Grape Seed Extract Grape Seed Extract

16 THE NATURAL THERAPIST Volume 26 No.3 THE NATURAL THERAPIST Volume 26 No.3THE NATURAL THERAPIST Volume 26 No.3

Grape Seed Extract (GSE) to; lower total cholesterol (TC), improve cardiovascular risk ratio by raising high-density lipoprotein (HDL) relative to low-density lipoprotein (LDL), and decrease the risk of frank cardiovascular disease (CvD) is suggested to be of clinical utility in the management of afflicted and at risk individuals.

The preceding suggestion is based on the validity of the following conditions:

An established relationship between 1. cardiovascular disease/s and dyslipidaemia exists. contemporary medical belief and 2. practice acknowledges an increased risk of cvD associated with dyslipidaemia and a justified need to remedy this condition. Statin based drugs are 3. commonly employed for dyslipidaemia and have considerable associated iatrogenic risks.GSe tends to lower total 4. cholesterol while relatively raising hDL compared to LDL. GSe is safe except for people with 5. grape allergy and favourably affects cvD risks by mechanisms other than dyslipidaemia modification.

Grape Seed Extract

Dr. James Langley

for Dyslipidaemia, Unfavourable Cardiovascular Risk Ratios & Cardiovascular Disease.

The legitimacy of the preceding stated conditions are examined within this presentation by reviewing literature relevant to:

Dyslipidaemia and cvD1. Pharmacological properties including; benefits, dangers or 2. risks associated with the clinical use of statins and GSe.The biological plausibility, clinical justification and optimal 3. dosage/s and form/s of GSe for dyslipidaemia and cvD.

cardiovascular risk factors other than those directly related to

very low-density lipoprotein (vLDL), LDL and hDL cholesterol while personally acknowledged will not be considered

within this document. Discussion about the polypeptide Apo(A) fractions of hDL, Apo(b)

fractions of LDL and the plasminogen-like lipoprotein Lp(A) composed of apo(A) and

apo(b)100 that is strongly associated with cardiovascular disease and resistant to most cholesterol lowering medicines except Niacin are not included (pagana 2008).

Similarly, other important dyslipidaemia and cvD therapeutic agents such as Niacin and omega 3 are not discussed within this article.

THE NATURAL THERAPIST Volume 26 No.3 THE NATURAL THERAPIST Volume 26 No.3THE NATURAL THERAPIST Volume 26 No.3 17

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Cholesterol and Cardiovascular Disease:

contemporary medicine accepts a pathologic role of elevated cholesterol in the genesis of arteriosclerosis and coronary artery disease in which, elevated LDL and vLDL penetrate the arterial wall by oxidative processes. oxidised LDL and vLDL are cytotoxic to endothelial cells and chemotactic to monocytes which promote their migration into the intima and sub-intimal compartment of arteries and the accumulation of lipids in foam and smooth muscle cells. Trapped foam cells die with an oxidative burst while lipid laden smooth muscle cells become hyperplastic and may bulge into the lumen exposing the sub-endothelium to platelet aggregation, mural thrombi formation and promote arteriosclerotic plaque. These plaques can progress to frank arterial stenosis or occlusion, and become stable by calcifying or spontaneously rupture, and cause coronary artery disease, cvD or acute ischemic events, including life-threatening myocardial infarction, cerebral vascular accidents and pulmonary embolisms. (beers & berkow 1999)

Total cholesterol equals vLDL plus LDL plus hDL. As most cholesterol is LDL high serum cholesterol is associated with cvD. Some laboratories only report total cholesterol, triglycerides and hDL as these measures allow calculation of vLDL by dividing triglycerides by five if <400, and LDL by subtracting HDL and the calculated vLDL value from total cholesterol. elevated LDL and vLDL cholesterol levels are directly related to cvD whereas elevated hDL is inversely related regardless of sex, age and ethnicity. Understanding lipoprotein fractions within total cholesterol provides a more accurate assessment of a patient’s coronary risk than consideration of total cholesterol. (mcphee & papadakis 2009)

