UNLV Retrospective Theses & Dissertations 1-1-2000 The effects of Bios Life and exercise on total cholesterol, serum low-density lipoprotein, and high-density lipoproteins Lori Jan Inderlied-Rucks University of Nevada, Las Vegas Follow this and additional works at: https://digitalscholarship.unlv.edu/rtds Repository Citation Inderlied-Rucks, Lori Jan, "The effects of Bios Life and exercise on total cholesterol, serum low-density lipoprotein, and high-density lipoproteins" (2000). UNLV Retrospective Theses & Dissertations. 1207. http://dx.doi.org/10.25669/wkee-r66y This Thesis is protected by copyright and/or related rights. It has been brought to you by Digital Scholarship@UNLV with permission from the rights-holder(s). You are free to use this Thesis in any way that is permitted by the copyright and related rights legislation that applies to your use. 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Contact UMI directly to order.Bell & Howell Information and Learning 300 North Zeeb Road, Ann Aitwr, Ml 48106-1346 USA 800-521-0600UMI*Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.THE EFFECTS OF BIOSLIFE AND EXERCISE ON TOTAL CHOLESTEROL, SERUM LOW DENSITY LIPOPROTEIN, AND HIGH DENSITY LIPOPROTEINSbyLori Jan Inderlied-RucksBachelor of Arts University of Pittsburgh 1996A thesis submitted in partial fuhilhnent o f the requirements for theM aster of Science in Exercise Physiology Departm ent of Kinesiology College of Health SciencesG raduate College University of Nevada, Las Vegas August 2000Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.UMI Number: 1403080Copyright 2000 by Inderlied-Rucks, Lori JanAll rights reserved.UMIUMI Microform 1403080 Copyright 2001 by Bell & Howell Information and Learning Company. All rights reserved . This microform edition is protected against unauthorized copying under Title 17, United S ta tes Code.Bell & Howell Information and Learning Com pany 300 North Zeeb Road P.O. Box 1346 Ann Arbor, Ml 48106-1346Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.Copyright by Lori Jan Inderlied-Rucks 2000 All Rights ReservedReproduced with permission of the copyright owner. Further reproduction prohibited without permission.UNTV Thesis ApprovalThe Graduate College University of Nevada, Las VegasJune 22 ^20 00The Thesis prepared byLori Jan Inderlied-RucksEntitledThe effects of BiosLife and Exercise on Total Cholesterol, Serum Low Density Lipoprotein, and High Density Lipoproteins___________is approved in partial fulfillment of the requirements for the degree of _________________ M a ste r o f S c ie n c e i n E x e r c is e P h y s io lo g ynation Comrrmtéemination Committee MemberGraduate College Factnty RepresentativeI i Examination Committee ChairDean o f the Graduate CollegePR/1017-53/1-00 11Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.ABSTRACTThe Effects of Bios Life and Exercise on Total Cholesterol, Serum Low Density Lipoprotein, and High Density LipoproteinbyLori Jan Inderlied-RucksLawrence A. Golding, PhJD. Examination Committee Chair, Distinguished Professor o f Kinesiology, University o f Nevada, Las VegasThe present study was designed to determine the effects of Bios Life, a nonprescription dietary fiber supplement, on serum lipoproteins and determine whether exercise accentuates this effect. Fifty male and female subjects (ages 30-60) participated in the study. Twenty-five subjects were exercising regularly in a supervised exercise program and the other twenty-five were sedentary. All participants where required to have a LDL-C o f 130 mg/dl or higher and none were on any cholesterol lowering medications. Blood was drawn three times at baseline, before the study started, 45 days into the program and at 90 days which was the end o f the study. Total cholesterol, HDL and LDL’s were analyzed by the Cholestech L.D.X. system. A mixed model ANOVA was used to analyze the data. The results indicated significant decreases in total cholesterol from baseline to 45 to 90 days (F = 18.29, p<0.05) with no significant difference between exercise and non-exercise groups (F = 0.20, p>0.05). The results also indicated significant decreases in LDL’s from baseline to 45 to 90 days (F = 21.60, p<0.05) with no significant difference between exercise and non-exercise groups (F =iiiReproduced with permission of the copyright owner. Further reproduction prohibited without permission.1.59, p>0.05). The analysis o f the HDL’s yielded no significant difference between exercise and non-exercise groups (F = 1.07, p>0.05) no r was there a significant difference from baseline to 45 to 90 days (F = 1.67, p>0).05). These results suggest that whether or not one participates in an exercise program B ios Life will decrease total cholesterol and LDL’s equally without c hanging HDL’s , which may help reduce the risk o f coronary heart disease.IVReproduced with permission of the copyright owner. Further reproduction prohibited without permission.TABLE OF CONTENTSABSTRACT............................................................................................................................... iiiLIST OF FIGURES.................................................................................................................. viiACKNOWLEDMENTS......................................................................................................... viiiCHAPTER 1 INTRODUCTION.............................................................................................. 1CHAPTER 2 LITERATURE REVIEW...................................................................................5Chemical Nature o f Cholesterol.............................................................................................5Production, Absorption, Transportation and Excretion...................................................... 6Metabolism...............................................................................................................................8Cholesterol and Age................................................................................................................ 8Diurnal and Seasonal Variations.......................................................................................... 10Cholesterol and Heart Disease............................................................................................. 11Cholesterol and Fiber............................................................................................................16Cholesterol and Exercise......................................................................................................22Cholesterol Lowering Drugs................................................................................................ 33Summary.................................................................................................................................36CHAPTER 3 METHODS........................................................................................................ 40Subjects..................................................................................................................................40Research Design.................................................................................................................... 41Statistical Design................................................................................................................... 41Pmcedure................................................................................................................................41Cholestech LDX.................................................................................................................... 44CHAPTER 4 RESULTS & DISCUSSION........................................................................... 48Total Cholesterol....................................................................................................................48Low Density Lipoprotein Cholesterol.................................................................................49High Density Lipoprotein Cholesterol................................................................................51CHAPTER 5 SUMMARY AND CONCLUSIONS.............................................................56Summary................................................................................................................................. 56Conclusions.............................................................................................................................57Recommendations................................................................................................................. 58Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.APPENDIX A ..........................................................................................................................59Instructions to Subjects....................................................................................................... 60Memorandum to Subjects.................................................................................................... 63APPENDIX B ..........................................................................................................................65Approval Letter from Institutionsl Review Board............................................................ 6 6Informed Consent................................................................................................................. 67APPENDIX C ..........................................................................................................................69Instructions o f Dietary Survey.............................................................................................70Helpful Measuring Guide.................................................................................................... 71Dietary Survey......................................................................................................................72Explanation o f Dietary Survey............................................................................................ 73List o f Minerals and Vitamins............................................................................................ 76APPENDIX D ..........................................................................................................................78Data Sheet............................................................................................................................. 79Raw D ata.............................................................................................................................. 82APPENDIX E ..........................................................................................................................85Physical Characteristics....................................................................................................... 8 6Body Composition Tables................................................................................................... 8 8Body Mass Index................................................................................................................. 89Waist/Hip Circumference.................................................................................................... 90Waist/Hip Ratio Percentile for Heart Disease...................................................................91BIBLIOGRAPHY................................................................................................................... 92VITA........................................................................................................................................107VIReproduced with permission of the copyright owner. Further reproduction prohibited without permission.LIST OF FIGURESFigure I Total Cholesterol over Tim e................................................................................ 49Figure 2 Total Cholesterol and Exercise Group................................................................. 49Figure 3 LDL Cholesterol over Time................................................................................. 50Figure 4 LDL Cholesterol and Exercise Group................................................................. 50Figure 5 HDL Cholesterol over Time................................................................................. 51Figure 6 HDL Cholesterol and Exercise Group................................................................. 52vnReproduced with permission of the copyright owner. Further reproduction prohibited without permission.ACKNOWLEDMENTSMy external gratitude to my graduate examing committee. Dr. Lawrence Golding, Dr. John Young, Dr. Richard Tandy and Dr. Richard Hoyt. Special thanks to Dr.Golding for his patients, knowledge and support.My thanks to Dr. Uhl, Lori Winchell, Dr. Susan Meacham, and Kelly Rucks for your donations and extra time spent on preparing this thesis. Without your help my research could not have been completed.My utmost gratitude to aU o f the subjects who volunteered their time to participate in this study. It was not always easy for them to drink the Bios Life, but they still continued to adhere to the program.To my husband Aaron, I thank you for your love, support, encouragement, time, patience and understanding through the ups and downs o f completing this study. I love you.To my family and closet jfriends Mom and Dad Inderlied, Lisa and David Peltz, Mark and Korri Inderlied, Matthew and Carrie Inderlied, Richard Miller, Bridgett Passauer, Katherine Goodman, Mama Youngberg and Anthony Santo thank you all for standing behind me and picking me up when the going got tough you are tmly my number one fens.A special thanks to Eugene Bailey, having you as my first cardiac patient, opened my eyes to a world o f strength, endurance and never giving up.V lllReproduced with permission of the copyright owner. Further reproduction prohibited without permission.To my grandparents Dr. and Mrs. H.F. Inderlied your love, passion and knowledge of medicine some how found its way to me. May your spirit and memory live in us all forever.IXReproduced with permission of the copyright owner. Further reproduction prohibited without permission.CHAPTER 1 INTRODUCTIONCoronary heart disease (CHD) is the leading cause o f death in the United States. The American Heart Association (AHA) statistics show that in 1993 there were 489,970 deaths from CHD. In 1998, as many as 1,500,000 Americans had a new or recurrent heart attack and about one third died. In 1993 artherosclerosis was the underlying cause of many o f the 639,710 heart attack and stroke deaths. In the U.S. approximately 96 million adults have total blood cholesterol levels o f over 200mg/dl and 37.8 million have levels greater than 240 mg/dl according to the AHA. These high levels are a major contributor to artherosclerosis and other types o f coronary artery disease. Due to its lifestyle etiology, CHD is expected to remain the leading cause o f death for future years. These statistics prove that CHD is a major public health problem and concern (Anderson, Zettwach, Feldman, Clark, Oeltgen & Bishop, 1988).It has been well documented that both high levels o f total serum cholesterol and specifically low-denshy lipoproteins (LDL-C cholesterol) are linked with coronary heart disease (Bridges, Anderson, Deakins, Dillon & Wood, 1992). From the epidemiological data from the Fram ingham Heart Study elevated total serum cholesterol was determined to be a major coronary risk factor. Larosa and associates (1990) studied 2,282 men and 2,845 women investigating CHD history and total cholesterol levels and concluded that there was definite evidence that high levels o f total cholesterol were associated with aReproduced with permission of the copyright owner. Further reproduction prohibited without permission.2high incidence o f CHD and that low levels o f total cholesterol were associated with a low incidence o f CHD (Larosa, Becker & Fitzgerald, 1990).The National Cholesterol Education Program (Expert Panel, 1993) recommends the following values for cholesterol in individuals to be:Total Cholesterol < 200mg/dlHDL > 35mg/dlLDL < 130mg/dlIndividuals with 200-239 mg/dl are considered borderline risk and those with total cholesterol greater than 240 are at abnormal risk. Increasing HDL and decreasing LDL reduces the risk o f CHD (Anderson, Riddell-Mason, Gustafson, Smith & Mackey, 1992). A lowfat diet was initially the main method o f reducing total cholesterol. New cholesterol lowering drugs are now commonly prescribed. Cholesterol lowering drugs were classified into bUe acids, sequestrates, nicotinic acids, statins, fibric acids and probucol (Anderson et al., 1988). The goals o f drug therapy was to lower total cholesterol, raise HDL’s and lower LDL’s. However, there were several major side effects. The side effects can range from itching o f the skin, gastrointestinal distress, liver