To say that the concerns about cholesterol are rampant would be quite an understatement. Infact, from much of the news and advertising, one would think that cholesterol is a poison ratherthan the essential component that it is. Yes, cholesterol is not only necessary for almost everycell in the body, but our bodies produce (not ingest) most of the cholesterol we use. Our mainconcern is with elevated blood (or serum) cholesterol and the secondary conditions, such aslipid peroxidation and atherosclerosis, caused by chronic increased levels of cholesterol in the

blood. Since there are thousands of articlesand reviews on cholesterol, this article willonly briefly cover the metabolism andpharmaceutical management of cholesterol,focussing primarily on the management ofcholesterol using natural ingredients.

Cholesterol: The Good, The Bad,and The UglyWe have all been guilty of reducing thewhole of cholesterol metabolism downinto “good” (HDL) cholesterol and “bad”(LDL) cholesterol. While this is a drasticover-simplification, it does help underscorethat not all cholesterol is hazardous toone’s health.

Since cholesterol is not soluble in theblood, it must be carried to and from theliver (the primary organ for synthesis andremoval of the body’s cholesterol) vialipoprotein particles. The difference betweenlipoprotein particles (LDL, IDL, VLDL, HDLetc) is not only their density, as the namesimply, but the composition of the proteinswithin the particle. Many of the diseasesassociated with hypercholesterolemia are aresult of genetic mutations in these proteinsor the cellular receptors that recognizethese proteins.

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MANAGING CHOLESTEROL:NATURALLY

A CONCISE UPDATE OF IMPORTANT ISSUES CONCERNING NATURAL HEALTH INGREDIENTS

Leading Causes of Death in the U.S. (1996)

Heart Disease

Cancer

Stroke

ADR

COPD

Accident

Pneu/Flu

Diabetes

HIV/Aids

0 100 200 300 400 500 600 700 800

733,834

32,655

544,278

160,431

110,000

106,146

93,874

82,579

61,559

Deaths in Thousands

“Leading causes of death in the United States for 1996as reported by the Centers for Disease Control,

modified by the adverse drug reaction (ADR) statisticsreported in JAMA, 1998; 279 (15): 1200-1205.

COPD is Chronic Obstructive Pulmonary Disease.Pneu/Flu is Pneumonia/Influenza.”

Edited By: Thomas G. Guilliams Ph.D.

2

The cholesterol and fatty acid portionof LDL particles are susceptible to oxidation,which can result in further free-radicaldamage to associated vessel walls andincreased adhesion leading to vessel damage,loss of elasticity (arteriosclerosis) and buildup of plaques along vessel walls(atherosclerosis). This has placed increasedserum cholesterol (and especially LDL) asone of the leading causes of heart disease,itself the leading cause of death in theWestern world.

The relative danger of elevated totalcholesterol (TC) should be assessed withconcurrent secondary risks such as smoking,obesity, family history, homocysteine levelsand others. According to the Adult TreatmentPanel II of the National CholesterolEducation Program (1), those with no heartdisease and relatively few secondary risksshould be assessed as follows: TC <200mg/dl are classified as desirable, TC from 200to 239 mg/dl are classified as border-linehigh, and those over 240 mg/dl are classifiedas high blood cholesterol. As secondary riskfactors are added, the relative risk ofcholesterol increases and should be treatedmore aggressively. HDL levels below 35mg/dl have also been associated with highrisk of CHD.

According to a recent publication, theguidelines set forth for cholesterol managementby this panel are being neglected by a majorityof physicians caring for heart patients (2). Whilethis was primarily a survey of Midwestern States,it likely reflects the treatment throughout therest of the United States. In fact, unless patientsask specifically for cholesterol screening, theyare unlikely to be tested on a consistent basis,even when they have previously been classifiedas having high cholesterol.