There are 5 classes of hDL; 2a, 2b, 3a, 3b and 3c, but only 2b is capable of reverse cholesterol transport and cardio-protection. hDL <40mg/dl is associated with low 2b, 40-60 minimal 2b and if >60 2b tends to dominate HDL profiles; 2b can be increased by cholesterol lowering Niacin but not statins. LDL has 7 classes, from the largest to the smallest; 1, 2a, 2b, 3a, 3b, 4a and 4b. The most commonly elevated LDL’s are 3a and 3b which are small enough to penetrate endothelial cells and promote atherosclerotic disease. LDL4 is especially dangerous and if >10% of total LDL nearly all patients have vascular events within months. vLDL is reported less arteriosclerotic than LDL, but can be converted to LDL within muscle cells, vLDL >25% of total cholesterol is a cardiovascular risk factor. The cardiovascular risk ratio, total cholesterol to hDL, ideally should be 3 and if >5 indicates increased cardiovascular risk. (pagana 2009)

Lowering cholesterol may reduce cardiovascular mortality and events in patients with known arteriosclerosis but not patients without arteriosclerotic disease (beers & berkow 1999: mcphee & papadakis 2009).

Treatment to lower cholesterol is currently recommended if there is a genetic propensity or familial history of cvD, premature

arteriosclerosis, very high LDL or triglycerides, or very low hDL (mcphee & papadakis 2009). The American heart Association recommends total LDL below 100 mg/dl and not above 160 mg/dl, has no definite goals for HDL and triglycerides but states HDL <50 mg/dl and triglycerides >150 mg/dl are criteria for metabolic syndrome (Lichtenstein et.al 2006). The cardiac risk ratio offers a useful index to monitor patient’s risk trends but tends

to overstate the protective effects of increasing hDL at low levels (mcphee & papadakis 2009) and not be reliable without considering other risk factors including obesity, smoking, hypertension and diabetes, as high LDL and low hDL are independent risk factors for cardiovascular disease (Gordon et.al. 1989: Kapur et.al. 2008).

The foregoing analysis is based on recent medical texts (beers m.h., berkow S. 1999: mcphee & papadakis 2009), recommendations of the American heart Association (Lichtenstein et.al 2006) and the research reviews cited (Gordon et.al.1989, Kapur et.al. 2008) and suggests there is a strong relationship between high LDL or vLDL and low hDL cholesterol with cardiovascular disease.

Cholesterol, Statin Drugs and Hypercholesterolemia:

cholesterol is essential for health and needed to synthesise; bile acids, vitamin D, steroid hormones, stabilise cell membranes, myelin and immune function (ellison 2006). Further, cholesterol comprises >half the dry weight of the cerebral cortex and is vital to neurological function and serotonin metabolism (Fallon & enig 2004). As stated in the preceding section, there is some evidence that lowering high cholesterol decreases cardiovascular events or mortality in arteriosclerotic patients but not in patients without arteriosclerosis. however, numerous epidemiological studies report increased mortality associated with low or lowering cholesterol (ellison 2006). The apparent disparity between decreased cardiovascular events or mortality and increased mortality appears to arise from reporting different measures and study populations.

Studies reporting decreased cardiovascular events or mortality usually report relative rather than absolute risk while those reporting increased mortality report total mortality, a much stronger measure of actual effect (ellison 2006). Similarly, studies finding decreased cardiovascular mortality associated with low or lowering cholesterol tend to suffer age and gender biases by reporting study populations composed of nearly exclusively middle aged males (ellison 2006: Walsh & pignone 2004). Whereas the numerous studies finding increased mortality associated with low or lowering cholesterol cited by ellison (ellison 2006) suffer age and selection biases by reporting elderly or disease specific populations. Collectively, the foregoing suggests that the preventative role of statin drugs for cardiovascular mortality is poorly supported by research except for middle aged males with known arteriosclerotic disease and that statins use appears associated with increased mortality in the elderly.

GRAPE SEED ExTRACT FoR DySLIPIDAEmIA, UNFAvoURAbLE CARDIovASCULAR RISK RATIoS AND CARDIovASCULAR DISEASE.

Dr. James Langley

THE NATURAL THERAPIST Volume 26 No.3 THE NATURAL THERAPIST Volume 26 No.3 19THE NATURAL THERAPIST Volume 26 No.3

Despite statins reliably lowering cholesterol they do not prevent early death from heart disease, heart attack or stroke (ellison 2006) or slow arteriosclerotic plaque formation (hecht & harman 2003). Statin drugs lower cholesterol by inhibiting hmG-coA reductase. This enzyme is involved in both the formation of cholesterol and other substances involved in important biochemical functions including; Ubiquinone (coQ10), squalene and dilochols. The heart requires high levels of coQ10 which has a critical role in energy supply via ATp production and cell respiration. coQ10 is also involved with; nerve conduction, muscle membrane integrity, collagen and elastin formation (Fallon & enig 2004). Dilochols are very important as they organise DNA synthesised proteins and cellular responses, while squalene demonstrates anti-cancer effects (Fallon & enig 2004).