toxic effects, and muscular damage due to interaction between drugs and blood clots (JAMA, 1993).Dietary therapy remains the first choice for treatment o f high cholesterol. There is evidence indicating that dietary fiber has important lipid lowering effects and may reduce risk o f CHD (Bell, Hectom, Reynolds & Hunninghake, 1990). Increasing Dietary fiber intake is an important therapeutic treatment for other specific conditions besides CHD such as diabetes, hyperlipidemia, hyperglyceridemia, hypercholesterolemia andReproduced with permission of the copyright owner. Further reproduction prohibited without permission.3intestinal disorders (Anderson, Gilinsky, Deakins, Smith, O’Neal, Dillion & Oeltgen,1991). Individuals consuming a diet high in fiber tend to have lower incidence o f myocardial infarction and sudden cardiac death (HaskeU, Spiller, Jensen, Ellis & Gates,1992).Dietary fiber is defined as “the endogenous components of plant materials in the diet that are resistant to digestion by enzymes produced by man” (Anderson, 1987).There are two main types o f fibers soluble and insoluble. In experimental studies, soluble fiber has been shown to reduce blood cholesterol levels. Soluble fiber increases the fecal excretion o f bUe acids, which may alter the quantity o f cholesterol absorbed by the intestine. The fibers fi’om fi’esh fimits, vegetables, legumes, oat bran and barley appear to have the most significance for reducing cholesterol levels (Haskell et al., 1992).Insoluble fiber, such as, wheat bran have essentially no effect on serum cholesterol levels.The general purpose o f dietary fiber as therapy is to reduce elevated serum cholesterol levels. This is achieved primarily by reducing fat intake and consuming a healthy diet, rich in fiber. Dietary therapy in conjunction with regular exercise is considered an essential element in therapy o f elevated serum cholesterol (Ready, 1996). Exercise has been shown to help in the promotion o f weight reduction which enhances LDL cholesterol lowering, reducing triglyceride, raising HDL, reduces blood pressure and decreasing the risk for diabetes mellitus (Grundy, 1986). Therefore, the combination o f regular exercise and diet rich in fiber should lower total cholesterol, increase HDL, decrease LDL and consequently reduce the risk o f CHD.The purpose o f this study was to investigate the effects o f Bios Life, a nonprescription dietary fiber supplement, on Total, LDL cholesterol and determine whetherReproduced with permission of the copyright owner. Further reproduction prohibited without permission.4exercise accentuates this effect. The null hypothesis is that exercise does not accentuate the effect o f Bios Life on Total Cholesterol, Low-Density Lipoproteins and High-Density Lipoproteins and the alternate hypothesis is that exercise accentuates the effect o f Bios Life on Total Cholesterol, Low-Density Lipoproteins and High-Density Lipoproteins.Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.CHAPTER!LITERATURE REVIEW An adult male weighing 70kg would have approximately 140g o f cholesterol present in the body with 8 g o f this in the plasma (Sabrine, 1977). The average synthesis of cholesterol in the body is about lOOOmg per day. The daily production is approximately 400mg from intestinal absorption and 600mg synthesized in the cells and the liver. An adult consuming a normal American diet ingests about lOOOmg per day. Every cell o f the body, except a mature red blood ceU, produces cholesterol (Sabrine, 1977). The liver is a major organ in cholesterol synthesis. The liver must synthesize and maintain control over the enzymes that convert acetyl coenzyme A to cholesterol. More than ninety percent o f the cholesterol in the body is found in the cell membrane.Chemical Nature o f Cholesterol At the end o f the eighteenth century a French chemist de Fourcroy described the compound now known as cholesterol by isolating a crystalline substance from the alcohol-soluble fraction o f human gallstones (Sabrine, 1977). About the same time another French chemist Chevreue detected it in human and animal bile (Sabrine, 1977). After the turn o f the century another French chemist Lecanu found cholesterol in the blood o f humans (Sabrine, 1977). De Fourcroy’s gave the name cholesterine from the Greek words Chole meaning bile and Steros meaning solid (Sabrine, 1977). The correctReproduced with permission of the copyright owner. Further reproduction prohibited without permission.6empirical formula (C2 7 H4 6 O) was published in 1888 by Reinitzer (Newsholme & Leech,1983).Cholesterol is probably the best known sterol, which is essential to the human body. “Cholesterol is found associated with the fets, but chemically it is not related to them. Cholesterol, a white waxy solid, is the principal sterol found in animal organisms” (Smolin & Grosvenor, 1997). Most o f the cholesterol found in the body occurs in free form, the unesterifred alcohol, which is precipitable by digitonin. The so-called bound cholesterol is found in much smaller portions; it is present as the ester o f long chain fatty acids. The largest amount o f cholesterol is found in muscle, nervous and connective tissue. It is needed to synthesize vitamin D, cholic acid which is part o f bile, some hormones, and cortisol which promotes glucose synthesis in the liver (Smolin & Grosvenor, 1997).Production, Absorption, Transportation and Excretion Cholesterol is not soluble in water therefore it can not enter the blood stream directly. Lipoproteins called chylomicron are formed to help cholesterol enter the blood stream (Williams, 1997). Chylomicrons are formed by combining triglycerides with cholesterol, free fatty acids, phospholipids, traces o f fat soluble vitamins, steroid hormones and lipoproteins (Williams, 1997). Once chylomicrons are produced they will carry lipids from the intestines and deliver triglycerides to body cells. On the surface o f cells, lining the blood vessels is lipoprotein lipase which breaks down the triglycerides too fetty acids which can be either used as fiiel or resynthesized into triglycerides for storage. After the breakdown o f chylomicron cholesterol and protein remain and returned to the liver (Smolin & Grosvenor, 1997).Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.7Crystalline cholesterol administered orally is absorbed in only small amounts unless some fatty material is also present in the intestine. This is not true with colloidal or amorphous cholesterol, which can be absorbed in the absence o f dietary fat. Bile and pancreatic juices are said to be two agents, which aid in the absorption o f cholesterol, because the combination o f cholesterol with bile acids increase the solubility of cholesterol in intestinal fluids. Pancreatic and intestinal enzymes hydrolyze cholesterol esters, which are later re-synthesized before reaching the lymph stream, the main route by which cholesterol is absorbed. Some cholesterol is absorbed directly into the blood stream; part o f the absorbed free cholesterol, but not the ester, is excreted in the bile; part is changed to coprosterol and eliminated later in the feces (Smolin & Grosvenor, 1997).Lipids are produced in the liver, by breaking down excess protein, carbohydrate or alcohol to produce either triglycerides or cholesterol. In the liver triglycerides, cholesterol, fatty acids and returned chylomicron are formed into very-low-density lipoprotein (VLDL) (Smolin & Grosvenor, 1997). VLDL carries a large lipid content, but also contains about ten to fifteen percent cholesterol formed in the liver from endogenous fat stores (Williams, 1997). VLDL transport lipids out o f the liver and delivers triglycerides to body cells. They must be broken-down by the enzyme lipoprotein lipase so that fatty acids can be taken up by the cells (Smolin & Grosvenor, 1997).Triglycerides are removed from VLDL leaving a smaller intermediate density lipoprotein (DDL) which contains mostly cholesterol. These IDL’s are either transported to the liver or formed into low-density lipoproteins (LDL’s). LDL’s are lipoproteins that transport cholesterol to cells. For LDL’s to be taken up by the cells, apoliprotein B, mustReproduced with permission of the copyright owner. Further reproduction prohibited without permission.8bind with the LDL receptor. A LDL receptor is a protein on the surface o f all cells, which binds to LDL particles and allows their contents to be taken up for uses by the cell (Smolin & Grosvenor, 1997).The body can not breakdown cholesterol esters, so it must be transported back to the liver where then it will be eliminated from the body as bile. This process is done by high-density lipoprotein (HDL). HDL’s are manufactured in the intestinal tract. They are then transported through blood to pick up cholesterol from cells so that the body can excrete it (Smolin & Grosvenor, 1997).MetabolismThe synthetic process o f cholesterol takes place in the liver and may occur in other organs. In all tissues except in the brain, cholesterol is continually regenerated. I f any organ can be singled out as the single most important to metabolize cholesterol and some amount o f plant sterols, it is the hver. It can both synthesize and destroy cholesterol. The breakdown and lose o f cholesterol can occur in four ways:1. By direct reduction to dihydrocholesterol or by passage through the intermediate cholesterone to dihydrocholesterol or coprosterol.2. By loss o f cholesterol in the feces.3. By conversion into steroid hormones.4. By conversion to bile acids in the liver.Cholesterol and AgeThere are a number o f variables that are important in determining or changing the level of blood cholesterol in the body. Throughout the day the level o f serum cholesterol remains for the most part constant, even though there is a large variation in the rate thatReproduced with permission of the copyright owner. Further reproduction prohibited without permission.9cholesterol enters and leaves the body (Winkel, Stratland & Bokelund, 1974). Over an extended period o f time the amount o f exdogensis cholesterol entering the body compared to cholesterol degradation will rise significantly (Hollister & Wright, 1956). This significant rise will eventually reach abnormal level o f cholesterol (Hollister & Wright, 1956).Females at birth have slightly higher levels o f plasma cholesterol than males. During childhood, adolescence and early adulthood there is very little difference in blood cholesterol between men and women (Syerberg & Hjome, 1973). In later life males tend to have higher serum cholesterol levels due to higher concentrations o f VLDL and LDL. Serum cholesterol levels tend to be lower in premenstrual women. After the age o f 50 male cholesterol levels tend to lower as females tend to raise slightly (Adlersberg, Schaefer, Steinberg & Wang, 1956). This rise in serum cholesterol levels in women is due to the fact that women going through menopause have lower levels o f estrogen. Estrogen is a cholesterol-lowering agent and the decrease o f estrogen during menopause is the cause o f rising serum cholesterol levels in women.At birth plasma levels o f cholesterol are usually low around 80mg/dl (Darmady, Fosbrooke & Llyod, 1972). Glueck, Heckman, Schoenfeld, Steiner and Pearce, (1971) studied the umbilical cord blood cholesterol in 1800 consecutive unselected live births and found it to be about 80mg/100 ml. After birth cholesterol rises rapidly to around 183 mg/100ml for the average male 20 to 29 years o f age depending mostly on diet (Fredrickson, Levy & Lees, 1967). Throughout life, cholesterol levels continue to rise slowly (Darmady, Fosbrooke & Lloyd, 1972). At about 50 years o f age serumReproduced with permission of the copyright owner. Further reproduction prohibited without permission.10cholesterol levels begin to plateau off. In men the level begins to drop slightly and in women blood cholesterol may continue to rise after 50 (Fredrick, Levy & Lees, 1967).Adlerberg and associates (1956) studied approximately 1,200 healthy males and females between the age o f 2 and 77 years. Their blood serum was analyzed fijr cholesterol in order to establish average lipid levels. It was found that in the age groups 3-12 and 53-57, the females have significantly higher cholesterol levels than men, whereas, in age groups 28-42 males have significantly higher levels than women. Adlersberg also compared the serum cholesterol levels between males and females at different age groups. The total serum cholesterol level of the males remained constant fi-om age 2 throughout 19. From the age 20 to 33 there was a significant increase o f total cholesterol level. No change was seen imtil after age 60. The total serum cholesterol level o f the females did not change significantly from age 2 through 32. From age 33 to 58 a significant increase o f 3.2 mg per lOOcc per year was seen. The difference in the serum cholesterol levels at the different age-trends between males and females may be the result from evidence showing that males at a young age start to show signs o f coronary artery disease and among women they tend to show signs o f coronary artery disease after the age o f 50 around the time o f menopause (Adlersberg, Schaefer,Steinberg & Wang, 1956).Diurnal and Seasonal Variations Several studies have examined seasonal fluctuations o f serum cholesterol in man. Fyfe, Dunnigan, Hamilton and Rae (1968) studied the seasonal variation o f 5,630 serum cholesterol and serum triglyceride on patients with confirmed or suspected ischemic heart disease. Serum cholesterol levels were at their peak in the spring, and fell progressivelyReproduced with permission of the copyright owner. Further reproduction prohibited without permission.11to the lowest level in autumn. Serum Triglyceride did not exhibit this kind o f seasonal fluctuation. This study concluded that the highest level o f serum cholesterol occur in the spring and the lowest in the autumn (Fyfe et al., 1968).Cholesterol and Heart DiseaseAtherosclerosis is the major disease affecting the heart and blood vessels, and is the leading cause o f death in the United States (Bierman & Chait, 1988). According to the International Atherosclerosis Project; observations were made on 19 different countries and race groups concluding that “practically aU persons have some degree o f atherosclerosis when examined at autopsy” (McHill, 1968). Atherosclerosis is a progressive disease throughout life. The severity which it develops seems to be due primarily to environmental conditions (Gresham, 1972). Since the 1960’s the number o f deaths from coronary artery disease has been declining at a fast rate but stül nearly half o f the deaths in this country are from blood vessel diseases (Lipid Research Clinics Program, 1984).Atherosclerosis is the result o f fatty cholesterol deposits in blood vessel walls; reducing elasticity and eventually blocking blood flow (Smolin & Grosvenor, 1997). It is a disorder o f the coronary arteries, cerebral arteries, iliac and femoral arteries and aorta that is responsible for coronary heart disease, stroke and peripheral arterial disease (Bierman & Chait, 1988). Atherosclerosis is characterized by the collection o f lipids in smooth muscle cells, macrophages o f the inner lining o f the walls o f arteries (Bierman & Chait, 1988).In 1833 Lobstein introduced the word atherosclerosis, athero meaning gruel or musk and scleroses meaning hardening o f the arteries (Katz & Stamler, 1953). MichaelReproduced with permission of the copyright owner. Further reproduction prohibited without permission.12Brown and Joseph Goldstein showed the connection between the discovery o f LDL receptors on cells with the development o f atherosclerosis (Smolin & Grosvenor, 1997). LDL receptors bind to LDL particles and help them to be absorbed by the cell. A high level o f LDL means there is too much cholesterol or not enough LDL receptors cells, this leads to cholesterol deposits in the artery walls causing atherosclerosis (Smolin & Grosvenor, 1997).Even though extensive studies have been done on atherosclerosis, there is stdl no known cause o f the exact events which initiate the buildup of cholesterol in arterial walls (Grundy, 1990). One theory is an injury to the arterial wall is caused by high blood pressure, viruses, chemicals or some other factor (Brown & Goldstein, 1984). Another theory suggests that the presence of high levels o f blood cholesterol causes injury to the arterial wall (Brown & Goldstein, 1984). Inside the artery wall, as the injury occurs, oxidized LDL cholesterol binds to scavenger receptors located on the surface o f the white blood cells. The white blood cells fill up with the oxidized LDL cholesterol and burst depositing cholesterol to form a fatty streak inside the artery wall. This process leads to an excessive amount o f cholesterol, smooth muscle cells and fibrous tissue called plaque. The