Managing Cholesterol There are essentially 5 ways toreduce elevated serum cholesterol.1. Decrease the dietary intake of

cholesterol, saturated fats,and trans fatty acids: Whileincreased levels of cholesterol in the diethave only a small direct effect on total

serum cholesterol levels, chronic ingestionof cholesterol will decrease liver LDLreceptors and keep serum levels high.This will be discussed further in the“Diet” section of Natural Approaches.

2. Increase bile production andsecretion while providing amechanism to bind andremove bile: Probably one of themost under-utilized ways to decrease serumcholesterol. Bile salts are synthesizedprimarily from cholesterol, and whensecreted from the liver to the gall bladder,bile includes more cholesterol. Usingcholoretics to stimulate bile production andsecretion along with bile acid sequesteringfibers is an extremely helpful way to reduceserum cholesterol levels.

3. Decrease the production ofcholesterol: Although every cell inthe body can synthesize cholesterol, thecells in the liver provide most of thecholesterol to the rest of the body. Whilefeedback loops exist linking cholesterolsynthesis with LDL receptor function andoverall fatty acid metabolism, limitingprecursors or reducing the amount (oractivity) of enzymes that producecholesterol is an effective approach toreducing cholesterol.

4. Increase the liver’s ability tobring in excess LDL particlesfrom the blood, while reducingit’s ability to secrete LDL par-ticles into the blood stream: Thiscan be done by increasing the amount ofLDL receptors on liver cells, whichdecreases de novo synthesis in the liverand gives the opportunity to remove thecholesterol via the bile or catabolicprocesses. Various processes also regulatethe amount of cholesterol (LDL particles)secreted into the blood. These pathwayscan be modified to reduce the amount ofLDL particles secreted.

5. Increase the cellular use andcatabolism of cholesterol: Thisspeaks for itself. Through exercise andproper fatty acid metabolism, the body will

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utilize its available cholesterol for cellmembranes and steroid hormones. Propercarbohydrate metabolism and blood sugarlevels will keep fatty acid metabolism (β-oxidation for energy) in balance and helpkeep cholesterol levels down.

The best way to maintain healthycholesterol levels or reduce already elevatedcholesterol levels is to use as many of theabove mechanisms as possible, simultan-eously. The potency of many pharmaceuticaldrugs makes this difficult, if not dangerous.The natural approach, on the other hand,would combine several ingredients, eachhaving an independentmechanism forreducing cholesterollevels at synergisticlevels (sometimes sub-therapeutic if consideredalone). Let us comparethese approaches.

TheDrugs: How TheyWorkBile acidsequestrants:Essentially this is a pharmaceuticallysynthesized fiber. Using a basic anionexchange resin (cholestyramine), and artificialcolors, sweeteners and flavors; BristolLaboratories produced Questran®.Cholestyramine adsorbs and combines withbile, limiting its reabsorption via theenterohepatic circulation. Side effects(constipation, gas, and intestinal pain) havelead to very low compliance. Nicotinic acid: The use of nicotinic acid(niacin) is considered one of the first steps inthe treatment of hypercholesterolemia.Usually 1-2 grams per day are given topatients with low HDL, high LDL or hightriglycerides. Nicotinic acid reduces theamount of VLDL and LDL particle

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production and excretion by the liver.Significant side effects (flushing, gastro-intestinal, and liver toxicity) have kept thistreatment from being used in a large numberof patients.

HMG-CoA reductase inhibitors(Statins): The most popular and wellknown of these has been lovastatin(Mevacor®), and now Lipitor®. These drugswork by inhibiting the enzyme 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA)reductase, an enzyme that converts HMG-CoAto mevalonate (one of the rate limiting steps

in cholesterolsynthesis). Theseshould be avoided inpatients with liverconditions and hasbeen shown to reducelevels of CoQ-10 (36),a necessary electrontransport componentof all tissues (especiallythe heart). Long-termeffect on steroidhormone synthesis isstill being researched.