Statin’s most common side effects are muscle pain, weakness and wasting or rhabdomyolysis precipitated by coQ10 depletion (Fallon & enig 2004). heart failure deaths in the United States of America more than doubled between 1989 and 1997 after statins were introduced in 1987. 2/3 of 20 patients with normal hearts given 20mg of Lipitor developed abnormalities in cardiac filling within 6 months, and 8 of 9 other human studies investigating statin induced coQ10 depletion found depletion with left ventricular function declines and other cardiac abnormalities (Langsjoen 2003). Neuropathic dysfunctions including polyneuropathy related weakness, tingling sensation, balance and walking difficulty are common in those taking statins for more than 1 year and often irreversible (Fallon & enig 2004). psychomotor, cognitive and memory impairments are also common in those taking statins (Tatley & Savage 2007) and reported in several statin studies (Fallon & enig 2004). Statin related carcinogenesis is found in all rodent studies to date at dosages comparable to human exposures, but human studies are inconclusive due to a lack of follow-up investigations with most human cancers developing over long time frames (Newman & hulley 1996). Despite this several controlled statin trials do report increased rates of cancer in the statin samples (ellison 2006). Statin induced hepatic failure and hepatitis is not uncommon especially in the elderly (Tuteja et.al 2008). Several other statin related side-effects appear wrongly reported within (Fallon & enig 2004: ellison 2006) including depression, suicide, immune compromise and premature death, as investigation of the source materials cited and or related searches finds these events appear more linked to low cholesterol rather than directly related to statin drugs.

The findings reported in this section are primarily based on two sources (Fallon & enig 2004: ellison 2006) both of which exhibit strong bias against statin drugs and at times were found to misreport their supporting literature. however, the aspects reported here are believed valid after reviewing their sources and other related information. In summary, statin drugs’ cholesterol lowering properties are undisputed similar to their inhibiting effects on coQ10, squalene and dilochol metabolisms. Statin’s primary and secondary effects have experimental, epidemiological and biological plausibility to precipitate dangerous side-effects including heart failure, multi-faceted neurological dysfunctions, cancer and liver failure. Increased surveillance for the occurrence or exacerbation of these conditions appears warranted in patients taking statin drugs as does coQ10 supplementation.


Dr. James Langley

Grape Seed Extract, Hypercholesterolemia and Cardiovascular Disease:

epidemiological studies show much less cvD despite otherwise similar risk factor profiles in those who consume red wine or the polyphenolic flavonoids resveratrol from grapes or proanthocyanidins from grape seeds (Das et.al. 1999). Grape seeds are one of the best known sources of polyphenolic flavonoids (Ghosh & Scheepens 2009) which improve endothelial function, inhibit platelet aggregation and increase LDL oxidation protection in humans (Folts 2002). Wine taken with food reduced postprandial rises in lipid hydropreoxidases and LDL oxidation, GSe proanthocyanidins appear to have the greatest antioxidant effect (Rasmussen et.al. 2005) and be more specific for peroxyl radicals, ph independent, active within the digestive tract, and inhibit postprandial rises in plasma oxidants as well as lipid deposition (Ursini & Sevanian 2002). GSe compared to grapes, grape juice and red wine shows a greater dose-dependent inhibition LDL oxidation in vitro; in vivo 300mg of GSe is much more effective than 200mg in increasing antioxidant activity (vinson et.al. 2001). 600mg of GSe is equal to 300ml of red wine or 1250mg of vitamin c in plasma antioxidant activity at 1 and 2 hours after ingestion and significantly increased plasma antioxidant activity with long-term supplementation and reduced total cholesterol, and LDL in subjects with hc but not subjects in normal plasma lipids (vinson et.al. 2001). 300mg of GSe showed significant increases in total antioxidant capacity in 20 subjects on standardised diets/lifestyle 30 and 60 minutes post ingestion twice daily from the first to the last day, day 5 (Nuttall et.al. 1998).

