LaSalle University
The Welfare State and the Paradoxical Shift
of Coronary Artery Disease Risk
Associated with Socioeconomic Status
A Dissertation Submitted to the Faculty of the Division of
the Nutritional Sciences
in Candidacy for the Degree of
Doctor of Philosophy
Department of Nutrition
By
Steven P. Petrosino
Columbus, Ohio
September 30, 1994
Acknowledgements
This author is indebted to the invaluable assistance of my friend and mentor,
Neurocardiologist Robert S. Eliot, M.D., F.A.C.C., one of the world's foremost
experts on stress, the heart, and human physiology, and upon whose important
research much of this paper is based.
I am also indebted to my friend Ever D. Grech, M.D., M.R.C.P. for assisting me in
my research in free radical theory, and for providing me access to his own unique
clinical research in the field.
And to Hari M. Sharma, M.D., F.R.C.P.C., expert in nutritional preventative
medicine and free radical theory, who has offered helpful insights and who has
shared his own important research on nutrition and degenerative disease with me.
Special thanks:
To my wife Lynn and my children Angela and Aaron for their constant love,
support and patience.
My gratitude to my friend Tate Antrim for computer technical support and
assistance during the course of my research, to Janet K. Bixel, M.D., endocrinologist
and authority in psychoendocrinology for her assistance in my research, and to my
friend Virgil C. Dias, Pharm D. for his support and valuable assistance.
ii
Preface
The decade of the sixties was characterized by radical and sweeping changes in
the United States. These alterations encompassed not only social aspects, but also
American lifestyle and nutrition. The early years of the decade of the sixties saw the
assassination of a President, the opening of the Vietnam war, the prohibition of
prayer in public schools, and a general moral and spiritual decline in America. The
early 1960s also ushered in Lyndon Johnsons' "Great Society" social welfare
programs, and set the stage for the Surgeon General of the United States' warning
against the health risks associated with smoking, and the American Heart
Association's well-publicized recommendation that Americans should limit their fat
and cholesterol intake.
There is one great paradox which occurred in this decade: Prior to the 1960s,
black Americans and other members of lower socioeconomic status displayed a
resistance to ischemic heart disease. Whites and members of the upper
socioeconomic strata more frequently fell prey to ischemic heart disease. After the
decade of the sixties, this situation was (and remains) reversed.
This paper will address the following Hypothesis: The American Social Welfare
System, which was designed to benefit the poor, is indirectly responsible for a
detrimental effect on the cardiovascular health of the American indigent who
depend upon the system. These consequences became evident in the decade of the
1960s and were exerted through modifications of lifestyle, environment, diet, and
family structure which were shaped and influenced by the American social welfare
system. The urban poor reacted differently and more slowly to consumer education
on diet, exercise and smoking than did the affluent. Both this factor and the inherent
stress, demoralization, hopelessness, and despair, engendered by the dependency of
the impoverished upon the social welfare system, were responsible for the
paradoxical and rapid shift in heart disease risk.
Stress exerts its detrimental cardiovascular effects more rapidly than does poor
diet, smoking, or lack of exercise, while further potentiating their destructive effects.
Stress contributed to the rapid development of adverse cardiovascular effects and
increased susceptibility to cardiovascular disease experienced by the indigent in the
decade of the sixties.
iii
Table of Contents
Acknowledgements..................................................................................... ii
Preface......................................................................................................... iii
Table of Contents....................................................................................... iv
List of Abbreviations.................................................................................. vii
Chapter:
I. Introduction..................................................................................... 2
Goal of this paper............................................................................. 6
II. Method............................................................................................. 7
III. Background: The Clinical Data.................................................... 9
Risk Factors for CAD ....................................................................... 9
The Paradox of SES as a CAD risk factor.......................................... 15