Others: Other drugsexist, such asClofibrate and

Gemfibrozil, which areused primarily for increased serumtriglycerides although they have some effectson both LDL and HDL levels. Some of thesehave quite serious side effects and are beingused only on difficult and high-risk patients.

In most cases, pharmaceutical drugsare unnecessary for the treatment ofhypercholesterolemia, (one obviousexception would be a patient withhomozygous familial hypercholesterolemia).The NCEP cholesterol recommendation wasto delay the use of pharmaceuticals in allpatients with high LDL and without otherhigh CHD risk factors (1). Thepharmaceutical companies have anotherapproach. Kohn and Roth say, “Many expertshave expressed concern that because of

“Many experts have expressed concernthat because of vigorous promotion by pharmaceutical companies, these

drugs are being urged on patients whomight have benefited from a less

aggressive approach. Worse yet, thereseems to be an increase in noncardiacrelated deaths in patents who havebeen placed on lipid-lowering drugs.Although the reason for this has notbeen discovered, it does suggest that

use of these drugs is not entirelyinnocuous and should not be undertaken

without adequate justification.”(3)

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NEWSPERSPECTIVES

IRONAdds To Heart Disease Risk.In the past several years, conflicting reports have beenpublished as to whether dietary iron has an influence on therisk of heart disease. Recent publications seem to link highblood levels of iron to the risk of heart attacks (1) anddietary iron to coronary heart disease (2). The first studyinvestigated the amount of body iron stores (usingTransferrin receptor to serum ferritin ratios) in relation tothe occurrence of acute myocardial infarctions in men. Afteradjusting for other risk factors, men in the highest thirdbody iron stores were 2.9 times more likely to have an acutemyocardial infarction than those in the lowest third. Thisreport confirmed previous studies by this group and others.

The second study investigated the associationbetween dietary iron intake and risk of coronary heart disease.Again, adjusting for other variables that adversely effect heartdisease, these researchers found a positive correlation betweenincreased iron intake and coronary disease in the elderly.Women over the age of 60 seemed to be particularly at risk(odds ratio 3.5) with increased iron levels.

Increased iron levels have been implicated in twomechanisms that increase risk of coronary disease,increased red blood cell adhesion and increased lipidperoxidation. Whether these are the only mechanismseffecting vascular conditions is still undetermined. Weanticipate that more studies will be conducted to investigatethe extent to which iron plays a role in heart disease. Whatdoes this mean for patients?

Iron deficiency is one of the most widely spreaddeficiencies in the world and requires serious attention andintervention. Fortunately, the same can not be said of mostof the U.S. population. With the advent of iron fortificationand the amount of red meat in the diet of most Americans,iron deficiency is not a common condition in the U.S. Thepopulation we are most concerned about is women withintheir child-bearing years. A recent study found that only10% of such women were iron deficient (3). While thisnumber is still quite high (over 7 million women), theseresults show that 90% of these women, considered the mostat risk, are not iron deficient. In men, iron deficiency isextremely rare in the U.S.

With these data in hand, it is stronglyrecommended that individuals should not add iron to asupplemental regimen unless they indeed have an irondeficiency. This is especially true if the individual is at anyincreased risk to cardiovascular disease. Unfortunately,many of the most common multi-vitamin products have10-20 mg of iron per tablet. Physicians should becomefamiliar with multivitamin/mineral products that areavailable without iron for the majority of their patient body.This will ensure that what is meant to help them, does notend up harming them.

1. Tuomainen TP, Punnonen K, Nyyssonen K, and Salonen JT. Association between bodyiron stores and the risk of acute myocardial infarction in men. Circulation 1998; 97(15):1461-1466

2. Tzonou A, Lagiou P, Trichopoulou A, Tsoutsos V, and Trichopoulos D. Dietary iron andcoronary heart disease risk: a study from Greece. Am J Epidemiol. 1998; 147(2):161-166.

