycoprotein as a possible target. Cancer Chemother Pharmacol. 1994;34(6):459-64.


14 Choi JA, Kim Jy et al. Induction of cell cycle arrest and apoptosis in human breast cancer cells by quercetin. Int J Oncol. 2001 Oct;19(4):837-44.


15 Asea A, Ara G, Teicher BA et al. Effects of the flavonoids drug quercetin on the response of human prostate tumours to hyperthermia in vitro and in vivo. Int J Hyperthermia. 2001 Jul-Aug;17(4):347-56.


16 Zhang X, Xu Q, Siaki I. Quercetin inhibits the invasion ands mobility of murine melanoma B16-Bl6 cells through inducing apoptosis via decreasing Bcl-2 expression. Clin Exp Metastasis. 2000;18(5):415-21.


17 Iitaka M et al. Induction of apoptosis and necrosis by zinc in human thyroid cancer cell lines. J Endocrinol. 2001 May;169(2):417-24.


18 Sciaudone MP et al. Chelation of zinc amplifies induction of growth hormone mRNA levels in cultured rat pituitary tumour cells. J Nutr. 2000 Feb;130(2):158-63.


19 Desser L. et al. Oral therapy with proteolytic enzymes decreases excessive TGF-beta levels in human blood. Cancer Chemother Pharmacol. 2001 Jul;47 Suppl:S10-5.


20 Eckert K et al. Effects of oral bromelain administration on the impaired immunocytotoxicity of mononuclear cells from mammary tumour patients. Oncol. Rep 1999 Nov-Dec;6(6):1191-9.


21 Zavadova E et al. Stimulation of reactive oxygen species production and cytotoxicity in human neutrophil in vitro and after oral administration of a polyenzyme preparation. Cancer Biother. 1995 Summer; 10(2):147-52.


22 Milenic DE et al. comparison of methods for the generation of immunoreactive fragments of a monoclonal antibody (B72.3) reactive with human carcinomas. J Immunol Methods.(1989)2;120(1):71-83.


23 Taussig SJ et al. Bromelain, the enzyme complex of pineapple and its clinical application. An update. J Ethnopharmacol. 1988, 22(2):191-203.


24 Gerard G. Anticancer treatment and bromelains. AGressologie. 1972;13(4):261-74.


25 Sakalova A et al. Retrolective cohort study of an additive therapy with an oral enzyme preparation in patients with multiple myeloma. Cancer Chemother Pharmacol. 2001 Jul;47 Suppl:S38-44.


26 Dale PS et al. Co-medication with hydrolytic enzymes in radiation therapy of uterine cervix: evidence of the reduction of acute side effects. Cancer Chemother Pharmacol. 2001 Jul;47 Suppl:S29-34.


27 Gujral MS et al. Efficacy of hydrolytic enzymes in preventing radiation therapy-induced side effects in patients with head and neck cancer. Cancer Chemother Pharmacol. 2001 Jul;47 Suppl:S23-8.


28 Popiela T et al. Double-blind pilot study on the efficacy of enzyme therapy in advanced colorectal cancer. Przegl Lek. 2000;57 Suppl 5:142.


29 Beers EP, Woffenden BJ, Zhao C. Plant proteolytic enzymes: possible roles during programmed cell death. Plant Mol Biol. 2000 Oct;44(3):399-415.


30 Brewer GJ. Copper control as an antiangiogenic anticancer therapy: lessons from treating Wilson’s disease. Exp Biol Med (Maywood). 2001 Jul;226(7):665-73.


31 Sprietsma JE. Modern diets and diseases: NO-zinc balance. Under Th1, zinc and nitrogen monoxide (NO) collectively protect against viruses, AIDS, autoimmunity, diabetes, allergies, asthma, infectious diseases, atherosclerosis and cancer. Med Hypothesis. 1999 Jul;53(1):6-16.


32 Yoon SO et al. Inhibitory effect of selenite on invasion of HT1080 tumour cells. J Biol hem. 2001 Jun 8;276(23):2085-92.


33 Chigbrow M, Nelson M. Inhibition of mitotic cyclin B and cdc2 kinase activity by selenomethionine in synchronized colon cancer cells. Anticancer Drugs. 2001 Jan;12(1):43-50.


34 Schrauzer GN. Anticarciogenic effects of selenium. Cell Mol Life Sci. 2000 Dec;57(13-14):1864-73.


35 Menter DG, Sabichi AL, Lippman SM. Selenium effects on prostate cell growth. Cancer Epidemiol Biomarkers Prev. 2000 Nov;9(11):1171-82.


36 Sundaram N et al. Selenium causes growth inhibition and apoptosis in human brain tumour cell lines. J neurooncol. 2000;46(2):125-33.


37 Redman C et al. Inhibitory effect of selenomethionine on the growth of three selected human tumour cell lines. Cancer Lett. 1998 Mar 13;125(1-2):103-10.


38 Redman C et al. Involvement of polyamines in selenomethionine induced apoptosis and mitotic alterations in human tumour cells. Carcinogenesis 1997 Jun; 18(6):1195-202.


39 Brigelius-Flohe R et al. utilization of selenium from different chemical entities for selenoprotein biosynthesis by mammalian cell lines. Biofactors 1995-96;5(3):125-31.


40 Daou DL. Natural anticarcinogens, carcinogens and changing patterns in cancer: some speculations. Environ Res. 1989; 50(2):322-40.

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Probiotics and Cancer Prevention

Written by Michelle Gillis B. H.Sc. (Naturopathy)


It has been estimated that 30-40 percent of all cancers can be prevented by appropriate dietary measures, physical activity, and maintenance of appropriate body weight. 1

When reading frightening statistics such as the one above, it is no wonder that integrative nutritional medicine has received a wealth of attention as a modality that may successfully prevent and/or assist in the treatment of cancer.


Henry Osiecki has spent a large component of his professional career devoted to researching and applying nutritional medicine to treat and support cancer patients whilst they undergo conventional cancer therapies such as chemotherapy, radiation and surgery. Many practitioners may already be familiar with some of Henry’s recommendations such as ketogenic and alkaline diets, digestive enzyme therapy and antioxidant support 2 . In regards to specific cancers such as colorectal cancer, Henry also suggests probiotic therapy, particularly formulas containing Lactobacillus acidophilus as in vivo and in vitro studies have demonstrated that this strain may have anti-tumour activity 3.


In the beginning of the 20th century, the Russian Nobel prizewinner Ellie Metchnikoff observed a higher life expectancy in Bulgarian persons who ate large amounts of fermented milk products. One hundred years later, the consumption of fermented milk products is still associated with several types of human health benefits 4.


Ingestion of viable probiotics and prebiotics is associated with anticarcinogenic effects. One theorized mechanism is via the detoxification of genotoxins in the gut. However, because of the complexity of cancer initiation, cancer progression and the exposure of cancer in the gut, many types of interactions may be envisaged 4. It is hypothesized that Lactobacilli inhibit carcinogenesis by:


Inactivating or inhibiting carcinogenic compounds in the gut

Decreasing the activity of β-glucoronidase, β-glucosidase and nitro-reductase; enzymes implicated in colon carcinogenesis

Improving immune competence

Stimulating the repair of carcinogen induced DNA damage

Inhibiting carcinogenic bacterial enzymes

Inhibiting pathogens by producing antimicrobial chemicals 2

Encouraging a lower colon pH through the production of short chain fatty acids 1





The bacteria that reside in the intestinal tract generally share a symbiotic relationship with their host. Beneficial bacteria manufacture natural antibiotics to keep pathogenic bugs in check and also produce some B group vitamins in the small intestine. These healthy little bugs support the function of the gastrointestinal tract by assisting digestion through the supply of extra enzymes, such as lactase, in the intestine. Beneficial bacteria can help strengthen gut immune function, where a great deal of exposure and interaction between the outside and internal world takes place. Evidence supports the use of beneficial bacteria to help prevent food allergies and to improve mineral absorption and maximize food utilization. Recently it has also been shown that they are potentially indicated in preventing cancer at various stages of development.


Lactobacillus casei is one particular strand that has been specifically investigated in two human trials assessing its use in superficial bladder cancer. In the first trial, the probiotic group had a 50% disease free time of 350 days, compared to 195 days in the control group. 5 The second trial reiterated that probiotics are superior to placebo, except in the instance of multiple recurring tumours 6.


Except for the two studies listed above, most of the research into probiotics and cancer has been animal studies, measuring markers of tumour growth in animals with chemically induced tumours. In one such study of rats, researchers demonstrated that probiotics can inhibit the formation of aberrant crypt foci, which is thought to be a pre-cancerous lesion in the colon. The most significant results were obtained when the probiotic strain was consumed with a fructooligosaccharide (FOS). Total aberrant crypt foci (chemically induced) were reduced by 74% in the probiotic treatment group with Bifidobacterium longum in combination with FOS 7.



A common complication in cancer patients treated with radiotherapy is acute diarrhea 8. In one study, a probiotic formulation containing strains such as L. casei, L. plantarum, L. acidophilus, B. longum, B breve and S. thermophilus was given to the treatment group whilst they received radiotherapy. In the placebo group, 52% of the patients developed diarrhea compared with 38% in the treatment group. Furthermore, patients with the placebo preparation developed more severe diarrhea. 9



The research into probiotics and disease is still an emerging avenue and warrants further investigation in not only animal but also human studies. What we do know is that there is a high degree of variation between the differing strains of bacteria and their reputed health benefits. However, as new methods for selecting and screening probiotics develop with technologic advances, it is envisaged that the exciting field of probiotic therapy will be able to advance rapidly along with our understanding of how they function in the body to reduce and prevent disease processes such as cancer.


1 Donaldson MS, Nutrition and cancer: a review of the evidence for an anti-cancer diet. Nutrtion Journal, 2004. 3: p. 19-40.


2 Osiecki H, The Physician's Handbook of Clinical Nutrition. 7th Ed ed. 2006, Brisbane, Australia: Bio Concepts Publishing.


3 Bauer G, Lactobacilli-mediated control of vaginal cancer through specific reactive oxygen species interaction. Med Hypotheses, 2001. 57(2): p. 252-257.


4 Wollowski I, Rechkemmer G, and Pool-Zobel BL, Protective role of probiotics and prebiotics in colon cancer. Am J Clin Nutr, 2001. 73: p. 451-455.


5 Aso Y and Akazan H, Prophylactic effect of Lactobacillus casei preparation on the recurrence of superficial bladder cancer. Urol Int, 1992. 49: p. 125-129.


6 Aso Y, et al., Preventative effect of a Lactobacillus casei preparation on the recurrence of superficial bladder cancer in a double-blind trial. Urol Int, 1995. 27: p. 104-109.


7 Rowland IR, et al., Effect of Bifidobacterium longum and inulin on gut bacterial metabolism and carcinogen-induced aberrant crypt foci in rats. Carcinogenesis, 1998. 19: p. 281-285.


8 Donner CS, Pathophysiology and therapy of chronic radiation-induced injury to the colon. Dig Dis, 1998. 16: p. 253-261.


9 Delia P, Sansotta G, and Donato V. et al, Prevention of radiation-induced diarrhea with the use of VSL 3, a new high-potency probiotic preparation. Eur J Gastroenterol Hepatol, 2002. 97: p. 2150-5152.

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Sports Nutrition - Not Only for Althetes.


Many athletes face both symptoms of exercise over‑training and under-recovery, which may be alleviated with proper nutrition and supplementation. However, supplementation is not only for athletes and body builders. While the average person attending a gym or playing a recreational sport may not suffer from over-training and under-recovery, they may experience muscle straining and increased injury due to poor training routines, lack of stretching or under-training.



Find the Energy

It is not always easy to find the energy, or motivation to exercise, especially after spending the day working or looking after young children. A herbal mix of adrenal tonics (adaptogens) may just make the difference, by reducing stress levels and increasing energy. Consider Korean Ginseng for a stronger stimulation; and Siberian Ginseng, Rhodiola or Withania as less stimulating adaptogens. A study found that extract equivalent to 400 mg of Korean Ginseng root for four weeks significantly improved fatigue. Side-effects were uncommon with only two subjects withdrawing from the study.1 Nervines including St John’s Wort, Oats and Skullcap may also be beneficial. While exercise is great for stress reduction, feeling stressed and anxious may reduce our desire to exercise. A multivitamin and mineral formulation containing all the B vitamins, selenium and alpha-lipoic acid for their antioxidant effects should be considered in order to maintain wellbeing and promote good health.