Diet and the Geographical Paradox of CAD among Populations...... 21
IV. Historical Background and Demographics...............................
23
Population Studies on CAD Mortality and American Longevity....... 23
Population Studies which Examined Acute versus Chronic CAD.... 25
Historical Events Effecting CAD Risk of Populations...................... 27
Historical Changes in Infant Mortality, Human Lifespan and SES.... 32
Race and Historical Changes in Life Expectancy............................ 33
A History of Pharmacologic Secondary Intervention Trials.............. 34
Population Studies which Examined Racial Differences in CAD...... 39
Racial Differences in the American Rural to Urban Migration.......... 49
Race and Demographics and Their Effect on SES.............................. 50
V. Demographic Theory and Discussion........................................... 52
Access to Medical Services and Quality of Care: Their Relationship to
SES and CAD Risk....................................................................... 52
Exercise, Daily Activity Levels, SES, and CAD Risk....................... 56
Diet and Demographics: Sources of Dietary Fat............................... 60
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VI. Physiology and CAD Risk............................................................. 90
Resting Heart Rate, Blood Pressure, Vasospasm, Left Ventricular
Mass and Function, Platelet Aggregation, Plasma Fibrinogen,
Catecholamines and CAD Risk.................................................. 90
Atherogenesis, Lipids, Abdominal Fat Deposition and Their
Relation to Stress, Hostility, and CAD Risk.................................. 96
iv
Table of Contents (continued)
VII. SES Associated Behaviors............................................................ 103
Abdication of Responsibility, Loss of Traditional Family Structure,
and Father Absence as an Influence on SES................................. 103
Supportive Social Relationships, the Intact Nuclear Family and
CAD Risk.................................................................................... 116
The Decline of Faith, Abandonment of Personal Responsibility, and
increased CAD Risk.................................................................... 118
Stress, Hostility, Rage and CAD Risk Factors................................. 120
Stress, Coping Skills, Environment and CAD................................... 123
Unemployment, Frustration, Fatalism, and CAD Risk.................... 138
Eating Habits, Family Gathering Traditions, and CAD Risk........... 142
Dietary Fat and Cholesterol Consumption...................................... 144
Changes in Carbohydrate Consumption.......................................... 148
Transfats and Hydrogenated Oil Consumption............................... 149
Obesity and Fat Consumption........................................................ 152
Obesity, Race, SES, and CAD Mortality........................................ 153
Diabetes, Fat Consumption............................................................. 155
Dietary Fiber Consumption, SES and CAD Risk............................ 158
Prevalence of Smoking, Attitudes to Smoking, and Access to Tobacco
Products by Adolescents............................................................. 163
Excessive Alcohol Consumption and SES....................................... 175
Destructive Personal Behaviors and their relationship to SES........ 180
VIII. Dietary Electrolyte, Mineral and Anti-Oxidant Vitamin and
Flavonoid Consumption and SES................................................ 182
Dietary Antioxidants, Recommended Daily Allowance, and SES... 182
Ratio of Dietary Sodium to Magnesium and Potassium in
Hypertension.............................................................................. 183
Dietary Calcium Intake, Hypertension, and CAD............................. 185
Dietary Iron Intake and CAD.......................................................... 187
Dietary Selenium Intake and CAD.................................................. 191
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Antioxidant Vitamins and CAD: Epidemiology................................. 195
Laboratory and Clinical Studies of Vitamin E.................................... 196
Laboratory and Clinical Studies of Vitamin C................................... 203
Laboratory and Clinical Studies of Beta Carotene............................. 207
Antioxidants and Their Effect on Serum Lipids................................ 211
Free Radical Theory....................................................................... 211
Antioxidants and Prevention of Oxidative Modification of LDL... 216
Laboratory and Clinical Studies of Folate and the B Vitamins....... 221
Laboratory and Clinical Studies of Flavonoids............................... 225
IX. Summary, Conclusions and Recommendations.........................
229
The Legacy of the Welfare State...................................................... 229
The Probable Cause of the Paradoxical Shift of SES associated
Risk............................................................................................239
Working Hypothesis......................................................................... 243
Recommendations to Reduce CAD risk associated with
Lower SES.................................................................................... 256
X. Appendix A (List of Figures)........................................................ 262
XI. Appendix B (List of Tables).......................................................... 264
XII. References....................................................................................... 265
XIII. Index................................................................................................ 344
Page 3
INDEX
An Exhaustive Index is available on
WPWIN\Steve\Welfare3.rpt
software disc:
Access Word Perfect, Install Disc, and Use Word Perfect
Edit/Search function.)