3. Looker AC, Dallman PR, Carroll MD, Gunter EW, Johnson CL. Prevalence of irondeficiency in the United States. JAMA 1997; 277(12):973-976

vigorous promotion by pharmaceuticalcompanies, these drugs are being urged onpatients who might have benefited from a lessaggressive approach. Worse yet, there seems tobe an increase in noncardiac related deaths inpatents who have been placed on lipid-lowering drugs. Although the reason for thishas not been discovered, it does suggest thatuse of these drugs is not entirely innocuousand should not be undertaken withoutadequate justification”(3). We could hardlyagree more. The use of dietary changes andproper use of natural ingredients can have adramatic effect on cholesterol levels as well asprovide other effects that benefit the patients

overall health. The use of these ingredientswill make the need for pharmaceuticalsunnecessary, except in rare, high-risk patients.

The Natural ApproachDiet and Exercise: While this topichas been covered over and over by thousandsof sources, it cannot be overemphasized.When a patient ingests large quantities of fat,cholesterol and refined sugars; theircholesterol levels will increase. Perhaps thegreatest offender to cholesterol managementhas come in like the Trojan Horse ... trans fattyacids. Trans fatty acids are formed by taking a

“healthy” polyunsaturated oil (liquid) andpartially saturating it with hydrogen atoms(partially hydrogenated) to make it moresolid (margarine, vegetable shortening). Thisprocess forms trans double bonds rather thanthe naturally occuring cis double bonds.Heating polyunsaturated oils (as with mostdeep frying) will not only produce trans fattyacids, but will produce oxidized oils. Theseunnatural fats effect the entire metabolism oflipids by slowing down enzymatic turnoverrates and producing secondary metabolitesthat require further conversion prior to theiruse or removal. The irony is that theseproducts have been considered healthierbecause they are cholesterol-free and madefrom polyunsaturated oils.

We recommend using poly-unsaturatedoils in their unheated, liquid form, and usingbutter, coconut or palm kernel oil (we knowthis is against current orthodoxy) inmoderation when cooking with oils. These oilsare already saturated and will not be altereddramatically by heating and the body shouldhave ample enzymatic machinery to handlethese fats in small doses. Olive oil is a slightexception, as it is only singly unsaturated.When using olive oil, add it with the fooditems (not to the hot pan alone) and do notreuse oil for deep-frying.

The benefits of exercise are obvious. Notonly will regular activity increase carbohydrateand lipid metabolism, it will stimulatehormonal and enzymatic activities whichbenefit fat metabolism. Since the work force ismoving increasingly away from strenuous laborand toward automated and sedentary activities,exercise has become a recreational activity. [Ournation’s youth are now moving to sedentaryrecreation (Nintendo etc.) making exercise laboronce again.]

Oxidized Cholesterol and Anti-oxidants: When cholesterol loseselectrons to oxygen, it becomes oxidized andchanges properties. This reaction can occuras cholesterol-rich food is being processed orcooked, as well as in LDL particles floatingaround in the blood. Researchers at theUniversity of California at San Franciscohave now confirmed that oxidized

cholesterol is much more likely to formplaques on arterial wall (atherosclerosis) (4).Oxidized cholesterol is not only moreadhesive, but can cause further damage toother lipid membranes by oxidative damage.

Significant ingestion of antioxidants isbecoming more popular to combat thedamage induced by cholesterol in its oxidizedform (5). One of the most beneficialantioxidant in this regard is Vitamin E. Thenatural form of vitamin E (d-α-tocopherol) isadded directly to LDL particles by the body toprevent and even reverse (reduce) theoxidized state of cholesterol. It is best to usethe natural form of Vitamin E, because whilethe artificial form (dl-α-tocopherol) is a usefulantioxidant in vitro, only approxamatly half ofthis is added to membranes and LDL particles.