In recent years, Coenzyme Q10 has gained considerable attention as a nutritional supplement capable of influencing cellular bioenergetics and counteracting free radical damage. CoQ10 improves energy (adenosine triphosphate - ATP) production in the mitochondria, acts as an essential antioxidant and supports the regeneration of other antioxidants, improves the stability, fluidity and permeability of membranes and stimulates cell growth and inhibits cell death.2

In athletes, CoQ10 deficiency may produce metabolic stress and free radical formation during times of intense training. Some studies have found CoQ10 to improve exercise performance and recovery, while others have been negative. It is possible that these inconsistent findings are due to the poor bioavailability of CoQ10 from particular supplements. CoQ10 is a large, hydrophobic molecule, which therefore limits its absorption and muscle tissue uptake. Various manufacturing techniques have been developed to improve the absorption of CoQ10 and a recent pilot study found that a enhanced form of CoQ10 resulted in higher muscle CoQ10 concentration, lower serum SOD (a marker of cellular antioxidant damage) and higher MDA (a marker of lipid peroxidation) levels during and following exercise. Two week supplementation also tended to increase time to exhaustion.2 The normal dosage of CoQ10 may be as high as 150 mg daily due to its poor bioavailability, however, when using a product with enhanced bioavailability, such as the micellised form, results may be achieved with a 50 - 100 mg daily dose.


Reduce the Oxidating Effects of Intense Exercise

Exercise training is known to increase free radical production, which potentially leads to muscle injury. Athletes can use ten times the amount of oxygen during activity, so oxidative stress on their cells is enormous. Vitamins C and E are well known antioxidants that may assist in the prevention of muscle cell damage. A pilot study found that vitamin C and E supplementation in soccer players reduced lipid peroxidation and muscle damage during high intensity efforts (p 


Reduce Inflammation and Muscle Ache, Protect Joints and Bones

Both over‑training and misguided exercise undertaken by an unfit person may result in acute or chronic inflammation. Over‑training, poor training and injury further result in arthritic changes.

Several studies have reported that the intake of fish oils is inversely associated with serum C-reactive protein concentrations. C-reactive protein is a marker of acute inflammation. A recent study involving 971 elderly Japanese men and women found that a greater intake of fish oils was related to a reduced prevalence of high CRP concentrations. These findings suggest that even very high intakes of omega 3 fatty acid may lower serum CRP concentrations and reduce inflammation.4 Fish oils

(3.2 g EPA and 2.2 g DHA) have also been shown to reduce exercise-induced bronchoconstriction and inflammation in athletes.5

Other anti-inflammatory compounds include herbs such as Boswellia, Devil’s Claw, Turmeric and Willow Bark. Nutrients for joint support include glucosamine, chondroitin sulphate, bromelain, rutin, and the minerals; silica, manganese and zinc. Products containing these ingredients can be given prophylactically as well as therapeutically.

The build-up of lactic acid is experienced by all who exercise and it causes pain and weakness in muscles. Muscular acidosis can be reduced by taking sodium bicarbonate (baking soda) or citrate (citric acid). Athletes may use pre-event loading with sodium bicarbonate and citrate to reduce the lactic acid build up. It is also possible to reduce muscular acidosis by adding 100 g baking soda to a warm bath. Epsom salts (magnesium sulfate) are also beneficial for muscle relaxation and detoxification by adding two cups to a warm bath. You can buy Epsom salts in bulk from your local pharmacy or supermarket. A diet high in fruits and vegetables and low in animal proteins will also help the body become less acidic. A good magnesium powder containing the appropriate cofactors is one of the best remedies for alleviating cramps and muscle aches.


Improve the Omega 6 to Omega 3 Ratio

Humans evolved consuming a diet containing approximately equal amounts of omega 6 and omega 3 essential fatty acids. In Western diets today, the ratio of omega 6 to omega 3 fatty acids ranges from approximately 10:1 to 20:1 instead of the traditional range of 1:1 to 2:1. Studies indicate that a high intake of omega 6 fatty acids shifts the physiological state to one that is prothrombotic and proaggregatory, characterised by increases in blood viscosity, vasospasm and vasoconstriction, and decreases in bleeding time. Omega 3 fatty acids, however, have anti-inflammatory, antithrombotic, antiarrhythmic, hypolipidaemic, and vasodilatory properties. Excessive free radical formation and trauma during high-intensity exercise leads to an inflammatory state that is made worse by the increased amount of omega 6 fatty acids in Western diets. Luckily, this can be counteracted by eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) found in omega 3. Anybody who is exercising may benefit from taking 1 - 2 g/day at a ratio of EPA:DHA of 2:1.6 This is around 800 - 1200 mg EPA and 400 - 600 mg DHA.


Fish Oils and Bone Mass Density

Fish oils, especially DHA, are also important for maintaining good Bone Mass Density (BMD). A study of 78 healthy young men found a positive correlation between omega 3 fatty acid concentrations and changes in BMD at the spine (p = 0.02). An even stronger correlation was found for DHA. Concentrations of DHA were positively associated with total BMD (p = 0.004) and BMD of the spine (p = 0.008).7

Improve Performance and Endurance

Athletes, especially body builders, are often looking for supplements which may enhance their athletic performance and endurance. These products are known as ergogenic aids and include creatine, HMB (beta-hydroxy-beta-methylbutyrate) and the hormones DHEA and androstenedione.



Promotes the production of lean muscle mass and • enhances athletic performance in sporting events encompassing explosive bursts of power.

Principally acts by increasing the availability of ATP to • muscles during exhaustive exercise. Prolonged activity stimulates further muscle development.

Increases the muscle fluid content which may stimulate • further protein synthesis in muscles.

May also help buffer muscle acidity, improve insulin-• sensitivity and reduce free radical damage

Creatine monohydrate is considered the most effective • and safe nutritional supplement available in terms of increasing high-intensity exercise capacity and lean body mass during training.

Adaptogens and tonics including Korean Ginseng, Withania and Schizandra can be used to improve stamina and endurance and reduce recovery time. In a randomised, double-blind, cross-over study, 18 healthy horses received a single dose of Schizandra concentrate (equivalent to 50 g of dried berries, standardised to contain 1.2% schisandrins) or placebo 30 minutes before a test race. For the race horses, the exercise consisted of an eight minute race over 5.6 km. The show-jump horses were taken over a 700 m obstacle course with 12 jumps. Treatment with Schizandra reduced heart rate and respiratory frequency, increased plasma glucose and decreased lactate levels in both exercise groups, although the effects were more marked in the race horse group. The Schizandra-treated show-jump horses completed the circuit in a shorter time than the controls. It was thought that Schizandra may cause a lower synthesis of lactate in muscles under anaerobic conditions and stimulate lactate clearance by the liver.8 Now you may not feel like running or jumping like a horse, but Schizandra may just give you or your patients a helping hand.

Korean Ginseng in combination with nutrients has been shown to improve exercise performance. Exercise performance was assessed on a treadmill according to the seven steps Bruce protocol. Physiological parameters were assessed before and after each step; and three, six and nine minutes after the end of the exercise. Maximal oxygen consumption, plasma lactate level, CO2 production, ventilation, and heart rate all significantly improved after Korean Ginseng, while no change was observed after placebo.9


Protein Powders

Consuming proteins and low GI carbohydrates pre- and post exercise promotes muscle gain. A low GI carbohydrate and sugar free diet is essential for maintaining a healthy body weight, however it is all about balance. Individuals who engage in regular exercise training need more protein than sedentary people. While it is possible for physically active individuals to obtain their daily protein requirements through a varied diet, supplemental protein in various forms including whey, is a practical way of ensuring adequate and quality protein intake for athletes. When part of a balanced, nutrient-dense diet, protein intakes at this level are not detrimental to kidney function or bone metabolism in healthy, active people. Specific amino acid supplements, such as branched-chain amino acids (leucine, isoleucine and valine), may improve exercise performance and recovery from exercise.


Lose Weight and Tone Up

Exercise and proper diet is essential to safe weight reduction. To lose fat a person needs to create a kilojoule deficit. However we often ‘reward’ ourselves after exercise in the gym with a large meal or a visit to the pub, which negates fat loss. The other extreme is also counterproductive. Severe kilojoule restriction is not as efficient as a moderate kilojoule restriction combined with a regular exercise program. It is important to make exercise fun and enjoyable, plus remember to fuel the body with enough kilojoules to provide energy to exercise. Eating a small breakfast and a big dinner tends to be fattening, whereas eating a substantial breakfast and lunch can help reduce fat gain. Adoption of a low-fat, vegan diet has been shown to be associated with a significant weight loss and increased insulin sensitivity in overweight menopausal women over a 14 week period.10 Herbs and nutrients to support weight loss include Coleus (may increase metabolism and promote lean body mass), Gymnema may stabilise blood sugar) and omega 3 (promotes weight loss). Avoid supplements with added sugars, especially fructose. Avoid soft drinks and fruit juices. Filtered water is more than adequate for most people during and after normal exercise. Almonds and other nuts are a good snack food as regular consumption of nuts may help to regulate body weight by suppressing appetite and fat absorption.11


SupplementDaily Dosage

Magnesium- 300 mg (powder formulation with cofactors)

CoQ10 - 50 mg (micellised form)

Vitamin C with flavonoids - 2 - 5 g

Multivitamin - 1 - 2 tablets (and mineral formulation with antioxidants, including selenium and alpha-lipoic acid)

Antioxidant - 1 - 3 tablets (mixed nutritional and herbal antioxidant)

Glucosamine - 1,500 mg (powder formulation with cofactors)

Omega 3 - 4 - 6 g



1 Le Gal M, Cathebras K. Phytother Res 1996; 10: 49-53

2 Cooke M, Iosia M et al. J Int Soc Sports Nutr 2008; 5: 8

3 Zoppi CC, Hohl R et al. Journal Int Soc Sports Nutr 2006; 3(2): 3-44

4 Niu K, Hozawa A et al. Am J Clin Nutr 2006; 84(1): 223-229

5 Mickleborough TD, Murray RL et al. Am J Respir Crit Care Med 2003; 168(10): 1181-1189

6 Simopoulos AP. Curr Sports Med Rep 2007; 6(4): 230-236

7 Högström M, Nordström P et al. Am J Clin Nutr 2007; 85(3): 647-648

8 Ahumada F, Hermosilla J et al. Phytotherapy Research 1989; 3(5): 175-179

9 Pieralisi G, Ripari P et al. Clin Ther 1991; 13(3): 373-382

10 Barnard ND, Scialli AR et al. Am J Med 2005; 118(9): 991-997

11 Coates AM, Howe PR. Curr Opin Lipidol 2007; 18(1): 25-30

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This study is quite flawed, but interesting none the less. Enjoy!


Life saving strength


The stronher you are, the longer you will live, a new strudy in the British Medical Journal has demonstrated.

In this long-term study, 8762 men underwent an initial complete physical examination, including measures of muscle strength. Muscle strength was assessed via a bench press, for upper body strength, and a seated leg-press, for lower body strength. In the almost 20 year follow up period, information on mortality was collected to assess any associations with muscle strength. Because those with higher muscle mass were likely to be fitter and live a healthier lifestyle existing medical conditions, lifestyle factors as well as cardiorespiratory fitness were accounted for to ensure that they did not cloud the results.

The adjusted data showed that increased muscle strength at base-line was associated with lower risk of death 20 years later from all causes, inclding heart disease and cancer.

The apparent protective effect of muscular strength against risk of death is likely to be linked to the benefits of higher muscle mass, as well as serving as a measure of the level of participation in resistance exercise.

Aerobic exercise has long been an important part of publich health recommendations. Evidence supporting the addition of resistance exercise to these recommendations continues to gather weight, for both improved wellbeing as well as chronic disease prevention.



Maintaining a health muscle mass provides many benedits. Muscle tissue increases the body's metabolic rate and insulin sensitivity via its constant demand for glucose and fatty acids from the blood. Having a reserve of muscle mass is also vital in acute illness, providing an immediate source of high quality protein for immune function and tissue repair. For these reasons, muscle mass has long been recognised as a biomarker of ageing - a biological parameter that will predict functional capability in later life.

Low muscle mass is common in patients, due to lack of exercise, protein deficient diets, or catabolic factors such as stress and chronic inflammation. Normal weight individuals are particularly at risk of low muscle mass going unrecognised, as their normal weight may be composed of a high percentage of fat and a low muscle percentage, termed sarcopenia.


Ruiz JR, Sui X, Lobelo F, Morrow JR Jr., Jackson AW, Sjostrom M, Blair SN. Association between muscular strength and mortality in men; prospective cohort study. BMJ. 2008 Jul 1;337a439.doi.1136/bmj.a439 - published online

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houghy what do you know about "Alpha Lipoic 200"


One of the guys at my gym said its one of the best antioxidants on the market.


He mentioned its good for your diet. But what i was wondering is what benefit it would be for me trying to get into bodybuilding?