Page 4
List of Abbreviations
AFDC................................................. Aid to families with dependent children
AHA................................................... American heart association
AMI................................................... Acute myocardial infarction
CAD................................................... Coronary artery disease
CHD................................................... Coronary heart disease
CHF................................................... Congestive heart failure
COPD................................................ Chronic Obstructive Pulmonary Disease
CVD................................................... Cardiovascular disease
CI....................................................... Confidence interval
D........................................................ Day
DL..................................................... Deciliter
DNA.................................................. Deoxyribonucleic acid
ECG................................................... Electrocardiogram
EDRF................................................. Endothelium derived relaxing factor
EMS................................................... Emergency Medical Service
EPA.................................................... Eicosapentaenoic acid
G......................................................... Gram
HDL................................................... High density lipoprotein cholesterol
HG..................................................... Mercury
HUD.................................................. Housing and urban development
IU....................................................... International units
L......................................................... Liter
LDL.................................................... Low density lipoprotein cholesterol
LDLOX................................................. Oxidized low density lipoprotein
LV...................................................... Left ventricle
MDA................................................. Malondialdehyde
MG.................................................... Milligram
MI...................................................... Myocardial infarction
ML..................................................... Milliliter
MMOL............................................... Millimole
MUFA............................................... Monounsaturated fatty acid
NIDDM............................................. Non insulin-dependent diabetes mellitus
NRC................................................... National research council
PUFA................................................. Polyunsaturated fatty acid
PVD................................................... Peripheral vascular disease
RDA................................................... Recommended daily allowance
Page 5
REDOX.............................................. Oxygen reduction system or reactant
SES..................................................... Socioeconomic status
SOD................................................... Superoxide Dismutase
SSI...................................................... Supplemental Security Income
TBARS.............................................. Thiobarbituric acid reactive substances
μG...................................................... Microgram
μM..................................................... Micromole
Page 6
I. Introduction
Observations by researchers in the first half of this century regarding dramatic
differences in Coronary Artery Disease (CAD) mortality between different
geographic areas raised questions about the possible association of mortality with
differing dietary habits or other environmental factors which are unique to certain
populations.1,2 Prior to Sir Alexander Fleming's discovery of a penicillin-
producing mold in 1928 and the first clinical use of penicillin in 1941, (and prior
to the subsequent proliferation of other widely-available antibiotic compounds by
1948, and vaccines in the 1950s), the major cause of death in the United States
was infectious disease. Currently, those diseases account for fewer than 3% of
deaths. In 1900, chronic degenerative diseases including cancer and CAD
accounted for only fourteen percent of deaths, while today they account for over
75 percent.3 Because CAD accounts for the vast majority of the chronic
degenerative disease-associated deaths, numerous clinical and epidemiological
studies have been conducted during the past four decades with the hope that these
diseases would respond as dramatically to medical interventions as did the
infectious diseases. The results of most of these medical intervention studies have
been disappointing,62 which, together with contemporary market pressures for
sweeping health care cost containment, has shifted the current investigational
emphasis to the realm of prevention through dietary and life-style modifications.
Research has identified at least nine risk factors for developing CAD, and most
of these cardiovascular risk factors can be altered through changes in diet or in
life-style [See Table 1].
Table 1: Risk Factors For Atherosclerosis
A. Not Reversible
1. Aging
2. Male sex
3. Positive family history of premature atherosclerosis
B. Potentially reversible
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1. Cigarette smoking
2. Physical inactivity
3. Hypertension*
4. Obesity*
5. Hyperlipidemia, hypercholesterolemia and/or
hypertriglyceridemia.*
6. Low levels of high-density lipoprotein (HDL)*
C. Other possible factors
1. Body build
2. Emotional stress
3. Personality type
* Influenced by diet
______________________________________________________________________
Adapted From: Bierman EL, Chait A. Nutrition and Diet in Relation to Hyperlipidemia and Atherosclerosis,
in: Shils ME, Modern Nutrition in Health and Disease, 7th ed., 1988:1285.
There is, however, a historical paradox facing researchers attempting to structure
clinical studies to evaluate the effects of these preventative modifications.
Clearly, coronary artery disease has historically increased in populations who
increasingly use tobacco products, have become sedentary, and who have adopted
diets rich in saturated animal fats and cholesterol. These increases in the
incidence of CAD and other chronic degenerative diseases typically parallel the
degree to which a population has adopted these at-risk practices. The United
States population suffered a dramatic increase in CAD mortality during the six
decades between 1900 and 1964 during which Americans increasingly embraced
these practices, and has been enjoying a consistent decline since widespread
changes in smoking and diet were adopted in the mid 1960s [see Fig. 1].
Indicative of the significant dietary changes which have occurred in the United
States within the last three decades, one recent survey reported that 13.5% of all
American households currently claim to have at least one vegetarian member.
This number represents an eight-fold increase from 1979 to 1992.890
Figure 1. Death Rate Due to Coronary Artery Disease, 1900-1988
Pooled data using early un-adjusted data and age-adjusted data, deaths per 100,000.
Page 8
_________________________________________________________________________________________________
Sources: Vital Statistics of the United States, Volume II Mortality, Part A; 1988; Moriyama IM, Grover M. Statistical studies
of heart diseases I. Heart diseases and allied causes of death in relation to age changes in the population. Public Health Rep
1948;63:537-545; Heart Disease and Tuberculosis. Public Health Reports 1946;61:1425; National Center for Health Statistics;
American Heart Association.