Other antioxidants have been shownto benefit oxidized cholesterol levels directlyor by “recharging” Vitamin E. One suchantioxidant would be α-Lipoic acid (formerlyknown as Thioctic acid). Having both fat-soluble and water-soluble components,Lipoic Acid is able to bridge the recharging ofVitamin E from Ascorbic Acid (a strictlywater-soluble antioxidant). Other excellentantioxidants include grape seed extracts,other flavonoid components, selenium,glutathione, N-acetyl cysteine, natural β-carotene, and zinc to name a few. We willhave expanded coverage of antioxidants andtheir use in subsequent newsletters.Supplemental Oils: One of the best waysto improve the body’s use of fatty acids is to giveit fresh oils high in essential fatty acids. Fresh flaxseed, evening primrose, borage, black currentseed and fish oils taken in bulk or capsule formis an excellent way to increase the properbalance of lipid metabolism and protect againstthe damage caused by oxidized cholesterol andtrans fatty acids. The oils should be as fresh aspossible and processed without chemicals orheat, as these polyunsaturated oils can go rancid(oxidized) and possibly add to the problem.Inositol Hexaniacinate: While the useof niacin is considered to be an excellent andconservative approach to cholesterolmanagement, the side effects have kept it fromits frequent use. Inositol Hexaniacinate (IH) is

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the only form of niacin not linked tosignificant side effects in clinical trials. IH is acentral inositol molecule with 6 niacin estersattached to its six-membered ring. It isunknown why this form works just like niacin(6), but without the side effects. Most of theresearch has used high doses (up to 4 gramsper day) of IH for the condition of intermittentclaudication (7, 8). Most have found that 1000to 1500 mg per day in divided doses is quiteadequate for lowering cholesterol, especiallywhen added to other cholesterol reducingnatural ingredients.Choloretics and natural fibers:One of the most underutilized naturalapproaches to reducing cholesterol is thecombined use of natural, bile sequesteringfibers such as psyllium or guar gum withpotent natural choloretics. There are manynatural products that willstimulate bile productionand secretion like dandelionroot, black radish root, beetleaf tops, silymarin etc. Oneof the best and most consistent would beGlobe artichoke (Cynara scolymus L.) extractcontaining 1-2% cynarin. A daily dose of 100-200 mg/day of a standardized artichoke extractwill force the liver to produce and dump bileinto the gall bladder and then into the smallintestines. The liver will then take morecholesterol from the blood via its LDLreceptors and produce more bile. When this iscombined with a bile-sequestering fiber, thebile is unable to reabsorb and is removed withthe stool. This should be a natural part of anyregimen dealing with liver conditions,especially when fat or cholesterol is involved.Garlic: Much has been written aboutgarlic’s (Allium sativum L.) ability to lowercholesterol, inhibit platelet aggregation andincrease fibrinolysis (18, 19, 20, 21). Garliccontains an odorless compound called alliin.When crushed or chewed the alliin contactsan enzyme called allinase, which convertsalliin to allicin, the active and strongsmelling component of garlic. Allicin andajoene seem to be able to interfere with theliver’s ability to synthesize cholesterol. Garlichelps prevent the oxidation of cholesterol andeven inhibits platelet aggregation. If your

patients can stand the smell, the best way totake garlic is fresh. Several cloves a day oughtto do it. Enteric coated tablets and capsulesare available which contain high amounts ofalliin and allinase, which produces allicinonce ingested and mixed in the smallintestines. 5-10 mg of allicin/day is sufficientfor most of the cardiovascular benefitsderived from garlic.Gugulipids: Gugulipids come from theresin of the mukul myrrh tree (Commiphoramukul). Used in India for centuries,gugulipids were researched significantlysince the 1960’s for obesity and lipiddisorders (23). The active ingredients are theguggulsterones, which can be extracted withethyl acetate and standardized. Gugulipidhas been shown to lower serum cholesteroland triglycerides, lower LDL and raise HDL

levels. It’s primary mode ofaction seems to be theability to increase thenumber of hepatic LDLreceptors (22). It has also