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this is houghy on spiros' computer


Alpha Lipoic Acid (Bioceuticals lipoec 200) is an excellent all purpose antioxidant. i would suggest a dietary antioxidant to everyone. pm me (on my normal account) if you want specific advice mate. i dont really have time at the moment to go through it all! sorry

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what if your allergic to fish oil tablets?

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houghy what do you know about "Alpha Lipoic 200"


Lipoic Acid


Best sources:

Broccoli, Kidney, Liver, Potatoes, Spinach, Tomatoes


Factors increasing demand:

Diabetes, Doxorubicin, Emphysema, Heart Disease, HIV ifnection, Liver disease


Functions Facilitated:

Metabolic antioxidant, helps recycle the antioxidants: vitamin c, e, coq10 and glutathione; improves ATP synthesis, increases t-lymphocyte production, increases t-helper :t suppressor ratio, inhibits the production of nuclear factor Kappa B, reduces insulin resitance and improves glucose metabolism, reduces neural damage associated with excitatory amino acid toxicity and diabetes, supports mitochondrial function, detoxifies the body of heavy metal pollutants eg. cadmium, lead, mercury; acts as a water soluble AND fat soluble antioxidant, reverses the declines in oxygen consumption and mitochondrial energy production associated with ageing, cofactor for mitochdonrial dehydrogenase, neuro-protective agent, elevates intracellular glutathione levels, regulates neuronal calcium homeostasis, regulates pro-inflammatory cytokines, cofactor for mitochondrial enzymes- catalyses oxidative decarboxylation of pyruvate, alpha ketoglutarate, alpha keto acids and brand chain amino acids; inhibits advanced glycation end products, inhibits pyruvate dehydrogenase kinase (PDK1>PDK4>PDK2>PDK3)- this inhibition stimulates mitochondrial burning of glucose and reducation in lactate production; may improve mitochondrial metabolism in cancer cells thus reducing proliferation.


Daily dosage:

SR- 100-600mg



Take 30 mins BEFORE meals. High doses of lipoic acid may compete with biotin in some reactions. Biotin supplementation is warranted with high dose lipoic acid supplementation.


Drugs affecting nutrient:

Gentamycin, doxorubucin



Unline the natural form, the S-lipoic acid does not improve cellular ATP levels. The R-form increases membrane fluidity while the S-form decreases fluidity.


The S-form potentiates the deterioration of the lens in diabetes.


Taken from: The Nutrient Bible: Seventh Edition. Henry Osiecki, Bioconcepts publishing



As for Alpha Lipoic 200, thats actually the name of a Bioceuticals Product, Lipoec 200:


Lipoec 200


Lipoec 200 contains pharmaceutical grade alpha-Lipoic acid, the only fat and water soluble antioxidant nutrient.



Alpha-Lipoic acid regenerates other antioxidants such as Glutathione, Coenzyme Q10 and Vitamins C and E

Scientific evidence supports its antioxidant benefits and heavy metal chelating function

It is a cofactor for many enzymes in the body and is necessary for cellular energy production

Alpha-Lipoic acid is involved in the metabolism of carbohydrates and in the conversion of food into energy


Each Capsule Contains:

R,S-alpha-Lipoic acid 200mg


That's taken from the Bioceuticals website.

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what if your allergic to fish oil tablets?


pm me

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Had a few pm's recently regarding Co enzyme Q10, so heres some info for you all


Co Enzyme Q10

(Ubiquinone - Ubecarenone - Co Q10)


Coenzyme Q10 is one of a family of naturally occurring fat-soluble substances known as quinones, which are essential for energy production in oxygen breathing species. It is an enzyme that acts in the mitochondria of the cell as an energy carrier and is necessary for adenosine triphosphate synthesis. Another important property of Coenzyme Q10 involves its role as a lipid-soluble antioxidant. It is located within the lipid compartment of mitochondrial membranes, a site of significant free radical production. Coenzyme Q10 has been widely researched since its discovery in the late 1950s. Much of the research has been done in Japan where use of Coenzyme Q10, known as ubidecarenone, equals that of the top 5 drugs. In humans, there are two sources of Coenzyme Q10. About half is derived from dietary sources, especially fatty meat and fish, and the other half is produced endogenously. Changes in dietary habits have led to decreased availability of Coenzyme Q10. These changes include restriction of foods containing Coenzyme Q10, and reduced absorption

of fat-soluble nutrients due to use of fat substitutes and increased levels of dietary fibre. During the same time, there has been an increased need for

antioxidants such as Coenzyme Q10. Supply from endogenous and exogenous sources decreases with age and supplementation may be necessary,

especially for elderly patients.


Helps maintain normal cardiovascular health

CoQ10 is essential for normal myocardial function, and CoQ10 supplementation has been shown to improve cardiac contractility, reduce, arrhythmia, dyspnoea, oedema, insomnia, vertigo and other symptoms of congestive heart failure. It has also been proven effective in reducing essential hypertension. CoQ10 improves myocardial tissue energetics and has been found to assist in idiopathic and ischaemic cardiomyopathies.


May assist blood circulation

Coenzyme Q10 (CoQ10) has a range of welldocumented actions on the cardiovascular system, which contribute to proper circulation. In a study of 109 patients with symptomatic essential hypertension presenting to a private cardiology practice, an average dose of CoQ10 (225 mg/day orally) was added to their existing antihypertensive drug regimen. Improvement in functional class, blood pressure control and myocardial function were observed, which was

attributed to an improvement in myocardial bioenergetics. Another study in 26 patients with essential hypertension, significant decrease in peripheral resistance thus improved peripheral circulation. Total peripheral resistances were 2,283 +/- 88 dyne.s.cm-5 before treatment and 1,627 +/- 158 dyn.s.cm-5 after treatment (P


May assist peripheral circulation

In an Italian study on CoQ10 a significant reduction in blood pressure and heart rate, both supine and sitting positions, was observed in a large number of

patients across 173 centres. According to the authors, this data confirms the results of earlier studies, in which a reduction in peripheral vascular resistances with CoQ10 therapy resulted in a significant decrease in blood pressure. Research has confirmed the antihypertensive effect of CoQ10 and found that the measured peripheral resistance was significantly reduced for 5 patients in a study group of 26. They concluded that the antihypertensive effect of the CoQ10 is probably based on a diminution of peripheral resistances. Such a reduction in peripheral vascular resistance by CoQ10 would be consistent with improving

peripheral circulation.


May assist in the management of sore gums

In the early 1970’s a correlation between CoQ10 deficiency and periodontal disease was reported in a number of studies, and it was suggested that CoQ10 supplementation would help treat the condition. Following this, in 1976, succinate dehydrogenasecoenzyme Q10 reductase activities were determined in mitochondria of gingival biopsies from 29 periodontal patients. A deficiency of 20-63% of CoQ10-enzyme activity was observed in the

biopsies of all 29 patients. In a study conducted in 1971 among 11 Japanese Men and Women aged 18-35 years old with minor to severe periodontitis, results indicated a therapeutic benefit of coenzyme Q10 (20-30mg daily) in many patients with severe and destructive periodontal disease. There was a decrease in

bleeding, redness, pain and swelling. A prospective study in 1975 [Wilkinson, Hansen et al] and a follow up double-blind randomised placebo-controlled trial in 1976 [Wilkinson et al], which administered CoQ10 as an adjunct treatment for patients receiving routine care for periodontitis, found significant improvements in periodontal scores between pre- and post-administration periods. In 1994 a trial conducted among Japanese male patients with adult periodontitis and 30 periodontal pockets showed significant improvements in the modified gingival index, bleeding on probing and peptidase activity derived from periodontopathic

bacteria were observed. The results suggest CoQ10 (topical in this study) improves adult periodontitis not only as a sole treatment but also in combination

with traditional nonsurgical periodontal therapy.


May help reduce the frequency of migraines

In an open clinical trial conducted in 2002 in 26 women and 6 men with a history of episodic migraine, it was demonstrated that the average number of days with migraine during the baseline period was 7.34 and this decreased to 2.95 after 3 months of therapy. (150mg per day). Mean reduction in migraine frequency after 1 month was 13.1% and this increased to 55.3% by the end of month 3. Mean migraine attack frequency was 4.85 during the baseline period and this decreased to 2.81 attacks by the end of the study period.


May assist in the management of migraine

In a 2005 double-blind, randomised, placebocontrolled trial comparing CoQ10 (3 x 100 mg/day) and placebo in 42 migraine patients, CoQ10 was significantly superior to placebo for attackfrequency, headache-days and days-with-nausea. The effect of CoQ10 was observed to begin after the first month with a maximum effect after 3 months. Its effects were most pronounced on attack frequency and gastrointestinal symptoms and weaker for the number of headache days and headache severity. No significant trends in favor of CoQ10 were observed for headache duration and acute anti-migraine drug consumption. The authors reported that CoQ10 is effective and excellently tolerated. Review articles of Clinical research published in 2006 have shown that coenzyme Q administration has been effectively used in the management and reduction of Migraines and pain associated with migraines without significant adverse events.


Protects against lipid peroxidation

The close proximity of CoQ10 in membranes to the unsaturated lipid chains enables it to act as a primary scavenger of free radicals. CoQ10 is present in many membranes in three to 30 times the concentration of tocopherol. The quinol form, which accounts for much of the CoQ10 in cell membranes, is a very effective antioxidant. More importantly, enzymes that are present in all membranes can readily reduce any CoQ quinone radicals generated by reaction with lipid or oxygen radicals. Results suggest that even though exercise increases plasma lipid peroxidation, CoQ10 elevates the ant oxidative capacity of plasma.


Restores vitamin E to its antioxidant form

The quinol form of CoQ10 can regenerate tocopheryl radicals produced by reaction with lipid or oxygen radicals, reducing them back to tocopherol. In the absence of CoQ10 in a membrane, tocopherol regeneration is very slow. Tocopherol regeneration can also occur in lowdensity lipoprotein where a small amount of coenzyme Q protects a larger amount of tocopherol.


Contains Coenzyme Q10, which is essential to mitochondrial energy production

Reversible redox reactions allow Coenzyme Q10 to readily interconvert between its oxidised, partially reduced, and fully reduced forms. These are the basis of its important antioxidant and vital electron and proton transport properties, which are essential to mitochondrial membrane stability and energy production


Helps maintain healthy cell membranes, cell integrity, and function

CoQ10 prevented collapse of the mitochondrial membrane potential after induction of oxidative stress. These results suggest that CoQ10 stabilizes the mitochondrial membrane. There is evidence that CoQ10 has a role in proton gradient formation in endomembranes and at the plasma membrane, as well as a role in the control of membrane structure and phospholipid status.


Source of Coenzyme Q10 where supplementation is required to offset the effects of HMG-CoA reductase inhibitors

HMG-CoA reductase is the rate-limiting enzyme in cholesterol synthesis. Because, this pathway is also shared with other compounds, including CoQ10, inhibition of HMG-CoA reductase leads to impairment of endogenous CoQ10 production. In their presentation at the Thirteen International Symposium On Drugs Affecting Lipid Metabolism in Italy in 1998, researchers Bliznakov and Wilkins, urged that during extended therapy with statins, CoQ10 supplementation should be considered to support cellular bioenergetic demand as well as minimize 3-hydroxy-3methylglutaryl coenzyme A (HMG-CoA) potential lipid eroxidative insult.


In a double blind placebo controlled trial conducted in 1993, it was found that treatment with the HMGCoA reductase inhibitors pravastatin or simvastatin

lowers both total cholesterol and CoQ10 plasma levels in both normal volunteers and hypercholesterolemic patients. A 1994 crossover study demonstrated that simvastatin lowers both LDL-C and apo B plasma levels, together with the plasma and platelet levels of CoQ10. Simultaneous treatment with CoQ10

prevented both plasma and platelet CoQ10 decrease, without affecting the cholesterol lowering effect of simvastatin. The results of a 2004 prospective study show that even brief exposure to atorvastatin causes a marked decrease in blood CoQ10 concentration. The authors suggest that widespread inhibition of CoQ10 synthesis could explain the most commonly reported adverse effects of statins, especially exercise intolerance, myalgia, and myoglobinuria.