plaque will collect calcium causing it to became hard. Blood clots wUl form around the plaque causing the artery to narrow and lose it’s elasticity. The artery becomes blocked and will no longer allow blood flow to supply oxygen and nutrients to the ceU, leading to the death o f cells (Smolin & Grosvenor, 1997).Atherosclerotic lesions in the coronary arteries lead to CHD, which is the most common and most serious o f cardiovascular diseases in middle-aged adults (National Research Coimcil, 1989). If atherosclerosis causes interference with blood flow to theReproduced with permission of the copyright owner. Further reproduction prohibited without permission.13myocardium a Myocardial Infarction results. One third o f aU myocardial infarction cases, coronary artery occlusion is the cause o f death in myocardial cells (National Research Council, 1989). Patients may also suffer from failure o f the heart to pump sufficient blood, known as congestive heart failure, or irregular heart beats, known as arrhythmias. The presence o f severe lesions in the coronary arteries will often cause angina pectoris, especially on exertion (National Research Council, 1989).Cholesterol has received much attention, especially in view o f the well known clinical fact that certain diseases and syndromes often associated with hypercholesteremia, including diabetes mellitus, the nephrotic syndrome, myxedema, and familial hypercholesteremia, predispose to premature atherosclerosis. In spite o f the fact that cholesterol levels are often above 260 mg in persons with atherosclerosis, there is evidence that a high proportion o f people develop atherosclerosis with blood levels in the normal range o f 125 to 260 mg (Barry, 1997).Incidence o f CHD varies widely from one country to another, which sparked the interest o f researchers to answer the question o f why cholesterol in blood and coronary heart disease is so different between countries (Frayn, 1996). Researchers started by looking at international coronary artery disease mortality data and autopsy records from cross-population studies which provided evidence supporting a significant association between CAD and dietary fat intake (Caggiula & Mustad, 1997). The Seven-Country study and the Japan-Honolulu-San Francisco study established the importance o f the fatty acid composition o f dietary fats with the link o f increased rates o f CHD.In the “Seven Country Study” dietary intake o f the participants was done by a 7- day food record and then a sample o f each food consumed was chemically analyzed. TheReproduced with permission of the copyright owner. Further reproduction prohibited without permission.14results showed in Finland and the United States total fat intake was 40% o f energy and in Japan it was 20% o f energy. Saturated Fatty Acid (SFA) intake ranged from 20% in the United States to less than 10% o f energy in Japan. This study was the first to show a strong correlation between SFA, coronary artery disease and death. This study showed that coronary artery disease rates were low despite moderately high total fat intakes, especially when SFA intakes were high (Keys, 1970).Three middle-aged men o f Japanese ancestry living in either Japan, Honolulu or San Francisco participated in a study observing the relation between SFA, cholesterol and heart disease. The intake o f total fat differed significantly among the three different cultures. In Japan the percent o f energy from fat was 15%, in Honolulu it was 33% and San Francisco participants SFA intake ranged from 7%, 13% and 38% (Kato, Tilloston, Nichaman, Rhodes & Hamilton, 1973). Coronary artery disease mortality was 1.7 times higher in Hawaii and 2.8 times higher in San Francisco than in Japan. Although no single dietary factor existed that is associated with coronary artery disease between and within aU different countries the mortality in these populations SFA and cholesterol are generally positively correlated with coronary artery disease (Kato et. al., 1973).There are specific differences in death rates from coronary artery disease among most industrialized countries (Shils & Young, 1988). The highest rate o f CAD in males between 35 and 74 years is seen in Finland and the United States. Eastern Europe and Japan are about one fifth o f that in the United States. These differences in CAD maybe due to genetic factors, but as seen with Japanese migrants to the United States they have rapidly accumulated the risk o f artherosclerosis through western diet and lack o f exercise (Shils & Young, 1988). Evidence suggests that cultural and environmental factorsReproduced with permission of the copyright owner. Further reproduction prohibited without permission.15including diet may have an important part in CAD, but genetics probably explains the difference in CAD among individuals from the same ethnic and cultural background (Shils & Young, 1988).There are a number o f conditions and habits that are correlated with the incidence o f CAD and these have been termed “coronary risk factors” (Dawber, 1975). Non- reversible risk factors or otherwise known as primary risk factors are aging, male sex and genetic traits: i.e. positive family history o f premature atherosclerosis (Dawber, 1975). Potentially reversible risk factors or Secondary risk factors are: cigarette smoking, hypertension, obesity, hyperlipidemia, hypercholesterolemia, hyperglycemia, diabetes mellitus, low levels o f HDL’s and sedentary lifestyle (JAMA, 1993). Other possible risk factors are body build, emotional stress and personality type (JAMA, 1993).Hyperlipidemia consists o f increased plasma levels o f cholesterol and/or triglycerides (Dawber, 1975). The elevated plasma hpid levels result from one or more abnormalities o f lipid metabolism or transport (Dawber, 1975). Hypercholesterolemia and hypertriglyceridemia seem to play an important role in the development of atherosclerosis.Hypercholesterolemia is associated with increased incidence o f premature CAD, but it’s importance varies in relation to age. The incidence o f myocardial infarction in individuals between the ages o f 30 and 49 with cholesterol levels greater than 260 mg/dl was three to five times higher than in individuals with cholesterol levels less than 2 0 0 mg/dl (Bierman & Ross, 1977).Hypertriglyceridemia has a significant relationship to CAD due to increased triglycerides and very low density lipoproteins (VLDL) (Assmann & Schulte, 1992).Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.16Individuals with elevated VLDL levels may have an increased risk for premature atherosclerosis due to the fact that high levels o f VLDL will be transformed into LDL and an even higher risk if the individual has other risk fectors such as diabetes, smoking and hypotensive (Assmann & Schulte, 1992).Goldstein (1973) studied the role o f genetics o f hyperlipidemia in atherosclerosis in 500 survivors o f myocardial infarctions. The study showed that approximately one half o f the males and two thirds o f females below the age o f 50 had either hypertriglycerdemia, hypercholesterolemia or both. In the individuals over 70 the presence o f atherosclerotic coronary disease was high, but no males and one fourth o f the females had hypertriglycerdemia or hypercholesterolemia. It appears that hyperlipidemia is more of a risk factor in individuals below the age o f 50, and for men and women over the age of 65, however, there is no evidence to support a correlation between hyperlipidemia and atherosclerosis (Goldstein, Hazzard, Schrott, Bierman & Motulsky, 1973).Cholesterol and Fiber Treatment o f high total blood cholesterol begins with dietary therapy. The goal of dietary therapy is to lower LDL-cholesterol to levels under 130 mg/dl if definite CHD or two other CHD risk factors are present (Expert Panel, 1993). The general purpose o f dietary therapy is to reduce elevated cholesterol levels while maintaining a healthy adequate diet. Modification o f the patient’s diet is an essential element of therapy (Expert Panel, 1993). One o f the important modifications to help reduce high levels o f cholesterol through diet is to increase the intake o f dietary fiber (Anderson et al., 1991).Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.17The effect o f fiber in various disease conditions has been studied for several years. British scientists in the 1960’s concluded that many diseases and disorders o f the Western society were related to a low intake o f dietary fiber (Council on Scientific Affairs, 1989). They compared Western cultures to rural Afirican blacks and found that cancer o f the colon and gastrointestinal disorders were rare in this society due to high- fiber diets and production o f soft stools in large volume (Council Scientific Affairs,1989). In Western cultures where life-styles and diet contain high amounts o f saturated fat and low amounts o f fiber the incidence o f heart disease is much higher (Council Scientific Affairs, 1989).Dietary fiber has been shown to have an important lipid lowering effects and may reduce risk for coronary artery disease (Anderson & Tietyen-Clark, 1986). Dietary fibers, are the endogenous components o f plant material in the diet that are resistant to digestion by enzymes produced by man (Pilch, 1987). Dietary fibers can be classified according to their water solubility. Most water insoluble fibers such as cellulose, cellulose-rich products and lignin (i.e. wheat bran) do not lower serum cholesterol concentrations o f humans or animals (Anderson, 1987). Water-soluble fibers (pectins, gums, and mucilages) and diets high in water-soluble fiber fi'om oats and bran decrease the glycémie response to foods and lower serum cholesterol concentrations (Anderson, 1987).The theories o f how fiber lowers cholesterol levels include the following: (1) Soluble fibers bind bile acids and other lipids and may interfere with micelle fijnnation in the small intestine resulting in alterations in the quantity o f cholesterol or fetty acids absorbed or altering the size o f lipoprotein particles formed by intestinal mucosa (CouncilReproduced with permission of the copyright owner. Further reproduction prohibited without permission.18on Scientific AflFairs, 1989). (2) Soluble fibers increase the fecal excretion o f bile acids and may interfere with cholesterol and bile acid homeostasis sufiiciently to affect hepatic secretion o f lipoproteins. (3) Soluble fibers fermented by colonic bacteria form gases and short chain fatty acids (Council on Scientific Affairs, 1989). Short Chain fatty acids are almost completely absorbed into the portal vein and could effect hepatic cholesterol synthesis (Council on Scientific Affairs, 1989). However various types o f dietary fiber have different effects on serum cholesterol (Anderson & Chen, 1979). Soluble fiber (Pectin, guar gum, barley and oat bran) have been shown to reduce blood cholesterol levels, when given in large amounts (Life Sciences Research OfiBce, 1987). The fibers fi-om fi-esh fimits, vegetables, legumes, oat bran and barley appears to have the most potential for reducing cholesterol levels (Life Sciences Research Office, 1987). Insoluble fibers such as wheat bran have a very small or no effect on serum cholesterol levels (Nutrition Committee, American Heart Association, 1988).Anderson and associates (1991) studied 20 hypercholesterolemic men admitted to a hospital metabolic ward. They were randomly divided into either an oat bran or wheat bran group for 21 days after a 7-day control-diet period. Both the control and treatment diets were designed to have the same energy content and nutrients, the only difference is in the amounts o f soluble fiber. After the 21 day o f treatment oat bran significantly decreased total cholesterol by 12.8% and lov/ density-lipoprotein cholesterol by 12.1%. Wheat bran had no significantly change. In both groups high density lipoprotein did not change significantly. They concluded that oat bran could have been effective in reducing the risk for CHD, since they found a significant reduction in total cholesterol and low density lipoproteins (Anderson et al., 1991).Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.19Kestin, Moss, Clifton and Nestel (1990) had similar findings on 24 mildly hypercholesterolemic men on the effects o f adding 11.8g dietary fiber per day from each o f three cereal brans (wheat, rice and oat) to a low-fiber diet for 4 weeks each. The subjects were placed on a low-fiber diet for 3 weeks and randomly allocated to consume the wheat, rice, or oat-bran supplement for 4 weeks in a double-blind crossover design. Altogether there were six orders o f treatment and the study lasted 90 days. At the end o f each period a fasted blood draw was done. Plasma total and low-density lipoprotein cholesterol concentrations were significantly lowered by oat bran. Oat bran significantly lowered the plasma total cholesterol concentration by 5.6%. This decrease was seen mainly in the LDL-cholesterol Auction. In both the rice and oat bran a slight increase was seen in the HDL cholesterol concentration o f 2.9% in rice bran and 4.0% in the oat bran when compared with the wheat bran. They concluded that an increase intake of fiber-rich foods from several sources might help prevent coronary heart disease and cancer. However, the consumption o f a single food source o f fiber such as oat bran or rice bran is unlikely to help lower plasma lipoprotein concentrations (Kestin, Moss, Clifton & Nestel, 1990).Oat-bran is a palatable cereal which is rich in water-soluble fiber (Kestin, Moss, Clifton & Nestel, 1990). Oat products, have important hypocholesterolemic properties as demonstrated in both humans and animals (Judd & Truswell, 1988). A 6 week study looking at oat-bran supplementation o f 50g per day in the diets o f 12 healthy young people showed a decrease o f serum cholesterol by 12% (Storch, Anderson & Young,1984). In studies using larger intakes o f oat bran serum total cholesterol lowered by 13-Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.2019% and LDL cholesterol lowered by 14-23% with no change seen in HDL cholesterol (Anderson, Story, Sieling, Chen, Petro & Story, 1984).Anderson et al. (1990) studied 12 men with high serum total cholesterol concentrations to determine the effects o f a ready-to-eat oat bran cereal on lipid concentrations. Subjects were randomly assigned to either 56g o f oat bran cereal or com flakes. Both diets were 43% o f energy from carbohydrate, 41% fat, 16% protein. After completing the first diet, subjects completed 2 weeks on the alternate diet. The oat bran cereal diet compared with the com flakes diet lowered semm total cholesterol by 5.4%. LDL cholesterol decreased by 8.5% and HDL cholesterol decreased by 3.3% on the oat bran diet (Anderson, Spencer, Hamilton, Smith, Tietyen, Bryant & Oeltgen, 1990).Kirby, Anderson, Sieling, Rees, Chen, Miller and Kay (1981) had similar findings on eight men who were fed control and oat bran diets with previously documented hypercholesterolemia. The men were fed two identical solid diets that only differed in the inclusion o f 1 OOg o f oat bran per day provided in muffins and hot cereals. Each 1 OOg o f the oat-bran preparation contained 26.4g o f plant fiber including 14.8g o f water- soluble fiber. The diets were randomized alternating each group to the other diet after 10 days. Serum concentrations o f total cholesterol, triglycerides and glucose were measured daily after a 10 hour fast. They measured plasma HDL cholesterol concentrations on 2 or 3 days at the end o f each dietary period and calculated values for LDL cholesterol. Patients tolerated both diets well and ate 94% o f the oat bran served. The non-bran control diets had a 5% increase on serum total cholesterol concentrations and in the oat bran group an 18% decrease in serum cholesterol concentrations. The decrease in total semm cholesterol was from a 14% reduction in LDL cholesterol whereas the cholesterolReproduced with permission of the copyright owner. Further reproduction prohibited without permission.21concentrations did not change. Concluding that palatable and inexpensive high fiber foods such as oat bran may have an important role in treating hypercholesterolemia.Anderson et al. (1984) examined 20 hypercholesterolemic men who were randomly allocated to oat-bran or bean supplemented diets for 21 days in a hospital metabolic ward. They developed control and experimental diets that were virtually identical in nutrient content and differed only in the amount o f plant fiber. The oat-bran diet provided lOOg o f oat bran per day served as hot cereal and five oat-bran muffins a day. Oat-bran diet supplied approximately 47g total plant fiber and 17g soluble fiber per day. The bean diet contained 115g o f dried bean per day, which provided approximately the same amount o f total plant fiber and soluble fiber as did the oat-bran diet. After the 21 days a 10 hour fasting blood draw was taken to measure serum cholesterol, triglyceride and HDL cholesterol. The subjects ate 98% of the oat bran provided and an average o f 88% o f the beans served. Subjects consumed the oat-bran without difficulty. The subjects who consumed the beans complained o f mild abdominal distension and gas production. Oat-bran diets decreased serum cholesterol concentrations by 19% and low- density hpoprotein cholesterol by 23%. Bean diets decreased serum cholesterol concentrations by 19% and low-density lipoprotein cholesterol by 24%. Oat-bran supplements and bean supplements had almost identical effects on serum total cholesterol by reductions o f approximately 19% and LDL cholesterol concentrations by about 24%. Neither diet was accompanied by substantial reductions in HDL cholesterol concentrations. They concluded that oat-bran or bean supplement might have substantial therapeutic benefits in the long-term management o f selected patients with hypercholesterolemia.Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.22These studies document the hypocholesterolemic effect o f soluble-fiber rich foods (Anderson & Chen, 1979). The lipid lowering effects o f soluble-ffbers such as guar gum, locust bean gum, pectin, oat bran, legumes and psyllium have all shown significant cholesterol lowering effects (Anderson et al., 1992). Considering the side effects of many cholesterol lowering drugs adding soluble fiber to the diet has been suggested as a safe, practical and cost effective alternative to help reduce serum cholesterol concentrations and may have a substantial impact in lowering the risk for CHD (Kinosian & Eisenberg, 1988; Witztum 1989, Anderson, Deakins, Floore, Smith & Whitis, 1990).Cholesterol and Exercise Individuals who engage regularly in cardio-respiratory activities are leaner and more physically fh in general than sedentary individuals. They also are reported to have higher plasma concentrations of high-density lipoprotein cholesterol (HDL-C) and lower concentrations o f total cholesterol, low-density lipoprotein cholesterol (LDL-C), very- low-density lipoprotein cholesterol (VLDL-C), and triglycerides than sedentary control subjects (Williams, Wood, Haskell & Vranizan, 1982). It is still uncertain whether physical activity can favorably influence the process o f coronary artery disease and coronary heart disease in human beings (Kramsch, Aspen, Abramowitz, Kreimendahl & Hood, 1981). Recent studies appear to support the belief that regular aerobic exercise may protect against premature cardiovascular disease (Kramsch et al., 1981). Observations firom early investigations indicated lower triglyceride concentration in endurance-trained subjects while total cholesterol was either not changed or only slightly different. However, it became evident that physical activity had an impact on the lipoprotein lipid distribution, and later investigations have focused on the measurement o fReproduced with permission of the copyright owner. Further reproduction prohibited without permission.23both the cholesterol and protein content associated with these various lipoproteins (Kendler, 1997). In most cases, regular participation in physical activity is associated with lower plasma triglyceride concentrations. Generally, when a person’s base line plasma triglyceride concentration is elevated endurance exercise training usually can reduce the high concentration (Thompson, CuUianane, Sady, Glynn, Chenevert & Herbert, 1991). The amount o f the concentration that is reduced is related to the pretraining concentration and the volume o f exercise completed during the training program (Guntelberg, Brennan, Holloszy, Schonfeld, Rennie & Weidman, 1977). Researchers believe that reduction in triglyceride concentrations result from both regular exercise and diet. Even though changing ones dietary intake can help with lowering triglyceride concentrations alone. It does not seem to be the absolute reason seen in people who are physically active (Kiens, Gad, Lithell & Vessby, 1981). This is portrayed especially in endurance athletes, extreme leanness is related to lower triglyceride concentrations (Hagan & Gettman, 1983).Holloszy, Skinner, Toro and Cureton, (1964) studied the effects o f a six month program o f endurance exercise on serum lipids o f middle-aged men. Two groups o f subjects were involved in this study. In group A. 15 men who all led sedentary lives for three or more years before the study participated in an organized exercise program consisting of pushups, sit-ups and distance running (2 to 4 miles) on an average o f 3.35 times per week for six months. In group B. 12 subjects did not exercise together with an instructor, but participated in a program o f distance running geared to their individual capacities and increasing progressively in intensity. Three festing blood sangles were taken on each subject over a seven day period to establish base line values. Total serumReproduced with permission of the copyright owner. Further reproduction prohibited without permission.24cholesterol levels were determined once a month, and phospholipids along with triglycerides measured every other month. AU three samples were taken over a seven day period after the study. The results o f the serum triglycerides fell from a mean pretraining o f208 ± 127 to 125 ± 78 mg. in both groups. The mean serum cholesterol and phospholipid levels did not change significantly with training. This reduction in serum triglycerides appears to occur within two to three hours after exercise and lasts for approximately two days. From their results they concluded that it would appear that serum triglyceride levels can be kept significantly lower by means o f regularly performed endurance exercise. This finding may represent one mechanism by which exercise possibly could protect against coronary heart disease. (HoUoszy, Skinner, Gelson & Cureton, 1964).Cholesterol is an important part o f ceU membrane and synthesis o f steroid hormones however; excess (high levels oQ cholesterol is also associated with development o f coronary artery disease. Studies have concluded differently on whether or not plasma cholesterol concentrations are lower in endurance-trained male and female athletes when compared to inactive control groups (Williams, Krauss, Wood, Lindgren, Giotas & Vraganizan, 1986).Factors such as body weight, percentage o f body fat and differences in fe»od intake are important considerations when evaluating the effects o f physical activity on plasma cholesterol concentration. Factors such as age and gender can play an important role in the difference o f plasma concentrations, which can effect whether or not physicaUy active individuals have lower plasma concentrations than do inactive individuals (Seals, Hagberg, Hurley, Ehsani & Holloszy, 1984).Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.25Studies comparing LDL-C concentrations in men and women athletes from various sports with those o f inactive subjects have produced mixed results (Thompson, Callinane, Sady, Flynn & Bernier, 1988). Tsopanakis, Kotsarellis and Tsopanakis (1986) found that athletes participating in power or speed-related events have LDL-C either similar or lower than those o f inactive controls. Stein, Michielli, Glantz, Sardy, Cohen, Goldberg and Brown (1989) found similar findings as Tsopanakis when studying the effects o f different exercise training intensities on lipoprotein cholesterol fractions in healthy middled-aged men. They reported that LDL-C concentrations are lower for men and women following endurance training. However, in one study conducted by Marti, Suter, Riesen, Tschopp, Wanner and Gutzwiller (1990) that looked at only men and another study conducted by Nikkila, Kuusi and Myllyen (1980) looked at both men and women long distance runners reported lower LDL-triglyceride concentrations in men but not in women when compared with inactive controls. However, a study conducted by Kuusela, Vautilainen, Kukkonen and Raurammaa (1980) compared Scandinavian lumberjacks with sedentary workers and concluded that lumberjacks have higher LDL- triglyceride concentration.Endurance-exercise training has been associated with increased HDL-C concentration, associating it with reduced CAD risk. There is a consensus, among cross- sectional studies that HDL-C concentrations are elevated typically 20-30% in endurance trained athletes when compared to inactive groups (Thompson, Lazarus, CuUianane, Henderson & Musliner, 1983). Some researchers have suggested a dose-response relationship between the amount o f exercise performed and how much HLD-C will increase (Rotkis, Cote, Coyle & Wilmore, 1982). Some researchers do not believe thatReproduced with permission of the copyright owner. Further reproduction prohibited without permission.26one bout o f exercise can have an effect on HDL-C increasing. Reasons for the discrepancy may be related to several factors: the length o f the training period, the volume o f training period, the volume o f training completed, changes in body composition, dietary intake, weight loss, and the pre-training HDL-C concentrations (Weltman, Matter & Stanford, 1980).Brownell, Bachorik and Ayerle (1982) studied the effect o f a 10 week exercise program on changes in plasma lipid and lipoprotein levels in 37 women and 24 men. Thirty-minute sessions were held three times weekly for 3 different groups of 15-25 subjects. The class was conducted by certified fitness instructors and focused on cardiopulmonary conditioning, flexibility, muscular strength and endurance. By the fourth week, the subjects were exercising at approximately 70% o f maximal heart rate for 15-20 minutes. The remaining time was used for warm-up, cool-down and stretching. Blood samples were obtained before and after the 10-week program. Results fi'om this study demonstrate that men and women differ in their lipid and lipoprotein responses to an exercise program Men showed significant reductions o f 4.4% in cholesterol 6% in LDL cholesterol and 9.5% in triglycerides and a 5.1% increase in HDL cholesterol. Women showed a 4.1% decrease in cholesterol with no significant changes in HDL cholesterol or LDL cholesterol and a 14.5% decrease in triglycerides. The results fi'om the study concluded that moderate exercise might have different effects on men and women (Thompson, Lararus, Cyllianane, Henderson & Musliner, 1983).Studies on exercise and lipid changes have proposed conflicting results between men and women. Studies o f men have shown consistent increases in HDL cholesterol during programs o f moderate or intensive exercise and have shown either a decrease orReproduced with permission of the copyright owner. Further reproduction prohibited without permission.27no significant change in triglyceride. The HDL/LDL ratio, an important predictor o f coronary heart disease, increased significantly in men, but did not change significantly in women when participating in an exercise program. Conclusions o f this matter suggests that a short-term exercise program in a work setting can improve plasma lipid and lipoprotein patterns more in men than in women (Brownell et al., 1982).In women, some studies showed no change in HDL cholesterol and a decrease in LDL cholesterol after moderate exercise (Lee, Nieman, Raval, Blankenship & Lee,1991). In addition, it is becoming increasingly apparent fi'om studies that the quantity and intensity o f physical activity required to have a positive change in lipoprotein levels may be varied (Leon, Connet, Jacobs & Rauramaa, 1987). For instance, it has been shown recently that more moderate levels o f activity can improve the lipoprotein profile by increasing HDL cholesterol levels and lowering LDL cholesterol levels (Duncan, Gordon & Scott, 1991). Researchers thought one would need to endurance train to show significant changes in cholesterol levels.King, Haskell, Young, Oka and Stefanick (1995) studied 149 men and 120 postmenopausal women to determine the two-year effects o f differing intensities and formats of endurance exercise on exercise participation rates, fitness, and plasma HDL cholesterol levels among healthy older adults. The subjects were randomly assigned to one o f four groups. (1) higher-intensity group-based exercise training (2) higher- intensity, home-based exercise training (3) lower-intensity home-based exercise training (4) a 1-year delayed treatment control condition that received an exercise training program during the second year. The primary purpose o f the second study year was to evaluate the maintenance o f changes that had occurred during the first year in the threeReproduced with permission of the copyright owner. Further reproduction prohibited without permission.28experimental conditions. It also allowed the researchers to look at long-term effects of the three different exercise-training conditions on variables such as lipoprotein levels that had not changed significantly during the first year. For the higher-intensity exercise training, three 40-minute endurance training sessions per week were prescribed at 73% to 88% o f peak treadmill max heart rate. For lower-intensity exercise, five 30-minute endurance training sessions per week were prescribed at 60% to 73%. Subjects assigned to the year delayed treatment control condition were requested not to change their activity habits during the initial 12-month study period. Changes in total cholesterol, HDL, LDL cholesterol and plasma triglycerides did not differ significantly between the three exercise training conditions versus the one-year wait-listed control group at the end o f 1 year. By the end o f the second year subjects in the two home-based training conditions showed small but significant HDL cholesterol increase fi'om baseline. The increases were the greatest for subjects in the lower-intensity condition, whose exercise prescription required more frequent exercise sessions per week. In all exercise conditions, increases in HDL cholesterol were associated with decreases in waist-to-hip ratio in both men and women. Concluding that frequency and length o f time needed to achieve HDL cholesterol change may be longer for older populations (King, Haskell, Young, Oka & Stefanick, 1995).Stein et al. (1989) studied the effects of different exercise intensities on lipoprotein cholesterol fiuctions in healthy middle-aged men. Forty-nine healthy men were randomly divided into four different groups o f exercise training. The subjects trained at either 65%, 75% or 85% o f their measured maximal heart rate. The fourth group was a 12 week non exercise control group. Fasting morning blood samples wereReproduced with permission of the copyright owner. Further reproduction prohibited without permission.29obtained from all subjects before and immediately after the exercise training or control period. Results o f the lipid profiles showed that total cholesterol did not change significantly in any o f the groups HDL cholesterol increased significantly in the 75% and 85% maximal heart rate training groups, but not in the other two groups. LDL cholesterol decreased significantly only in the 75% group. No significant differences were seen with in any o f the groups for VLDL cholesterol or triglyceride levels. Concluding that an aerobic exercise at 75% maximal heart rate, 30 minutes per session, 3 days a week for 12 weeks results in a 19% increase in HDL cholesterol and an 22% decrease in LDL cholesterol (Stein et al., 1989).Elevated levels o f plasma high-density-lipoprotein (HDL) may be associated with a lowered risk o f coronary heart disease (Gordon, Castelli, Hjortland, Kannel & Dawber, 1977). Several studies have indicated that vigorous exercise training may result in elevated HDL cholesterol levels in young and middle aged men (Lopez, Vial, Balart & Arroyave, 1974). The concept o f elevated HDL levels resulting from exercise has been combined with the idea o f the effect which dietary modification may have on HDL levels (Sacks, Castelli, Donner & Kass, 1975). Some researchers have suggested that moderate alcohol intake and a reduction caloric intake will increase HDL levels. Hartung, Foreyt, Mithcell, Vlasek and Gotto (1980) studied 59 healthy middle aged marathon runners, 85 joggers and 74 inactive men and observed the relation between diet and plasma lipids and lipoprotein levels in all o f these men. The inactive subjects were men selected randomly from the general population who indicated that they did not exercise regularly. They participated in a diet-education study and were randomized into a control group. The marathon runners had aU completed a 26.2 mile marathon during the 12 months beforeReproduced with permission of the copyright owner. Further reproduction prohibited without permission.30the study and continued to train heavily. They reported an average o f 40 miles per week. The joggers ran at least 2 miles three times per week. Blood was drawn in the morning after a 12 to 16 hour fast. Height, weight, tricep skinfold and blood pressure were also measured and a comprehensive questionnaire was completed during the visit on the fi>od- intake-record section the subject was asked how many servings o f each food he ate daily weekly, monthly or yearly. The marathon runners and joggers did not differ substantially fi’om the inactive subjects in their reported dietary habits, although they had significantly higher HDL-cholesterol levels. The positive relation between distance running and HDL cholesterol was significant. The distance ran was the best predictor o f both HDL cholesterol and the ratio o f HDL to total cholesterol Concluding that it is primarily the jogging and running, rather than diet that elevated HDL to a level associated with significant reduction o f coronary risk (Hartung, Foreyt, Mitchell Vlasek & Gotto, 1980).Hartung, Squires and Gotto (1981) found similar results in studying the effects of chronic exercise training on plasma HDL cholesterol on 18 male coronary patients. Exercise training was conducted three times weekly for 20 minutes, increasing to 40 minutes per session at an intensity utilizing 70% to 85% o f the maximal heart rate for a period o f 3 months. None o f the patients were placed on a specific diet. Blood was drawn at the start o f the study ft) Ho wing a 12 to 14 hour fast and then again at the end of the 3 months. Hartung found similar results fi’om the previous study he conducted a year earlier. Moderate physical activity ft)r 3 months can contribute to increases in HDL-C in patients with coronary artery disease without dietary intervention or significant change in total cholesterol triglycerides and body weight (Hartung, Squires & Gotto, 1981).Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.31Regular participation in physical activity as well as single exercise session can alter lipoprotein metabolism, plasma lipid and lipoprotein concentrations and lipid transport (Durstine & Haskell, 1994). The understanding of the precise mechanisms responsible for these changes is not totally clear. There is evidence indicating that other factors including diet composition adiposity, weight loss, plasma volume change, and hormone and enzyme activity interact with exercise to alter the rates o f synthesis, transport and clearance of lipid and lipoproteins from the blood (Durstine & Haskell,1994).Lipoprotein Lipase (LPL) is responsible for delipidation of chylomicron and VLDL molecules and promotes the clearance o f fatty acids and glycerol from the vascular compartment for either storage or use as substrate in energy metabolism (Durstine & Haskell, 1994). Cross-sectional studies indicate that endurance-trained runners at rest have higher plasma concentrations o f LPL activity than less active controls (Thompson et al., 1991). Inactive men, after undergoing endurance-exercise training, usually have significantly lower adipose tissue and LPL activity than compared to their adipose tissue when they were inactive. (Peltonen, Mamiemi, Hietanen, Vuori & Ehnholm, 1981).Studies evaluating a single exercise session indicates that it increases LPL activity. Depletion o f intramuscular triglyceride stores by endurance exercise may promote secretion and/or synthesis o f LPL by muscle cells (Oscari, Essig & Palmer, 1990). Kanter, Cullinane, Sady, Herbert and Thompson (1987) studied 21 trained and untrained men on the effect o f a single exercise session on lipid and lipoprotein concentrations and on plasma lipoprotein lipase. After the trained and untrained subjectsReproduced with permission of the copyright owner. Further reproduction prohibited without permission.32performed a single prolonged session o f endurance cycling exercise both groups had higher LPL activity.Studies show that increased LPL activity results in increased HDL synthesis and also indicates that exercise training also prolongs the survival o f HDL (Durstine & Haskell 1994). The survival time o f HDL protein was 27% longer in the circulation o f physically active men, compared with inactive men (Herbert, Bemier, Cullinane, Edelstein, Kantor & Thompson, 1984). Endurance training increases the half-life of apoliproteins A-I and A-H in active men (Thompson et al., 1988). Researchers have concluded the increase o f HDL associated with endurance training is a result o f both increased synthesis and survival.Other factors should be considered when evaluating the impact o f a single session o f exercise or exercise training on lipoprotein metabolism. Controversy exists about the effect of dietary modification on lipoproteins (Sacks et al., 1975). Some researchers have suggested that moderate alcohol intake or caloric restriction resulting in weight loss may elevate HDL (HuUey, Cohen & Widdowson, 1977). Reduced body fat and increased leanness are important outcomes o f exercise training. Leanness has been associated with lower hepatic lipase activity in physically active people (Wood & Stefenick, 1990). Increasing one’s exercise and changing one’s diet will help reduce body fat and prevent the incidence o f high cholesterol and occurrence o f heart disease.The adipose distribution shown by waist-to-hip girth ratio (WHR) is associated with altered lipoproteins (Durstine & H askell 1994). Abdominal adiposity with a WHR greater than 1.0 in nonobese males is associated with lower HDL-C concentration (Barakat, Burton, Carpenter, Holbert & Israel 1980). Studies have shown subjects withReproduced with permission of the copyright owner. Further reproduction prohibited without permission.33abdominal adiposity to have plasma LDL characteristics that look almost identical to the LDL plasma o f subjects with CAD (Peeples, Carpenter, Israel & Barakat, 1989). This may suggest, as a result o f endurance training, a selective loss o f abdominal fat versus other areas (gluteal), a reduction in the WHR could perhaps reduce CAD risk (Peeples et. a l 1989).Physical activity has a positive effect on the lipid and lip>oprotein concentrations. In normal men and women increased physical activity is associated with lower plasma triglyceride concentrations (Durstine & Haskell, 1994). The dominant changes in lipoproteins associated with endurance training are increased HDL-C, HDL2-C and apoliprotein A-I concentration (Durstine & Haskell, 1994). Exercise-induced reductions in LDL-C are only minor without change in adiposity or dietary fat cholesterol intake (Durstine & Haskell 1994).Cholesterol Lowering DrugsPatients whose LDL cholesterol levels remain high even with extensive dietary therapy and exercise should be considered for drug treatment. Dietary therapy should be at least six months long before drug treatment is started (The Expert Panel 1988). Individual with elevated LDL cholesterol levels above 220 mg/dl and/or with confirmed coronary heart disease, diet and exercise should not be the only therapy considered (The Expert Panel 1988). After the required six months o f dietary therapy, to establish adequate baseline values, drug therapy should be initiated. (The Expert Panel 1988).There are about fourteen types o f cholesterol lowering drugs, which are grouped into categories based on their action. Bile acid sequestrates: cholestyramine and colestipal action binds acids in the GI tract, forming an insoluble complex resulting inReproduced with permission of the copyright owner. Further reproduction prohibited without permission.34increased clearance o f cholesterol binded to bile acids eliminated in the feces. Some o f the most common side effects are nausea, constipation, abdominal discomfort, rashes and skin irritations (Hopfer, 1995).Nicotininc acid generally known as Niacin helps lower cholesterol levels by decreasing lipoprotein and triglyceride synthesis by inhibiting the release o f free fatty acids from adipose tissue and decreasing hepatic lipoprotein synthesis. Generally it decreases blood lipids. Some major side effects are nausea and flushing o f the face and neck (Hopfer, 1995).Fibric acids: clofibrate, fenofibrate, gemfibrozil and benzafibrate works by decreasing triglyceride production by the liver and increases HDL lipoproteins. Major side effects consist o f diarrhea and abdominal pain (Hopfer, 1995).Probucol is one o f the most common cholesterol drugs prescribed to date. It may decrease transport o f cholesterol from intestine or interfere with cholesterol synthesis. Also it may increase fecal excretion o f cholesterol and bile acids. The most common side effects are diarrhea, bloating, abdominal pain, nausea and vomiting (Hopfer, 1995).There are four HMG-CoA reductase inhibitors available on prescription in the United States. Pravastin (provachol), Fluvastatin (lescol), and two of the newest and most common prescribed Lovastatin (mevacor) and Simvastatin (zocor). Also known as “statins” these agents slow the progression o f coronary artery disease and have actually been shown to induce regression o f artherosclerotic lesions in CAD patients (Pedersen,1995). These drugs act by inhibiting the hepatic enzyme HMG-CoA reductase, which leads to an increase in the hepatic production o f cholesterol receptors. These receptors pull cholesterol out o f the blood stream, thus reducing serum cholesterol levelsReproduced with permission of the copyright owner. Further reproduction prohibited without permission.35(Thompson et al.,1995). Statins have been associated with some skeletal muscle con^laints (myositis and rhabdomyolysis). The most common side effects include headache, abdominal pain, constipation, and diarrhea (Kobashigawa et al., 1995).Patients should incorporate diet, weight control, exercise and stop smoking to lower cholesterol levels and the risk of CHD before any drug therapy is considered (Expert Panel, 1993). I f these methods fail and cholesterol levels are not lowered drug therapy should then be considered.Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.36SummaryCholesterol is probably the best known sterol, which is essential to the human body. It is found associated with the fats, but chemically it is not related to them. Cholesterol, a white waxy solid, is the principal sterol found in animal organisms. The largest amount o f cholesterol is found in muscle, nervous and connective tissue. It is needed to synthesis vitamin D, cholic acid which is part o f büe, some hormones, and cortisol which promotes glucose synthesis in the liver. The daily production is approximately 400 mg from intestinal absorption and 600mg synthesized in the cells and the Uver. In the human body every cell, except a mature red blood ceU, produces cholesterolThe synthetic process o f cholesterol takes place in the liver and may occur in other organs. In all tissues expect in the brain, cholesterol is continually regenerated. If any organ can be singled out as the single most important to metabolize cholesterol and some amount o f plant sterols, it is the liver. It can both synthesize and destroy cholesterol. The breakdown and lose o f cholesterol can occur in four ways:1. By direct reduction to dihydrocholesterol or by passage through the intermediate cholesterone to dihydrocholesterol or coprosterol2. By loss o f cholesterol in the feces.3. By conversion into steroid hormones.4. By conversion to bile acids in the liver.There are a number o f variables that are important in determining or changing the level o f blood cholesterol in the body. Throughout the day the level o f serum cholesterol remains for the most part constant, even through there is a large variation in the rate thatReproduced with permission of the copyright owner. Further reproduction prohibited without permission.37cholesterol enters and leaves the body. Females at birth have slightly higher levels o f plasma cholesterol than males. During childhood, adolescence and early adulthood there is very little difference in blood cholesterol between men and women. In later life males tend to have higher serum cholesterol levels due to higher concentrations o f VLDL and LDL. Serum cholesterol levels tend to be a lower in premenstrual women. After the age o f 50 male cholesterol levels tend to lower whereas females tend to rise slightly.Artherosclerosis is the major disease affecting the heart and blood vessels, and is the leading cause o f death among middle-aged adults in the United States. Artherosclerosis is the result o f fatty cholesterol deposits in blood vessels walls, reducing elasticity and eventually blocking blood flow. It is a disorder o f the coronary arteries, cerebral arteries, iliac and femoral arteries and aorta that is responsible for coronary heart disease, stroke and peripheral arterial disease.Treatment o f high cholesterol begins with dietary treatment. There is evidence indicating that dietary fiber has important hpid lowering effects and may reduce risk of CHD. Increasing dietary fiber intake is an important therapeutic treatment for other specific conditions besides CHD, such as diabetes, hyperlipidemia, hyperglyceridemia, hypercholesterolemia and intestinal disorders. Soluble fiber has been shown to reduce blood cholesterol levels. Soluble fiber increases the fecal excretion o f bile acids, which may alter the quantity o f cholesterol absorbed by the intestine. The fibers fi’om firesh fruits, vegetables, legumes, oat bran and barley appear to have the most significance for reducing cholesterol levels.Individuals who engaged regularly in cardio-respiratory activities are leaner and more physically fit in general than sedentary individuals. They also cholesterol (HDL-C)Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.38and lower concentrations o f total cholesterol, low-density lipoprotein cholesterol (LDL- C), very-low-density lipoprotein cholesterol (VLDL-C) and triglycerides than sedentary control subjects- Regular participation in physical activity as well as a single exercise session can alter lipoprotein metabolism, plasma lipid and lipoprotein concentrations and lipid transport. The understanding o f the precise mechanisms responsible for these changes is not totally clear. There is evidence indicating that other factors including diet composition adiposity, weight loss, plasma volume change, and hormone and enzyme activity interact with exercise to alter the rates o f synthesis, transport and clearance o f lipid and lipoproteins from the blood.Patients who cholesterol levels do not lower with dietary and exercise therapy drug intervention should be considered as a method o f lowering these high levels. There are fourteen types o f cholesterol lowering drugs which are grouped into categories based on the action they perform in the body; bile acid séquestrants, nicotininc acids, Fibric acids, probucol and HMG-CoA. The goals o f drug therapy are to lower total cholesterol, raise HDL’s and lower LDL’s. However, there are several major side effects. They range from itching o f the skin, gastrointestinal distress, liver toxic effects, muscular damage due to interaction between drugs and blood clots.In summary, coronary heart disease (CHD) is the leading cause o f death in the United States (JAMA, 1995). While factors such as obesity, diabetes, smoking, sedentary living and hypertension have been shown to influence CHD risk, serum cholesterol seems to have the strongest correlation with CHD (Genest & Cohn, 1995). The real aim o f any cholesterol management intervention is to lower circulating cholesterol fractions. The National Cholesterol Education Program Guidelines state thatReproduced with permission of the copyright owner. Further reproduction prohibited without permission.39exercise along with a high fiber diet, weight loss and medication should be included in the management o f high cholesterol filetions. It is important to know not only the interactive effect o f exercise and diet on lipoprotein metabolism but also the interactions between exercise and various classes o f lipid medications now used in treatment.Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.CHAPTERSMETHODSSubjectsFifty (50) male and female subjects volunteered to participate in this study. Twenty-five were exercising regularly in a supervised exercise program and the other 25 were sedentary. The twenty-five exercising subjects belonged to two formal exercise programs. Twenty were from the Adult fitness program at the University o f Nevada Las Vegas (UNLV). This program starts at a low level o f intensity and progresses in intensity each week. Subjects meet as a group five days a week Monday through Friday. The supervised exercise program consists o f four components: 1) warm-up and stretching, 2) strength and muscular endurance, 3) cardiovascular or aerobic, and 4) cool down. The warm-up period includes 5 to 7 minutes o f flexibility exercises, consisting o f bending, stretching and twisting. Exercises for muscular strength and endurance include push-ups, sit-ups and chest raising. For the aerobic pwrtion o f the class the women do bench steps and jogging, and the men do bench steps and swimming. The final part o f the program is a cool down period; these exercises are similar to the warm up exercises. The other five were participating in their own exercise program at least 3 times a week for duration of 30 minutes and at an intensity o f 70 % or more o f their max heart rate. The twenty-five sedentary subjects were recruited from the Las Vegas community and the UNLV faculty40Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.41and staff. All subjects had an LDL-C o f 130 mg/dl or higher and were not on any cholesterol lowering medications. This study was approved by the Institutional Review Board (See Appendix B).Research DesignThe study was divided into a pre-experimental period, an experimental period and a post experimental period.1). The 7 day pre-experimental period was for collecting baseline data.2). The experimental period was 90 days in duration during which time the subjects ingested the experimental fiber.3). The post-experimental period was when final testing was done.There were three testing periods. Test 1 (T l) during the pre-experimental period. Test 2 (T2) 45 days after starting the experimental period and Test 3 (T3) test during the post- experimental period.Statistical DesignThis study was a 2 (Group) by 3 (Time) mixed model with repeated measures design with exercise being between subjects and time being within subjects. The two levels o f exercise were exercise and non-exercise. The three levels o f time were baseline, 45 days and 90 days. The dependent measures o f interest were Total Cholesterol, Low- Density lipoproteins (LDL’s) and High-Density lipoproteins (HDL’s).Procedure Pre-experimental Period During this period o f approximately one week the testing (T l) included a 12-hour fasting blood sample. A lipid profile determined Total Cholesterol, HDL-C, LDL-C,Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.42VLDL-C, Cholesterol/HDL Ratio and Triglycerides. This lipid profile served as their baseline blood profile if it was greater than 130 mg/dl. Since an LDL-C greater than 130 mg/dl was required to be in the study. If the LDL-C was less than 130mg/dl they were eliminated fi-om the study. During this pre-experimental period, subjects were briefed on the study, questions were answered and they read and signed an informed consent form (Appendix B). Written information about Bios Life 2 was distributed to subjects (Appendix A). Height and weight was measured and Body Mass Index was calculated. Waist girth and hip girth were measured firom which a waist to hip ratio was calculated. Body fat was determined by bioimpedance analysis. A six-minute walk test was administered. The six-minute walk test was used to determine “fimctional exercise capacity”, which is defined as a patient’s ability to undertake physical demanding activities encountered in everyday life that are not reflected by conventional exercise testing.Experimental Period During this 90-day experimental period the subjects in the exercise group exercised a minimum o f three times a week and took the prescribed dosage of Bios Life2. The non-exercise group took the prescribed amount o f Bios Life 2 and did not change their regular routine or eating habits. After 45 days all tests (T2) were repeated exactly as performed in T l . This was Test 2 (T2).Post-experimental Period During this period all tests were again administered: Test 3 (T3). Test T3 was administered as soon after the experimental period as possible. However, the subjects continued the experimental protocol until they were tested.Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.43BiosLife 2BiosLife 2 is a dietary fiber in the form o f a powder and packaged in 4.5-gram packets. It was mixed with eight-ounces o f water or finit juice and one packet was taken twice per day. It was taken 15 minutes prior to breakfast and dinner. (See appendix A for ingredients). A dietary survey was completed on all subjects to determine the amount o f fiber in their normal diet. (Appendix C). I f the diet was low in fiber subjects were introduced to the Bios Life supplement gradually by taking one-half the normal dose for the first three to four days. Subjects reported to the laboratory every two weeks during the experimental period. During this time weight was taken and questions were asked about the subject’s adherence to the experiment protocol and reported any side effects o f the Bios Life. Every two weeks the subjects brought back their used and (any unused packages) fi-om the prior two weeks. This was used to determine compliance.Six-minute Walk Test To determine a level o f cardio-respiratory fitness a submaximal six-minute walk test was given. The six-minute walk test was done on a measured course. The distance covered in six minutes was recorded and conqiared to national norms. The number o f stops (or rest periods) during the walk were also recorded. The outdoor course, where the test was administered, was on a concrete walkway and consisted o f 283 feet and 8 inches per lap. In the center o f the course was a courtyard, which was surrounded by concrete benches. These benches not only served as course markers they also provided a place to sit i f a rest was needed. The subjects were encouraged to walk as far as they could in the 6-minute period but were allowed to stop and rest if necessary. The distance and the number o f stops were recorded for each subject.Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.44Anthropometrical Measurements Height was taken without shoes with an anthropometer to the nearest quarter o f an inch. Subjects were instructed to stand as tall as possible, feet together and looking straightforward. Weight was measured, without shoes and minimal clothes, on a physicians balance scale to the nearest quarter o f a pound. Body Mass Index was computed from formula o f body weight in kilograms divided by height in meters squared (BW (kg)/HT (m)^). Men with a BMI greater than 27, and women with a BMI greater than 26.9 were considered overweight. (Appendix E). Waist girth was measured in centimeters at the narrowest circumference and hip girth was taken at the largest circumference. A waist to hip ratio o f greater than .9 was considered obese (See appendix E for risks).BMI and waist to hip ratio are commonly used in epidemiology studies to describe the degree o f fatness in a population. Although these measurements were taken at T l, T2 and T3 they are measurements that do not usually reflect body composition changes in an individual over time, but were used to describe the population.Bioimpedance Analysis (BIA)Bio impedance analysis was done using the Bio Analgesics system A low-grade electric current is passed through the body, which is resisted, by body water. This resistance is measured in Ohms. This resistance is used in an equation to determine total body water. Total body water is then used to calculate per cent body fet.Cholestech LDXThe cholestech LDX Analyzer is a small size (5”x 5” x 8”) lightweight (21b) instrument designed for point o f service lipid analysis. The analyzer uses a disposableReproduced with permission of the copyright owner. Further reproduction prohibited without permission.45cassette that needs only 35 uL blood sangles, which can easily be obtained by a fingerstick. The cassette contains a well into which the blood is pipetted, a glass fiber screen, four optical windows, a reagent impregnated bar allowing four separate reactions and a magnetic code bar to communicate with the analyzer. The blood is separated by the glass fiber screen that allows only the plasma into a reservoir. The system than uses reflectance photometry to obtain lipid results. The instrument has a display window that guides the user and displays the results, which are available within four minutes (Drimmer et al., 1995).Optics Check Cassette Test Procedure Before any procedure is performed the analyzer must be tested. The Cholestech Optics Check Cassette should be ran once each day before patient samples are tested and after the cholestech L.D.X System has been moved or serviced. One should never use the Cholestech L.D.X Optics Check Cassette that has become damaged or altered in anyway. The cassette is placed in the analyzer and the test is run. The analyzer will automatically perform the optics check. Once the test is complete four numbers will appear on the screen and if they are within the acceptable range (80-105) a blood sample can be ran.Performing a Fingerstick The patient was asked to sit quietly for five minutes before the blood sanple was taken. Gloves were worn while working with the blood sample and the samples were placed into the biohazard box when the test was completed. A capillary plunger was placed into the end o f a cholestech capillary tube with the red mark and set aside. To help increase blood flow, the fingers and hands were warm to the touch. I f not the capillary puncture was done on center fingers that has been thoroughly cleaned with anReproduced with permission of the copyright owner. Further reproduction prohibited without permission.46alcohol swab. The area was thoroughly dried with a gauze pad before pricking the finger. Then the center fingers were firmly pricked with the lancet. The finger was squeezed gently to obtain a large drop of blood. The first drop o f blood was wiped away due to the fact it may contain tissue fluid. The finger was gently squeezed again while holding it downward until a second large drop of blood forms. The puncture should provide a firee- flowing drop o f blood. The capillary tube was held horizontally by the end with the plunger, then touched to the drop o f blood without touching the skin. The tube will fill by capillary action up to the black mark. A very important step is not to collect air bubbles. The excess blood was wiped off and then the patient applied pressure to the puncture until the bleeding stopped.Performing the TestThe fingerstick sample was analyzed within 5 minutes after the collection or the blood wUl clot. The cassette was taken out of the refiigerator and warmed up to room temperature for 10 minutes before opening. The Analyzer is plugged in and warmed up. The cassette was removed from its pouch and held by the short sides only. Do not touch the black bar or the brown magnetic stripe. The cassette was placed on a flat surface. Press run on the analyzer first so that a self-test can be ran. Once a Self-Test is ok the cassette drawer will open and load cassette will appear on screen. Use the Cholestech capillary tube to place sample into the test cassette sample well. Keep the cassette level after the sample has been applied. Immediately place the cassette into the drawer o f the analyzer. The black reaction bar must free toward the analyzer. The brown magnetic strip must be on the right. By pressing run the drawer will close and the testing begins. When the test is conqileted, the analyzer will beep and the screen will display the data.Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.47Everything that came into contact with blood including the cassette was placed into a biohazardous container. The results were recorded on the appropriate form.Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.CHAPTER 4RESULTS & DISCUSSIONMean total cholesterol and low-density lipoproteins were analyzed using a 2 (group) by 3 (time) analysis o f variance (ANOVA) procedure with repeated measures on the second factor. All statistical analysis was done using the SAS system.Total CholesterolThe test for interaction was not significant F = 0.00, p = .9985. The ANOVA did however yield a significant main effect for time, (F = 18.29, p = .0001), with means for the exercise group being 242, 233,222 and the means for the non-exercise group being 246, 237, 226 for baseline, 45 days and 90 days, respectively (see figure 1). Tukey’s test was used to determine the nature o f the difference. This indicated a significant decrease in total cholesterol at each measure baseline, 45 and 90 days in both exercising and nonexercising groups.The ANOVA did not yield a significant main effect for group, (F = 0.20, p = .6540), with means being 232, 236 for exercise and non-exercise, respectively (see figure2). Therefore, there was a significant decrease in total cholesterol for the exercise and non-exercise groups, but there was no significant difference between exercise and nonexercise.48Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.4921u1260250240230220210200190Figure 1 Total Cholesterol over Time-Exercise-Non-ExerciseBaseline 45 Days 90 Days270 _ 250 # 2 3 0■S5 210 U5 190O170150Figure 2 Total Cholesterol and Exercise GroupExercise Non-Exercisea Baseline ■ 45 Days □ 90 DaysLow Density Lipoprotein Cholesterol The test for interaction was not significant F = 0.72, p = .4896. The ANOVA did however yield a significant main effect for time, (F = 21.60, p = .0001), with means for the exercise group being 161, 154, 139 and the means for the non-exercise group being 151,144, 135 for baseline, 45 days and 90 days, respectively (see figure 3). Tukey’s test was used to determine the nature of the difference.Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.50Figure 3 LDL Cholesterol over Time170 12Io£160 -150 -Ô 140130 -_ i3120 iBaseline 90 Days45 Days-♦—Exercise-•—Non-ExerciseTimeThis indicated a significant decrease in LDL cholesterol at each measure from baseline to 90 days in both exercising and non-exercising groups. The ANOVA did not yield a significant main effect for group, (F = 1.59, p = .2128), with means being 151, 158 for exercise and non-exercise respectively (see figure 4). Therefore, there was a significant decrease in LDL cholesterol for the exercise and non-exercise groups, but there was no significant difference between the exercise and non-exercise.Figure 4 LDL Cholesterol and Exercise Group180 160 2 140I 120 ® 100U 806040200B Baseline ■ 45 Days □ 90 DaysExercise Non-ExerciseReproduced with permission of the copyright owner. Further reproduction prohibited without permission.51High Density Lipoprotein Cholesterol The test for interaction was not significant (F = 1.06, p > 0.05). The ANOVA did not yield a significant main effect for time, (F = 1.67, p>0.05), with means for the exercise group being 51, 49, 46 and the means for the non-exercise group being 54, 52,53 for baseline, 45 days and 90 days, respectively (see figure 5).Figure 5 HDL Cholesterol over Time60 -,I 55 -so 50 -O_iQX45 -40Baseline 45 Days 90 Days-♦— ExerciseNon-ExerciseTimeTherefore, there was no significant difference in the HDL cholesterol levels from baseline to 45 days, from 45 days to 90 days and from baseline to 90 days in both exercising and non-exercising groups. The ANOVA did not yield a significant main effect for group, (F = 1.07, p>0.05), with means being 49, 53 for exercise and nonexercise, respectively (see figure 6). Therefore, there was no significant difference in HDL cholesterol for the exercise and non-exercise groups, nor was there a significant difference between exercise and non-exercise.Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.5260 -,- 50 2î 40 J 30j 20 -IOz 10 0Figure 6 HDL Cholesterol and Exercise GroupExercise Non-ExerciseH Baseline ■ 45 Days □ 90 DaysIn the present study, serum total cholesterol and low-density lipoprotein cholesterol was significantly reduced in both exercise and non-exercising groups after taking three months o f the dietary fiber supplement. Total serum cholesterol concentrations in the exercise group were reduced by 7.96%, and in the non-exercise by 7.84%. Low-density lipoprotein concentrations in the exercise group were reduced by 13.3% and in the non-exercise group decreased by 10.46%. Similar reductions in total cholesterol have been reported in other studies using insoluble fibers, such as pectin, guar gum, psyllium, legumes, oat bran and locust bean gum. Van Horn, Liu, Parker, Emidy, Liao, Pan, Giumetti, Hewitt and Stamler (1986) supplemented the diet o f healthy volunteers on a low-fet diet with 4g soluble fiber from either oatmeal or oat bran. Serum total cholesterol was reduced by 5% after 6 weeks on just a low fet diet and an additional 3% reduction after 6 more weeks after adding either oatmeal or oat bran (Van Horn et al., 1986). Jensen, Spillar, Gates, Miler and Whitman (1993) also foimd similar findings with patients who took a mixture o f guar gum, pectin, psyllium and locust bean gumReproduced with permission of the copyright owner. Further reproduction prohibited without permission.53three times a day and the subjects experienced a 10% reduction in serum TC and a 14% reduction in serum LDL (Jensen et aL, 1993).Total cholesterol and serum LDL cholesterol were lowered in both the exercise and non-exercise groups without significantly afifecting serum HDL cholesterol levels. In the exercise group serum HDL levels were reduced by 8.42% and 1.63% ia the nonexercise group. This was also observed by Anderson and associates (1992) who studied 44 hypercholesterolemic male and female participants. After one week baseUne period, subjects were assigned to consume either 114g per day o f a psyllium-flake or wheat bran- fiake cereal ft>r 6 weeks. Fasting HDL cholesterol levels did not change significantly during the six weeks (Anderson et al., 1992). In a similar study Anderson (1984) also ft)und that in thirty-five hypercholesterolemic men with total cholesterol higher than 260 mg/dl who were placed in either a oat bran diet, dried bean diet or canned bean diet for 21 days. Twelve participants were placed in the oat-bran diet which the consumed between 50 to 100 g o f oat bran daily as hot cereal or oat bran muffins. Eleven participants were placed in the dried bean diet group, which they consumed 100 g o f navy or pinto beans served in soup. The last twelve participants were placed in the canned bean diet in which they consumed 120 g o f canned beans from Campbell’s Pork and Beans. HDL cholesterol concentrations had a non-significant decrease o f 6% as for the dried and canned beans there was a significant decrease in HDL concentrations.In this study the effect o f the exercise on the participant’s total, low-density lipoprotein, and high-density lipoprotein serum cholesterol levels was also of interest. It has been well documented that individuals who engaged in regular cardiovascular concentrations that place them at low risk for developing coronary artery disease. StudiesReproduced with permission of the copyright owner. Further reproduction prohibited without permission.54demonstrating this lower risk include the results o f world class marathon runners having exceptionally high plasma HDL cholesterol and relatively low total cholesterol, LDL cholesterol and triglyceride concentrations. These findings indicate that individuals who participate in regular strenuous exercise achieve increases in HDL levels helping reduce the risk o f cardiovascular disease. Huttunen, Lansimis, Voutilainen, Ehnhohn, Hietanen, Penttila, Siitonen and Raurama (1990) reported a significant increase in HDL cholesterol by 19%, whereas plasma total cholesterol, LDL cholesteroL and triglyceride levels were decreased by 10% in a group o f middle-aged men who performed aerobic exercise 3 to 4 days a week for 16 weeks.Analysis of data from the present study shows that participants performing regular aerobic exercises three times a week for a duration o f 30 minutes and at an intensity o f 70% or more o f their predicted max heart rate had no greater decrease in lipid serum concentrations then those in the non-exercising participants. As shown in figure 1 and 2 total cholesterol decreased 7.96% in the exercising group and 7.84% in the nonexercising group and LDL decreased 13.3% in the exercise group and 10.46% in the nonexercising group. HDL concentration decreased 8.42% in the exercise group and 1.63% in the non-exercise group (see figure 3). Generally, when a person’s lipid levels are high, regular exercise training can usually reduce high levels o f total and LDL cholesterol. The exercise group’s lack o f response to have an even larger decrease in total and LDL cholesterol concentrations when compared to the non exercise group might be explained by the feet that each participant in the exercise group had been exercising for 6 months or longer before entering the study. One might hypothesis that they may have already lowered their cholesterol levels to the extent in which exercise can affect them DietaryReproduced with permission of the copyright owner. Further reproduction prohibited without permission.55therapy in conjunction with regular exercise is considered an essential element in therapy o f elevated serum cholesterol levels. In this study, patients at risk for coronary heart disease exhibited significant reductions in serum cholesterol after using Bios Life.Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.CHAPTERSSUMMARY AND CONCLUSIONS SummaryAn increase in the incidence o f coronary heart disease has lead to an increased interest in preventive measures. Since there is a strong relationship between high fiber diet, regular exercise and coronary heart disease, health professionals support a high fiber diet and regular exercise as a contributing factor in reducit^ this incidence.It has been well documented that both high levels o f total serum cholesterol and specifically low-density lipoproteins are linked with coronary heart disease. Epidemiological data from the Framingham Heart Study indicate that elevated total serum cholesterol is a major coronary risk factor. Larosa and associates (1990) studied CHD histoiy and total cholesterol in 2,282 men and 2,845 women and concluded that there was definite evidence that high levels o f total cholesterol were associated with an increase in the incidence o f CHD and that conversely low levels o f total cholesterol were associated with a low incidence o f CHD (Larosa et al., 1990).The general purpose o f dietary fiber supplementation as therapy is to reduce elevated serum cholesterol levels. This is achieved primarily by reducing fet intake and consuming a healthy diet, rich in fiber. Dietary therapy in conjunction with regular exercise is considered an essential element in therapy o f elevated serum cholesterol56Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.57(Ready, 1996). Exercise has been shown to help in the promotion o f weight reduction, which enhances LDL cholesterol lowering, reducing triglyceride, raising HDL, reduces blood pressure and decreasing the risk o f diabetes mellitus. Therefore, the combination o f regular exercise and diet rich in fiber can lower total cholesterol, increase HDL, decrease LDL and consequently reduce the risk o f CHD.The purpose o f this study was to investigate the effects o f Bios Life, a nonprescription dietary fiber supplement, on Total and LDL cholesterol and determine whether exercise accentuates this effect. Fifty (50) male and female subjects volunteered to participate. Twenty-five were exercising regularly in a supervised exercise program and the other 25 were sedentary. A 12-hour fasting blood sample was taken prior to the study to obtain a baseline value and again at 45 and 90 days. Subjects had to have LDL- C greater than 130 mg/dl to participate in the study. Both groups took 4.5 gram packets of Bios Life twice a day. Neither group changed their regular routine or eating habits.Mean total cholesteroL low-density Upoproteins and high-density lipoproteins were analyzed using a 2 (group) by 3 (time) analysis o f variance (ANOVA) procedure with repeated measures on time. All statistical analysis was done using the SAS system.The results o f this study showed that total cholesterol and low-density lipoproteins concentrations decreased significantly from baseline to 90 days. This was true whether or not the subject was in the exercise group or non-exercising group. ConclusionsThe following conclusions can be drawn from this study:1. Exercise did not accentuate the effect o f Bios Life.Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.58RecommendationsThe following are recommendations for future studies:1. Since there was no significant difference between the exercise and non-exercise groups it is suggested that the participants in the exercise group not be involved in an exercise program prior to the study. Both groups should take the Bios Life, but the participants in the exercise group start an exercise regimen at the beginning o f a study.2. Bios Life did decrease total cholesterol and LDL levels over the 90 days but not to the same extent as some o f the other drugs like probucol, niacin, pravastin, and zocor. As reported in the existing literature, further research over a greater amount o f time may be needed to see if time would allow for a greater decrease in total cholesterol and LDL levels with Bios Life users.Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.APPENDIX AINSTRUCTIONS TO SUBJECTS MEMORANDUM TO SUBJECTS59Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.ouReproduced with permission of the copyright owner. Further reproduction prohibited without permission.61PURPOSEIt has been documented that high levels of total serum cholesterol have been linked with coronary heart disease. However, reductions in the low-density lipoprotein fraction of total cholesterol are linked with reduction in myocardial inferction and sudden cardiac death. There is evidence indicating that dietary fiber can lower serum cholesteroL Individuals consuming a diet high in fiber tend to have a lower incidence of myocardial inferction and sudden cardiac death. This study will the effects of Bios Life 2 a dietary fiber supplement on serum IqmiHotems, and determine whether exercise potentates this effect.PRODUCTThe natural dietary fiber supplement consisted o f a mixture based on a patented formula (# 4,824,672) and (# 4,883,788) titles "hfethod and C on^sition for Reducing Serum Cholesterol’ manufoctured by Rexall Showcase International under the trade name Bios Life Natural This patented formula consisted of pectin, guar gum, gum arable, oat fiber, and locust bean, gum. This product also contains various vitamins (beta carotene, vitamin E, vitamin C, niacinamide, vitamin B-12, pyridoxine HCl, riboflavin, thiamine HCl, biotin, and folic acid). In addition, diromium polynicotinate and selenomethionine were added to enhance the metabolic a^>ects of the product To improve palatability, Stevia, a natural fiber with known natural sweet effects, was added to the product mix.METHODSAs a volunteer for this study your LDL cholesterol level must be greater than 130 mg/dl and keep particÿating in a frmnal exercise program at least three times per week.Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.62You will givea 12-far. âsting blood sanq>le baseline, 30,60 and 90 days. Also at these time periods heigln and we^ht will be taken and Bogiith will be measured and waist to bq> ratio will be computed. Body fat will be detomined by lnoinq)edance anafysis. A six-minute walk test will be administered.For the next 90 days you will mix Bios Life 2 a dietary fiber with an eight-ounce glass of water, fruit juice or Gatomde. It will be taken 15 minutes prior to breakfrst and dinner. Weekly questioning to monitor adherence to the fiba* statement will administoed.Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.63U N IV E R S IT Y O F NEVADA, LA S V EG A S COLLEGE OF HEALTH SCIEN CESDEPARTMENT OF KINESIOLOGY EXERCISE PHYSIOLOGY BOX 4 5 3 0 3 4 LAS VEGAS, NV 8 9 1 5 4 -3 0 3 4M E M O R A N D U MDATE: 9/15/98_________________________TO: ______ Subjects for Cholesterol lowering study__________________FROM: Lawrence A. Golding. E-mail: T.AnmlHlnpfS)ani com and Lori inderiiedSU BJEC T:_____ Requirements for the study______________________________The Exercise Physiology Laboratory Is about to start a study on the effect o f a non-prescription fiber preparation, which Is claimed to reduce LDL Cholesterol. Total cholesterol Is m ade up o f iow-denslty lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C). The popular literature refers to LDL a s the "bad” cholesterol and the HDL as the "good” cholesterol.This study will Investigate the effect of taking th is supplem ent In people who are exercising and in people who are sedentary. All subjects m ust have a LDL cholesterol of more than 130mg/dl.You have been Identified a s som eone who is exercising regularly (the adult exercise program) but who has a LDL cholesterol greater than 130mg/dl. We would like you to volunteer to be a su b jec t The details of the study are a s follows:1. The study will be 90 days in duration.2. A llpid profile will be done prior to the study starting, after 45 days and again at the end of the study.3. During those sam e 3 times the following m easurem ents will be taken:I. Percent fat by Bioimpedance. This only requires two electrodes to be placed on your wrist and ankle. A very low-grade electric current (from a 9voK battery, which you will not feel) will pass between the electrodes and impedance will be m easured from which percent fat Is calculated. This is done in street clothes only requiring the right shoe and sox to be removed.II. Height and welghLIII. Waist and hip girthhr. A Sminute walk will be done for time.V. Every two weeks you will be asked to come to the laboratory to pick up your two week supply o f Blosllfe and return the empty packages from the previous two weeks. This is the way we document that you have taken the Bloslife. If you m iss a dose, simply bring back the full package and we canTdcplione; (702M 9S-3766 FAX, (702)-895-4191Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.64record w hat you m issed. When you com e in weight will be taken and a modified percent fat through bioim pedance will be done. This modified procedure only requires you to hold and Instrument in your hand, vl. Prior to starting, you will be asked to complete a simple questionnaire to determ ine how much fiber you are presently consuming In your normal dally diet.Enclosed Is an Informed consent form which explains the above. If you arewilling to participate please sign the form, have your signature w itnessed and return it in the enclosed, self addressed stamped envelope.Telephone; (702)-895-3766 FAX, (702)-895-4191Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.APPENDIX BAPPROVAL LETTER FROM INSTITUTIONAL REVIEW BOARDINFORMED CONSENT65Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.TJNTV66DATE: May 11, 1998TO: Lori J. Inderiied (KIN)M/S: 3034FROM: ' Dr. William E. Schulzeo^^'VDirector, Office of Sponsored Programs and y Member, Biomedical Sciences Committee UNLV Institutional Review BoardRE: Status of Humcui Subject Protocol entitled:"The Effect of Bios Life, a Non-prescription Cholesterol-Lowering Substance and a Combination of Bios Life and Exercise on Serum Lipids : “OSP #504s0498-013bThis memorandum is official notification that the protocol for the project referenced above has been approved by the Biomedical Sciences Committee of the Institutional Review Board. This approval is approved for a period of one year from the date of this notification, and work on the project may proceed.Should the use of human subjects described in this protocol continue beyond a year from the date of this notification, it will be necessary to request an extension.If you have any questions or require any assistance, please Marsha Green at 895-1357.cc: L. Golding (KIN-3034) OSP FileOffice of Sponsored Programs 4505 Maryland Parkway • Box 451037 • Las Vegas, Nevada 89154-1037 (702) 895-1357 • FAX (702) 895-4242Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.67CONSENT TO PARTICIPATE IN RESEARCH UNIVERSITY OF NEVADA, LAS VEGAS EXERCISE PHYSIOLOGY LABORATORYTITLE OFTHE STITDYi The effect o f Bk>s Life axid a combination o f Bios Life and exercise on total cholesterol,serum bw density lipoprotein, and serum high density Iqx>piotein will be invest^ated.PURPOSEIt has been weU documented that high fevels o f total serum cholesterol have been linked with coronary heart disease. However, reductbns in the b w density lipoprotein feactbn ̂ o f total cholesterol are linked with reductbn In myocardial inferctbn and sudden cardiacdeath. There is evidence iixiicating that dietary fiber can bwer serum cholesteroL I bxlividuals consuming a diet high in fiber tend to have a bwer incidence o f nyocardialinferctbn and sudden cardiac death. This study will mvestigate the effects of B bs Life, a _ dietary fiber stqrplement on serum lipoproteins, and determine whether exercises potentiates this effect.yPROCEDURESIf you decide to partbipate in this Study you will report to eifirer the Exercise Pfaysbbgy L Laboratory or the Cardbvascular Center of Southern Nevada fer an explanatbn of the^ study. A six mmute walk test will be given as well as weight arxi body percent fet taken.Four times during the study you win report to the bbod lab fer a 12 hour festing bbod ' sarr^te to be collected. There is no cost to you as a pattbq>ant fer any tests done in thisproject The details o f the study areas felbwed:V Pretreatmem Period: A 12 hour fisting bbod sanyb will be taken fiom each) partbqrant to determine if they fiilfiU the cholesterol arb lipoprotein criteria. The criteriato partbqrate is ones LDL must be 130 mg/dl or greater. Orx% 50 participants are f identified body fet and weight will be takerL A six mmute walk wUl be administered todetermine aerobb capacity.Treatment Perbd: The group wfil be randomly divided in two grouns: The R control groiç will not be exercising and wfll remain on tfaerrcurreittdiet. Theexperimental grorq) win continue, their regular exercise program at least three