Dietary and lifestyle changes do not immediately yield discernable effects upon
CAD morbidity and mortality. A plateau of coronary artery disease mortality
occurred in the mid to late 1960s, and the sweeping dietary and lifestyle changes
instituted by a significant portion of the American population within this decade
became evident within the following decade. While death from non-
cardiovascular diseases (non-CVD) have remained steady, age-adjusted mortality
due to stroke and coronary heart disease (CHD) has declined rapidly and
consistently since 1972 [see Fig. 2].
Figure 2: Decline in Age-Adjusted Mortality From All Causes Since 1972
__________________________________________________________________
From: Joint National Committee on the Detection, Evaluation, and Treatment of High Blood Pressure, Arch Int Med 1993;153:158.
National Center for Health Statistics data calculated by the National Heart, Lung, and Blood Institute.
These results, however, have not been consistent for all subgroups of Americans.
Page 9
Enigmatically, during the period of 1900 through 1964, blacks and poor
Americans of all ethnic groups had a lower risk of CAD than the wealthy [see Fig.
3], however in the mid 1960s, as the CAD mortality rate of the rest of the nation
reached a plateau and subsequently began to plummet, the CAD mortality rate of
indigent Americans surpassed that of the affluent, and the gap has subsequently
been widening [see Fig. 7].4,393,394,395,396,397
A study conducted by Cassel et al49 is noteworthy because it examined the
incidence of coronary heart disease by ethnic group, social class, and sex from
1960 to 1962, [see Fig. 3], and conducted a follow-up in 1967 through 1969.
During the initial period of observation, researchers were able to document the
"excess prevalence found in the high social class," but noted that during the course
of the study the class differences were disappearing in favor of a lower trend of
CAD among the high social class.
Figure 3. Prevalence of Coronary Artery Disease, 1960-1962
Age-adjusted prevalence rates per 1,000 population
Prevalence By Race and Sex Prevalence by Social Class
_______________________________________________________________
Cassel JC. Review of 1960 through 1962 Cardiovascular Disease Prevalence Study. Arch Intern Med 1971;128:890-895
The Goal of this Paper
Page 10
This paper will attempt to identify the risk factors for CAD and the forces which
differentially altered them within the last three decades, causing a "risk factor
shift" between members of low and high socioeconomic status (SES). This paper
will also attempt to identify those risk factors for CAD which are more prevalent
among young members of lower SES, and those which are more prevalent among
older members of higher SES, and investigate their potential impact on the
established paradoxical shift of SES-associated CAD mortality which occurs
between age groups. This paper will further examine the span of influence of the
American social welfare system and other contemporary sociological influences
upon these forces of alteration and will attempt to demonstrate a cause and effect
relationship using previous epidemiologic and clinical data.
II. Method
In Phase I, an initial group of studies potentially relevant to the question of the
association between SES, stress, and the incidence CAD was retrieved through
computer searches of the following databases (1960 through 1994): Medline, BRS
Colleague, Catline, Dissertation Abstracts International, and government
document indices. A maximally broad keyword scheme was used ("cardiac,"
"cardiovascular," "coronary heart disease," or "coronary artery disease;" "blacks"
or "minority;" "psychological factors," "stress," and the word stem "psych;" and
"socioeconomic status," "social class," "indigent," "poverty," or "poor"). Library
searches were conducted using Index Medicus for additional references between
1890 and 1960. Computer and manual searches were then augmented with a
bibliographic review of retrieved manuscripts.
In Phase II, a broad database search was conducted for the nine generally
accepted risk factors for CAD, and these sources were also augmented by a
bibliographic review of the manuscripts. Factors with the potential to magnify the
deleterious effects of these known risk factors were identified through exhaustive
Page 11
literature review, and these factors were subsequently indexed, searched, and
cross-referenced.
In Phase III, a database search (Social Work, Psychological Abstracts), and
extensive library searches were conducted for review articles on the American
social welfare system and upon welfare reform recommendations. These reviews
were cross-referenced using retrieved bibliographies, and were augmented using
current data bases from the Vital Statistics of the United States.
In Phase IV, a casual-comparative research methodology was utilized to
demonstrate a cause-and-effect relationship between identified CAD risk factors
specific to blacks or to the indigent and exacerbating environmental factors
potentially influenced by or documented to have been influenced by the American
social welfare system. This comparison was accomplished using the retrieved
epidemiologic, statistical, and clinical data.