Supplementation with CO Q 10 can be of assistance when dieting, during exercising or losing weight

Results of a Swedish Trial conducted in 1997 (18 Swedish men & Women where tested on aerobic and anaerobic physical performance over 22 days) show that on an anaerobic (10 × 10 s) cycling test, the placebo group showed a significantly greater improvement after a supplementation and training

16-08-02 period (P

Tolerance of Middle-Aged, Untrained Men a trial was conducted in 15 subjects using 150mg of CoQ10 daily. Results showed that the subjective perception of

vigor (visual analog scale 1-10 where, 10 = very energetic, and 0 = very, very unenergetic) increased (p

treatment protected skeletal muscles against injury caused during exercise, but not against damage related with inflammatory processes after



Another controlled study using 150mg of coenzyme Q10, showed that during exercise, there was a pronounced acidosis with delayed kinetics of postexercise recovery for blood lactate, pH, PCr, and PCr/Pi ratio. Oxygen uptake during exercise was reduced while the lowering of the ventilatory threshold indicated an early activation of glycolysis. The observations indicate an improvement of mitochondrial function and a shift from high to low glycolytic activity in both patients consequent to CoQ treatment. COQ10 is beneficial for energy production while maintaining a weight loss program.



Factors increasing demand:

Antidepressants, beta blocker drugs, cancer, candida infections, chemotherapy, cholesterol lowering drugs (statin's), diabetes, ageing, HIV infection, Ischaemic heart disease, muscular dystrophy, Parkinson's disease, radiation.



SR 90-600mg

Most products will come in 100-150mg. I have seen dosages taken in the grams!!! Especially in Parkinson's disease research

As with all lipid soluble supplements, take with a fatty meal to increase absorption.

If you're looking for a Co Q10 supplement be prepared to pay through the arse for it, its quite expensive.

Nutrition Care make a good 100mg CoQ10. They have recently spent alot of time and money researching a new capsule/delivery system which seems the goods. Bioceuticals make a pretty good 150mg.


Functions facilitated:

Acts as a lipid antioxidant, cofactor in several metabolic pathways (particlularly oxidative respiration), lowers blood pressure, improves the energetics of the immune cellular system, increases igG levels in response to infection, prevents cellular depletion of ATP, reduces aldosterone secretion and inhibits the effects of angiotensin, reduces blood viscosity and fibrinogen levels, reduces low density lipoprotein (LDL) peroxidation during oxidative stress, improves cardiac bioenergetics, protects ATPase protein frm oxidation, normalises cancer cells, spares vitamin E, stabilises mycocardial calcium ion channels, strengthens the heart.


Co Q10 is a cofactor in oxidative phosphorylation through the electron transport chain. It transfers electrons from flavo-proteins to cytochromes.


Deficiency may cause or be associated with:

Angina, cardiomyopathy, diabetes, fatigue, heart disease, heart failure, muscular dystrophy, infection, periodontal disease.


Side effects:

Diarrhoea, dizziness, epigastric discomfort, occasional nausea (over 250mg)


Drug interactions:

Adriamycin, antidepressants, beta-blockers, doxorubicin, HMG-CoA reductase inhibitors, glaucoma drugs, lovastatin, phenothiazines, pravastatin, statins.


Synergistic nutrients:

Lipoic acid, Vitamin E, Vitamin C, Selenium, Glutathione

For synthesis of CoQ10 - tyrosine, folate, vitamins b2, b3, b5, b6, b12 and c.


Target tissues:

Heart, liver, kidney, pancreas

Because CoQ10 is part of the electron transport chain and plays a role in aerobic cellular respiration, coq10 is found in the highest concentration in organs with high energy requirements.



1. Braun, L. and M. Cohen, Coenzyme Q10, in Herbs

and Natural SupplementsAn evidence-based guide.

2005, Elsevier Mosby Sydney. p. 132-138.

2. Madit, Comparative bioavailability of CoQ 10

formulations: Licaps™ formulation versuscurrent

commercial formulations. Pfizer internal data, 2004.

3. Baggio, E., et al., Italian multicenter study on the

safety and efficacy of coenzyme Q10 as adjunctive

therapy in heart failure. CoQ10 Drug Surveillance

Investigators. Mol Aspects Med, 1994. 15 Suppl: p.


4. Langsjoen, P., et al., Treatment of essential

hypertension with coenzyme Q10. Mol Aspects Med,

1994. 15 Suppl: p. S265-72.

5. Jones, K., et al., Coenzyme Q-10 and cardiovascular

health. Altern Ther Health Med, 2004. 10(1): p. 22-

30; quiz 31.

6. Digiesi, V., et al., Coenzyme Q10 in essential

hypertension. Mol Aspects Med, 1994. 15 Suppl: p.


7. Gian Paolo Littarru*, et al., Deficiency of Coenzyme

Q10 in Gingival Tissue from Patients with

Periodontal Disease. Proc. Nat. Acad. Sci. USA

1971. 68(10): p. pp. 2332-2335,.

8. Hanioka, T., et al., Effect of topical application of

coenzyme Q10 on adult periodontitis. Mol Aspects

Med, 1994. 15 Suppl: p. s241-8.

9. Rozen TD, et al., Open label trial of coenzyme Q10 as

a migraine preventive. Cephalalgia. , 2002. 22(2): p.


10. Sandor, P.S. and J. Afra, Nonpharmacologic

treatment of migraine. Curr Pain Headache Rep,

2005. 9(3): p. 202-5.

11. Tepper, S.J.B., Marcelo; Rapoport, Alan; Sheftell,

Fred, Alternative therapies: evidence-based

evaluation in migraine. Headache Care,, October

2006 Volume 3( Numbers 2-3): p. pp. 57-64(8).

12. Evans, R.W. and F.R. Taylor, "Natural" or

alternative medications for migraine prevention.

Headache, 2006. 46(6): p. 1012-8.

13. Crane, F.L., Biochemical Functions of Coenzyme

Q10. J Am Coll Nutr, 2001. 20(6): p. 591-598.

14. Kaikkonen, J., et al., Effect of combined coenzyme

Q10 and d-alpha-tocopheryl acetate supplementation

on exercise-induced lipid peroxidation and muscular

damage: a placebo-controlled double-blind study in

marathon runners. Free Radic Res, 1998. 29(1): p.


15. Somayajulu, M., et al., Role of mitochondria in

neuronal cell death induced by oxidative stress;

neuroprotection by Coenzyme Q10. Neurobiol Dis,

2005. 18(3): p. 618-27.

16. Emile G. Bliznakov, M.D. and P.D. David J. Wilkins,

Biochemical and Clinical Consequences of Inhibiting

Coenzyme Q10 Biosynthesis

by Lipid-Lowering HMG-CoA Reductase Inhibitors (Statins):

A Critical Overview. Presented in part at the 13th International


On Drugs Affecting Lipid Metabolism, Florence, Italy,, 1998.


17. Ghirlanda, G., et al., Evidence of plasma CoQ10-

lowering effect by HMG-CoA reductase inhibitors: a

double-blind, placebo-controlled study. J Clin

Pharmacol, 1993. 33(3): p. 226-229.

18. Bargossi, A.M., et al., Exogenous CoQ10

supplementation prevents plasma ubiquinone

reduction induced by HMG-CoA reductase inhibitors.

Mol Aspects Med, 1994. 15 Suppl: p. s187-93.

19. Rundek, T., et al., Atorvastatin decreases the

coenzyme Q10 level in the blood of patients at risk for

cardiovascular disease and stroke. Arch Neurol,

2004. 61(6): p. 889-92.

20. Malm, C., et al., Effects of ubiquinone-10

supplementation and high intensity training on

physical performance in humans. Acta Physiol Scand,

1997. 161(3): p. 379-84.

21. Shimomura, Y., et al., Protective effect of coenzyme

Q10 on exercise-induced muscular injury. Biochem

Biophys Res Commun, 1991. 176(1): p. 349-55.

22. Bendahan D, D.C., Vanuxem D, Confort-Gouny S,

Figarella-Branger D, Pellissier JF, Kozak-Ribbens G,

Pouget J, Serratrice G, Cozzone PJ., 31P NMR

spectroscopy and ergometer exercise test as evidence

for muscle oxidative performance improvement with

coenzyme Q in mitochondrial myopathies. Neurology.

. 1992. 43(3 part 1): p. 628-9.

23. Riley, R.E., Popular weight loss diets. Health and

exercise implications. Clin Sports Med, 1999. 18(3):

p. 691-701, ix.

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I've decided to do a series on Amino Acids commonly found in health food stores sold individually. Because it would take me forever and a day to do them all, I'll just do the ones relevant to weight training and fitness.




(Alpha amino propionic acid)


Sold in stores as Beta Alanine. Alanine is a non-essential amino acid, meaning it can be produce endogenously (created by the body).

Acts as a buffer preventing acid build up in the muscle, gives an energy kick.


Factors increasing demand:



Functions facilitated:

Activates glucagon release, anti-ketogenic, contributes to thymus growth, cytoprotective of kidney cells, helps metabolise tryptophan and b6, increases lymphocyte division, inhibitor of pyruvate kinase, increases synthesis of HSP70 (stress protein), inhibitory neurotransmitter, regulator of glucose metabolism, source of energy for muscle and brain and strengthens immune system by increasing antibody production.


Therapeutic uses:

Athletes, Hypoglycaemic, kidney stone prevention, poor immunity, post exercise ketosis. (there are mroe but im listing only the relevant ones)


Daily dosage:

SR 200-600mg

i have seen alot higher dosing in sports supplements. like up around 6g daily




The effects of 10 weeks of resistance training combined with beta-alanine supplementation on whole body strength, force production, muscular endurance and body composition.


Kendrick IP, Harris RC, Kim HJ, Kim CK, Dang VH, Lam TQ, Bui TT, Smith M, Wise JA.

University of Chichester, College Lane, Chichester, West Sussex PO196PE, UK. i.kendrick@chi.ac.uk


Carnosine (Carn) occurs in high concentrations in skeletal muscle is a potent physico-chemical buffer of H+ over the physiological range. Recent research has demonstrated that 6.4 g x day(-1) of beta-alanine (beta-ala) can significantly increase skeletal muscle Carn concentrations (M-[Carn]) whilst the resultant change in buffering capacity has been shown to be paralleled by significant improvements in anaerobic and aerobic measures of exercise performance. Muscle carnosine increase has also been linked to increased work done during resistance training. Prior research has suggested that strength training may also increase M-[Carn] although this is disputed by other studies. The aim of this investigation is to assess the effect of 10 weeks resistance training on M-[Carn], and, secondly, to investigate if increased M-[Carn] brought about through beta-ala supplementation had a positive effect on training responses. Twenty-six Vietnamese sports science students completed the study. The subjects completed a 10-week resistance-training program whilst consuming 6.4 g x day(-1) of beta-ala (beta-ALG) or a matched dose of a placebo (PLG). Subjects were assessed prior to and after training for whole body strength, isokinetic force production, muscular endurance, body composition. beta-Alanine supplemented subjects increased M-[Carn] by 12.81 +/- 7.97 mmol x kg(-1) dry muscle whilst there was no change in PLG subjects. There was no significant effect of beta-ala supplementation on any of the exercise parameters measured, mass or % body fat. In conclusion, 10 weeks of resistance training alone did not change M-[Carn].


PMID: 18175046 [PubMed - indexed for MEDLINE]



beta-Alanine supplementation augments muscle carnosine content and attenuates fatigue during repeated isokinetic contraction bouts in trained sprinters.


Derave W, Ozdemir MS, Harris RC, Pottier A, Reyngoudt H, Koppo K, Wise JA, Achten E.

Dept. of Movement and Sport Sciences, Ghent Univ., Watersportlaan 2, B-9000 Ghent, Belgium. Wim.derave@ugent.be


Carnosine (beta-alanyl-l-histidine) is present in high concentrations in human skeletal muscle. The ingestion of beta-alanine, the rate-limiting precursor of carnosine, has been shown to elevate the muscle carnosine content. We aimed to investigate, using proton magnetic resonance spectroscopy (proton MRS), whether oral supplementation with beta-alanine during 4 wk would elevate the calf muscle carnosine content and affect exercise performance in 400-m sprint-trained competitive athletes. Fifteen male athletes participated in a placebo-controlled, double-blind study and were supplemented orally for 4 wk with either 4.8 g/day beta-alanine or placebo. Muscle carnosine concentration was quantified in soleus and gastrocnemius by proton MRS. Performance was evaluated by isokinetic testing during five bouts of 30 maximal voluntary knee extensions, by endurance during isometric contraction at 45% maximal voluntary contraction, and by the indoor 400-m running time. beta-Alanine supplementation significantly increased the carnosine content in both the soleus (+47%) and gastrocnemius (+37%). In placebo, carnosine remained stable in soleus, while a small and significant increase of +16% occurred in gastrocnemius. Dynamic knee extension torque during the fourth and fifth bout was significantly improved with beta-alanine but not with placebo. Isometric endurance and 400-m race time were not affected by treatment. In conclusion, 1) proton MRS can be used to noninvasively quantify human muscle carnosine content; 2) muscle carnosine is increased by oral beta-alanine supplementation in sprint-trained athletes; 3) carnosine loading slightly but significantly attenuated fatigue in repeated bouts of exhaustive dynamic contractions; and 4) the increase in muscle carnosine did not improve isometric endurance or 400-m race time.