been implicated to increase bile secretionand decrease cholesterol synthesis, possiblydue to the increased LDL receptors on livercells. As a single ingredient, patients shouldtry to get 50-75 mg of guggulsterones per dayin divided doses (24, 29). Much less (10-25mg/day) can be used when added withsynergistic ingredients for long-termcholesterol management.Tocotrienols: Tocotrienols are veryclosely related to Vitamine E (tocopherols).Found abundantly in rice bran oil and palmoil, tocotrienols may play a significant role inthe natural approach to cholesterolmanagement. A significant body of researchis available which shows direct reduction ofserum cholesterol (25, 26, 27, 28) with theingestion of gamma-tocotrienols as well asclosely related compounds. The mechanismis thought to be a suppression of the enzymeHMG-CoA reductase, but rather thaninhibiting the enzyme (leading to build upof the enzyme as well as other precursors),tocotrienols increase the breakdown of theenzyme. Available in soft gel capsules,tocotrienols should be an adjunct therapywith capsule and tablet form

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“Tocotrienols are sure to be one of the leading natural products

in the next decade.”

hypercholesterolemia products.Pantethine: As a precursor to Coenzyme A,a necessary component of the lipid catabolicprocess, pantethine would be a logical additionto lipid lowering regimens. Interestingly,pantethine has been shown to lowertriglycerides and LDL while increasing HDL by amechanism other than the coenzyme A portionof the molecule (9). Pantethine is thought toinhibit cholesterol synthesis (35) as well asaccelerate fatty acid break down in themitochondria. When using pantethine as asingle product, doses of 900 mg are indicated.Sub-therapeutic doses can work synergisticallywith other ingredients to reduce cholesterol andtriglyceride levels.Chromium: As we mentioned previously,proper carbohydrate metabolism is tied tolipid metabolism. Chromium has been usedfor a long time to increase insulin’s effect.Known as GTF (Glucose Tolerance Factor), aniacin derivative of chromium has been usedto help reduce serum glucose levels and movethe body into a state of lipid catabolism. Thisprimarily helps reduce triglycerides and tosome extent cholesterol. Chromiumsupplementation has been shown to increaseHDL and decrease total cholesterol andtriglycerides (34, 35). 100-200 mcg of

chromium is more than sufficient to improveglucose tolerance and work synergisticallywith the other natural ingredients mentioned.

ConclusionSince heart disease is the number one causeof death in the western world, and increasedserum cholesterol one of the major riskfactors, we cannot overlook naturalapproaches to treating this condition.Decreasing dietary intake of cholesterol,trans fatty acids and refined sugars is afoundation for any natural approach. Usinga wide variety of natural ingredients tosynergistically take advantage of theirdifferent cholesterol lowering properties isthe best natural approach to managingcholesterol. Since the treatment will last foryears, safety is a major concern. Using thesenatural ingredients, in sub-therapeutic, butsynergistic doses will ensure good results,low side effects, and increased patientcompliance. Becoming familiar with theseingredients and how they work for differentmetabolic types will make your approach tocholesterol management quit dynamic andwill soon become the standard.