III. Background: The Clinical Data
Risk Factors for Coronary Artery Disease
Coronary artery disease remains the number one cause of death in the United
States, regardless of race,14,17,21,37,217 and mortality rates from cardiovascular
diseases in the United States are among the highest in the world. 35,61,294
Approximately 20% of American men and 5% of women will have symptomatic
CAD by age 60,17,21 and of all Americans who died in 1989, CAD was listed as the
cause of death in 43% of the cases.217
The recognized risk factors for coronary artery disease include
hypertension,14,17,21,32,35 hyperlipidemia,5,14,17,28,32,35,36,400,401
smoking,6,14,17,21,32,33,35,53,79,81,95,96,97 diabetes,14,17,21,32,34,80,81,82 family history of
premature CAD,14,17,21,32,34 a sedentary lifestyle with minimal aerobic
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exercise,13,14,17,21,34,35,80,87,291,292,293,385,386,466,511,512,513,514,515,516,517
stress,10,14,17,21,34,35,57,80,145,148,149,164,165,166,168,169,225,226,229,230,231,232,351,493,494,495,496,688,689,6
90,692, 693, 701,709,714,734,735,736,738,739,740 aggressive personality,10,14,17,21,34,35,57,698 and
obesity.14,17,21,34,145,172,181 According to epidemiologic studies, these risk factors
influence only about 50% of overt cases of coronary heart disease.274 Only
recently has lower socioeconomic status, (SES), been recognized as a potential
risk factor for coronary artery disease among Americans.4,112,113,114,115,725,726,727
Race as a CAD Risk Factor
Some researchers have postulated that the association between lower SES and
heart disease is due to inherent racial CAD risk factors,14,16,225 since blacks
comprise the largest segment of the American minority population,11,42 have lower
average incomes than whites,11 are more likely to live in the most impoverished
areas,11 are at greater risk for developing hypertension, CAD, renal failure, stroke,
left ventricular hypertrophy, cardiac arrest, and sudden cardiac
death,14,15,16,19,20,37,38,39,40,41,178,314,942 experience more rapid disease
progression,14,15,16,19,20,37,38,39,40,41 have been shown to have more underlying
disease,175,180,182,942 and are more likely to succumb to
CAD.14,15,16,19,20,37,38,39,40,41,178,179,313 Other theories attempt to link socioeconomic
risk factors with dietary inadequacies or environmental differences, such as
limited access to health care,47,177,358,359,360,361 that more frequently accompany
lower socioeconomic status. While the latter theories may have validity, the
assumption that minority racial status is a causative factor for CAD (especially
among blacks) lacks scientific basis. A genetic basis for increased CAD
susceptibility of blacks has not been identified to date,35,38,442,444 nor have older
post-mortem416,419,427,444,450,451,456 or recent angiographic
studies135,362,363,364,365,366,367,368 demonstrated greater prevalence of detectable
coronary artery lesions in blacks compared to white persons. Blanche and
Page 13
Handler,427 in discussing the lower incidence of CAD in American blacks in
contrast to whites in 1950, noted that degenerative changes in the coronary vessels
developed more slowly in blacks, and Gilbert and Gillman812 in their discussion of
diet and disease in the African Bantu in 1944, cautioned against "attributing a
racial factor to any differences in the incidence of disease amongst the black and
white people," and suggested that diet was the major contributor to the observed
differences.
The current correlation with increased incidence of CAD in blacks does not
establish causality, and particularly in light of the inconsistencies involving this
correlation, and the existence of numerous confounding variables. Black men and
women with four or less years of grade school education have an age-adjusted
mortality rate 75% higher than blacks with five or more years of college[see Fig.
4].4,129
Figure 4. All Cause Mortality by Education and Race
A mortality study of 1.3 million persons 25 years of age and older, 1979-1985.
__________________________________________________________
From: Rogot E, Sorlie P, et al. A mortality study of 1.3 million persons by demographic, social and economic factors:
1979-1985 follow-up. National Institutes of Health. 1992. NIH Publication No. 92-3297:1-5.
After 14 years of follow-up, black men of high socioeconomic status who
participated in the Charleston Heart Study had CAD and infarction rates half those
of black or white men of lower socioeconomic status.142
Page 14
In a prospective analysis of over 4,000 blacks and whites living in the Piedmont
region of North Carolina,114 a subgroup of black women who had the highest
education levels was found to have the highest total life expectancy and a
widening advantage over similarly educated white women with increasing age.