PMID: 17690198 [PubMed - indexed for MEDLINE]



Effect of creatine and beta-alanine supplementation on performance and endocrine responses in strength/power athletes.


Hoffman J, Ratamess N, Kang J, Mangine G, Faigenbaum A, Stout J.

Dept. of Health and Exercise Science, The College of New Jersey, Ewing, NJ 08628, USA.


The effects of creatine and creatine plus beta-alanine on strength, power, body composition, and endocrine changes were examined during a 10-wk resistance training program in collegiate football players. Thirty-three male subjects were randomly assigned to either a placebo (P), creatine ©, or creatine plus beta-alanine (CA) group. During each testing session subjects were assessed for strength (maximum bench press and squat), power (Wingate anaerobic power test, 20-jump test), and body composition. Resting blood samples were analyzed for total testosterone, cortisol, growth hormone, IGF-1, and sex hormone binding globulin. Changes in lean body mass and percent body fat were greater (P


PMID: 17136944 [PubMed - indexed for MEDLINE]

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(2-amino - 5-guanidinopentanoic acid)


Sold in stores in the L form (L-arginine).


Daily dosage:

SR 1-6g.

Contraindicated for those with herpes or psuedomonas as it promotes their growth (unless lysine is also given)

L-Arginine may aggravate the effects of cardiac shock.


Factors increasing demand:

Diabetes, high protein diets, infection, injury, intestinal disease, liver failure, lead poisoning, low birth weight infants, poor renal function, sepsis, stress.


Deficiency may cause or be associated with:

Decreased growth, delayed puberty, fatty liver, glucose intolerance, gut infections, hyper-ammonia, infertility, increases urinary orotate excretion, muscle weakness, skin rashes.


Functions facilitated:

ammonia detoxification, glycogenesis, methylation; enhances protein synthesis and thymus gland activity; inhibits ornithine decarboxylase, immunomodulator, increases creatine clearance and glomerular filtration rate, stimulates t lymphocyte, involved in collagen, creatine, creatinine, elastin, glucagon, haemoglobin, insulin and vasopressin synthesis; precursor of ornithine and urea; precursor of polyamines required for proliferative responses characteristic in healing; metabolised to L-proline - major constituent of collagen; reduces the toxicity of protein loading; stimulates the immune system by significantly increasing natural killer (NK) and lymphocyte activated killer cell cytotoxicity, stimulates the release of gastrin, growth hormone and insulin; blocks tumour formation, stimulates acetyl glutamate synthesis; substrate for the enzymes: arginase, arginine-glycine transaminase, myotrophin synthase, arginine decarboxylase and nitric oxide synthetase; wound healing.


Syngergistic nutrients:

Aspartic acid, leucine, glycine, lysine, proline, glutamine, manganese, methionine, ornithine, vitamin b6, folic acid,, vitaminc, biopterin, citrulline.


The pathways linking arginine, glutamine and proline are bi-directional.


Lysine and ornithine compete with arginine for uptake in the brain.


Drugs affecting nutrient:

Steroids, cyclosporin A, puromycin amino nucleoside, glyceryl trinitrate.






Beneficial effects of a long-term oral L-arginine treatment added to a hypocaloric diet and exercise training program in obese, insulin-resistant type 2 diabetic patients.


Lucotti P, Setola E, Monti LD, Galluccio E, Costa S, Sandoli EP, Fermo I, Rabaiotti G, Gatti R, Piatti P.

Diabetology, Endocrinology and Metabolic Disease Unit, Fondazione Centro San Raffaele del Monte Tabor, Milan, Italy.


Because chronic L-arginine supplementation improves insulin sensitivity and endothelial function in nonobese type 2 diabetic patients, the aim of this study was to evaluate the effects of a long-term oral L-arginine therapy on adipose fat mass (FM) and muscle free-fat mass (FFM) distribution, daily glucose levels, insulin sensitivity, endothelial function, oxidative stress, and adipokine release in obese type 2 diabetic patients with insulin resistance who were treated with a combined period of hypocaloric diet and exercise training. Thirty-three type 2 diabetic patients participated in a hypocaloric diet plus an exercise training program for 21 days. Furthermore, they were divided into two groups in randomized order: the first group was also treated with L-arginine (8.3 g/day), and the second group was treated with placebo. Although in the placebo group body weight, waist circumference, daily glucose profiles, fructosamine, insulin, and homeostasis model assessment index significantly decreased, L-arginine supplementation further decreased FM (P

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Just breaking my amino acid series to post something from an email i received today. I am subscribed to a website by Dr. Joseph Mercola, he sends out updates of current research and articles etc, alot of it is just advertising for his own supplement range, but there is quite alot of good information on there. I suggest anyone subscribe to it, go to www.mercola.com



Avoid Flu Shots With the One Vitamin that Will Stop Flu in Its Tracks


Another influenza season is beginning, and the U.S. Center for Disease Control and Prevention (CDC) will strongly urge Americans to get a flu shot. In fact, the CDC mounts a well-orchestrated campaign each season to generate interest and demand for flu shots.


But a recent study published in the October issue of the Archives of Pediatric & Adolescent Medicine found that vaccinating young children against the flu appeared to have no impact on flu-related hospitalizations or doctor visits during two recent flu seasons.


At first glance, the data did suggest that children between the ages of 6 months and 5 years derived some protection from vaccination in these years. But after adjusting for potentially relevant variables, the researchers concluded that "significant influenza vaccine effectiveness could not be demonstrated for any season, age, or setting" examined.


Additionally, a Group Health study found that flu shots do not protect elderly people against developing pneumonia -- the primary cause of death resulting as a complication of the flu. Others have questioned whether there is any mortality benefit with influenza vaccination. Vaccination coverage among the elderly increased from 15 percent in 1980 to 65 percent now, but there has been no decrease in deaths from influenza or pneumonia.


There is some evidence that flu shots cause Alzheimer’s disease, most likely as a result of combining mercury with aluminum and formaldehyde. Mercury in vaccines has also been implicated as a cause of autism.



Three other serious adverse reactions to the flu vaccine are joint inflammation and arthritis, anaphylactic shock (and other life-threatening allergic reactions), and Guillain-Barré syndrome, a paralytic autoimmune disease.


One credible hypothesis that explains the seasonal nature of flu is that influenza is a vitamin D deficiency disease.


Vitamin D levels in your blood fall to their lowest point during flu seasons. Unable to be protected by the body’s own antibiotics (antimicrobial peptides) that are released by vitamin D, a person with a low vitamin D blood level is more vulnerable to contracting colds, influenza, and other respiratory infections.


Studies show that children with rickets, a vitamin D-deficient skeletal disorder, suffer from frequent respiratory infections, and children exposed to sunlight are less likely to get a cold. The increased number of deaths that occur in winter, largely from pneumonia and cardiovascular diseases, are most likely due to vitamin D deficiency.


Unfortunately, now, for the first time, flu vaccination is also being pushed for virtually all children -- not just those under 5.


This is a huge change. Previously, flu vaccine was recommended only for youngsters under 5, who can become dangerously ill from influenza. This year, the government is recommending that children from age 6 months to 18 years be vaccinated, expanding inoculations to 30 million more school-age children.


The government argues that while older children seldom get as sick as the younger ones, it's a bigger population that catches flu at higher rates, so the change should cut missed school, and parents' missed work when they catch the illness from their children.


Of course, this policy ignores the fact that a systematic review of 51 studies involving 260,000 children age 6 to 23 months found no evidence that the flu vaccine is any more effective than a placebo.



LewRockwell.com October 3, 2008

EMS Responder September 9, 2008

WebMD October 6, 2008

Archives of Pediatric and Adolescent Medicine October 2008; 162(10):943-51


Mercola's Comments


Back in 2005, The Federal Advisory Committee on Immunization Practices (ACIP) recommended that all children between 6 months and 5 years old receive flu shots each year. Now they have expanded their guidelines to include children up to 18 years, which means everyone except those between the ages of 19-49, who are in good health, are urged to get a flu shot.


It should come as no surprise to find out that a majority of the ACIP members who came up with these guidelines have financial ties to the vaccine industry, and stand to gain personally for every additional person getting a yearly injection. It’s actually the only explanation that makes any sense for recommendations as insane as these.


Three Reasons to Reconsider Flu Shots


There are three major reasons why this government push to vaccinate 84 percent of the U.S. population with a yearly flu vaccine is so incomprehensible:


1. The majority of flu shots contain 25 micrograms of mercury; an amount considered unsafe for anyone weighing less than 550 pounds! And which groups are most sensitive to the neurological damage that has been associated with mercury? Infants, children, and the elderly.


2. No studies have conclusively proven that flu shots prevent flu-related deaths among the elderly, yet this is one of the key groups to which they’re pushed.


3. If you get a flu shot, you can still get the flu (or flu-like symptoms). This is because it only protects against certain strains, and it’s anyone’s guess which flu viruses will be in your area.


So why would you take a flu shot – EVERY YEAR -- that has NEVER been proven to be effective, that can give you the very illness you’re trying to prevent, and has potential long-term side effects that are far worse than the flu itself?


The powers that be have done an excellent job of instilling fear into the population so they believe that they must get a shot to stay healthy, but the simple reality is it’s doing you more harm than good.


And, even if the flu vaccine could effectively prevent the flu, there have been several examples in past years where government health officials have chosen the incorrect influenza strains for that year’s vaccine. In 2004, the National Vaccine Information Center described how CDC officials told everyone to line up for a flu shot that didn't even contain the influenza strain causing most of the flu that year.


Two-Thirds of This Year’s Flu Vaccines Contain a Full-Dose of Mercury


According to Dr. Donald Miller, MD, two-thirds of this year’s flu vaccines contain 25 micrograms of thimerosal. Thimerosal is 49 percent mercury by weight.


Each dose of these flu vaccines contains more than 250 times the Environmental Protection Agency’s safety limit for mercury.


By now, most people are well aware that children and fetuses are most at risk of damage from this neurotoxin, as their brains are still developing. Yet the CDC still recommends that children over 6 months, and pregnant women, receive the flu vaccine each year.


In addition to mercury, flu vaccines also contain other toxic or hazardous ingredients like:


Formaldehyde -- a known cancer-causing agent

Aluminum -- a neurotoxin that has been linked to Alzheimer’s disease

Triton X-100 -- a detergent

Phenol (carbolic acid)

Ethylene glycol (antifreeze)

Various antibiotics: neomycin, streptomycin, gentamicin – which can cause allergic reactions in some people

The Evidence Against Flu Vaccines


For those of you who are still unconvinced, know that there’s plenty of scientific evidence available to back up the recommendation to avoid flu vaccines – if nothing else, then for the simple reason that they don’t work, and don’t offer any real benefit to offset their inherent health risks. For example:


A brand new study published in the October issue of the Archives of Pediatric & Adolescent Medicine found that vaccinating young children against the flu had no impact on flu-related hospitalizations or doctor visits during two recent flu seasons. The researchers concluded that "significant influenza vaccine effectiveness could not be demonstrated for any season, age, or setting" examined.



A study published in the Lancet just two months ago found that influenza vaccination was NOT associated with a reduced risk of pneumonia in older people. This supports a study done five years ago, published in The New England Journal of Medicine.



Research published in the American Journal of Respiratory and Critical Care Medicine last month also confirms that there has been no decrease in deaths from influenza and pneumonia, despite the fact that vaccination coverage among the elderly has increased from 15 percent in 1980 to 65 percent now.



Last year, researchers with the National Institute of Allergy and Infectious Diseases, and the National Institutes of Health published this conclusion in the Lancet Infectious Diseases: “We conclude that frailty selection bias and use of non-specific endpoints such as all-cause mortality have led cohort studies to greatly exaggerate vaccine benefits.”



A large-scale, systematic review of 51 studies, published in the Cochrane Database of Systematic Reviews in 2006, found no evidence that the flu vaccine is any more effective than a placebo in children. The studies involved 260,000 children, age 6 to 23 months.

Might Influenza be Little More Than a Symptom of Vitamin D Deficiency?


Vitamin D, “the sunshine vitamin,” may very well be one of the most beneficial vitamins there is for disease prevention. Unfortunately it’s also one of the vitamins that a vast majority of people across the world are deficient in due to lack of regular exposure to sunshine.


Published in the journal Epidemiology and Infection in 2006, the hypothesis presented by Dr. John Cannell and colleagues in the paper Epidemic Influenza and Vitamin D actually makes a lot of sense.