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REFERENCES1. NCEP. Summary of the Second Report of the National Cholesterol Education Program (NCEP)Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults.JAMA.1993; 269:3015-30232. McBride P. Et. al. Primary care practice adherence to National Cholesterol Education Programguidelines for patients with coronary heart disease.Arch Intern Med, 1998; 158(11):1238-12443. Cohn, R.M. and Roth,K.S. Biochemistry and Disease. 1996.Williams & Wilkins Publishers, Baltimorepg 280.4. Staprans I. Et. al. Oxidized cholesterol in the diet accelerates the development of aorticatherosclerosis in cholesterol-fed rabbits.Arterioscler Thromb Vasc Biol. 1998; 18(6):977-9835. Mosca L. Et. al.Antioxidant nutrient supplementation reduces the susceptibility of low densitylipoprotein to oxidation in patients with coronary artery disease.J Am Coll Cardiol. 1997;30(2):392-3996. El-Eneim AMA. Et. al. The role of nicotinic acid and inositol hexaniacinate as anticholesterolemicand antilipemic agents. Nutr. Rep Intl. 1983; 28:899-9117. O’Hara J, Jolly P, and Nicol C.The therapeutic efficacy of inositol nicotinate (Hexapol) inintermittent claudication: a controlled trial. Brit J Clin Pract. 1988; 42:377-3938. Kiff R, and Quick CR. Does inositol nicotinate (Hexapol) influence intermittant claudication? Acontrolled trial. Brit J Clin Pract. 1988; 42:141-59.Wittwer C. Et. al. Pantethine lipomodulation: evidence for cysteamine mediation in vitro and invivo. Atherosclerosis. 1987; 68(1-2):41-4910. Maggi G, Donati C, and Criscuoli G. Pantethine: a physiological lipomodulating agent, in thetreatment of hyperlipidemias. Curr Ther Res. 1982; 32:380-611. Galeone F. Et. al. The lipid-lowering effect of pantethine in hyperlipidemic patients: a clinicalinvestigation. Curr Ther Res. 1983; 34:383-9012. Superko H. Et. al. Effects of solid and liquid guar gum on plasma cholesterol and triglycerideconcentrations in moderate hypercholesterolemia.Am J Cardiol. 1988; 62(1):51-5513. Glore S. Et. al. Soluble fiber and serum lipids: a literature review. J Am Diet Assoc. 1994;94(4):425-43614.Anderson JW. Dietary fiber, lipids and atherosclerosis.Am J Cardiol. 1987; 60(12): 17G-22G15. Sprecher D. Et al. Efficacy of psyllium in reducing serum cholesterol levels inhypercholesterolemic patients on high or low fat diets.Ann Intern Med. 1993; 119 (7 pt 1): 545-55416. Bell L. Et al. Cholesterol-lowering effects of psyllium hydrophilic mucilloid.Adjunct therapy to aprudent diet for patients with mild to moderate hypercholesterolemia.JAMA. 1989; 261(23):3419-342317. Levin E. Et al. Comparison of psyllium hydrophilic mucilloid and cellulose as adjuncts to aprudent diet in the treatment of mild to moderate hypercholesterolemia.Arch Intern Med. 1990;150(9):1822-182718. Sumiyoshi H. [New pharmacological activities of garlic and its constituents] [Abstract only,Article in Japanese]. Nippon Yakurigaku Zasshi. 1997; 110 (S1): 93P-97P.

