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Critical Reviews in Food Science and Nutrition Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/bfsn20
Dietary fiber and coronary heart disease James W. Anderson Whitis a
a b
c
d
e
, Dee A. Deakins , Tammy L Floore , Belinda M. Smith & Sarah E.
f
Chief, Metabolic‐Endocrine Section , VA Hospital ,
b
Professor of Medicine and Clinical Nutrition in the Department of Medicine , University of Kentucky , Lexington c
Research Nurse Coordinator for the Metabolic Research Group in the Department of Medicine , University of Kentucky , Lexington d
Research Nurse in the Metabolic Research Group in the Department of Medicine , University of Kentucky , Lexington e
Research Dietitian in the Department of Behavioral Science , University of Kentucky , Lexington f
Cardiovascular Research Coordinator in the Department of Behavioral Science, College of Medicine , University of Kentucky , Lexington Published online: 29 Sep 2009.
To cite this article: James W. Anderson , Dee A. Deakins , Tammy L Floore , Belinda M. Smith & Sarah E. Whitis (1990) Dietary fiber and coronary heart disease, Critical Reviews in Food Science and Nutrition, 29:2, 95-147, DOI: 10.1080/10408399009527518 To link to this article: http://dx.doi.org/10.1080/10408399009527518
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Food Science and Nutrition lifestyle factors, and dietary fiber on major causes of death in the U.S. We review evidence relating dietary fiber to CHD specifically as it pertains to cardiovascular risk, hypercholesterolemia, hypertriglyceridemia, hypertension, and regression of atherosclerotic disease. In addition, we provide a historical perspective on dietary fiber, review possible mechanisms of action, and discuss therapeutic and practical applications. The interrelationship of dietary fiber intake, diabetes, and obesity are discussed elsewhere.16
Dietary Fiber And Coronary Heart Disease James W. Anderson, Dee A. Deakins, Tammy L Floore, Belinda M. Smith, and Sarah E. Whitis
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I. INTRODUCTION
B. New Found Popularity of Dietary Fiber For centuries the health benefits of dietary fiber consumption were related to the well-recognized effects on fecal bulk and bowel regularity. Pioneering work by Trowell22 and Burkitt23 indicated that many diseases of modern society might be related to dietary changes such as reduced dietary fiber intake. These observations suggested that dietary fiber intake may protect against such diseases as diabetes, hypertension, CHD, and obesity.24 Subsequent studies revealed that other fiber-rich foods such as oat bran and beans have important effects on serum cholesterol.25 These studies, combined with traditional wisdom, indicate that wheat bran and other foods with fecal bulking action are important in gastrointestinal function, while foods rich in water-soluble fiber have important metabolic effects on glucose and lipid metabolism.24
A. Importance and Significance of Coronary Heart Disease Cardiovascular disease (CVD) is the major cause of death in the U.S. and in most Western countries. Despite the recent sharp decline in the death rate from CVD,1 it still accounts for 759,000 deaths yearly2 in the U.S. (Table 1) or one death every 32 s.3 In 1988, the estimated U.S. financial cost for heart disease, including medical services, institutional costs, medications, and lost productivity, exceeded $83.7 billion annually.3 Certain characteristic factors greatly increase risk for CVD. The seven major modifiable risk factors for heart disease can be divided into two categories: lifestyle related and diet related. The lifestyle-related risk factors include cigarette smoking, inactivity, and poor stress management.4 The diet-related risk factors include hyperlipidemia, hypertension, diabetes, and obesity. Of the hyperlipidemias, hypercholesterolemia has moved to the forefront as a major risk factor for coronary heart disease (CHD).5 About 60% of men aged 20 to 50 years have serum cholesterol values above 200 mg/dl (Figure I). 6 Of this 60%, three quarters have cholesterol levels between 200 to 250 mg/dl, levels that can usually be reduced by dietary intervention. The remaining one quarter with levels above 250 mg/dl most likely have a genetic component. Thus, about 75% of individuals with hypercholesterolemia should respond to dietary intervention. One single dietary choice is emerging that may significantly prevent or qualitatively manage all four diet-related CHD risk factors: dietary fiber. Intensive nutrition intervention with diets high in complex carbohydrates and water-soluble fiber reduces serum cholesterol 20 to 32% and fasting serum triglycerides 10 to 20%. 7 U A high-fiber diet has been shown to lower systolic blood pressure 11% and diastolic blood pressure 10% in hypertensive individuals.12 High fiber intake also lowers plasma glucose levels in diabetic11-13 and nondiabetic individuals9 and significantly reduces insulin requirements of diabetic individuals.14 High fiber intake promotes weight loss and maintenance through increased satiety.15-16 In addition to managing these risk factors, recent data suggest that dietary fiber may independently protect against CHD. 1719 Thus, combining dietary fiber with a low-fat diet such as the American Heart Association (AHA) Diet can further reduce risk for developing heart disease.20-21 Table 1 summarizes the effects of diet, exercise, other
C. Existing Fiber Recommendations for Populations In the last decade, a consensus diet recommendation emerged: the U.S. Senate Select Committee recommended
J. W. Anderson received a B.A. degree from West Virginia University in Morgantown; a M.S. degree from Mayo Graduate School in Rochester, Minnesota; and a M.D. degree from Northwestern University in Evanston, Illinois. Dr. Anderson is currently Chief, Metabolic-Endocrine Section at the VA Hospital and Professor of Medicine and Clinical Nutrition in the Department of Medicine at the University of Kentucky in Lexington. D. A. Deakins received a B.S. in Nursing degree from the University of Tennessee in Knoxville and a M.S. degree from the University of Louisville in Louisville, Kentucky. Ms. Deakins is currently the Research Nurse Coordinator for the Metabolic Research Group in the Department of Medicine at the University of Kentucky in Lexington. T. L. Floore received a B.S.N. degree from Berea College in Berea, Kentucky. Ms. Floore is currently a Research Nurse in the Metabolic Research Group in the Department of Medicine at the University of Kentucky in Lexington. B. M. Smith received a B.A. degree from Eastern Kentucky University in Richmond. Ms. Smith is currently a Research Dietitian in the Department of Behavioral Science at the University of Kentucky in Lexington. S. E. Whitis received B.S., B.S.N., and M.S. degrees from the University of Kentucky in Lexington. Ms. Whitis is currently the Cardiovascular Research Coordinator in the Department of Behavioral Science, College of Medicine, University of Kentucky in Lexington.
1990
95
Critical Reviews In Table 1 Estimated Total Deaths and Contributing Factors for The 10 Leading Causes of Death in The U.S., 1987 Rank 1 2 3 4 5
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6 7 8 9
10
Contributing factors
Cause of death Heart diseases Cancers Strokes Unintentional injuries Chronic obstructive lung diseases Pneumonia and influenza Diabetes mellitus Suicide Chronic liver-diseases and cirrhosis
D, E, L, F D, L, F D, E, L, F L L
Atherosclerosis
Number
Percent of total deaths
759,400 476,700 148,700 92,500 78,000
35.7 22.4 7.0 4.4 3.7
L D, E, F L L
68,600 37,800 29,600 26,000
3.2 1.8 1.4 1.2
D, E, L, F
23,100
1.1 100.00 All causes
2,125,100
Note: D = diet, E = exercise, L = lifestyle, and F = fiber. Adapted from U.S. Department of Health and Human Services, The Surgeon General's Report on Nutrition and Health, U.S. Government Printing Office, Washington, D.C., 1988.
tow«r 168
182
193
203
213
221
232
245
264 higher
SERUM CHOLESTEROL, mg/dl FIGURE 1. CHD mortality related to serum cholesterol. (Adapted from Assmann, G., Expanding Horizons in Atherosclerosis Research, Schlierf, G. and Mori, H., Eds., SpringerVerlag, New York, 1987, 105. With permission.)
Americans increase intake of complex carbohydrate and fiber and decrease intake of saturated fat and cholesterol.26 The National Research Council of the National Academy of Sciences27 recommended maintaining or increasing consump96
tion of complex carbohydrates. Most recently, the Surgeon General's 1988 Report on Nutrition and Health2 promoted lowfat, low-cholesterol dietary patterns, emphasizing consumption of vegetables, fruits, and whole grain products — foods rich
Volume 29, Issue 2
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Food Science and Nutrition in complex carbohydrates and fiber and relatively low in calories. The report also emphasized consumption offish, poultry prepared without skin, and lean meats. Several national health organizations make fiber related dietary recommendations. The AHA recommends a diet high in complex carbohydrate but with no specifications for fiber intake.28 Using the Nutritionist HI computer analysis software package, which was upgraded by the addition of our fiber values,29 we calculated that the Phase I AHA Guideline provides approximately 21 g fiber per 2000 kcal. More specific fiber recommendations are made by the National Cancer Institute, which recommends intake of 25 to 35 g fiber per d,30 and by the British National Advisory Committee on Nutrition Education,31 which recommends 30 g/d of total dietary fiber with emphasis on cereal fiber. Other national health organizations recommending specific fiber amounts per day include the American Diabetes Association32 (25 g fiber per 1000 kcal) and the HCF Nutrition Research Foundation33 (10 to 13 g fiber per 1000 kcal). Table 2 compares the recommendations of these organizations. D. Types of Fiber Different types of fiber are distinguished by their differing physiological properties and systemic effects. Dietary fiber is grouped into two categories: water soluble and water insoluble.34 Water soluble fiber will dissolve in hot water; insoluble fiber will not. Examples of soluble fiber include pectin, gums, certain hemicelluloses, and storage polysaccharides. Fruits, oats, barley, and legumes contain more soluble fiber than other foods. Insoluble fiber includes cellulose, lignin, and many hemicelluloses. Vegetables, wheat, and most grain products contain primarily insoluble fibers.29-35 Soluble and insoluble fiber function differently in the body.34 Soluble fiber increases intestinal transit time, delays gastric emptying, and slows glucose absorption. These and other actions lower postprandial blood glucose concentrations, decrease serum cholesterol, and produce other metabolic effects. Insoluble fiber decreases intestinal transit time, increases fecal bulk, delays glucose absorption, and slows starch hydrolysis. These effects alter gastrointestinal function, but do not lower serum glucose or cholesterol.