They raise the possibility that influenza is a symptom of vitamin D deficiency!


The vitamin D formed when your skin is exposed to sunlight regulates the expression of more than 2,000 genes throughout your body, including ones that influence your immune system to attack and destroy bacteria and viruses. Hence, being overwhelmed by the “flu bug” could signal that your vitamin D levels are too low, allowing the flu virus to overtake your immune system.


How to Prepare For Flu Season Without Getting a Flu Shot


I often find that some of the simplest explanations are the truest, and this sounds about as simple as it gets. And, getting appropriate amounts of sunshine (or taking a vitamin D supplement when you can’t get healthy amounts of sun exposure) is one of my KEY preventive strategies against the cold and flu, as it has such a strengthening effect on your immune system.


Interestingly, last week the American Academy of Pediatrics doubled its recommended dose of vitamin D. Unfortunately this is still a woefully inadequate recommendation as the dose should be TEN times larger. Rather than going from 200 to 400 units per day, it should have increased to about 2,000 units per day.


For most of you reading this it is “vitamin D winter,” which means there simply isn’t enough sunshine to make significant amounts of vitamin D, so you will need to use a tanning bed or take oral supplements.


Although supplements are clearly inferior to sunlight or safe tanning beds, I am becoming more convinced of the value of vitamin D supplements as they are less potentially toxic than my initial impression, and they are certainly more convenient and less expensive than a tanning bed.


For those in the winter with no or very limited exposure to sunshine, 4,000-5,000 units per day would seem appropriate for most adults. If you are very heavy you may need to double that dose, and for children the dose can be half that.


The key though is to make sure you monitor your vitamin D levels by blood testing, to make sure your levels are therapeutic and not toxic.


I advocate getting your vitamin D levels tested regularly, but as I reported recently, you now need to beware of where you’re getting your test done. For an in-depth explanation of what you MUST know before you get tested, please read my updated article Test Values and Treatment for Vitamin D Deficiency.


You can also use vitamin D therapeutically to TREAT the flu. But please understand that if you are taking the above doses of vitamin D the odds of you getting the flu are VERY remote. The dose of vitamin D you can use would be 2,000 units per kilogram of body weight (one pound is 0.45 kg). The dose would be taken once a day for three days.


This could be a very large dose if you were very heavy (2-300,000 units per day) This is the dose that Dr. John Cannell, founder of the Vitamin D Council, has been using very successfully for a number of years.


I have not received a flu shot nor had the flu in over 20 years. Here are the other “secrets” I use to keep the flu (and other illnesses) at bay:


Eat right for your nutritional type, including avoiding sugar

Eliminate sugar from your diet

Eat garlic regularly

Consume a high-quality krill oil daily


Get adequate sleep

Address emotional stress

Wash your hands regularly (but not excessively)

Another useful supplement you could try, should you come down with a case of the flu, is olive leaf extract, which you can find in most any health food store.


Olive leaf extract has been found to be a potent broad-spectrum antiviral agent, active against all viruses tested, including numerous strains of influenza and para-influenza viruses.




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I had a request for information on Creatine, so here it is. unbiased information on creatine. I wont suggest whether people should or shouldn't take it, ill give you the info and you make up your own minds. fair enough.....




(Alpha-methyl guanidino acetic acid)


Creatine is synthesised in the kidney, liver and pancreas from three different amino acids: arginine, glycine and methionine. It is converted into creatinine before elimination by the kidneys.



Muscle meats


Factors increasing demand:

Cardiac Surgery, high intensity exercise, vegetarian diets.


Target organs:

Skeletal muscle, cardiac tissue, smooth muscle, brain, kidney, sperm.


Daily dosage:

SR 1/5g

Acute loading for sport: 20g for two days, or 5g for 5 days in divided doses.

Note: About 1-2g of creatine are biosynthesised daily and another 1-2g are obtained from diet.

Creatine is contraindicated in those with renal failure or renal disorders such as nephrotic syndrome.


Synergistic nutrients:

Arginine, glycine, methionine, leucine, chromium, carbohydrate loading.


Side effects:

Weight gain, cramps, dehydration, diarrhoea, dizziness.


Functions facilitated:

Attenuates corticosteroid induced muscle wasting, improves bioenergetics of heart muscle, improves muscle protein synthesis, improves working memory and general intelligence, improves mitochondrial bioenergetics, improves neurological protection against ischaemia and oxidant insult, improves training capacity, reduces muscle lactate during exercise.


Precursor of phosphocreatine - a hgih energy intermediate.

-Phosphocreatine inhibits enzymes in the glycolytic pathway, including: glyceraldehyde-3-phosphate dehydrogenase, phosphofructo-kinase and pyruvate kinase.


Twelve weeks of resistance training combined with creatine supplemetation increases muscle fibre diameter by 35% in both type 1 and type 2 muscle fibres in men versus 6-15% in placebo supplemenation resistance trained subjects.



Effect of creatine supplementation and resistance-exercise training on muscle insulin-like growth factor in young adults.

Burke DG, Candow DG, Chilibeck PD, MacNeil LG, Roy BD, Tarnopolsky MA, Ziegenfuss T.

Department of Human Kinetics, St. Francis Xavier University, Antigonish, NS, Canada.


The purpose of this study was to compare changes in muscle insulin-like growth factor-I (IGF-I) content resulting from resistance-exercise training (RET) and creatine supplementation (CR). Male (n=24) and female (n=18) participants with minimal resistance-exercise-training experience (=1 year) who were participating in at least 30 min of structured physical activity (i.e., walking, jogging, cycling) 3-5 x/wk volunteered for the study. Participants were randomly assigned in blocks (gender) to supplement with creatine (CR: 0.25 g/kg lean-tissue mass for 7 days; 0.06 g/kg lean-tissue mass for 49 days; n=22, 12 males, 10 female) or isocaloric placebo (PL: n=20, 12 male, 8 female) and engage in a whole-body RET program for 8 wk. Eighteen participants were classified as vegetarian (lacto-ovo or vegan; CR: 5 male, 5 female; PL: 3 male, 5 female). Muscle biopsies (vastus lateralis) were taken before and after the intervention and analyzed for IGF-I using standard immunohistochemical procedures. Stained muscle cross-sections were examined microscopically and IGF-I content quantified using image-analysis software. Results showed that RET increased intramuscular IGF-I content by 67%, with greater accumulation from CR (+78%) than PL (+54%; p=.06). There were no differences in IGF-I between vegetarians and nonvegetarians. These findings indicate that creatine supplementation during resistance-exercise training increases intramuscular IGF-I concentration in healthy men and women, independent of habitual dietary routine.


PMID: 18708688 [PubMed - in process



Low-Dose Creatine Combined with Protein during Resistance Training in Older Men.

Candow DG, Little JP, Chilibeck PD, Abeysekara S, Zello GA, Kazachkov M, Cornish SM, Yu PH.

1Faculty of Kinesiology and Health Studies, University of Regina, Regina, Saskatchewan, CANADA; and 2College of Kinesiology,3College of Pharmacy and Nutrition, and 4Department of Psychiatry, Neuropsychiatry Research Unit, University of Saskatchewan, Saskatoon, Saskatchewan, CANADA.


PURPOSE:: To determine whether low-dose creatine and protein supplementation during resistance training (RT; 3 d.wk; 10 wk) in older men (59-77 yr) is effective for improving strength and muscle mass without producing potentially cytotoxic metabolites (formaldehyde). METHODS:: Older men were randomized (double-blind) to receive 0.1 g.kg creatine + 0.3 g.kg protein (CP; n = 10), creatine (C; n = 13), or placebo (PLA; n = 12) on training days. Measurements before and after RT included lean tissue mass (air-displacement plethysmography), muscle thickness (ultrasound) of elbow, knee, and ankle flexors and extensors, leg andbench press strength, and urinary indicators of cytotoxicity (formaldehyde), myofibrillar protein degradation [3-methylhistidine (3-MH)],and bone resorption [cross-linked N-telopeptides of type I collagen (NTx)]. RESULTS:: Subjects in C and CP groups combined experienced greater increases in body mass and total muscle thickness than PLA (P


PMID: 18685526 [PubMed - as supplied by publisher]



Ergogenic effects of creatine in sports and rehabilitation.

Hespel P, Derave W.

Research Center for Exercise and Health, Faculty of Kinesiology and Rehabilitation Sciences, K.U. Leuven, Leuven, Belgium.


The daily oral ingestion of supplementary creatine monohydrate can substantially elevate the creatine content of human skeletal muscle. This chapter aims to summarize the current knowledge regarding the impact muscle creatine loading can have on exercise performance and rehabilitation. The major part of the elevation of muscle creatine content is already obtained after one week of supplementation, and the response can be further enhanced by a concomitant exercise or insulin stimulus. The elevated muscle creatine content moderately improves contractile performance in sports with repeated high-intensity exercise bouts. More chronic ergogenic effects of creatine are to be expected when combined with several weeks of training. A more pronounced muscle hypertrophy and a faster recovery from atrophy have been demonstrated in humans involved in resistance training. The mechanism behind this anabolic effect of creatine may relate to satellite cell proliferation, myogenic transcription factors and insulin-like growth factor-1 signalling. An additional effect of creatine supplementation, mostly when combined with training, is enhanced muscle glycogen accumulation and glucose transporter (GLUT4) expression. Thus, creatine may also be beneficial in sport competition and training characterized by daily glycogen depletion, as well as provide therapeutic value in the insulin-resistant state.


PMID: 18652080 [PubMed - indexed for MEDLINE]




The regulation and expression of the creatine transporter: a brief review of creatine supplementation in humans and animals.

Schoch RD, Willoughby D, Greenwood M.

Exercise and Biochemical Nutrition Laboratory, Baylor University, Waco, TX. Ryan_Schoch@baylor.edu.


ABSTRACT : Creatine monohydrate has become one of the most popular ergogenic sport supplements used today. It is a nonessential dietary compound that is both endogenously synthesized and naturally ingested through diet. Creatine ingested through supplementation has been observed to be absorbed into the muscle exclusively by means of a creatine transporter, CreaT1. The major rationale of creatine supplementation is to maximize the increase within the intracellular pool of total creatine (creatine + phosphocreatine). There is much evidence indicating that creatine supplementation can improve athletic performance and cellular bioenergetics, although variability does exist. It is hypothesized that this variability is due to the process that controls both the influx and efflux of creatine across the cell membrane, and is likely due to a decrease in activity of the creatine transporter from various compounding factors. Furthermore, additional data suggests that an individual's initial biological profile may partially determine the efficacy of a creatine supplementation protocol. This brief review will examine both animal and human research in relation to the regulation and expression of the creatine transporter (CreaT). The current literature is very preliminary in regards to examining how creatine supplementation affects CreaT expression while concomitantly following a resistance training regimen. In conclusion, it is prudent that future research begin to examine CreaT expression due to creatine supplementation in humans in much the same way as in animal models.


PMID: 18500965 [PubMed - in process]

PMCID: PMC2129152




Effect of a pre-exercise energy supplement on the acute hormonal response to resistance exercise.

Hoffman JR, Ratamess NA, Ross R, Shanklin M, Kang J, Faigenbaum AD.

Department of Health and Exercise Science, College of New Jersey, Ewing, New Jersey, USA. hoffmanj@tcnj.edu


The effect of a pre-exercise energy sport drink on the acute hormonal response to resistance exercise was examined in eight experienced resistance trained men. Subjects were randomly provided either a placebo (P: maltodextrin) or the supplement (S: combination of branched chain amino acids, creatine, taurine, caffeine, and glucuronolactone). Subjects performed 6 sets of no more than 10 repetitions of the squat exercise at 75% of their 1 repetition maximum (1RM) with 2 minutes of rest between sets. Blood draws occurred at baseline pre-exercise, immediately post- (IP), 15 minutes post- (15P), and 30-minutes post (30P) exercise for measurement of serum growth hormone, total and free testosterone, cortisol, and insulin concentrations. Although significant differences were seen only at set 5, the total number of repetitions and training volume tended (p = 0.08) to be higher with S compared to P. Serum growth hormone and insulin concentrations were significantly higher at 15P and IP, respectively, in S compared to P. Results suggest that a pre-exercise energy S consumed 10 minutes before resistance exercise can enhance acute exercise performance by increasing the number of repetitions performed and the total volume of exercise. The enhanced exercise performance resulted in a significantly greater increase in both growth hormone and insulin concentrations, indicating an augmented anabolic hormone response to this pre-exercise S.


PMID: 18438227 [PubMed - indexed for MEDLINE]




Randomized controlled trial of dietary creatine as an adjunct therapy to physical training in chronic obstructive pulmonary disease.