The authors, citing previous scholarship,346 concluded that educational level and
socioeconomic status are alterable risk factors, and that at least part of the
disadvantage associated with lower SES relates to poorer health practices in this
group.114 Several additional studies have demonstrated that men with the lowest
annual incomes have a mortality rate as much as twice that of men in the highest
income categories studied, regardless of race[see Fig. 5].143,144
Figure 5: All Cause Mortality by Income in Subjects Age 25 Years and Older
______________________________________________________
Adapted from Rogot et al.143
Unemployment, Residence in Poverty Areas, and CAD Risk
Living in areas of high unemployment has been proposed as an accurate
identifier for members of lower socioeconomic status,120,125 however this method
of identification is not consistently reliable. In one study by Berkman and co-
workers,238 which compared an area of poverty with an affluent area, the
incidence of hypertension was 50% higher in the poor area, regardless of social
interaction, medical care, smoking or other identified CAD risk factors. Among a
group of more affluent people who chose to live in the poverty area, the pattern of
Page 15
hypertension was more closely related to that seen within the poor area rather than
to that of a high SES group with a similar income living in an affluent area.
Because relatively few members of high SES groups, (regardless of race), choose
to live in poverty areas, this data suggests that the increased mortality generally
seen among lower socioeconomic classes may be related to greater exposure to
certain environmental factors within poverty areas which are more common to
members of low SES, rather than to risk factors associated with race.114,225,346
The finding that hostile environment and material deprivation predict CAD
mortality more accurately than social class has been validated by several
additional researchers.182,382,629
Although more blacks than whites are unemployed per capita, there is evidence
that it is stress associated with unemployment, rather than risk factors associated
with race, lack of income, or the availability of affordable medical care which
increases CAD mortality among the unemployed. Unemployed workers are up to
fifty percent more likely to suffer sudden cardiac death, and are more likely to die
from any cause than their employed counterparts [see Fig. 6] regardless of
race.4,10,49,70,116,117,118,119,140,143,144
Figure 6. All Cause Mortality by Employment Status of Subjects
Age-adjusted mortality rates per 1,000 population, ages 25 to 64 years.
_____________________________________________________________
From: Rogot E, Sorlie P, et al. A mortality study of 1.3 million persons by demographic, social and economic factors:
1979-1985 follow-up. National Institutes of Health. 1992. NIH Publication No. 92-3297:1-5.
Page 16
In addition to an increased risk of death, the unemployed are significantly more
likely to be depressed122,123,124 or be hospitalized for serious mental illness,120,121
independent of their racial status.
In the Rancho-Bernardo Study, Kritz-Silverstein and associates380 examined the
relationship between employment status and CAD risk factors in middle-aged
women, and found an increased risk of CAD which was associated with
unemployment. These researchers noted that women who were employed smoked
less cigarettes, drank less alcohol, had significantly lower total cholesterol and
fasting plasma glucose levels, and exercised more than unemployed women.
The association of unemployment with increased CAD risk in both men and
women has not only been seen in America, but also has been demonstrated across
diverse cultures in nine industrialized countries.116 Education, income, place of
residence, and employment status seem to overcome or modify the "risk factor"
associated with race.
The Paradox of Socioeconomic Status as a CAD Risk Factor
The indigent clearly were not always the highest at-risk group for developing or
dying from heart disease. Prior to 1960, the affluent had a significantly greater
risk for sudden coronary death and CAD mortality than did the
poor.4,129,132,301,369,377,378,379 In fact, the late-nineteenth century surgeon, Sir William
Osler described angina pectoris as being an "affliction of the wealthy". 377 As
early as 1937, White418 stated "race, temperament, social and economic status, and
occupation appear to have some slight bearing on the incidence of coronary
disease," and observed that blacks and members of lower socioeconomic status
rarely developed CAD. In 1939, Burch and Voorhies419 stated that "coronary
occlusion and angina pectoris, along with other cardiovascular states such as
hypertension, have been associated with high tension living conditions and
occupations requiring considerable responsibility and intelligence, e.g., the
Page 17
physician, banker, and lawyer." The following year, Crile,458 writing on
"Diseases Peculiar to Civilized Man," argued that the existence of a racial or class
distribution of hypertension suggested that urban stress may induce hypertension
because the highest known prevalence is among "those who struggle with the
complexities and pressures of civilization," and the lowest prevalence is among
aboriginal natives. Similarly in Europe, the 1950 decennial Occupational
Mortality statistics of England and Wales449 demonstrated a susceptibility of the
professional and executive social class and a resistance of the unskilled lower
class to the development of CAD and subsequent cardiovascular mortality.