II. DIETARY FIBER AND HEALTH A. The Dietary Fiber Hypothesis Dietary fiber is defined as the endogenous components of plant materials in the diet, predominantly nonstarch polysaccharides and lignin, which are resistant to digestion by human enzymes.36 The dietary fiber hypothesis developed by Burkitt and Trowell was summarized by Southgate37 into the following two statements:
1.
2.
"A diet that is rich in foods which contain plant cell walls (for example, high-extraction cereals, fruits, and vegetables) is protective against a range of diseases, in particular those prevalent in affluent Western communities (for example, constipation, diverticular disease, large bowel cancer, coronary heart disease, diabetes, obesity, and gallstones)." "In some instances a diet providng a low intake of plant cell walls is a causative factor in the etiology of these diseases and in others it provides the conditions under which other etiological factors are more active."
B. Historical Perspective For more than 20 centuries the merits of brown vs. white bread have been debated.38-39 While potential health benefits and intestinal effects of dietary fiber have been recognized by observant physicians and others for centuries, the full health implications of dietary fiber have emerged in only the last quarter century. The term dietary fiber was apparently coined by Hipsley40 in 1953. While there was a great deal of information buried in the medical and lay literature prior to 1970, the health implications of dietary fiber were made known to the medical and world community through the tireless efforts of Burkitt and Trowell.41 The history of dietary fiber has been chronicled by Burkitt42-43 and others*" 6 and can arbitrarily be divided into these phases: (1) early history, (2) clinical observations, (3) epidemiologic associations, and (4) research investigations. Table 3 summarizes some of the major historical events. The Bible provides an early written record of the apparent benefits of a high-fiber diet. Daniel and his companions appeared healthier after 10 d of eating vegetables and drinking water than other young men who ate the king's rich food and drank wine (Table 3). Hippocrates, the Father of Medicine, recommended eating wholemeal bread "for its salutary effect upon the bowel". 45 Thirteen centuries later, the Persian physician Hakim noted the benefits of wholewheat chuppatis.42 More recently, Stubs,47 Tyron,48 and Shakespeare (Coriolanus, Act I, Scene I) recognized the health benefits of wholemeal bread containing the wheat bran. Jonathan Swift, better known as the author of Gulliver's Travels, published a book for the general public on human stools. He observed that large, soft stools were viewed with favor, while small, round, hard stools were viewed with disfavor and seemed to flourish mainly around universities.43 As an outgrowth of his physiologic observations regarding gastric function, Beaumont concluded that "too highly nutritive diet is probably as fatal to prolongation of life and health, as that which contains an insufficient quantity of nutriment."49 Graham,50 and Kellogg51 in the U.S. and Allinson52 in Great Britain popularized whole meal bread. In the 20th century, a series of clinicians5362 documented the benefits and safety of wheat bran for laxation and colon function. The report of Painter and colleagues63 stimulated further studies of dietary fiber and gastrointestinal function. 1990
97
Critical Reviews In Table 2 Recommendations for Fiber and Carbohydrate Intake for Healthy Americans by Eight Major Health Organizations Total dietary fiber g/d
Carbohydrate % total kcal
Dietary Goals for the United States, 2nd ed. U.S. Senate Select Committee on Nutrition and Human Needs, 1977 The Surgeon General's Report on Nutrition and Health:' Summary and Recommendations, 1988
n/s
48
Increase intake of complex carbohydrate, "naturally occurring sugars", and fiber
n/s
n/s
National Advisory Committee on Nutrition Education: Proposal for Nutrition Guidelines for Health Education in Britain Recommended Dietary Allowances, 9th ed. Committee on Dietary Allowances, Food and Nutrition Board, National Research Council National Academy of Scienes, 1980 NCI Dietary Guidelines: Rationale. National Cancer Institute, National Institutes of Health, U.S. Department of Health and Human Services, 1988 Dietary Guidelines for Healthy American Adults, American Heart Association, 1988 Nutritional Recommendations and Principles for Individuals with Diabetes Mellitus, American Diabetes Association, 1988 High Fiber-High Carbohydrate Dietary Guidelines, HCF Diabetes Foundation, 1988
30
50
Increase intake of whole grain foods and cereal products, vegetables (including dried beans and peas), and fruits Increase cereal fiber intake, encourage fruits and vegetables
n/s
n/s
Maintain or increase consumption of complex carbohydrate, specifically from vegetables, fruits, whole-grain cereals
20—30, no>35
n/s
Eat fiber from a variety of food sources: vegetables, fruits, wholegrain cereals
n/s
50 or more
Emphasize complex carbohydrates: vegetables, fruits, and grains
40 or 25 per 1000 kcal
55—«i
Substitute unrefined carbohydrates with fiber for low-fiber, highly refined carbohydrate
20—35, 10—13 per 1000 kcal
50—60
Encourage both soluble and insoluble fiber intake
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Title and organization
Fiber-related recommendations
Note: n/s = none specified.
Walker, Burkitt, Cleave, and Trowell (Table 3) share honors as the modern pioneers of dietary fiber. Walker64 noted South African blacks from rural homelands had a lower incidence of certain gastrointestinal and metabolic disorders than did urban blacks and Caucasians. He suggested that the low prevalence of these disorders might be related to the high fiber intake of the rural blacks. Cleave,62 while serving as a medical officer on a battleship, reported that wheat bran intake was an effective and inexpensive way of treating the constipation that greatly troubled seagoing sailors. Subsequently, he developed the hypothesis that many of the diseases of Western people related to the consumption of fiber-depleted, refined sugars and flours.65 His books66"68 were not widely accepted in medical circles until Burkitt endorsed these ideas.44 Burkitt69 first became interested in fiber by noting that diseases responsible for emergency abdominal surgery in Great
98
Britain were rare in Africa. Subsequently, his interest in fiber was stimulated by Cleave.42 Burkitt has actively studied fiber since 1969 and remains a vigorous spokesman.70 In his medical textbook, Trowell71 listed the diseases that were common among Western people but rare in Africa. After returning to Great Britain, Trowell critically reviewed the literature and developed and refined several disease hypotheses related to the dietary fiber hypothesis.39-7274 In the early 1960s, clinical investigations (Table 3) and animal studies75 documented the hypocholesterolemic effects of pectin,76 guar,77 and psyllium78 in humans and animals. Other investigators noted that oatmeal bread79 or beans80 had important hypocholesterolemic effects in humans and animals. These studies of dietary factors affecting serum cholesterol developed independently of the evolving hypothesis relating to dietary fiber and merged with the dietary fiber research field in the early 1970s.
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Food Science and Nutrition Table 3 (continued) Some Major Observations in The History of Dietary Fiber
Table 3 Some Major Observations in The History of Dietary Fiber
Observation
Observation 1960
Early History 800 B.C.
400 B.C. 900 A.D.
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1585 1683
1773 1883 1837 1885 1923
DANIEL and companions appeared healthier after 10 days of eating vegetables than other youth after eating royal dishes (Daniel 1:8—16) HIPPOCRATES recommended wholemeal bread for the bowel43 HAKIM noted that wholemeal chuppatis passed through the intestine faster than chuppatis made from refined flour42 STUBS observed that poor men eating brown bread appeared healthier than wealthier men eating daintier food47 TYRON indicated that wholemeal bread stimulated bowel activity48 SHAKESPEARE wrote about the beneficial effects of fiber for the gastrointestinal tract. (Coriolanus, Act I, Scene I) SWIFT stated that large soft stools were viewed more favorably than small, round, hard stool43 BEAUMONT suggested that vegetable fiber intake probably prolonged life and health49 GRAHAM wrote an influential book on the health benefits of wholemeal ("Graham") bread50 ALUNSON preached that brown bread was the true staff of life52 KELLOGG promoted whole grain and bran cereals51
1975
Research Investigations 1961
1962 1965 1965 1965
Clinical Observations 1909 1910 1926 1932 1941 1942 1936 1937 1941 1972
TROWELL itemized diseases common among Western people but rare in Africa, and suspected that the bulky stools passed by Africans were protective against these diseases71 BURKITT AND TROWELL formalized the dietary fiber hypothesis73
HURST recommended wholemeal bread for treating constipation53 GALLANT used coarse wheat bran to treat constipation54 MCCARRISON recommended whole wheat flour, fruit, and vegetables for their health benefits55 COWGILL AND ANDERSON reported that wheat bran intake increased stool weight and aided taxation*' FANTUS and colleagues performed studies indicating that wheat bran did not iiritate the intestine17 HOPPERT AND CLARK demonstrated the long-term benefits of wheat bran for bowel activity60 WILLIAMS AND OLMSTEAD reported on the fecal-bulking effect of different high-fiber foods59 DIMOCKreportedthat All Bran cereal alleviated constipation" CLEAVE used Miller's bran to treat constipation of sailors at sea 62 PAINTER AND COLLEAGUESreportedthat wheat bran provided benefits for patients with diverticulosis63
KEYS AND COLLEAGUESreportedthe hypocholesterolemic effects of pectin administration to humans76 WELLS AND ERSDOFF document the cholesterol-lowering effects of pectin in rats75 DE GROOTAND COLLEAGUES reported the hypocholesterolemic effects of rolled oat intake for humans79 GROEN AND COLLEAGUES reported the hypocholesterolemic effects of bean intake for humans'0 FAHRENBACH AND COLLEAGUESreportedthe hypocholesterolemic effects of guar or pectin administration to humans77 GARVIN AND COLLEAGUES reported the hypocholesterolemic effects of psyllium administration to humans78
C. Evolution, Dietary Fiber, and Western Diseases Table 4 presents estimations of the dietary fiber and nutrient content of the human diet from the late paleolithic period to the present time. One of the most striking changes is the progressive reduction in dietary fiber intake. While the stone age individual had a high intake of wild meat and a high protein intake, the intake of fruits and vegetables also was very high, resulting in a high fiber intake.81-82 Knowledge of food intake in 18th century Great Britain is limited, but estimates of potato and wheat intake,83 as well as information about the milling of wheat flour,84 allows estimation of dietary fiber intake. Dietary fiber intake was estimated for the years 1909—1913 and 1947—1949 85 - 86 by the method described in detail elsewhere.87 Based on such observations, Trowell72 suggests that reduced intake of complex carbohydrates and dietary fiber has significantly contributed to the increased prevalence of coronary heart disease in Western people when compared with the prevalence in hunter gatherers.