Deacon SJ, Vincent EE, Greenhaff PL, Fox J, Steiner MC, Singh SJ, Morgan MD.

Institute for Lung Health, Department of Respiratory Medicine, Allergy and Thoracic Surgery, University Hospitals of Leicester NHS Trust, Glenfield Hospital, Leicester LE39QP, UK. sarah.deacon@uhl-tr.nhs.uk


RATIONALE: Skeletal muscle strength and bulk are reduced in patients with chronic obstructive pulmonary disease (COPD) and influence quality of life, survival, and utilization of health care resources. Exercise training during pulmonary rehabilitation (PR) can reverse some of these effects. In athletes and healthy elderly individuals, dietary creatine supplementation (CrS) has been shown to augment high-intensity exercise training, thereby increasing muscle mass. OBJECTIVES: This article examines the effect of CrS on functional exercise capacity and muscle performance in people with COPD. METHODS: One hundred subjects with COPD (mean [sD] age, 68.2 [8.2] yr; FEV(1), 44.0 [19.6] %predicted) were randomized to a double-blind, placebo-controlled, parallel group trial of CrS during 7 weeks of PR encompassing aerobic and resistance exercises. Subjects ingested creatine (22 g/d loading for 5 d; maintenance, 3.76 g/d throughout PR) or placebo. Baseline, postloading, and postrehabilitation measurements included pulmonary function, body composition, peripheral muscle strength, and functional performance (shuttle walking tests). A volunteer subgroup (n = 44) had pre- and postloading quadriceps muscle biopsies. MEASUREMENTS AND MAIN RESULTS: Eighty subjects completed the trial (38 creatine, 42 placebo). All outcome measures significantly improved after PR. There were no significant differences between groups post-PR (mean [sD] change in incremental shuttle walk distance, 84 [79] m in the creatine group vs. 83.8 [60] m in the placebo group; P = 1.0; knee extensor work, 19.2 [16] Nm [Newton meters] in the creatine group vs. 19.5 [17] Nm in the placebo group; P = 0.9). Muscle biopsies showed evidence of creatine uptake. CONCLUSIONS: This adequately powered, randomized, placebo-controlled trial shows that CrS does not augment the substantial training effect of multidisciplinary PR for patients with COPD. Clinical trial registered with https://portal.nihr.ac.uk/Pages/NRRArchiveSearch.aspx (NO123138126).


PMID: 18420964 [PubMed - indexed for MEDLINE]




The potential benefits of creatine and conjugated linoleic acid as adjuncts to resistance training in older adults.

Tarnopolsky MA, Safdar A.

Department of Pediatrics and Medicine, McMaster University, HSC-2H26, 1200 Main St. W., Hamilton, ON L8N 3Z5, Canada. tarnopol@mcmaster.ca


Human aging is associated with a significant reduction in muscle mass (sarcopenia) resulting in muscle weakness and functional limitations in the elderly. Sarcopenia has been associated with mitochondrial dysfunction and the accumulation of mtDNA deletions. Resistance training increases muscle strength and size and can increase mitochondrial capacity and decrease oxidative stress in older adults. Creatine monohydrate (CrM) and conjugated linoleic acid (CLA) have biological effects that could enhance some of the beneficial effects of resistance training in older adults (i.e., up arrow fat-free mass, down arrow total body fat). We have completed two resistance-training studies with CrM alone and CrM+CLA supplementation in older adults to evaluate the independent effects of exercise and dietary supplements, as well as their interactive effects. Our studies, and several others, have found that CrM enhanced the resistance exercise mediated gains in fat-free mass and strength. More recently, we found that the addition of CLA also lead to a significant reduction of body fat after six months of resistance training in older adults. Older adults have fewer wild-type mtDNA copies and higher amounts of mtDNA deletions as compared with younger adults in mature skeletal muscle; however, these deletions are not seen in the satellite cell-derived myoblast cultures. These findings, and the fact that mtDNA deletions are lower and wild-type mtDNA copy number is higher after resistance training in older adults, suggests that activation of satellite cells secondary to resistance exercise-induced muscle damage can dilute or "shift" the proportion of mtDNA genotype towards that of a younger adult. Recent evidence suggests that CrM supplementation in combination with strength training can enhance satellite cell activation and total myonuclei number per muscle fiber in young men. Future studies are required to determine whether the mitochondrial adaptations to resistance exercise in older adults are further enhanced with CrM supplementation and whether this is due to increased recruitment of satellite cells. It will also be important to determine whether these changes are maintained over a longer time period.


PMID: 18347674 [PubMed - indexed for MEDLINE]





Timing of creatine or protein supplementation and resistance training in the elderly.

Candow DG, Chilibeck PD.

Faculty of Kinesiology and Health Studies, University of Regina, Regina, SK S4S 0A2. darren.candow@uregina.ca


Muscle loss with age has a negative effect on strength and functional independence. Age-related loss of muscle is the result of decreased muscle fiber number and size, which are functions of altered hormonal status, physical inactivity, and variations in nutritional intake. Resistance training has a positive effect on muscle mass and strength in the elderly. Studies of protein or creatine supplementation for increasing muscle mass and strength in older individuals are equivocal. The timing of nutritional supplementation may be more important than the absolute daily intake of supplements. Protein or creatine ingestion proximate to resistance-training sessions may be more beneficial for increasing muscle mass and strength than ingestion of protein or creatine at other times of the day, possibly because of increased blood flow and therefore increased transport of amino acids and creatine to skeletal muscle.


PMID: 18347671 [PubMed - indexed for MEDLINE]





The Effects of Creatine and Whey Protein Supplementation on Body Composition in Men Aged 48 to 72 Years during Resistance Training.

Eliot KA, Knehans AW, Bemben DA, Witten MS, Carter J, Bemben MG.

A.W. Knehans, Department of Nutritional Sciences, University of Oklahoma Health Sciences Center, Box 26901, Oklahoma City, Oklahoma 73190, Phone: (405) 271-2113, E-mail: allen-knehans@ouhsc.edu.


Objectives: Creatine and whey protein are supplements believed to have an ergogenic effect. Very little is known regarding the effects of these dietary supplements in older men. The purpose of this study was to determine the effect of creatine and whey protein supplements, consumed independently and in combination, on total and regional body composition in middle-aged men during a resistance-training program. Design, Setting, Participants: Forty-two men were randomly assigned to four groups to receive supplements according to a double-blind protocol. Groups consumed their supplements three times per week immediately following their resistance training sessions. The groups were: 1) placebo (480 ml of Gatorade); 2) creatine (480 ml of Gatorade plus 5 grams of creatine); 3) whey protein (480 ml of Gatorade plus 35 grams of whey protein powder); and 4) whey protein/creatine (480 ml of Gatorade plus 5 grams of creatine and 35 grams of whey protein powder). All groups participated in resistance training 3 times per week for 14 weeks. Measurements: At the beginning and end of the study, total and regional measures of body composition (DXA) and total (TBW), intracellular (ICW), and extracellular (ECW) body water (Multifrequency BIA) were measured and 3-day diet records were completed. Results: There were significant training effects for regional arm fat (decrease), regional arm bone free-fat free mass (BF-FFM - increase), total body BF-FFM (increase), ICW (increase), and ECW (increase) but no significant group effects and only one significant group by training interaction (ECW). There were no significant changes for total calorie, carbohydrate, fat or protein intake for any of the groups from prestudy to post-study testing. Conclusion: The results from this study suggest that supplementation with creatine, whey protein, or a combination of creatine and whey protein, when combined with resistance training in middleaged men, have no added benefit to changes that occur to body composition due to resistance training alone.


PMID: 18309444 [PubMed - in process]




Creatine supplementation does not reduce muscle damage or enhance recovery from resistance exercise.

Rawson ES, Conti MP, Miles MP.

Department of Exercise Science and Athletics, Bloomsburg University, Bloomsburg, Pennsylvania 17815, USA. erawson@bloomu.edu


Previous studies have shown that creatine supplementation reduces muscle damage and inflammation following running but not following high-force, eccentric exercise. Although the mechanical strain placed on muscle fibers during high-force, eccentric exercise may be too overwhelming for creatine to exert any protective effect, creatine supplementation may protect skeletal muscle stressed by a resistance training challenge that is more hypoxic in nature. The purpose of this study was to examine the effects of short-term creatine supplementation on markers of muscle damage (i.e., strength, range of motion, muscle soreness, muscle serum protein activity, C-reactive protein) to determine whether creatine supplementation offers protective effects on skeletal muscle following a hypoxic resistance exercise test. Twenty-two healthy, weight-trained men (19-27 years) ingested either creatine or a placebo for 10 days. Following 5 days of supplementation, subjects performed a squat exercise protocol (5 sets of 15-20 repetitions at 50% of 1 repetition maximum [1RM]). Assessments of creatine kinase (CK) and lactate dehydrogenase activity, high-sensitivity C-reactive protein, maximal strength, range of motion (ROM), and muscle soreness (SOR) with movement and palpation were conducted pre-exercise and during a 5-day follow up. Following the exercise test, maximal strength and ROM decreased, whereas SOR and CK increased. Creatine and placebo-supplemented subjects experienced significant decreases in maximal strength (creatine: 13.4 kg, placebo: 17.5 kg) and ROM (creatine: 2.4 degrees , placebo: 3.0 degrees ) immediately postexercise, with no difference between groups. Following the exercise test, there were significant increases in SOR with movement and palpation (p


PMID: 18076246 [PubMed - in process]

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Thanks for that info Houghy. Just a quick question though, what sort of percentage of serious lifters use creatine? Is it commonly used, or more often by the man-on-the-street?

I used it years ago with my brother, but I ditched as I wasn't willing to give up coffee.


BTW went into VitaminMe on Elizabeth St yesterday for protein and the guy serving there was a BIG boy. Someone on here (Simon?) works at the Chaddy store, wonder if he knows this bloke.

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I dont follow the diets/supplementation of the more well known or pro lifters mate so im not really sure sorry. Maybe Simon could answer both questions for ya, hes right into that scene, and yeah he works at the chadstone store so he might know who it is.


though i doubt it, the dumb *milkshake* had me walking up and down elizabeth street tryin to find that shop when we were at bourke street mall cause he knew there was one around. we literally did 5 laps of elizabeth st looking for it before we called sensis and asked the number :lol: turned out it was on the other side of bourke st towards flinders, who woulda thought.

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I have always had positive effects from creatine. However after the loading phase the effects seem to taper off so i never stay on it for very long. I think I'll try some high dose creatine use (over a 6-8 week period) soon and post up how it goes.

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interesting creatine info. what do you conclude from those studies?


i conclude its probably much of a muchness mate.


there seems to be alot of mixed press on creatine, having never taken it myself id have to say the jury is still out.


however, what nick said about the effects AFTER the loading phase seems to be the common consensus.

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Hi Houghy would you be able to recommend a good value for money multivitamin and fish oil that i can get over the counter?


I went looking for the ones you listed, on vitaminme.com and couldnt find any, i assume they are part of the practioner range

if possible i would prefer not to have to go see someone everytime i want vitamins/fish oil lol


Cheers for any help

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fusion do a really good off the shelf multivitamin

blackmores have quite a good high strength fish oil, i think its called omega joint care or something like that, contains around 500mg of EPA and is steam processed to reduce reflux and odour and for purification.



also, good news for anyone looking at buying coenzyme q10. prices SHOULD be dropping substantially.

i was speaking to a friend who is a rep for Blackmores practitioner range and she mentioned a few studies done recently that will change the price of co q10.

originally there were 2 ways of sourcing coq10 in mass quantities and that was through either tobacco or yeast. the cheaper companies usually used the tobacco and yeast was considered the superior form. however, some recent studies have shown no change in efficacy between the two. being that tobacco is a much cheaper alternative, alot of companies will most probably be shifting towards this for their production (dont quote me on this, this is just the information i was given, but thats good news if it goes ahead as coq10 prices have always been what let it down)

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a recent pilot study found that a enhanced form of CoQ10 resulted in higher muscle CoQ10 concentration, lower serum SOD (a marker of cellular antioxidant damage) and higher MDA (a marker of lipid peroxidation) levels during and following exercise.


What the? So this better form of CoQ10 lowered Super Oxide Dismutase and increased lipid peroxidation. And the author is sayingthat is beneficial? LOL


SOD is not a marker of Cellular antioxidant damage is IS your bodies primary antioxidant against Super Oxide which is a natural by-product of ATP generation in the mitocondria.

Any decrease in SOD will also increase lipid peroxidation as Super Oxide is a pre cursor to peroxynitrite... so that makes sense but actually shows that this CoQ10 may be worse.


LOL im keen to read that study.