A randomised double blind placebo controlled study investigating 200mg GSe or 200mcg chromium polynicotinate or both per day found reduced total cholesterol principally from LDL reduction in the GSe -2.5%, chromium -10% and combination -16.5% groups with no significant change in HDL and triglycerides between the groups over a 2 month period (preuss et.al 2000). Another similar study reports a 20% drop of LDL in the combination group and 60% of the group receiving GSe showed a >50% reduction of autoantibodies to oxidised LDL compared to only 10% in the chromium polynicotinate group (bagchi et.al. 2003). consistent with the preceding findings 600mg of GSE in a placebo controlled randomised blinded crossover design study of 32 type 2 diabetics

over 4 weeks found significantly decreased total cholesterol p=0.05 with insignificant changes in hDL and triglycerides (Kar 2009). however, clifton reported no significant changes in lipid profiles in a double blinded randomised crossover of control and active ingredient/s study testing 2gms of GSe in yoghurt per day during a 12 week period but did find increased flow mediated dilation in the GSe groups. clifton’s combining GSe with yoghurt, lack of medication and alcohol consumption exclusion criteria, poorly designed diet, and employing several previously undocumented measures suggest caution in accepting his findings in regard to the clinical use of GSE (Clifton 2004). These findings collectively strongly suggest that GSe raises the ratio of hDL to total cholesterol by virtue of lowering LDL.

The improved lipid profile effects of GSE have also been demonstrated in many rat and rabbit studies that additionally



Dr. James Langley

report a very strong anti-arteriosclerotic effect and other cardio protective actions including; decreased platelet aggregation, improved endothelial function and eNoS (Nassiri-Asi & hosseinzadch 2009: bagchi et.al 2003 ).

GSe is proanthocyanidins rich and more importantly they occur in readily absorbable forms including catechin monomers, proanthocyanidin dimers and simple phenolic compounds. proanthocyanidins appears the most important substances in grapes for cardio protection but a synergistic response from other constituents cannot be excluded. human inability to digest and metabolise polymeric proanthocyanidins explains why GSe’s in vitro responses are often reproducible in vivo unlike the polymeric forms unless injected intravenously, which appear more effective in vitro (Ramussen et.al. 2005).

Proanthocyanidins are anti-inflammatory and inhibit monocyte adhesion involved in arteriosclerosis, in vivo only the monomer and dimer forms are relevant and have been demonstrated in several recent human studies (Ramussen et.al. 2005) in contrast to clifton’s (clifton 2004) hscRp, TNF-a, vcAm-1 and IcAm-1 findings. Red wine and grape polyphenols have convincingly shown beneficial vasodilator effects in humans by increasing intracellular ca activating eNoS. however, in vitro results do not find monomer and dimer proanthocyanidins effective only trimers and larger, thus the agent involved maybe a metabolic by-product that has still not been identified. Platelet derived growth factor (pDGF) is a potent mitogenic and chemotactic agent involved in all stages of arteriosclerosis that is inhibited by red but not white wine polyphenols, however enriching white wine with GSe to mimic the mash fermentation of red wine inhibits pDGF suggesting the mash fermentation of red wine releases active compounds in grape seeds. (Ramussen et.al. 2005)

Database searches for iatrogenic, side effects and toxicity with grape seed extract searched on pubmed, US FDA and Australian TGA found no references to noxious effects from GSe. Similar to several animal studies (Yamakoshi et.al. 2002: Wren et.al. 2002: Ray et.al. 2001). Further, I recently contacted a GSe supplement manufacturer who informed of recent TGA labelling changes wherein GSe 12,000mg capsules can now be labelled 2 per day for the general public.

Summary of Grape Seed Extract Dyslipidaemia and Cardiovascular Disease Findings:

Despite relatively few human trials on GSe it does have an established role in the management of human hc wherein it appears to improve the cardiovascular risk ratio by selectively lower LDL the most undesirable fraction of total cholesterol while maintaining hDL and vLDL. GSe also has established benefits to endothelial function, platelet aggregation, inflammatory monocyte adhesion and oxidation of LDL. epidemiological and clinical research suggests that whole GSE is the most beneficial form despite in vitro findings suggesting poorly absorbed polymeric proanthocyanidins are more efficient. Further, the lack of societal experience and regulatory body findings of toxicity, and the dose dependent nature of GSe effects reported suggest that higher doses in keeping with the current TGA labelling recommendations will be more beneficial than the lower doses reported herein. personal clinical experience of the TGA’s currently approved dosage, for 20+ years, also supports GSe having a beneficial role in the management of dyslipidaemia and CVD afflicted patients, and prompted the preparation of this presentation.