Epidemiologic Associations 1947
1952
1956
III. DIETARY FIBER AND CORONARY HEART DISEASE
WALKER noted a relationship between dietary fiber intake, large stool, and the low incidence of certain gastrointestinal and metabolic diseases64 BURKLTT pointed out the rarity among Africans of most of the diseases responsible for emergency abdominal surgery in Great Britain" CLEAVE blamed many of the diseases of civilization on the intake of highly refined or fiber-depleted carbohydrate foods such as sugar and flour65
A. Risk Factors for Coronary Heart Disease (CHD) 1. Concept of CHD Risk Factors The Framingham study fostered the concept of risk factors for CHD.88 Risk factors are defined as epidemiologically identifiable relationships between physical or environmental char-
1990
99
Critical Reviews In Table 4 Changes in Diet Composition Since Paleolithic Times
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Year Country Protein, g/d Carbohydrate, g/d Fat, g/d Dietary fiber, Total, g/d Soluble, g/d
10,000 BC 7 169 227 47
1770 Great Britian 60 364 35
1863 Great Britian 50 338 48
1909—1913 U.S 59 283 72
1947—1949 U.S. 59 250 87
100 35
49 16
25 8
28 10
15 5
acteristics of an individual and CVD.89 No single factor has been identified that provides absolute immunity to CHD, or, when present, guarantees that disease will occur.90 Using multiple risk factors appears to be a more accurate method of assessing risk for developing CHD.91 Figure 2 depicts the 22fold increase in CHD risk that occurs when three potent risk factors are present in young males.89 600 r- Men Age 40
1977—1978 U.S. 78 212 92 11.9 4.3
and (2) nonmodifiable (constitutional) risk factors. Major modifiable risk factors for CHD include hyperlipidemia, hypertension, smoking, diabetes mellitus, obesity, physical inactivity, and poor stress management.93 Alterations in one or more of these risk factors may affect the probability of developing CHD. This probability can be converted to a risk ratio, as shown in Table 5, providing a predictive value for the occurrence of C H D 89.90.94-101 A risk ratio defines the increased probability of the development of CHD by establishing a relationship between a normal sample and a sample with the risk factor. The nonmodifiable risk factors for CHD include male sex, older age, family history of premature CHD, and the presence of definite CHD in the individual.93102 3. Relationship of Specific Risk Factors to CHD Risk
Average Risk High Blood Pressure High Cholesterol Smokes Cigarettes
No
Yes
Yes
Yes
No
No
Yes
Yes
No
No
No
Yes
FIGURE 2. Relative risk of cardiovascular disease among persons with multiple risk factors. (Reprinted from Prog. Cardiovasc. Dis., 26, 320, 1983. With permission.)
Relationships between risk factors may be assessed in two ways. First, comparing the absolute risk of any individual with other individuals provides a practical risk-assessment method for those concerned with the reliable prediction of CHD risk. Second, risk for CHD assures neither a zero nor a 100% probability. Rather, risk factors occupy a continuum along which risk varies with intensity of the risk factor. The Lipid Research Clinics study provides an example of the operation of risk factors on a continuum by demonstrating that a 1% reduction in serum cholesterol levels leads to a 2% reduction in CHD risk.92 2. Categories of Risk Factors The identifiable risk factors for CHD can be divided into two categories: (1) modifiable (lifestyle-related) risk factors
100
a. CHOLESTEROL
Hypercholesterolemia is a potent risk factor for CHD.93 Several epidemiologic studies have demonstrated the relationship between serum cholesterol levels and CHD risk.92103 Figure 1 illustrates the rise in CHD risk with serum cholesterol elevations. Measurable increases in risk occur with cholesterol elevations as shown in Table 5. 94 For example, middle-aged men with serum cholesterol levels above 245 mg/dl demonstrate nearly a threefold increase in CHD risk.95 b. TRIGLYCERIDES
Aberg et al.104 suggest that elevated serum triglycerides are linked to increased risk for CHD. Data from the Framingham study suggest serum triglyceride values may be useful as a predictor of the development of CHD in women.105 Other investigators106-107 question the independent impact of elevated triglycerides on CHD risk, except in the presence of diabetes.108 Since an association between serum triglyceride levels and CHD has been suggested, treatment of hypertriglyceridemia in the presence of other risk factors is prudent. c. HIGH-DENSITY LIPOPROTEIN (HDL) CHOLESTEROL
Serum HDL cholesterol is inversely related to risk for CHD.109 This protective function of HDL cholesterol may be related to its role in the transport of cholesterol from peripheral tissues to the liver.110 The Framingham data indicate that every 10 mg/dl increase in HDL cholesterol results in a 33 to 50%
Volume 29, Issue 2
Food Science and Nutrition Table 5 Risk Ratios for Coronary Heart Disease Risk ratio Risk factor Serum cholesterol/(mg/dl) and risk for CHD
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Serum cholesterol (mg/dl) and risk for CHD
HDL cholesterol (mg/dl) and risk for CHD
Range
M
=sl81 182—202 203—220 221—244 ^245 >200 200—219 220—239 240—259 260+ 65 60 55
1.0 1.8 2.6 3.7 5.8 — — —
50
Systolic blood pressure (mm/Hg) and risk for CHD
Cigarette smoking and average annual incidence of CHD according to number of cigarettes smoked daily Percent of ideal body and risk for CHD Diabetes mellitus and risk for cardiovascular disease Physical activity and average annual incidence of CHD Fibrinogen levels (mg/dl) and cardiovascular disease risk
Serum uric acid (mg/100 ml) and incidence of CHD
45 40 74—119 120—139 140—150 160—179 180—300 Nonsmoker WHC
Ref. 45, 284, 286
IpH.T WHC Variable effect on WHC 4 Motility I Micelle formation | Bile acid pool size | Gastric emptying | Cation exchange, binding | Bile acid excretion i Serum and tissue cholesterol f1 Bacterial growth t Conversion 1° to 2° bile acids | Short chain fatty acids production f Density, i binding j Fecal bulk, t bowel effects Heating may alter fermentability or 1 ion exchange ability t Grinding, 1 WHC
1990
287—289
285, 289—2!
293—295
45 45 45, 285, 287 287
115
Critical Reviews In Table 14 Gastrointestinal Effects of Fiber
Mouth Stomach Small Intestine
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Large Intestine
Food intake Satiety Gastric emptying Absorption of nutrients Mobility Transit time Intestinal morphology and cell proliferation Fecal weight Stool frequency Transit time Fecal constituents Bacterial metabolism Intraluminal pressures
etary fibers may contribute to alterations in gastrointestinal function. These effects may work individually or collectively to lower serum cholesterol. 3. Proposed Mechanisms for Hypocholesterolemic Effects The hypocholesterolemic effect of certain dietary fibers has been well documented; however, the mechanisms have not. The physicochemical and gastrointestinal effects of various dietary fibers may lower serum cholesterol by the following proposed mechanisms: 1. 2. 3. 4.
Modification of bile acid absorption and metabolism Interference with lipid absorption and metabolism Production of short-chain fatty acids (SCFA) from fiber fermentation in the colon Alterations in concentrations of or sensitivity to insulin and other hormones
a. MODIFICATION OF BILE ACID ABSORPTION AND METABOLISM
Early research by Eastwood and Hamilton310 noted that bile acids bind strongly to vegetable fiber. This observation led to the hypothesis that dietary fiber may bind bile acids and increase their fecal excretion. A subsequent increased demand for cholesterol in the bile acid synthetic pathways diverts cholesterol away from the lipoprotein synthetic pathways,311 thereby reducing serum cholesterol. Subsequent investigators verified these observations36-290-312314 noting, however, that several fibers such as lignin,242-289 pectin311 and beans8 have varying relationships between the binding and excretion of bile acids and their hypocholesterolemic effect. Although inconsistencies have been observed, a reasonably consistent relationship exists between the in vitro binding of certain dietary fibers and their cholesterol-lowering ability.313 The gelling and viscosity properties of gums and pectins may play a further role in serum cholesterol reduction by in-
116
Ref.