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Herbs and Nutrients to promote healthy joints


The holistic approach to maintaining joint health will involve dietary, supplemental and other lifestyle interventions such as corrective exercises. The use of appropriate herbs and nutrients should focus on:

• Providing the key building blocks to protect and regenerate the joint tissue

• Reducing inflammation of the joint tissue

• Providing complementary antioxidant support to the joint specifically and the body as a whole

Protecting and Repairing Joint Tissue

The cartilage between joints acts as a natural shock absorber and maintains lubrication of the joint surfaces, thereby protecting bones and tissues from the impact associated with movement. In particular, the degeneration of this cartilage and bone surface can result in crippling osteoarthritic pain typified by the pain of localised inflammation, damaged joint tissue and reduced mobility.1

Of particular importance in repairing and maintaining health of the specialised components of the joint, are GAGs (glycosaminoglycans). These are long, unbranched molecules of repeating pairs of sugar units. GAGs play a critical role in both the structure of the cartilage itself and their presence in the matrix of the joint cavity is testament to their highly viscous nature, which makes them ideal as lubricating agents that aid proper joint mobility. Anage-related reduction in GAG content typically occurs inosteoarthritic degeneration of the cartilage and joint matrix.2



Glucosamine is an amino sugar that is crucial for the construction of GAGs that are responsible for maintaining the structure and integrity of the articular cartilage in joints. Supplemental glucosamine is seen as one of the primary treatments of choice for relieving the pain of osteoarthritis for its multifaceted ability to maintain healthy joint structure and function.

• Provides the structural building blocks to aid GAG homeostasis within the joint

• Stimulates the body’s own synthesis of GAGs and proteoglycans in the cartilage matrix

• Inhibits certain enzymes that are associated with breakdown of cartilage

• Aids in reducing joint inflammation, thereby helping ease the pain of osteoarthritis

Clinical evidence suggests that glucosamine helps benefitpeople with arthritic pain of the hip or knee by maintainingthe joint space and may help rebuild damaged cartilage.2 This compares favourably with other forms of treatment suchas the use of Non Steroidal Anti Inflammatory Drugs (NSAIDs),which generally only favour reducing joint inflammation, but have no role in maintaining or rebuilding joint structure.3


Salts of glucosamine hydrochloride (GH) and glucosamine sulphate (S-GS) are the primary supplementary forms of glucosamine.

• Glucosamine is the active component

• Both GH and S-GS are fully ionised when digested in the stomach and therefore absorbed via similar mechanisms

• GH is the starting material from which S-GS is manufactured

• GH is approximately 83 per cent active glucosamine; S-GS is approximately 58 per cent active glucosamine

• In a tablet with limited space for active glucosamine and other active constituents, the tablet containing GH will offer a higher amount glucosamine than the S-GS form

Therapeutic Dose: Glucosamine taken at 500 mgthree times daily is regarded as an effective therapeutic dose.4

Potential Drug-Nutrient Interactions: No regulatory restrictions apply to glucosamine. However, it is important to consider that there is some evidence glucosamine may potentiate the INR value in susceptible individuals undergoing concomitant treatment with warfarin. Until further research clarifies the extent of this interaction, glucosamine should be closely monitored in patients on warfarin therapy.

clinical information for practitioners

Protecting the health of weight bearing joints is a primary goal in any healthy ageing program. The causes of degeneration of these joints and resulting osteoarthritic pain can be multifactorial and include secondary to injury, repetitive joint use, or conditions such as obesity. The main issue to remember is maintaining healthy joints can be achieved and any degeneration of the joints needs to be addressed at the earliest symptoms.


Chondroitin Sulfates

Chondroitin sulfates (CS) are a class of GAGs and as such, play a major role in providing the structural components of articular cartilage. Oral CS may aid in the stimulation of the production of cartilage by:

• Increasing GAG concentration

• Increasing synovial fluid viscosity

• Reducing the activity of enzymes involved in the breakdown of cartilage3

Other synergistic actions of CS relate to its suspected antioxidant capability in inhibiting the detrimental effect ofreactive oxygen species that degrade joint cartilage andcollagen (see antioxidant minerals section below). It improvesblood circulation to joints, which enables antioxidants and glucosamine to enter inflamed joints to stimulate the repair process. Although the intestinal absorption of CS is much lower than that of glucosamine (10 – 15 per cent versus90 – 98 per cent), some studies have shown very good results (in reducing pain and increasing range of motion) from long-term treatment with CS.

Therapeutic Dose: Studies on CS suggest typical therapeutic dose is in the range of 800 – 1,200 mg per day. Oral CS at such doses have been shown to be superior to placebo in the temporary reduction of osteoarthritic pain of the knees, as measured by a reduction in pain, walking time, pain medication use and joint mobility.5-7


Reducing Inflammation of the Joint Tissue

Devil’s Claw (Harpagophytum procumbens): This southern African desert herb has been traditionally used as a therapy for treating various conditions including fever, malaria and indigestion. The key constituents of Devil’s Claw root are the iridoid glycosides, with harpagoside being the primary active of medical interest.

Currently, the major uses of Devil’s Claw revolve around its anti-inflammatory and pain relieving properties, especially for joint conditions, back pain and headache. There is good scientific evidence supporting the use of Devil’s Claw for the short-term treatment of pain related to degenerative joint disease or osteoarthritis (8 – 12 weeks). As with glucosamine, use of Devil’s Claw may be equally effective as drug therapies such as NSAIDs, or may allow for reduced dosing of NSAIDs when used concomitantly.

Several double-blind clinical trials have been conducted for osteoarthritis or rheumatic problems of the hip or knee using various preparations of Devil’s Claw. Compared toplacebo, Devil’s Claw reduced the intensity of pain, increasedspinal mobility and was accompanied by reducing dosages of ibuprofen. Devil’s Claw was as effective or slightly better than phenylbutazone in improving pain relief, and as effective as the slow-acting analgesic, diacerein in improving spontaneous pain and mobility. The dosage of Devil’s Claw provided 30 – 60 mg/day of iridoid glycosides, usually standardised to harpagoside. Treatment ranged from 4 – 20 weeks. Devil’s Claw is well tolerated with mild gastrointestinal disturbance occurring as rare adverse events. It may be advisable to avoid the use of Devil’s Claw in those with gastric and duodenal ulcer.8,9


Bromelain and Rutin: Bromelain is typically established as a digestive supplement for its proteolytic enzymes and thereby as a support for enhancing digestive function. However, an alternative therapeutic application of bromelainis in the reduction of systemic inflammation, particularly with attention to relieving the pain of osteoarthritis.10 Several preliminary studies suggest that when taken orally, bromelain can reduce inflammation or pain caused by inflammation. Research into this anti-inflammatory action compares bromelain favourably against established NSAIDs. A therapeutic anti-inflammatory dose for bromelainis believed to be 200 – 400 mg daily, however it does offer a synergistic anti-inflammatory action at lower doses.

Rutin is a member of the bioflavonoid family of phytonutrientsand offers complementary antioxidant and anti-inflammatoryaction. Flavonoids in general may have a direct anti-inflammatory action by decreasing adhesion of inflammatorycells to endothelial cells, reducing peroxidise release and by inhibiting the metabolism of arachidonic acid, one of the initiating fatty acids of a general inflammatory response.11


Complementary Antioxidant Support

Antioxidant Minerals: Oxidative stress is considered as a major contributor to the development of pain, inflammation and degradation of cartilage tissue associated with osteoarthritis.12 Evidence links a significant reduction in humancartilage in patients with osteoarthritis and a reduction in oneof the body’s primary antioxidants, superoxide dismutase.13 Antioxidant minerals include zinc, manganese, copper and selenium. Though not antioxidants in themselves, these minerals help comprise antioxidant enzymes, including superoxide dismutase and the consequent reduction in damage caused by reactive oxygen species can aid and promote healthy joint function.



Osteoarthritic pain is not a condition that needs to be considered as a normal part of ageing. It can effectively be managed with the correct use of nutritional and herbal intervention, however this course of action needs to be initiated as early as possible when symptoms first arise. Justas the cause of osteoarthritic pain may be multifactorial inits cause, the use of therapeutic nutrients and herbs shouldalso be multifaceted. Nutrients that support the maintenanceand rebuilding of joint cartilage and associated tissue includeglucosamine and chondroitin sulfate. To complement these, include an anti-inflammatory focus provided by an effectiveherb such as Devil’s Claw and synergistic phytonutrientsincluding bromelain and rutin. Finally, antioxidant nutrients provide the third component of maintaining joint health byhelping control damage caused by reactive oxygen species.



1 Goldring MB, Goldring SR. J Cell Physiol 2007; 213(3): 626-34

2 Matheson AJ, Perry CM. Drugs Aging 2003; 20(14): 1041-60

3 Thie NM, Prasad NG, Major PW. J Rheumatol 2001; 28(6): 1347-55

4 Clegg DO, Reda DJ et al. N Engl J Med 2006; 354(8): 795-808

5 Morreale P, Manopulo R, Galatie M, et al. J Rheumatol 1996; 23: 1385-1391

6 Mazieres B, Combe B, Phan Ban A, et al. J Rheumatol 2001; 28: 173-81

7 Bucsi L, Poor G. Osteoarthritis Cartilage 1998; 6: S31-S36

8 Grant L, McBean DE, Fyfe L et al. Phytother Res 2007; 21(3): 199-209

9 ESCOP Monographs: The Scientific Foundation for Herbal Medicinal Products, 2nd Edition. ESCOP, European Scientific Cooperative on Phytotherapy, Exeter, 2003.

10 Brien S, Lewith G, Walker A et al. Evid Based Complement Altern Med 2004; 1(3)251-7

11 Nijveldt RJ, van Nood E et al. AJCN 2001; 74: 418-25

12 Henrotin YE, Bruckner P, Pujol JP. Osteoarthritis Cartilage 2003; 11(10): 747-55

13 Regan E, Flannelly J et al. Osteoarthritis Rheum 2005; 52(11): 3479-91

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Good read Houghy, thanks.


I'm currently on a few of the metagenics range. Ive noticed vast improvements using them too. I started off with a total detox using 2 tubs of - Nutritional Food, Ultra Clear Plus.


The metagenics products I use are for general health, to restore health and other problems I'm trying to restore back to normal;



- Inflavonoid Intensive Care - I hurt my back a while back and this really helps the pain to go away when I'm on it.

- Ultra Probioplex

- Ultra Flora Restore DF

- Male Essentials Multivitamin and mineral

- Mitochondrial Complex - Its got that Coenzyme Q10 mentioned earlier in the articles.

- Allergenics Respiratory Relief Formula

- Metazinc - Can't actually take this as I get really dizzy?? Any reason why Houghy/Mitch? I was advised to not take it.


+ Innovative Therapies, Luteol Plus.


I was also taking Herbal extracts which contained fenugreek, goldenseal, grindelia. This was mainly to rid my asthmatic symptoms. It worked however my aunt who is a naturopath has now put me on some Chinese (or was it Japanese????) medicine. Its called Saposhnikovia & astragalus formula 520 - Yu ping Feng San.


Anyway, I'm about to take the journey to Buffville (lol) and was curious to know if you can see any medicine I'm taking will affect the way I train?





Edited by Rx3ej20

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Don't know why you are feeling dizzy on zinc. If your not deficient, don't take it. It might be a zinc/copper thing but its not typical or it may be more of a gastric response to the zinc (which can irritate a bit in some people). It can make you feel a bit off if you take it on empty stomach etc. try it with food. You should be taking it at night before bed ideally.


Yu Ping Feng San is great for lungs and immune system, particularly if you are prone to atopy / allergies / getting colds often etc. and are prone to being out of breath or find your pores open easily (break out in sweats like your pores won't stay shut). Its used in chinese medicine to strengthen the Lung and Wei Qi (defensive Qi)


none of that should effect the way you train at all.

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Don't know why you are feeling dizzy on zinc. If your not deficient, don't take it. It might be a zinc/copper thing but its not typical or it may be more of a gastric response to the zinc (which can irritate a bit in some people). It can make you feel a bit off if you take it on empty stomach etc. try it with food. You should be taking it at night before bed ideally.


Yu Ping Feng San is great for lungs and immune system, particularly if you are prone to atopy / allergies / getting colds often etc. and are prone to being out of breath or find your pores open easily (break out in sweats like your pores won't stay shut). Its used in chinese medicine to strengthen the Lung and Wei Qi (defensive Qi)


none of that should effect the way you train at all.


Thanks for the reply Mitch,


Yeah Ive tried all different things with the Zinc and it all still made me dizzy? I think you're right when you say it may of irritated me. I haven't taken it since anyhow.


Re the yu ping, yes its for colds and allergies (asthma) and it works a treat.


Its good to know it wont effect me, cheers.



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