Conclusion/s:

high LDL or vLDL, or low hDL is clearly involved with cvD and life threatening cardiovascular conditions. contemporary medical opinion indicates that hypercholesterolemia warrants intervention and statin based drugs are the most frequently employed cholesterol lowering agent. Statins’ risks appear greater than their benefits for many people, as their risks are present for all but benefits for females and the aged lack definitive evidence or appear very questionable. Despite GSe not being found in this review to lower total cholesterol as much as statins it has a more selective action against the most harmful fraction LDL, and many other cardiovascular and health benefits unlike statins. Further, the dose dependent nature of reported GSe effects do not rule out the possibility of greater cholesterol lowering results at higher doses, as allowed by current TGA guidelines. critical appraisal of the findings presented herein support GSE’s role in the management of dyslipidaemia and cvD, and provide evidence based information to assist practitioners and patients consideration of GSe’s inclusion within the clinical management these conditions.

Acknowledgements: I would like to thank Dr. Sonya brownie DipAppScNat (AcadNatTher), GradDipSc (otago University), phD(ScU) for her valuable guidance in the preparation of this presentation. List of References

bagchi D., Sen c.K., Ray S.D., Das D.K., bagchi m., preuss 1. h.G. and vinson J.A. (2003) molecular mechanisms of cardioprotection by a novel grape seed proanthocyanidin extract. Fundamental and molecular mechanisms of mutagenesis: mutation Research. Science Direct electronic Journal collection. volume / issue 523-524 pg 87-97beers m.h., berkow R. (1999) The merck manual 17th edn. 2. merck Research Laboratories, Whitehouse Station, New Jerseyclifton, p. m. (2004) effect of grape seed extract and quercetin 3. on cardiovascular and endothelial parameters in high-risk subjects. Journal of biomedicine & biotechnology. 5, 272–278.Das D. K., Sato m., Ray p. S., maulik G.. (1999) cardioprotection 4. of red wine: Role of polyphenolic antioxidants. Drugs exp. clinical. Res. 25, 115–120ellison S. (2006) hidden Truth About cholesterol-Lowering 5. Drugs. health myths exposed, LLc.Fallon S. & enig m. G. (2004) Dangers of Statin Drugs: What 6. You haven’t been Told About popular cholesterol-Lowering medicines. Wise Traditions. Weston A. price Foundation. http://www.westonaprice.org/moderndiseases/statin.html viewed on 1st may 2009Folts, J. D. (2002) Potential health benefits from the flavonoids 7. in grape products on vascular disease. Adv. exp. med. biol. 505, 95–111.Ghosh D. and Scheepens A. (2009) vascular action of 8. polyphenols. molecular Nutrition Food Res. 2009, 53, 322 – 331Gordon D.J., Probstfield J.L., Garrison R.J., Neaton J.D., Castelli 9. W.p., Knoke J.D., Jacobs D.R., bangdiwala S. and Tyroler h.A. (1989). high-density lipoprotein cholesterol and cardiovascular disease. Four prospective American studies. circulation. Journal of the American heart Association. Number 79 pages 8-15, Dallas, Texas hecht h.S. & harmann Sm. (2003) “Relation of aggressiveness 10. of lipid-lowering treatment to changes in calcified plaque burden by electron beam tomography.” American Journal of cardiology. Aug 1;92(3):334-6.