Effect
Sites
46, 296, 297 46, 288, 298 46, 287, 299, 300—303, 320
235, 287, 304—307
creasing the excretion of entrapped bile acids and subsequently decreasing bile acids available for micelle formation.312 These fibers may also act as bile-acid binding resins that further enhance bile acid excretion.313-316 The most common postulate is that fibers that significantly decrease serum cholesterol levels increase fecal bile acid excretion, and vice versa. Alterations in the ratio of primary to secondary bile acids289 or bile acid secretion rates317 affect changes in bile acid metabolism. Several dietary fibers increase the fecal excretion of chenodeoxycholic acid and decrease the fecal excretion of cholic acid in rats289 and humans.262 Chenodeoxycholic acid and its derivatives may alter hepatic cholesterol synthesis and are not as well absorbed as cholic acid. Therefore, changes in the ratio of chenodeoxycholic to cholic acid could affect cholesterol metabolism.289-318-319 Relatively little is known about the effect of different dietary fibers on bile acid secretion rates due to the lack of quantitative measurements. Pectin supplements increased the biliary secretion of 14C-deoxycholic metabolites of taurocholic acid, while cellulose and lignin produced little or no effect when studied by Hillman and associates.317 Most investigators agree that modifications in bile acid absorption and metabolism play a key role in the hypocholesterolemic effects of some dietary fibers such as oat gum and pectin, but other mechanisms are involved as well. The quantitative contribution of alterations in bile acid absorption and metabolism to the cholesterol-lowering effect of dietary fibers is yet to be determined.
b. INTERFERENCE WITH LIPID ABSORPTION AND METABOLISM
Dietary fibers may exert their hypocholesterolemic effect by interfering with lipid absorption from the small intestines and altering lipid metabolism. Possible mechanisms include changes in gastric function, altered digestive enzymes activity, changes in intestinal motility and content mixing, alterations in the intestinal absorptive surface, changes in lymphatic blood
Volume 29, Issue 2
Food Science and Nutrition Table 15 Proposed Mechanisms for The Hypocholesterolemic Effect of Fiber
contents, delaying their absorption to more distal sites in the small intestines.303-320 Altered fat absorption rates may further interfere with cholesterol synthesis by delaying the chylomicron triglyceride peaks.323
Ref.
Mechanism
c. PRODUCTION OF SHORT-CHAIN FATTY ACIDS (SCFA) Modify bile add absorption and metabolism Increase bile acid binding
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Increase fecal bile acid excretion Alter ratio of primary:secondary bile acids Change bile acid secretion rates Interfere with Iipid absorption and metabolism Alter gastric function Decrease available bile acids Interfere with micelle formation Alter digestive enzymes Change intestinal motility/mixing of intestinal contents Increase fecal fat excretion Alter intestinal absorptive surface Morphology and function Unstirred water layer Change lymphatic blood flow Increase short-chain fatty add (SCFA) production Increase portal vein SCFA concentrations of propionate Propionate inhibits Iipid regulatory enzymes Increase fecal SCFA excretion Increase perpherial acetate Hormonal effects on Iipid metabolism Decrease serum insulin Decrease serum glucagon Increase perpherial insulin sensitivity Decrease gastrointestinal hormones/pancreatic hormones
289, 290, 310, 312, 313, 315, 317 36 262, 289, 318, 319 317
288, 298, 320 289 313, 316 299, 320, 321 287 322 302 300
328, 357 325, 326 59, 304—306 330
332—336 338, 339 222, 227, 332, 337 339, 340
flow, decreases in availability of bile acids, and interference with micelle formation. Both animal320 and human288-298 studies suggest that soluble fiber may decrease gastric emptying, delaying the emptying of nutrients into the small intestines.307 Dietary fibers may alter digestive enzymes by changing pH, viscosity, absorption, and other fiber-enzyme interactions,321 thereby decreasing digestion of Iipid in the upper small intestine.299-320 Decreased motility in the small intestine may decrease nutrient absorption by changing the thickness of the unstirred water layer300-301 and by altering morphologic and functional properties of the intestinal absorptive mucosal cells.302-303 The effect of fibers on intestinal capillary and lymphatic flow is not known, but could also play a role in Iipid synthesis. Fiber may interfere with dietary fat absorption by binding the bile acids289 necessary for optimal micelle formation313-316 and increasing fecal fat excretion.237-322 Viscous fibers may sequester both the Iipid and bile acid components of intestinal
Dietary fibers are fermented in the colon by a variety of bacteria. The end products of this fermentation process are SCFA such as acetate, butyrate, and propionate. These SCFA, especially propionate, might contribute to the hypocholesterolemic effects of certain dietary fibers by interfering with hepatic cholesterol metabolism.204 Supporting data for this hypothesis have been obtained from rat studies. Propionate fed to rats significantly reduced serum cholesterol.295-324 Studies using isolated rat liver cells demonstrated that propionate concentrations as low as 0.25 vaM significantly inhibited cholesterol synthesis in rat hepatocytes309 (Figure 9). Previous studies using pharmacologic doses of propionate and its derivatives demonstrated inhibition of hepatic Iipid regulatory enzymes in vivo and in vitro.325-326 However, several studies324-327-328 report that physiologic levels of propionate do not contribute to the hypocholesterolemic effects of pectin or oat bran, and that other physiologic effects may potentiate the cholesterol-lowering effects of SCFA.329 Although many studies document increased fecal excretion of SCFA with increased dietary fiber intake,59-304-306 few studies have examined the effects of SCFA on hepatic cholesterol synthesis in humans. Pomare and associates330 found peripheral serum acetate concentrations to rise in humans and remain elevated for several hours after feeding 20 g of pectin. Carefully controlled studies are needed to resolve the controversy regarding the role of propionate in cholesterol metabolism and to examine the effect of different dietary fibers on SCFA metabolism in humans. d. HORMONAL EFFECTS OF LIPID METABOLISM
Key hormones such as insulin and glucagon make important contributions to Iipid metabolism by affecting rates of hepatic cholesterol and Iipid synthesis.331 Insulin serves as a key regulatory hormone responsible for Iipid metabolism from adipose tissue and the liver, and Iipid synthesis by body tissues. Glucagon antagonizes these effects. High-carbohydrate, high-fiber diets lower insulin requirements in both diabetic11-227-332 and nondiabetic subjects.333"336 Increased fiber intake also improves peripheral insulin sensitivity of diabetic222'227-337 and nondiabetic subjects.338 Lower ambient insulin concentrations may reduce hepatic cholesterol and fatty acid synthesis.274 High intake of dietary fiber reduces serum glucagon levels in both diabetic339 and nondiabetic individuals.338 Lower glucagon concentrations would allow insulin to act in an unopposed fashion. Other pancreatic and gastrointestinal hormones are also reduced by increased fiber intake.339340 1990
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Critical Reviews In 100
\
Control
IESIS
!
± - 50 >- *w
I
CO
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co
0
1
1
.5
10
25
mM PROPIONATE FIGURE 9. Effect of propionate on de novo cholesterol synthesis from '•'C-acetate (5 mM) in isolated rat hepatocytes. *Significantly differs from control (p
"5 * 60 % u "5 Downloaded by [New York University] at 18:35 17 June 2015
c
40
20 Control diet
High-carbohydrate high-fiber diet I 10 Days
FIGURE 11. Serum triglyceride response of hypertriglyceridemic men to weight-maintaining HCF diets. (Reprinted from Anderson, J. W., Nutrition Management of Metabolic Conditions: Professional Guide to HCF Diets, 1986. With permission.)
diets that were not vegetarian. Typical vegetarian diets contain about 40 g of dietary fiber per day with about 40% of fiber coming from cereal sources and about 60% coming from fruits, legumes, and vegetables.369 HCF diets differ from vegetarian diets in many ways. HCF diets distinguish between soluble and insoluble fiber content and usually contain at least 40 to 45 g/d375 and as much as 65 g/d12 of total dietary fiber. The following studies focused on the effect of HCF diets on blood pressure. Wright and colleagues376 compared fiber intake and blood pressure in 94 healthy individuals and noted that those with high-fiber intakes had significantly lower blood pressures than those with low-fiber intakes. When 17 healthy volunteers increased their fiber intake modestly by making high-fiber substitutions for low-fiber foods, blood pressure dropped significantly over a 4-week period. In 1983, 12 nonobese, insulin-dependent diabetics were admitted to our metabolic ward to evaluate responses to highfiber diets.12 Six patients had no history of hypertension. The remaining six had a history of systolic blood pressure measurements exceeding 150 mmHg; four were being treated with 122
antihypertensive medications that were continued throughout the study. Average blood pressures were 10% lower on the high-fiber diet (Figure 13). Dodson and colleagues studied various forms of high-fiber, low-fat, low-sodium diets.356-375-377 After treating375 53 diabetic patients with mild hypertension for 1 month with a 35 to 40 g fiber diet comprised of 15% fat, 20% protein, 65% unrefined carbohydrate, 0 to 5% refined carbohydrate, and 40 to 50 mmol sodium per d, they observed a 6.8% reduction in diastolic blood pressure (p 121-398 Liu and colleagues398 compiled data on 20 economically advanced countries based on per capita food consumption. Estimated fiber intake was inversely related to CHD mortality rate. Populations consuming a vegetarian-type diet also have reduced mortality incidence.399 A study by Kromhout and colleagues19-400 of 871 Netherlands men reported that mortality from CHD was approximately four times higher in men with lower fiber intakes than men with higher fiber intakes. The effect was independent of other dietary variables and remained significant after multivariate adjustment for other risk factors. The authors concluded that a diet containing at least 37 g dietary fiber per day may be protective against CHD.19 Khaw and Barrett-Connor121 noted a 6 g increase in daily fiber intake was associated with a 25% reduction in ischemic heart disease mortality (p
Critical Reviews in Food Science and Nutrition Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/bfsn20
Dietary fiber and coronary heart disease James W. Anderson Whitis a
a b
c
d
e
, Dee A. Deakins , Tammy L Floore , Belinda M. Smith & Sarah E.
f
Chief, Metabolic‐Endocrine Section , VA Hospital ,
b
Professor of Medicine and Clinical Nutrition in the Department of Medicine , University of Kentucky , Lexington c
Research Nurse Coordinator for the Metabolic Research Group in the Department of Medicine , University of Kentucky , Lexington d
Research Nurse in the Metabolic Research Group in the Department of Medicine , University of Kentucky , Lexington e
Research Dietitian in the Department of Behavioral Science , University of Kentucky , Lexington f
Cardiovascular Research Coordinator in the Department of Behavioral Science, College of Medicine , University of Kentucky , Lexington Published online: 29 Sep 2009.