Examining CAD prevalence data gathered from 1962 to 1964, Cassel and
colleagues49 stated: "It is clear from these analyses that black males are definitely
protected in some fashion from coronary heart disease..." As late as 1964, upward
mobility was still being associated with an increased risk of heart disease. 459 After
1960 and through the present, a steady increase in mortality among members of
lower SES has been coinciding with reductions in upper SES mortality in both
Europe301,457 and the United States.4,112,301,379 By the mid to late 1960s, mortality
from CAD in both the United States and the United Kingdom was more common
in the lower socioeconomic classes than in the higher,4,301,379 and there is
significant evidence that this inverse relationship between SES and cardiovascular
disease has subsequently been widening [see Fig.7].4,393,394,395,396,397
Cassel et al49 were some of the first researchers to document a paradoxical shift
of socioeconomic status-associated CAD risk factors in the rural Evans County
Georgia Heart Study, a biracial cohort study which examined the incidence of
CAD in rural Georgians from 1960 to 1967.
Figure 7: A Graphic Representation of the Paradoxical 1964 Risk Factor
Shift
Comparative Mortality Per 100,000 Due to Diseases of the Heart
Page 18
_____________________________________________________________
Adapted from Keil,4 and Vital Statistics of the United States.216,217
Analyzing this same data, Kaplan and associates510 concluded that in 1960 the
more affluent upper-half of the socioeconomic class range was found to have age-
adjusted rates of CAD which were more than twice as high as those who where in
the lower-half of the socioeconomic class range. By 1967, however, this social
class difference had disappeared, and this equalizing of the CAD rates for the two
social class groups was primarily "achieved by an increase in the rates for the
"lower" social class men (particularly the younger men), rather than a decrease in
the "higher" social class." Furthermore, the researchers noted that these changes
in CAD risk associated with those of lower SES occurred primarily during a rapid
transition in rural Evans County Georgia from a rural agrarian society to a more
modern, urbanized, and industrialized economy.510 High-coronary risk patterns of
living which were previously "characteristic of the more favored segments of
white society" were being adopted by low SES whites, and to a lesser extent by
low SES blacks. Specifically, Cassel et al49 noted that changes in lifestyle were
occurring more slowly in lower class blacks than in lower class whites while both
groups were living in rural areas, but adverse lifestyle changes among blacks
accelerated following the black migration to urban centers, and resulted in an
increased incidence of CAD within this group which was detected by the
researchers by 1967. Kaplan, Cassel et al510 stated that although no evidence of
major changes in diet among blacks was detected prior to 1967, increases in
Page 19
tobacco consumption, the adoption of a more sedentary lifestyle, and
"psychosocial factors" which accompanied social mobility and urbanization might
be implicated in the shift of coronary risk. Building upon previous research, the
authors hypothesized that powerlessness,948 role and value conflicts,948 disruption
of relationships,949 reduction in family ties,949 anomie (or the breakdown of social
norms and values),952 alienation,950 the loss of social support,951 and social
isolation951 are powerful stressors which have been associated with social
mobility, and that these factors have the potential for eliciting adverse
"neuroendocrine changes".510 Kaplan, Cassel, and their co-workers further
suggested that these alterations might be responsible for the selective adverse
cardiovascular changes in the health status within the lower socioeconomic class
which was socially more vulnerable to these effects of change. The authors
concluded that migration and upward social mobility among those of higher SES
did not increase cardiovascular risk within this group because of an inherently
greater degree of social support and stability which resulted in a "comfortable
acculturation" following the "successful acquisition of new lifestyles."
Subsequent reanalysis of the Evans County data in 1980 by Morgenstern379
affirmed the conclusions of previous researchers, and also attributed the reversal
of risk associated with socioeconomic status to changes in certain urban
populations "following a period of rapid socioeconomic change or
"modernization"."
Figure 8: Incidence of CAD per 1,000 in White Males by Age and Social
Class, 1960 through 1962 and 1967 through 1969.
Page 20
_____________________________________________________________
From: Cassel et al.173
This reanalysis by Morgenstern further revealed that the association of CAD risk
and lower socioeconomic status demonstrated an age-related cross-over effect and
was reversed with increasing age [see Fig. 8]. When incidence rates were
stratified by age, it became evident that younger men of high socioeconomic status
had lower CAD rates than their poorer counterparts, but older men of high
socioeconomic status had a higher incidence of CAD than similarly aged men of
lower status. A similar crossover trend was seen in a Piedmont region of North
Carolina study by Guralnik and co-workers114 of over 4,000 blacks and whites. In
this study, researchers found that through the age of 65, black men had a lower
total life expectancy than white men, however both black men and women 75
years of age and older had greater total life expectancy than whites, and these
differences were larger after adjusting for education.
In a population-based, ten-year study of 1.5 million northwestern American
whites, blacks, urban American Indians and Alaskan natives by Grossman and
co-workers,302 average death rates per 100,000 were 120% higher among urban
blacks between the ages of 25 to 44 years than urban whites, however this
negative trend seemed to slow with increasing age and disappeared by age 65.