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Kapur N.K., Ashen D., blumenthal R.S. (2008). high density 11. lipoprotein cholesterol: an evolving target of therapy in the management of cardiovascular disease. vascular health and Risk management 4(1) pages 39-57. Dove medical press LimitedKar p., Laight D., Rooprai h.K., Shaw K.m. and cummings 12. m. (2009) effects of grape seed extract in Type-2 diabetic subjects at high cardiovascular risk: A double blind randomized placebo controlled trial examining metabolic markers, vascular tone, inflammation, oxidative stress and insulin sensitivity. Diabetic medicine “Accepted Article 26th march 2009”; doi: 10.1111/j.1464-5491.2009.02727.xLangsjoen p. h. & Langsjoen A. m.(2003) The clinical use of 13. hmG co-A reductase inhibitors (statins) and the associated depletion of the essential co-factor coenzyme Q10: a review of pertinent human and animal data. biofactors 2003;18(1-4):101-11 oxford, england. Lichtenstein A.h., Lawrence J.A., brands m., carnethon m., 14. Daniels S., Franch h.A, Franklin b., Kris-etherton p., harris W.S., howard b., Karanja N., Lefevre m., Rudel L., Sacks F., horn L.v., Winston m. and Wylie-Rosett J. (2006). Diet and Lifestyle Recommendations Revision 2006: A Scientific Statement from the American heart Association Nutrition committee. circulation. Journal of the American heart Association. Number 114 pages 82-96, Dallas, Texasmcphee S.J., papadakis m.A. (2009) 2009 current medical 15. Treatment & Diagnosis. mcGraw hill medical, New Yorkministry of public health (2007) public health Statistics A.D. 16. 2006. bangkok, ThailandNassir-Asi m. & hosseinzadch h. (2009) Review of the 17. pharmacological effects of vitis vinifera (Grape) and its bioactive compounds. phytotherapy Research published online in Wiley Interscience (www.interscience.wiley.com) DoI: 10.1002/ptr.2761Newman T. b. & hulley S. b. (1996) carcinogenicity of lipid 18. lowering drugs. Journal of the American medical Association Jan 3;275(1):55-60Nuttall S.L., Kendall m.J., bombardelli e. and morazzoni (1998) 19. An evaluation of the antioxidant activity of a standardized grape seed extract, Leucoselect. Journal of clinical pharmacy and Therapeutics (1998) 23, 385–389pagana K. D. & pagana T. J. (2009) mosby’s Diagnostic and 20. Laboratory Test Reference 9th edn. mosby elsevier, chinapreuss, h. G., Wallerstedt, D., Talpur, N., Tutuncuoglu, S. o., 21. echard b., myers A., bui m. and bagchi D. (2000) effects of niacin-bound chromium and grape seed proanthocyanidin extract on the lipid profile of hypercholesterolemic subjects: A pilot study. Journal of medicine. 31, 227–46Rassmussen S.e., 22. Frederlksen h., Krogholm K.S. and poulsen L. (2005) Dietary proanthocyanidins: occurrence, dietary intake, bioavailability, and protection against cardiovascular disease. molecular Nutrition Food Res. 49, 159 – 174 * 2nd Floor, 234 Swanston Street, Melbourne Vic 3000 ( (03) 9663 8822 : [email protected] w www.chinabooks.com.au

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Ray S., bagchi D., Lim p.m., bagchi m., Gross S.m., Kothari 23. S.c., preuss h.G. and Stohs S.J. (2001) Acute and longterm safety evaluation of a novel Ih636 grape seed pranthocyanidin extract. Resource community of molecular pathology and pharmacology. mar-Apr;109(3-4):165-97Tatley m. & Savage R. (2007) psychiatric adverse reactions with 24. statins, fibrates and ezetimibe: implications for the use of lipid-lowering agents. Drug Safety 30(3):195-201Tuteja S., pyrsopoulos N. T., Wolowich W. R., Khanmoradi 25. K., Levi D. m., Selvaggi G., Weisbaum G., Tzakis A. G. and Schiff e. R. (2008) Simvastatin-ezetimibe-induced hepatic failure necessitating liver transplantation. pharmacotherapy. Sep;28(9):1188-93. Ursini F. & Sevanian A. (2002) Wine polyphenols and optimal 26. nutrition. Annals of the New York Academy of Sciences. may;957:200-9.vinson, J. A., proch, J., bose, p., (2001) mega natural gold 27. grapeseed extract: In vitro antioxidant and in vivo human supplementation studies, Journal of . medicinal Food 4, 17–26.Walsh, J.m. & pignone, m. (2004) Drug Treatment of 28. hyperlipidemia in women. Journal of the American medical Association. may 12;291(18):2243-52Wren A.F., cleary m., Frantz c., melton S. and Norris L. (2002) 29. 90-day oral toxicity of a grape seed extract (Ih636) in rats. Journal of Agricultural Food chemistry. mar 27;50(7):2180-92Yamakoshi J., Saito m., Kataoka S. and Kikuchi m. (2002) Safety 30. evaluation of proanthocyanidin rich extract od grape seeds. Food and chemical Toxicology. may; 40(5):599-607


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