To cite this article: James W. Anderson , Dee A. Deakins , Tammy L Floore , Belinda M. Smith & Sarah E. Whitis (1990) Dietary fiber and coronary heart disease, Critical Reviews in Food Science and Nutrition, 29:2, 95-147, DOI: 10.1080/10408399009527518 To link to this article: http://dx.doi.org/10.1080/10408399009527518
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Food Science and Nutrition lifestyle factors, and dietary fiber on major causes of death in the U.S. We review evidence relating dietary fiber to CHD specifically as it pertains to cardiovascular risk, hypercholesterolemia, hypertriglyceridemia, hypertension, and regression of atherosclerotic disease. In addition, we provide a historical perspective on dietary fiber, review possible mechanisms of action, and discuss therapeutic and practical applications. The interrelationship of dietary fiber intake, diabetes, and obesity are discussed elsewhere.16
Dietary Fiber And Coronary Heart Disease James W. Anderson, Dee A. Deakins, Tammy L Floore, Belinda M. Smith, and Sarah E. Whitis
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I. INTRODUCTION
B. New Found Popularity of Dietary Fiber For centuries the health benefits of dietary fiber consumption were related to the well-recognized effects on fecal bulk and bowel regularity. Pioneering work by Trowell22 and Burkitt23 indicated that many diseases of modern society might be related to dietary changes such as reduced dietary fiber intake. These observations suggested that dietary fiber intake may protect against such diseases as diabetes, hypertension, CHD, and obesity.24 Subsequent studies revealed that other fiber-rich foods such as oat bran and beans have important effects on serum cholesterol.25 These studies, combined with traditional wisdom, indicate that wheat bran and other foods with fecal bulking action are important in gastrointestinal function, while foods rich in water-soluble fiber have important metabolic effects on glucose and lipid metabolism.24
A. Importance and Significance of Coronary Heart Disease Cardiovascular disease (CVD) is the major cause of death in the U.S. and in most Western countries. Despite the recent sharp decline in the death rate from CVD,1 it still accounts for 759,000 deaths yearly2 in the U.S. (Table 1) or one death every 32 s.3 In 1988, the estimated U.S. financial cost for heart disease, including medical services, institutional costs, medications, and lost productivity, exceeded $83.7 billion annually.3 Certain characteristic factors greatly increase risk for CVD. The seven major modifiable risk factors for heart disease can be divided into two categories: lifestyle related and diet related. The lifestyle-related risk factors include cigarette smoking, inactivity, and poor stress management.4 The diet-related risk factors include hyperlipidemia, hypertension, diabetes, and obesity. Of the hyperlipidemias, hypercholesterolemia has moved to the forefront as a major risk factor for coronary heart disease (CHD).5 About 60% of men aged 20 to 50 years have serum cholesterol values above 200 mg/dl (Figure I). 6 Of this 60%, three quarters have cholesterol levels between 200 to 250 mg/dl, levels that can usually be reduced by dietary intervention. The remaining one quarter with levels above 250 mg/dl most likely have a genetic component. Thus, about 75% of individuals with hypercholesterolemia should respond to dietary intervention. One single dietary choice is emerging that may significantly prevent or qualitatively manage all four diet-related CHD risk factors: dietary fiber. Intensive nutrition intervention with diets high in complex carbohydrates and water-soluble fiber reduces serum cholesterol 20 to 32% and fasting serum triglycerides 10 to 20%. 7 U A high-fiber diet has been shown to lower systolic blood pressure 11% and diastolic blood pressure 10% in hypertensive individuals.12 High fiber intake also lowers plasma glucose levels in diabetic11-13 and nondiabetic individuals9 and significantly reduces insulin requirements of diabetic individuals.14 High fiber intake promotes weight loss and maintenance through increased satiety.15-16 In addition to managing these risk factors, recent data suggest that dietary fiber may independently protect against CHD. 1719 Thus, combining dietary fiber with a low-fat diet such as the American Heart Association (AHA) Diet can further reduce risk for developing heart disease.20-21 Table 1 summarizes the effects of diet, exercise, other
C. Existing Fiber Recommendations for Populations In the last decade, a consensus diet recommendation emerged: the U.S. Senate Select Committee recommended
J. W. Anderson received a B.A. degree from West Virginia University in Morgantown; a M.S. degree from Mayo Graduate School in Rochester, Minnesota; and a M.D. degree from Northwestern University in Evanston, Illinois. Dr. Anderson is currently Chief, Metabolic-Endocrine Section at the VA Hospital and Professor of Medicine and Clinical Nutrition in the Department of Medicine at the University of Kentucky in Lexington. D. A. Deakins received a B.S. in Nursing degree from the University of Tennessee in Knoxville and a M.S. degree from the University of Louisville in Louisville, Kentucky. Ms. Deakins is currently the Research Nurse Coordinator for the Metabolic Research Group in the Department of Medicine at the University of Kentucky in Lexington. T. L. Floore received a B.S.N. degree from Berea College in Berea, Kentucky. Ms. Floore is currently a Research Nurse in the Metabolic Research Group in the Department of Medicine at the University of Kentucky in Lexington. B. M. Smith received a B.A. degree from Eastern Kentucky University in Richmond. Ms. Smith is currently a Research Dietitian in the Department of Behavioral Science at the University of Kentucky in Lexington. S. E. Whitis received B.S., B.S.N., and M.S. degrees from the University of Kentucky in Lexington. Ms. Whitis is currently the Cardiovascular Research Coordinator in the Department of Behavioral Science, College of Medicine, University of Kentucky in Lexington.
1990
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Critical Reviews In Table 1 Estimated Total Deaths and Contributing Factors for The 10 Leading Causes of Death in The U.S., 1987 Rank 1 2 3 4 5
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6 7 8 9
10
Contributing factors
Cause of death Heart diseases Cancers Strokes Unintentional injuries Chronic obstructive lung diseases Pneumonia and influenza Diabetes mellitus Suicide Chronic liver-diseases and cirrhosis
D, E, L, F D, L, F D, E, L, F L L
Atherosclerosis
Number
Percent of total deaths
759,400 476,700 148,700 92,500 78,000
35.7 22.4 7.0 4.4 3.7
L D, E, F L L
68,600 37,800 29,600 26,000
3.2 1.8 1.4 1.2
D, E, L, F
23,100
1.1 100.00 All causes
2,125,100
Note: D = diet, E = exercise, L = lifestyle, and F = fiber. Adapted from U.S. Department of Health and Human Services, The Surgeon General's Report on Nutrition and Health, U.S. Government Printing Office, Washington, D.C., 1988.
tow«r 168
182
193
203
213
221
232
245
264 higher
SERUM CHOLESTEROL, mg/dl FIGURE 1. CHD mortality related to serum cholesterol. (Adapted from Assmann, G., Expanding Horizons in Atherosclerosis Research, Schlierf, G. and Mori, H., Eds., SpringerVerlag, New York, 1987, 105. With permission.)
Americans increase intake of complex carbohydrate and fiber and decrease intake of saturated fat and cholesterol.26 The National Research Council of the National Academy of Sciences27 recommended maintaining or increasing consump96
tion of complex carbohydrates. Most recently, the Surgeon General's 1988 Report on Nutrition and Health2 promoted lowfat, low-cholesterol dietary patterns, emphasizing consumption of vegetables, fruits, and whole grain products — foods rich
Volume 29, Issue 2
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Food Science and Nutrition in complex carbohydrates and fiber and relatively low in calories. The report also emphasized consumption offish, poultry prepared without skin, and lean meats. Several national health organizations make fiber related dietary recommendations. The AHA recommends a diet high in complex carbohydrate but with no specifications for fiber intake.28 Using the Nutritionist HI computer analysis software package, which was upgraded by the addition of our fiber values,29 we calculated that the Phase I AHA Guideline provides approximately 21 g fiber per 2000 kcal. More specific fiber recommendations are made by the National Cancer Institute, which recommends intake of 25 to 35 g fiber per d,30 and by the British National Advisory Committee on Nutrition Education,31 which recommends 30 g/d of total dietary fiber with emphasis on cereal fiber. Other national health organizations recommending specific fiber amounts per day include the American Diabetes Association32 (25 g fiber per 1000 kcal) and the HCF Nutrition Research Foundation33 (10 to 13 g fiber per 1000 kcal). Table 2 compares the recommendations of these organizations. D. Types of Fiber Different types of fiber are distinguished by their differing physiological properties and systemic effects. Dietary fiber is grouped into two categories: water soluble and water insoluble.34 Water soluble fiber will dissolve in hot water; insoluble fiber will not. Examples of soluble fiber include pectin, gums, certain hemicelluloses, and storage polysaccharides. Fruits, oats, barley, and legumes contain more soluble fiber than other foods. Insoluble fiber includes cellulose, lignin, and many hemicelluloses. Vegetables, wheat, and most grain products contain primarily insoluble fibers.29-35 Soluble and insoluble fiber function differently in the body.34 Soluble fiber increases intestinal transit time, delays gastric emptying, and slows glucose absorption. These and other actions lower postprandial blood glucose concentrations, decrease serum cholesterol, and produce other metabolic effects. Insoluble fiber decreases intestinal transit time, increases fecal bulk, delays glucose absorption, and slows starch hydrolysis. These effects alter gastrointestinal function, but do not lower serum glucose or cholesterol.