times per \ week.? Each grotq) will be instructed to consume 4.5gofB bs Life beferebreakfest anddinner by stirring the contents o f one packet into an 8oz glass o f half water arxi half juice arxi drink immediately. This will be done 15 minutes prbr to Ixeakfest and dinner everyday fer the length o f the study. Partbipants wOl have a festing lipid panel conqrleted 30,60 arxi 90 days later. Also weight, aerobb capacity arxi body percent fet will be measured at 30,60 arxi 90 days.RISKSThe risks o f taking B bs Life are m m im al. This is an non-prescriptive dietary siqrplement administered comnaonly be cardbbgists. Efowever, using this product may result in mild gastroirrtestinal distress, increases stool volume, Hkrrhm*, constipatbn, abdominalReproduced with permission of the copyright owner. Further reproduction prohibited without permission.68cranqnngor^ipetitesiqrpressioa Ifyou experience any ofthese side affects, please repent to the leseardier as soon as possible and also consult your plqrsician if necessary.BENEHTSThe benefits include a reduction in LDL-C and increase in HDL-C. The exercise group will benefit fix>m the physical effect o f exercise, and the value o f exercise combined with ingestion o f Bios Life win be known.COWFTDENTf ALITYYour particpetionm and the results o f this study wiUremamconfidentiaL On^ those parties dhectfy related whh the coUection and analysis o f data wfll have access to your file. Iffhe data is presented in a scientific journal or conférence you wOl be referred to by aparticipam number not your name.RIGHT TO REFUSE OR WITHDRAWALYour particpation in this sturfŷ is strictfy voluntary. You nay withdraw consent or refiise to participate at any tinae.QUESTIONSAny questions you have about the study it's purpose, dmagn, methodology, procedures arxi significance will be addressed to your satisfictioa If you have additioral questions please feel fiee to contact Lori hxlerlied or Dr. Goldirg at 895*3766 or Chetri Epstein Director o f the Cardiac Rehabilitation program at 254-2400.For questions regarding the r%hts o f research participants you rray contact the OfBce of Sponsored Programs at 895-1357.You will be given a s%ned arxi dated copy o f this fimn fer you records.I UNDERSTAND THE RESEARCH PROCEDURE AND HAVE DECIDED TO VOLUNTEER AS A RESEARCH SUBJECT. I HAVE READ THE PROVIDED INFORMATION AND ALL QUESTIONS REGARDING THE EXPERIMENT HAVE BEEN ANSWERED TO MY SATISFACTION. I UNDERSTAND THAT I HAVE THE RIGHT TO WITHDRAW FROM THIS STUDY AT ANY TIME WITHOUT RECRIMINATION.Name o f Particpant (print) Signature DateName o f Witness ^xrint) Signature DateReproduced with permission of the copyright owner. Further reproduction prohibited without permission.APPENDIX CINSTRUCTIONS OF DIETARY SURVERY HELPFUL MEASURING GUIDE DIETARY SURVEY EXPLANATION OF DIETARY SURVEY LIST OF MINERALS AND VITAMINS69Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.70UNLVUniversity o f Las Vegas Nevada Inderiied Cholesterol/Bios Life Study Instructions on Dietary SurveyFor three days you wül write down everything you eat including beverages in the first column. In the second column you will put down the amount o f your servings. Attached to the dietary survey there is a helping guide, this allows you to figure out the exact serving size. The third column you will write down how you prepared the food. For example: You baked chicken in the oven. Remember to count what you might have marinated the chicken in and also how you coated the baking pan. The last column is for any comments that you might want to add for the nutritionist who wül be analyzing the survey.Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.GnEHWlEIKrk w m m71A “Helping” HandW h a t^ a F o o d G u id e P y n m id s e r v in g ? ^Abiir MuM-ColummBasic Compononts VhaamAHE 928J3RE 116%Ctlories 1466.19 70% A-CtiMeBaid 220.04RE Fhnride -m gPMcm 43j6g 74% A-ReHmri SS.S9RECaiboi^dnles 230.27g S2% TlmmmBl 1.07mg 102% Ino 14J6mg 96%Dietmy Fiber 15.76 g 75% Megnomm 256.44 mg 92%SohM eFta 3.95 g 1 11' i|iirillFniiW lkP71lï Mangasem 4.25 mg 121%InSoiobieFiber 6.74gSagv-ToOl 147.41g P b a jto » 533.81 mg 67%Moooacdurides 18.41 g V| _DiaodBiides 15J8g VimmmC 320.18mg 534% Sdenmm T3T$0d ^ 80%OtherCubs 55A )g ^UMlÊDaS^^SIBSSÊfSmH Sodmm 1777.85 n« 74%g g g B W B @ S S g |B K i^ |% VkmmnEe, 5.23mg ^SBSS^^Sm msSÊSSÊÊm s^mFoWc lS3J3mcg 102% OOMTFalSonegi3FmtyAddi 0.63 g Omeg,6Fm^AdL__________mg/dlmg/dl EDDL/RATTO___________mg/dl_______mg/dl#LAPSNUMBER OF PACKETS OF BIOSLIFE RETURNED FULL EMPTYDATE TEST STARTEDNEXT SCHEDULED APPOINTMENT COMMENTS:C o lleg e o f H ea lth S c ie n c e s D e p a r tm e n t o f K inesio logy 4 5 0 5 M ary land P a rk w a y • B o x 4 5 3 0 3 4 • L a s V eg a s , N ev a d a 8 9 1 5 4 -3 0 3 4 (702) 8 9 5 -0 9 9 6 • FAX (702) 8 9 5 -1 5 0 0Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.82Exercise GroupRaw Data Total CholesterolNon-Exercise GroupBaseline 45 Davs 90 Davs Baseline 45 Davs 90 DaSubject 1 284 270 250 Subject 26 240 237 228Subject 2 196 196 180 Subject 27 205 200 200Subject 3 186 190 180 Subject 28 200 200 200Subject 4 204 203 200 Subject 29 260 240 210Subject 5 316 239 277 Subject 30 220 210 200Subject 6 246 250 248 Subject 31 359 313 253Subject 7 249 230 225 Subject 32 283 255 230Subject 8 279 272 273 Subject 33 280 270 240Subject 9 197 225 199 Subject 34 221 211 190Subject 10 227 227 228 Subject 35 250 240 250Subject 11 218 211 190 Subject 36 210 210 200Subject 12 246 220 235 Subject 37 228 240 237Subject 13 209 188 183 Subject 38 265 265 260Subject 14 230 209 200 Subject 39 264 250 244Subject 15 287 378 293 Subject 40 234 246 212Subject 16 217 218 200 Subject 41 246 236 212Subject 17 210 209 200 Subject 42 246 246 246Subject 18 246 230 200 Subject 43 290 290 280Subject 19 230 230 200 Subject 44 210 210 210Subject 20 288 270 270 Subject 45 222 200 214Subject 21 213 200 200 Subject 46 240 237 237Subject 22 222 177 200 Subject 47 205 205 205Subject 23 269 279 280 Subject 48 283 255 255Subject 24 222 200 205 Subject 49 284 270 250Subject 25 359 313 253 Subject 50 210 210 210Mean Std. Dev. Std. Error242 41.560197 8 J 120395233.3644.5980948.9196188222.7635.189108167.037821633Mean Std. Dev. Std. Error246.236.9244727.3848945237.8429.7625045.9525009226.9223.8919794.7783958Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.83Exercise GroupRaw Data LDL CholesterolNon-Exercise GroupBaseline 45 Davs 90 Davs Baseline 45 Davs 90 DavsSubject 1 206 197 160 Subject 26 138 129 137Subject 2 133 133 120 Subject 27 132 140 130Subject 3 132 130 125 Subject 28 130 130 130Subject 4 141 139 130 Subject 29 180 170 130Subject 5 189 165 140 Subject 30 146 136 126Subject 6 142 173 149 Subject 31 236 196 139Subject 7 162 150 140 Subject 32 158 114 114Subject 8 177 173 150 Subject 33 160 160 140Subject 9 173 142 140 Subject 34 131 124 120Subject 10 154 154 172 Subject 35 140 135 135Subject 11 154 150 130 Subject 36 140 141 130Subject 12 143 113 120 Subject 37 137 138 129Subject 13 155 117 136 Subject 38 180 180 175Subject 14 139 124 112 Subject 39 139 139 130Subject 15 219 296 211 Subject 40 140 143 136Subject 16 134 133 120 Subject 41 149 146 131Subject 17 134 136 129 Subject 42 138 138 138Subject 18 140 136 129 Subject 43 158 158 154Subject 19 140 140 130 Subject 44 141 140 141Subject 20 171 161 161 Subject 45 138 137 149Subject 21 172 162 146 Subject 46 138 129 129Subject 22 140 123 126 Subject 47 132 132 132Subject 23 170 155 145 Subject 48 158 114 114Subject 24 174 164 131 Subject 49 206 197 160Subject 25 236 196 139 Subject 50 141 140 141Mean 161.2 154.48 139.64 Mean 151.44 144.24 135.6Std. Dev. 27.971712 36.766289 20.605177 Std. Dev. 25.270338 21.6781 13.400871Std. Error 5.5943424 7.3532578 4.1210355 Std. Error 5.0540677 4.3356199 2.6801741Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.84Exercise GroupRaw Data HDL CholesterolNon-Exercise GroupBaseline 45 Davs 90 Davs Baseline 45 Davs 90 DavsSubject 1 58 54 50 Subject 26 60 60 82Subject 2 49 49 46 Subject 27 54 56 50Subject 3 25 20 54 Subject 28 54 54 54Subject 4 48 51 30 Subject 29 60 60 48Subject 5 56 66 53 Subject 30 54 54 50Subject 6 61 61 71 Subject 31 56 55 59Subject 7 64 54 64 Subject 32 64 63 50Subject 8 62 48 44 Subject 33 56 56 50Subject 9 23 27 45 Subject 34 54 43 54Subject 10 31 31 36 Subject 35 54 54 50Subject 11 31 30 31 Subject 36 54 52 50Subject 12 82 84 58 Subject 37 82 60 60Subject 13 23 31 29 Subject 38 34 34 29Subject 14 59 51 50 Subject 39 61 61 61Subject 15 43 60 39 Subject 40 32 34 36Subject 16 50 45 47 Subject 41 39 39 41Subject 17 58 58 51 Subject 42 60 60 60Subject 18 45 45 45 Subject 43 64 64 62Subject 19 65 65 50 Subject 44 50 50 50Subject 20 70 60 60 Subject 45 22 19 27Subject 21 54 50 46 Subject 46 60 60 60Subject 22 55 31 29 Subject 47 54 54 54Subject 23 86 94 60 Subject 48 64 63 63Subject 24 28 26 27 Subject 49 60 60 82Subject 25 56 55 59 Subject 50 48 40 46Mean 51.28 49.84 46.96 Mean 54 52.2 53.12Std. Dev. 17.145262 17.747488 11.890052 Std. Dev. 12.086494 11.25833 12.80403(Std. Error 3.4290523 3.5494976 2.3780104 Std. Error 2.4172988 2.251666 2.5608072Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.APPENDIX EPHYSICAL CHARACTERISTICS BODY COMPOSTION TABLES BODY MASS INDEX WAIST/HIP CIRCUMFERENCE W AIST/mP RATIO PERCENTILE FOR HEART DISEASE85Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.CD■DOQ.CgQ.■DCDC/)C/)8■DCD3.3"CDCD■DOQ.CaO3"OoCDQ.■DCDC/)C/)Exercise GroupPhysical Characteristics of ParticipantsSex Age Height Weight BMI Waist to Hip Ratio Bioimpedance % Fat 6-Minute Walk TestYears Inches Pounds OhmsSubject 1 Male 50 70 215 31 0.8 400 21.3 7 lapsSubject 2 Female 32 63 138 24.5 0.8 478 24.2 8 lapsSubject 3 Male 58 69 170 25 0.9 486 19.7 8 lapsSubject 4 Male 53 73 250 31 0.6 486 36.8 8 lapsSubject 5 Female 50 68 163 24 0.75 557 29.7 6 lapsSubject 6 Male 36 71 156 22 0.8 477 13.9 8 lapsSubject 7 Female 63 71 186 26 0.75 586 33.1 6 lapsSubject 8 Male 50 73 246 33 1 403 23 6 lapsSubject 9 Male 59 71 178 25 0.9 462 17.6 7 lapsSubject 10 Female 59 64 120 21 0.8 400 21 5 lapsSubject 11 Female 53 63 166 29 0.9 586 37.8 6 lapsSubject 12 Male 56 72 200 28 0.8 496 29 7 lapsSubject 13 Male 59 69 177 26 0.8 496 27 7 lapsSubject 14 Female 47 64 171 29 0.75 483 32.7 6 lapsSubject 15 Male 47 70 188 27 0.85 451 19.8 6 lapsSubject 16 Male 64 68 131 20 1.1 531 13.8 6 lapsSubject 17 Male 54 61 153 29 0.8 464 23.8 6 lapsSubject 18 Male 60 69 190 28 0.8 470 24.2 6 lapsSubject 19 Female 52 67 155 23 0.8 581 30.5 7 lapsSubject 20 Female 48 66 162 26 0.9 580 31 6 lapsSubject 21 Female 50 60 132 26 0.9 581 21 6 lapsSubject 22 Male 59 68 156 23 0.9 467 16.1 8 lapsSubject 23 Female 30 67 142 22 0.8 389 16.1 7 lapsSubject 24 Male 65 72 257 30 1.1 486 36 5 lapsSubject 25 Male 45 71 166 23 0.75 478 16.1 9 lapsMean 51.96 68 174.72 26.06 0.842 490.96 24.608 6.68Standard Dev, 9.18 3.71 36.25 3.41 0.11 60.47 7.37 1.03Standard Error 1.84 0.74 7.25 0.68 0.02 12.09 1.47 0.21CD■DOQ.CgQ.■DCDC/)C/)8■DNon-Exercise GroupPhysical Characteristics of Participants33"CDCD■DOQ.CaO3"OOCDQ.■DCDC/)C/)Sex AgeYearsHeightInchesWeightPoundsBMI Waist to Hip Ratio BioimpedanceOhms% Fat 6-Minute Walk TestSubject 26 Female 57 67 141 22 0.8 648 28.8 7 lapsSubject 27 Male 56 62 131 24 0.8 648 28.8 6 lapsSubject 28 Female 60 70 180 26 1 423 16.1 8 lapsSubject 29 Male 59 68 140 21 0.8 477 13.9 7 lapsSubject 30 Male 50 72 205 28 0.9 486 28 6 lapsSubject 31 Female 46 60 120 23 1 300 18 6 lapsSubject 32 Female 40 62 130 24 1 400 23 7 lapsSubject 33 Female 30 70 221 30 1.1 535 15 7 lapsSubject 34 Female 60 70 174 25 1.1 386 17.1 6 lapsSubject 35 Male 56 74 250 30 1.1 586 27 6 lapsSubject 36 Male 51 66 140 24 0.8 486 23 6 lapsSubject 37 Male 40 62 140 25 0.9 424 12 4 lapsSubject 38 Female 48 68 131 35 0.9 648 28.6 5 lapsSubject 39 Male 57 72 186 25 0.9 500 26 5 lapsSubject 40 Female 36 64 140 24 0.7 480 25 8 lapsSubject 41 Female 38 62 146 27 0.9 464 28.6 4 lapsSubject 42 Male 45 70 200 29 1 500 24.6 7 lapsSubject 43 Female 55 61 205 35 1 486 31.1 4 lapsSubject 44 Female 39 58 150 30 I 486 26.7 7 lapsSubject 45 Male 36 67 166 25 0.9 423 16.1 8 lapsSubject 46 Female 57 64 154 26 0.7 646 28 7 lapsSubject 47 Male 52 67 283 40 1.2 537 34.4 7 lapsSubject 48 Female 44 64 126 21 0.7 648 28.8 8 lapsSubject 49 Female 30 67 142 22 0.8 389 16.1 7 lapsSubject 50 Male 59 68 156 23 0.9 467 16.1 8 lapsMean 48.04 66.2 166.28 26.56 0.916 498.92 23.232 6.44Standard Dev. 9.69 4.16 41.28 4.71 0.13 94.86 6.36 1.26Standard Error 1.94 0.83 8.26 0.94 0.03 18.97 1.27 0.2588BODY COMPOSmON (% BODY FAT) FOR MEN*Age% ile 20-29 30-39 40-49 50-59 60+99 52.4 S5.2 <6.6 <8.8 57.795 5.2 9.1 11.4 12.9 13.1 S90 7.1 11.3 13.6 15.3 15.365 8.3 12.7 15.1 16.9 17.280 9.4 13.9 16.3 17.9 18.4 E75 10.6 14.9 17.3 19.0 19.370 11.8 15.9 18.1 19.8 20.365 12.9 16.6 18.8 20.6 21.160 14.1 17.5 19.6 21.3 22.0 G55 15.0 18.2 20.3 22.1 22.650 15.9 19.0 21.1 22.7 23.545 16.8 19.7 21.8 23.4 24.340 17.4 20.5 22.5 24.1 25.0 F35 18.3 21.4 23.3 24.9 25.930 19.5 22.3 24.1 25.7 26.725 20.7 23.2 25.0 26.6 27.620 22.4 24.2 26.1 27.5 28.5 PIS 23.9 25.5 27.3 28.8 29.710 25.9 27.3 28.9 30.3 31.25 29.1 29.9 31.5 32.4 33.4 VP1 236.4 235.6 237.4 238.1 241.3N = 1342 5611 5724 3275 984TOTAL N = 16936'Data provided by (he Instituie lor Aerobics Research, Dallas. TX (1994). S, superior E. excellent; G. good; F. lair: P. poor VP. very poor.BODY COMPOSITION (% BODY FAT) FOR WOMEN*Age•/• ile 20-29 30-39 40-49 50-59 60+99 55.4 57.3 <11.6 511.6 <15.495 10.8 13.4 16.1 18.8 16.8 S90 14.5 15.5 18.5 21.6 21.185 16.0 16.9 20.3 23.6 23.580 17.1 18.0 21.3 25.0 25.1 E75 18.2 19.1 22.4 25.8 26.770 19.0 20.0 23.5 26.6 27.565 19.8 20.8 24.3 27.4 28.560 20.6 21.6 24.9 28.5 29.3 G55 21.3 22.4 25.5 29.2 29.950 22.1 23.1 26.4 30.1 30.945 22-7 24.0 27.3 30.8 31.840 23.7 24.9 28.1 31.6 32.5 F35 24.4 26.0 29.0 32.6 33.030 25.4 27.0 30.1 33.5 34.325 26.6 28.1 31.1 34.3 35.520 27.7 29.3 32-1 35.6 36.6 P15 29.8 31.0 33.3 36.6 38.010 32.1 32.8 35.0 37.9 39.35 35.4 35.7 37.8 39.6 40.5 VP1 240.5 240.0 245.5 250.8 &47.0N = 638 TOTAL N = 41071336 1175 708 250'Data provided by the Institute for Aerobics Research, Dallas. TX (1994). S. superior E. excellent- o. good; F. fair P. poor VP, very poor.Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.■ooQ.c8Q.■oCDC/)o'3OCD8■Dv 287 328Less than 20 20 -25 26 to 27 Higher than 27Weight gain Acceptable range for most people but Escalating Dramatic risk of health problemsmay be advisabie potential heaith probiems with weight gain Health risks90180 701706016030 6015080LU 140 LU90 W HRlU0.6LUU .LL 1300.7100500.81200.9110110120=1— 4010013090140801503060cmcmReprinted from: Bray GA and Gray DS: Obesity. Part 1 —Pathogenesis. Western JesternM ed 149:429-441. 1988.Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.911.10-11.0 -oMIS 0 9-̂f t0.8A^ 0.70.6 —MENVery High RUcUoderat* RiskLow Riskloih30th70thI — r20-29 30-39 40-49 50-59Age (yr) WOMEN60-69IVery High Risk30ttl Smsimc £ 0.840-4920-29 30-39Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.BIBLIOGRAPHYAdlersberg, D., Schaefer, L., Steinberg, A. & Wang, C. (1956). Age, sex, serum lipids, and coronary artherosclerosis. The Journal o f the American Medical Association. 162. 619-622.Anderson, J., & Chen, W. (1979). Plant fiber: carbohydrate and lipid metabolism. The American Journal o f Clinical Nutrition. 32. 346-363.Anderson, J., Story, L., Sieling, B., Chen, W., Petro, M. & Story, J. (1984). Hypocholesterolemic effects o f oat-bran or bean intake for hypercholesterolemic men. The American Journal o f Clinical Nutrition. 40. 1146-1155.Anderson, J., & Tietyen-Clark, J. (1986). Dietary fiber hyperlipidemia, hypertension and coronary heart disease. The American Journal Gastroenterol 81. 907- 919.Anderson, J. (1987). Dietary fiber, lipids and atherosclerosis. The American Journal of Cardiology. 60. 17G-22G.Anderson, J. & Bridges, S. (1988). Dietary fiber content o f selected foods. The American Journal o f Clinical Nutrition. 47. 440-447.Anderson, J., Zettwoch, N., Feldman, T., Tietyen-Clark, J., Oeltgen, P. & Bishop, C. (1988). Cholesterol-lowering effects o f psyllium hydrophilic mucilloid for hypercholesterolemic men. Archives Internal Medicine. 148. 292-296.92Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.93Anderson, J., Deakins, D., Floore, T., Smith, B., & White, S. (1990). Dietary fiber and coronary heart disease. Critical Review Food Science Nutrition. 29. 95-147.Anderson, J., Spencer, D., Hamilton, C., Smith, S., Tietyen, J., Bryant, C. & Oeltgen, P. (1990). Oat-bran cereal lowers serum total and LDL cholesterol in hypercholesterolemic men. The American Journal o f Clinical Nutrition. 52. 495-499.Anderson, J., Gilinsky, N., Deakins, D., Smith, S., O ’Neal, D., Dillion, D. & Oeltgen, P. (1991). Lipid response of hypercholesterolemic men to oat-bran and wheat- bran intake. The American Journal o f Clinical Nutrition. 54. 678-683.Anderson, J., Riddell-Mason, S., Gustafeon, N., Smith, S. & Mackey, M. (1992). 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