19. Silagy C and Neil A. Garlic as a lipid lowering agent- a meta-analysis. J Royal College PhysLondon. 1994; 28:39-4520.Warshafsky S, Kramer R and Sivak S. Effects of garlic on total serum cholesterol.Ann Inter Med1993; 119:599-60521. Holzgartner H, Schmidt U and Kuhn U. Comparisons of the efficacy and tolerance of a garlicpreparation vs. bezafibrate.Arzneim-Forch Drug Res. 1992; 42:1473-722. Singh V. Et al. Stimulation of low density lipoprotein receptor activity in liver membrane ofguggulsterone treated rats. Pharmacol Res. 1990; 22(1):37-4423. Nityanand S, Srivastava J, and Asthana O. Clinical trials with gugulipid.A new hypolipidaemicagent. J Assoc Physicians India. 1989; 37(5):323-32824. Singh R, Niaz M, and Ghosh S. Hypolipidemic and antioxidant effects of Commiphora mukul asan adjunct to dietary therapy in patients with hypercholesterolemia.Cardiovasc Drugs Ther. 1994;8(4):659-66425. Sugano M and Tsuji E. Rice bran oil and cholesterol metabolism.J Nutr. 1997; 127(3):521S-524S26. Qureshi A. Et al. Response of hypercholesterolemic subjects to administration of tocotrienols.Lipids. 1995; 30(12):1171-727. Qureshi A. Et al. Dietary tocotrienols reduce concentrations of plasma cholesterol,apolipoprotein B, thromboxane B2, and platelet factor 4 in pigs with inherited hyperlipidemias.AmJ Clin Nutr. 1991; 53(4):1042S-1046S28. Qureshi A. Et al. Lowering of serum cholesterol in hypercholesterolemic humans by tocotrienols(palmvitee). Am J Clin Nutr. 1991; 53(4):1021S-1026S29. Lata S. Beneficial effects of Allium sativum,Allium cepa, and Commiphora mukul onexperimental hyperlipidemia and atherosclerosis- a comparative evaluation.J Postgrad Med.1991; 37(3):132-13530. Kamat J. Et al. Tocotrienols from palm oil as effective inhibitors of protein oxidation and lipidperoxidation in rat liver microsomes. Mol Cell Biochem. 1997; 170(1-2):131-731.Tomeo A. Et al.Antioxidant effects of tocotrienols in patients with hyperlipidemia and carotidstenosis. Lipids. 1995; 30(12):1179-8332. Parker R. Et al. Tocotrienols regulate cholesterol production in mammalian cells by posttranscriptional suppression of 3-hydroxy-3-methylglutaryl-coenzyme A reductase.J Biol Chem.1993; 268(15):11230-833. Pearce B. Et al. Inhibitors of cholesterol biosynthesis. Hypocholesterolemic and antioxidantactivities of benzopyran and tetrahydronaphthalene analogues of the tocotrienols.J MedChem. 1994; 37(4):526-4134. Lee N and Reasner C. Beneficial effect of chromium supplementation on serum triglyceridelevels in NIDDM. Diabetes Care. 1994; 17(12):1449-5235. Cighetti G. Et al. Modulation of HMG-CoA reductase activity by pantetheine/pantethine.Biocheim Biophys Acta. 1988; 963(2):389-39336. Mortensen S. Et al. Dose-related decrease of serum coenzyme Q10 during treatment withHMG-CoA reductase inhibitors. Mol Aspects Med. 1997; 18 Suppl:S137-S144

IN MY OPINIONAs many of you are aware, the approach to using natural medicines is quit different than current standardmedical approaches. It’s not just what’s in the capsule that is different, it can be everything from the patientinterview, diagnosing techniques, treatment modalities, and medications given. Those who think that“natural medicine” is simply replacing the pharmaceutical magic bullets with herbal or natural magicbullets are missing the point. Human beings are complex. When the body begins to show symptoms ofdisease, rarely are those symptoms directly linked with a single primary cause. Usually the symptoms willappear within the system of the body that is weakest in that individual, but your diagnosis and treatmentmay start elsewhere. Your goal is health, not merely lack of symptoms.

Preventative medicine is no longer truly preventative, but a management of sub-clinical conditions.We are told that atherosclerosis begins at a very young age in the United States (this was confirmed by the18-25 year old men, autopsied after being killed in the Korean War). Taking flavonoid antioxidants,vitamin E and other lipid protecting natural ingredients may prevent an eventual cardiac event, but is trulybeginning to reverse a sub-clinical blockage of the arteries. This is why natural medicine needs to beconsider all aspects of the individual when diagnosing and treating.

For instance… if bowel elimination is poor, the liver will be adversely affected. If the liver isperforming sub-optimally, all sorts of “unrelated” functions in the body can be affected (hormoneimbalances, serum glucose levels, heartburn to name a few). One could spend a lot of time treating eachsymptom until it was alleviated and another manifest, while the more simple increase of bowel transit timesmay help alleviate a host of symptoms.

Remember that natural medicine is no more ”wholistic“ (sic) than other systems of medicine unlessthe one administering it makes it so. You need to understand a whole range of diagnosing, treatment, andnatural ingredient options to become the best resource for your patients. It would be a tragedy to limitnatural medicine to just herbal alternatives to prescription drugs.

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