II. DIETARY FIBER AND HEALTH A. The Dietary Fiber Hypothesis Dietary fiber is defined as the endogenous components of plant materials in the diet, predominantly nonstarch polysaccharides and lignin, which are resistant to digestion by human enzymes.36 The dietary fiber hypothesis developed by Burkitt and Trowell was summarized by Southgate37 into the following two statements:
1.
2.
"A diet that is rich in foods which contain plant cell walls (for example, high-extraction cereals, fruits, and vegetables) is protective against a range of diseases, in particular those prevalent in affluent Western communities (for example, constipation, diverticular disease, large bowel cancer, coronary heart disease, diabetes, obesity, and gallstones)." "In some instances a diet providng a low intake of plant cell walls is a causative factor in the etiology of these diseases and in others it provides the conditions under which other etiological factors are more active."
B. Historical Perspective For more than 20 centuries the merits of brown vs. white bread have been debated.38-39 While potential health benefits and intestinal effects of dietary fiber have been recognized by observant physicians and others for centuries, the full health implications of dietary fiber have emerged in only the last quarter century. The term dietary fiber was apparently coined by Hipsley40 in 1953. While there was a great deal of information buried in the medical and lay literature prior to 1970, the health implications of dietary fiber were made known to the medical and world community through the tireless efforts of Burkitt and Trowell.41 The history of dietary fiber has been chronicled by Burkitt42-43 and others*" 6 and can arbitrarily be divided into these phases: (1) early history, (2) clinical observations, (3) epidemiologic associations, and (4) research investigations. Table 3 summarizes some of the major historical events. The Bible provides an early written record of the apparent benefits of a high-fiber diet. Daniel and his companions appeared healthier after 10 d of eating vegetables and drinking water than other young men who ate the king's rich food and drank wine (Table 3). Hippocrates, the Father of Medicine, recommended eating wholemeal bread "for its salutary effect upon the bowel". 45 Thirteen centuries later, the Persian physician Hakim noted the benefits of wholewheat chuppatis.42 More recently, Stubs,47 Tyron,48 and Shakespeare (Coriolanus, Act I, Scene I) recognized the health benefits of wholemeal bread containing the wheat bran. Jonathan Swift, better known as the author of Gulliver's Travels, published a book for the general public on human stools. He observed that large, soft stools were viewed with favor, while small, round, hard stools were viewed with disfavor and seemed to flourish mainly around universities.43 As an outgrowth of his physiologic observations regarding gastric function, Beaumont concluded that "too highly nutritive diet is probably as fatal to prolongation of life and health, as that which contains an insufficient quantity of nutriment."49 Graham,50 and Kellogg51 in the U.S. and Allinson52 in Great Britain popularized whole meal bread. In the 20th century, a series of clinicians5362 documented the benefits and safety of wheat bran for laxation and colon function. The report of Painter and colleagues63 stimulated further studies of dietary fiber and gastrointestinal function. 1990
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Critical Reviews In Table 2 Recommendations for Fiber and Carbohydrate Intake for Healthy Americans by Eight Major Health Organizations Total dietary fiber g/d
Carbohydrate % total kcal
Dietary Goals for the United States, 2nd ed. U.S. Senate Select Committee on Nutrition and Human Needs, 1977 The Surgeon General's Report on Nutrition and Health:' Summary and Recommendations, 1988
n/s
48
Increase intake of complex carbohydrate, "naturally occurring sugars", and fiber
n/s
n/s
National Advisory Committee on Nutrition Education: Proposal for Nutrition Guidelines for Health Education in Britain Recommended Dietary Allowances, 9th ed. Committee on Dietary Allowances, Food and Nutrition Board, National Research Council National Academy of Scienes, 1980 NCI Dietary Guidelines: Rationale. National Cancer Institute, National Institutes of Health, U.S. Department of Health and Human Services, 1988 Dietary Guidelines for Healthy American Adults, American Heart Association, 1988 Nutritional Recommendations and Principles for Individuals with Diabetes Mellitus, American Diabetes Association, 1988 High Fiber-High Carbohydrate Dietary Guidelines, HCF Diabetes Foundation, 1988
30
50
Increase intake of whole grain foods and cereal products, vegetables (including dried beans and peas), and fruits Increase cereal fiber intake, encourage fruits and vegetables
n/s
n/s
Maintain or increase consumption of complex carbohydrate, specifically from vegetables, fruits, whole-grain cereals
20—30, no>35
n/s
Eat fiber from a variety of food sources: vegetables, fruits, wholegrain cereals
n/s
50 or more
Emphasize complex carbohydrates: vegetables, fruits, and grains
40 or 25 per 1000 kcal
55—«i
Substitute unrefined carbohydrates with fiber for low-fiber, highly refined carbohydrate
20—35, 10—13 per 1000 kcal
50—60
Encourage both soluble and insoluble fiber intake
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Title and organization
Fiber-related recommendations
Note: n/s = none specified.
Walker, Burkitt, Cleave, and Trowell (Table 3) share honors as the modern pioneers of dietary fiber. Walker64 noted South African blacks from rural homelands had a lower incidence of certain gastrointestinal and metabolic disorders than did urban blacks and Caucasians. He suggested that the low prevalence of these disorders might be related to the high fiber intake of the rural blacks. Cleave,62 while serving as a medical officer on a battleship, reported that wheat bran intake was an effective and inexpensive way of treating the constipation that greatly troubled seagoing sailors. Subsequently, he developed the hypothesis that many of the diseases of Western people related to the consumption of fiber-depleted, refined sugars and flours.65 His books66"68 were not widely accepted in medical circles until Burkitt endorsed these ideas.44 Burkitt69 first became interested in fiber by noting that diseases responsible for emergency abdominal surgery in Great
98
Britain were rare in Africa. Subsequently, his interest in fiber was stimulated by Cleave.42 Burkitt has actively studied fiber since 1969 and remains a vigorous spokesman.70 In his medical textbook, Trowell71 listed the diseases that were common among Western people but rare in Africa. After returning to Great Britain, Trowell critically reviewed the literature and developed and refined several disease hypotheses related to the dietary fiber hypothesis.39-7274 In the early 1960s, clinical investigations (Table 3) and animal studies75 documented the hypocholesterolemic effects of pectin,76 guar,77 and psyllium78 in humans and animals. Other investigators noted that oatmeal bread79 or beans80 had important hypocholesterolemic effects in humans and animals. These studies of dietary factors affecting serum cholesterol developed independently of the evolving hypothesis relating to dietary fiber and merged with the dietary fiber research field in the early 1970s.
Volume 29, Issue 2
Food Science and Nutrition Table 3 (continued) Some Major Observations in The History of Dietary Fiber
Table 3 Some Major Observations in The History of Dietary Fiber
Observation
Observation 1960
Early History 800 B.C.
400 B.C. 900 A.D.
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1585 1683
1773 1883 1837 1885 1923
DANIEL and companions appeared healthier after 10 days of eating vegetables than other youth after eating royal dishes (Daniel 1:8—16) HIPPOCRATES recommended wholemeal bread for the bowel43 HAKIM noted that wholemeal chuppatis passed through the intestine faster than chuppatis made from refined flour42 STUBS observed that poor men eating brown bread appeared healthier than wealthier men eating daintier food47 TYRON indicated that wholemeal bread stimulated bowel activity48 SHAKESPEARE wrote about the beneficial effects of fiber for the gastrointestinal tract. (Coriolanus, Act I, Scene I) SWIFT stated that large soft stools were viewed more favorably than small, round, hard stool43 BEAUMONT suggested that vegetable fiber intake probably prolonged life and health49 GRAHAM wrote an influential book on the health benefits of wholemeal ("Graham") bread50 ALUNSON preached that brown bread was the true staff of life52 KELLOGG promoted whole grain and bran cereals51
1975
Research Investigations 1961
1962 1965 1965 1965
Clinical Observations 1909 1910 1926 1932 1941 1942 1936 1937 1941 1972
TROWELL itemized diseases common among Western people but rare in Africa, and suspected that the bulky stools passed by Africans were protective against these diseases71 BURKITT AND TROWELL formalized the dietary fiber hypothesis73
HURST recommended wholemeal bread for treating constipation53 GALLANT used coarse wheat bran to treat constipation54 MCCARRISON recommended whole wheat flour, fruit, and vegetables for their health benefits55 COWGILL AND ANDERSON reported that wheat bran intake increased stool weight and aided taxation*' FANTUS and colleagues performed studies indicating that wheat bran did not iiritate the intestine17 HOPPERT AND CLARK demonstrated the long-term benefits of wheat bran for bowel activity60 WILLIAMS AND OLMSTEAD reported on the fecal-bulking effect of different high-fiber foods59 DIMOCKreportedthat All Bran cereal alleviated constipation" CLEAVE used Miller's bran to treat constipation of sailors at sea 62 PAINTER AND COLLEAGUESreportedthat wheat bran provided benefits for patients with diverticulosis63
KEYS AND COLLEAGUESreportedthe hypocholesterolemic effects of pectin administration to humans76 WELLS AND ERSDOFF document the cholesterol-lowering effects of pectin in rats75 DE GROOTAND COLLEAGUES reported the hypocholesterolemic effects of rolled oat intake for humans79 GROEN AND COLLEAGUES reported the hypocholesterolemic effects of bean intake for humans'0 FAHRENBACH AND COLLEAGUESreportedthe hypocholesterolemic effects of guar or pectin administration to humans77 GARVIN AND COLLEAGUES reported the hypocholesterolemic effects of psyllium administration to humans78
C. Evolution, Dietary Fiber, and Western Diseases Table 4 presents estimations of the dietary fiber and nutrient content of the human diet from the late paleolithic period to the present time. One of the most striking changes is the progressive reduction in dietary fiber intake. While the stone age individual had a high intake of wild meat and a high protein intake, the intake of fruits and vegetables also was very high, resulting in a high fiber intake.81-82 Knowledge of food intake in 18th century Great Britain is limited, but estimates of potato and wheat intake,83 as well as information about the milling of wheat flour,84 allows estimation of dietary fiber intake. Dietary fiber intake was estimated for the years 1909—1913 and 1947—1949 85 - 86 by the method described in detail elsewhere.87 Based on such observations, Trowell72 suggests that reduced intake of complex carbohydrates and dietary fiber has significantly contributed to the increased prevalence of coronary heart disease in Western people when compared with the prevalence in hunter gatherers.
Epidemiologic Associations 1947
1952
1956
III. DIETARY FIBER AND CORONARY HEART DISEASE
WALKER noted a relationship between dietary fiber intake, large stool, and the low incidence of certain gastrointestinal and metabolic diseases64 BURKLTT pointed out the rarity among Africans of most of the diseases responsible for emergency abdominal surgery in Great Britain" CLEAVE blamed many of the diseases of civilization on the intake of highly refined or fiber-depleted carbohydrate foods such as sugar and flour65
A. Risk Factors for Coronary Heart Disease (CHD) 1. Concept of CHD Risk Factors The Framingham study fostered the concept of risk factors for CHD.88 Risk factors are defined as epidemiologically identifiable relationships between physical or environmental char-
1990
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Critical Reviews In Table 4 Changes in Diet Composition Since Paleolithic Times
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Year Country Protein, g/d Carbohydrate, g/d Fat, g/d Dietary fiber, Total, g/d Soluble, g/d
10,000 BC 7 169 227 47
1770 Great Britian 60 364 35
1863 Great Britian 50 338 48
1909—1913 U.S 59 283 72
1947—1949 U.S. 59 250 87
100 35
49 16
25 8
28 10
15 5
acteristics of an individual and CVD.89 No single factor has been identified that provides absolute immunity to CHD, or, when present, guarantees that disease will occur.90 Using multiple risk factors appears to be a more accurate method of assessing risk for developing CHD.91 Figure 2 depicts the 22fold increase in CHD risk that occurs when three potent risk factors are present in young males.89 600 r- Men Age 40
1977—1978 U.S. 78 212 92 11.9 4.3
and (2) nonmodifiable (constitutional) risk factors. Major modifiable risk factors for CHD include hyperlipidemia, hypertension, smoking, diabetes mellitus, obesity, physical inactivity, and poor stress management.93 Alterations in one or more of these risk factors may affect the probability of developing CHD. This probability can be converted to a risk ratio, as shown in Table 5, providing a predictive value for the occurrence of C H D 89.90.94-101 A risk ratio defines the increased probability of the development of CHD by establishing a relationship between a normal sample and a sample with the risk factor. The nonmodifiable risk factors for CHD include male sex, older age, family history of premature CHD, and the presence of definite CHD in the individual.93102 3. Relationship of Specific Risk Factors to CHD Risk
Average Risk High Blood Pressure High Cholesterol Smokes Cigarettes
No
Yes
Yes
Yes
No
No
Yes
Yes
No
No
No
Yes
FIGURE 2. Relative risk of cardiovascular disease among persons with multiple risk factors. (Reprinted from Prog. Cardiovasc. Dis., 26, 320, 1983. With permission.)
Relationships between risk factors may be assessed in two ways. First, comparing the absolute risk of any individual with other individuals provides a practical risk-assessment method for those concerned with the reliable prediction of CHD risk. Second, risk for CHD assures neither a zero nor a 100% probability. Rather, risk factors occupy a continuum along which risk varies with intensity of the risk factor. The Lipid Research Clinics study provides an example of the operation of risk factors on a continuum by demonstrating that a 1% reduction in serum cholesterol levels leads to a 2% reduction in CHD risk.92 2. Categories of Risk Factors The identifiable risk factors for CHD can be divided into two categories: (1) modifiable (lifestyle-related) risk factors
100
a. CHOLESTEROL
Hypercholesterolemia is a potent risk factor for CHD.93 Several epidemiologic studies have demonstrated the relationship between serum cholesterol levels and CHD risk.92103 Figure 1 illustrates the rise in CHD risk with serum cholesterol elevations. Measurable increases in risk occur with cholesterol elevations as shown in Table 5. 94 For example, middle-aged men with serum cholesterol levels above 245 mg/dl demonstrate nearly a threefold increase in CHD risk.95 b. TRIGLYCERIDES
Aberg et al.104 suggest that elevated serum triglycerides are linked to increased risk for CHD. Data from the Framingham study suggest serum triglyceride values may be useful as a predictor of the development of CHD in women.105 Other investigators106-107 question the independent impact of elevated triglycerides on CHD risk, except in the presence of diabetes.108 Since an association between serum triglyceride levels and CHD has been suggested, treatment of hypertriglyceridemia in the presence of other risk factors is prudent. c. HIGH-DENSITY LIPOPROTEIN (HDL) CHOLESTEROL
Serum HDL cholesterol is inversely related to risk for CHD.109 This protective function of HDL cholesterol may be related to its role in the transport of cholesterol from peripheral tissues to the liver.110 The Framingham data indicate that every 10 mg/dl increase in HDL cholesterol results in a 33 to 50%
Volume 29, Issue 2
Food Science and Nutrition Table 5 Risk Ratios for Coronary Heart Disease Risk ratio Risk factor Serum cholesterol/(mg/dl) and risk for CHD
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Serum cholesterol (mg/dl) and risk for CHD
HDL cholesterol (mg/dl) and risk for CHD
Range
M
=sl81 182—202 203—220 221—244 ^245 >200 200—219 220—239 240—259 260+ 65 60 55
1.0 1.8 2.6 3.7 5.8 — — —
50
Systolic blood pressure (mm/Hg) and risk for CHD
Cigarette smoking and average annual incidence of CHD according to number of cigarettes smoked daily Percent of ideal body and risk for CHD Diabetes mellitus and risk for cardiovascular disease Physical activity and average annual incidence of CHD Fibrinogen levels (mg/dl) and cardiovascular disease risk
Serum uric acid (mg/100 ml) and incidence of CHD
45 40 74—119 120—139 140—150 160—179 180—300 Nonsmoker WHC
Ref. 45, 284, 286
IpH.T WHC Variable effect on WHC 4 Motility I Micelle formation | Bile acid pool size | Gastric emptying | Cation exchange, binding | Bile acid excretion i Serum and tissue cholesterol f1 Bacterial growth t Conversion 1° to 2° bile acids | Short chain fatty acids production f Density, i binding j Fecal bulk, t bowel effects Heating may alter fermentability or 1 ion exchange ability t Grinding, 1 WHC
1990
287—289
285, 289—2!
293—295
45 45 45, 285, 287 287
115
Critical Reviews In Table 14 Gastrointestinal Effects of Fiber
Mouth Stomach Small Intestine
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Large Intestine
Food intake Satiety Gastric emptying Absorption of nutrients Mobility Transit time Intestinal morphology and cell proliferation Fecal weight Stool frequency Transit time Fecal constituents Bacterial metabolism Intraluminal pressures
etary fibers may contribute to alterations in gastrointestinal function. These effects may work individually or collectively to lower serum cholesterol. 3. Proposed Mechanisms for Hypocholesterolemic Effects The hypocholesterolemic effect of certain dietary fibers has been well documented; however, the mechanisms have not. The physicochemical and gastrointestinal effects of various dietary fibers may lower serum cholesterol by the following proposed mechanisms: 1. 2. 3. 4.
Modification of bile acid absorption and metabolism Interference with lipid absorption and metabolism Production of short-chain fatty acids (SCFA) from fiber fermentation in the colon Alterations in concentrations of or sensitivity to insulin and other hormones
a. MODIFICATION OF BILE ACID ABSORPTION AND METABOLISM
Early research by Eastwood and Hamilton310 noted that bile acids bind strongly to vegetable fiber. This observation led to the hypothesis that dietary fiber may bind bile acids and increase their fecal excretion. A subsequent increased demand for cholesterol in the bile acid synthetic pathways diverts cholesterol away from the lipoprotein synthetic pathways,311 thereby reducing serum cholesterol. Subsequent investigators verified these observations36-290-312314 noting, however, that several fibers such as lignin,242-289 pectin311 and beans8 have varying relationships between the binding and excretion of bile acids and their hypocholesterolemic effect. Although inconsistencies have been observed, a reasonably consistent relationship exists between the in vitro binding of certain dietary fibers and their cholesterol-lowering ability.313 The gelling and viscosity properties of gums and pectins may play a further role in serum cholesterol reduction by in-
116
Ref.
Effect
Sites
46, 296, 297 46, 288, 298 46, 287, 299, 300—303, 320
235, 287, 304—307
creasing the excretion of entrapped bile acids and subsequently decreasing bile acids available for micelle formation.312 These fibers may also act as bile-acid binding resins that further enhance bile acid excretion.313-316 The most common postulate is that fibers that significantly decrease serum cholesterol levels increase fecal bile acid excretion, and vice versa. Alterations in the ratio of primary to secondary bile acids289 or bile acid secretion rates317 affect changes in bile acid metabolism. Several dietary fibers increase the fecal excretion of chenodeoxycholic acid and decrease the fecal excretion of cholic acid in rats289 and humans.262 Chenodeoxycholic acid and its derivatives may alter hepatic cholesterol synthesis and are not as well absorbed as cholic acid. Therefore, changes in the ratio of chenodeoxycholic to cholic acid could affect cholesterol metabolism.289-318-319 Relatively little is known about the effect of different dietary fibers on bile acid secretion rates due to the lack of quantitative measurements. Pectin supplements increased the biliary secretion of 14C-deoxycholic metabolites of taurocholic acid, while cellulose and lignin produced little or no effect when studied by Hillman and associates.317 Most investigators agree that modifications in bile acid absorption and metabolism play a key role in the hypocholesterolemic effects of some dietary fibers such as oat gum and pectin, but other mechanisms are involved as well. The quantitative contribution of alterations in bile acid absorption and metabolism to the cholesterol-lowering effect of dietary fibers is yet to be determined.
b. INTERFERENCE WITH LIPID ABSORPTION AND METABOLISM
Dietary fibers may exert their hypocholesterolemic effect by interfering with lipid absorption from the small intestines and altering lipid metabolism. Possible mechanisms include changes in gastric function, altered digestive enzymes activity, changes in intestinal motility and content mixing, alterations in the intestinal absorptive surface, changes in lymphatic blood
Volume 29, Issue 2
Food Science and Nutrition Table 15 Proposed Mechanisms for The Hypocholesterolemic Effect of Fiber
contents, delaying their absorption to more distal sites in the small intestines.303-320 Altered fat absorption rates may further interfere with cholesterol synthesis by delaying the chylomicron triglyceride peaks.323
Ref.
Mechanism
c. PRODUCTION OF SHORT-CHAIN FATTY ACIDS (SCFA) Modify bile add absorption and metabolism Increase bile acid binding
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Increase fecal bile acid excretion Alter ratio of primary:secondary bile acids Change bile acid secretion rates Interfere with Iipid absorption and metabolism Alter gastric function Decrease available bile acids Interfere with micelle formation Alter digestive enzymes Change intestinal motility/mixing of intestinal contents Increase fecal fat excretion Alter intestinal absorptive surface Morphology and function Unstirred water layer Change lymphatic blood flow Increase short-chain fatty add (SCFA) production Increase portal vein SCFA concentrations of propionate Propionate inhibits Iipid regulatory enzymes Increase fecal SCFA excretion Increase perpherial acetate Hormonal effects on Iipid metabolism Decrease serum insulin Decrease serum glucagon Increase perpherial insulin sensitivity Decrease gastrointestinal hormones/pancreatic hormones
289, 290, 310, 312, 313, 315, 317 36 262, 289, 318, 319 317
288, 298, 320 289 313, 316 299, 320, 321 287 322 302 300
328, 357 325, 326 59, 304—306 330
332—336 338, 339 222, 227, 332, 337 339, 340
flow, decreases in availability of bile acids, and interference with micelle formation. Both animal320 and human288-298 studies suggest that soluble fiber may decrease gastric emptying, delaying the emptying of nutrients into the small intestines.307 Dietary fibers may alter digestive enzymes by changing pH, viscosity, absorption, and other fiber-enzyme interactions,321 thereby decreasing digestion of Iipid in the upper small intestine.299-320 Decreased motility in the small intestine may decrease nutrient absorption by changing the thickness of the unstirred water layer300-301 and by altering morphologic and functional properties of the intestinal absorptive mucosal cells.302-303 The effect of fibers on intestinal capillary and lymphatic flow is not known, but could also play a role in Iipid synthesis. Fiber may interfere with dietary fat absorption by binding the bile acids289 necessary for optimal micelle formation313-316 and increasing fecal fat excretion.237-322 Viscous fibers may sequester both the Iipid and bile acid components of intestinal
Dietary fibers are fermented in the colon by a variety of bacteria. The end products of this fermentation process are SCFA such as acetate, butyrate, and propionate. These SCFA, especially propionate, might contribute to the hypocholesterolemic effects of certain dietary fibers by interfering with hepatic cholesterol metabolism.204 Supporting data for this hypothesis have been obtained from rat studies. Propionate fed to rats significantly reduced serum cholesterol.295-324 Studies using isolated rat liver cells demonstrated that propionate concentrations as low as 0.25 vaM significantly inhibited cholesterol synthesis in rat hepatocytes309 (Figure 9). Previous studies using pharmacologic doses of propionate and its derivatives demonstrated inhibition of hepatic Iipid regulatory enzymes in vivo and in vitro.325-326 However, several studies324-327-328 report that physiologic levels of propionate do not contribute to the hypocholesterolemic effects of pectin or oat bran, and that other physiologic effects may potentiate the cholesterol-lowering effects of SCFA.329 Although many studies document increased fecal excretion of SCFA with increased dietary fiber intake,59-304-306 few studies have examined the effects of SCFA on hepatic cholesterol synthesis in humans. Pomare and associates330 found peripheral serum acetate concentrations to rise in humans and remain elevated for several hours after feeding 20 g of pectin. Carefully controlled studies are needed to resolve the controversy regarding the role of propionate in cholesterol metabolism and to examine the effect of different dietary fibers on SCFA metabolism in humans. d. HORMONAL EFFECTS OF LIPID METABOLISM
Key hormones such as insulin and glucagon make important contributions to Iipid metabolism by affecting rates of hepatic cholesterol and Iipid synthesis.331 Insulin serves as a key regulatory hormone responsible for Iipid metabolism from adipose tissue and the liver, and Iipid synthesis by body tissues. Glucagon antagonizes these effects. High-carbohydrate, high-fiber diets lower insulin requirements in both diabetic11-227-332 and nondiabetic subjects.333"336 Increased fiber intake also improves peripheral insulin sensitivity of diabetic222'227-337 and nondiabetic subjects.338 Lower ambient insulin concentrations may reduce hepatic cholesterol and fatty acid synthesis.274 High intake of dietary fiber reduces serum glucagon levels in both diabetic339 and nondiabetic individuals.338 Lower glucagon concentrations would allow insulin to act in an unopposed fashion. Other pancreatic and gastrointestinal hormones are also reduced by increased fiber intake.339340 1990
117
Critical Reviews In 100
\
Control
IESIS
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I
CO
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co
0
1
1
.5
10
25
mM PROPIONATE FIGURE 9. Effect of propionate on de novo cholesterol synthesis from '•'C-acetate (5 mM) in isolated rat hepatocytes. *Significantly differs from control (p
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c
40
20 Control diet
High-carbohydrate high-fiber diet I 10 Days
FIGURE 11. Serum triglyceride response of hypertriglyceridemic men to weight-maintaining HCF diets. (Reprinted from Anderson, J. W., Nutrition Management of Metabolic Conditions: Professional Guide to HCF Diets, 1986. With permission.)
diets that were not vegetarian. Typical vegetarian diets contain about 40 g of dietary fiber per day with about 40% of fiber coming from cereal sources and about 60% coming from fruits, legumes, and vegetables.369 HCF diets differ from vegetarian diets in many ways. HCF diets distinguish between soluble and insoluble fiber content and usually contain at least 40 to 45 g/d375 and as much as 65 g/d12 of total dietary fiber. The following studies focused on the effect of HCF diets on blood pressure. Wright and colleagues376 compared fiber intake and blood pressure in 94 healthy individuals and noted that those with high-fiber intakes had significantly lower blood pressures than those with low-fiber intakes. When 17 healthy volunteers increased their fiber intake modestly by making high-fiber substitutions for low-fiber foods, blood pressure dropped significantly over a 4-week period. In 1983, 12 nonobese, insulin-dependent diabetics were admitted to our metabolic ward to evaluate responses to highfiber diets.12 Six patients had no history of hypertension. The remaining six had a history of systolic blood pressure measurements exceeding 150 mmHg; four were being treated with 122
antihypertensive medications that were continued throughout the study. Average blood pressures were 10% lower on the high-fiber diet (Figure 13). Dodson and colleagues studied various forms of high-fiber, low-fat, low-sodium diets.356-375-377 After treating375 53 diabetic patients with mild hypertension for 1 month with a 35 to 40 g fiber diet comprised of 15% fat, 20% protein, 65% unrefined carbohydrate, 0 to 5% refined carbohydrate, and 40 to 50 mmol sodium per d, they observed a 6.8% reduction in diastolic blood pressure (p 121-398 Liu and colleagues398 compiled data on 20 economically advanced countries based on per capita food consumption. Estimated fiber intake was inversely related to CHD mortality rate. Populations consuming a vegetarian-type diet also have reduced mortality incidence.399 A study by Kromhout and colleagues19-400 of 871 Netherlands men reported that mortality from CHD was approximately four times higher in men with lower fiber intakes than men with higher fiber intakes. The effect was independent of other dietary variables and remained significant after multivariate adjustment for other risk factors. The authors concluded that a diet containing at least 37 g dietary fiber per day may be protective against CHD.19 Khaw and Barrett-Connor121 noted a 6 g increase in daily fiber intake was associated with a 25% reduction in ischemic heart disease mortality (p