There was only a 4% increase in all-cause death rate per 100,000 for urban blacks
over the age of 65 versus urban whites (who were of somewhat higher average
SES) within the same age group. U.S. Census Data confirms that age reverses the
Page 21
risk associated with CAD among blacks and whites. Elderly black males and
females demonstrate a lower mortality rate per 100,000 population than whites for
both acute and chronic heart disease, but only after age 85. Similarly, mortality
from all forms of ischemic heart disease is lower among blacks after age 65, and
mortality from acute myocardial infarction is lower after age 54 in black males,
and after age 84 in black females than among whites of similar ages.216 Clearly,
environmental factors exist which have the potential to increase CAD risk. There
is evidence that these factors may vary in their prevalence, intensity, or effect
between socioeconomic groups as well as between age groups.
These data indicate that although socioeconomic status and race may currently
be associated risk factors for CAD, since this association has not remained
constant, they cannot be recognized as causative risk factors.
Diet and the Geographical Paradox of CAD Mortality among Population
Groups
The relationship of diet and CAD mortality is complex. Traditionally, the
influence of diet on CAD risk factors has been attributed to alterations in serum
low density lipoprotein (LDL) cholesterol concentrations moderated by dietary
cholesterol, saturated fatty acids, and soluble fiber.819,891 Animal and plant foods,
however, are highly complex "chemical cocktails" which contain many other
natural or additive substances which may positively or negatively impact upon
CAD risk, including flavonoids, isoflavones, phytosterols, tocotrienols, arginine,
folacin, phytochemicals, phytoestrogens, antioxidant vitamins and minerals,
antioxidant co-factors, electrolytes and other essential minerals, transfats, heme
iron and chemical additives and contaminants.
Saturated fat consumption has been the single dietary variable which has been
most studied by previous research. Increases in the incidence of CAD and other
chronic degenerative diseases within large population groups typically parallel the
Page 22
degree to which a population has adopted certain at-risk practices, including a diet
high in saturated animal fat and cholesterol.528,529,530,531,532 Numerous
epidemiologists have successfully linked the dietary fat and saturated fat
consumption of entire populations to the incidence of CAD within that
population.2,35,36,53,376,444,451,476,522,526,527
The Paradox of Finland, France, and Greenland
The associations between dietary fat consumption and CAD are typically strong,
however there are three notable exceptions which constitute a paradox. Finland
consistently demonstrates the highest level of CAD mortality, and France and
Greenland are among the countries with the lowest, despite having comparably
high intakes of dietary fat [see Figures 11 and 15].35,61,476,527,528,529,608 Because
Finland is an industrialized nation whose population generally enjoys better
economic conditions than the countries of Poland, Romania, and Yugoslavia
(which are countries that enjoy significantly lower rates of CAD mortality,61,476,527
and whose populations consume less fat,476) this further sheds doubt on SES as a
causative risk factor for CAD.
IV. Historical Background and Demographics
Population Studies on CAD Mortality and American Longevity
A gradual rise in the rate of death from CAD between 1900 and 1940 was first
documented in a series of U.S. Public Health Service reports published between
1946 and 1951.315,316,317,407,408,409 Many of the early statistical studies of CAD were
predominantly conducted with white subjects, and were rarely stratified for SES.
In the first of these reports, a 1946 Public Health Report editorial409 briefly
mentioned that total deaths reported due to heart disease in the United States had
increased from 303,724 in 1934 to 418,062 in 1944--an (unadjusted) escalation of
38 percent. In 1948, Moriyama and Grover315 documented a rise in age-adjusted
CAD mortality from 168 deaths per 100,000 in 1900 to 239 in 1920; and
Page 23
subsequently climbing to 339 per 100,000 in 1940. From 1950 through 1963, age-
adjusted mortality from CAD increased an additional 19 percent.371,372 After six
decades of consistent increases,36,376,388,389,390 Epstein318 reported in 1965 that
overall CAD mortality was leveling. Borhani and Hechter319 showed in 1964
that for the first time in this century, ischemic heart disease mortality in California
had begun a sudden decline as sharp as its abrupt rise after 1920. This same
phenomenon which was first seen in California, subsequently was documented to
have occurred throughout the rest of the nation about a decade later. From 1960
through 1970, the rate of death from heart disease in the United States began to
slow and plateau, and since 1970 it has been declining. 3,62,63,325 In subsequent
analyses of the onset of this decline in CAD mortality at the state level rather than
at the national level, it became evident that states with the poorest socioeconomic
conditions (in terms of income, education, and occupation) were from two to ten
times more likely to have experienced a later onset in this decline [see Fig.
9].398,399 In a recent population study by Davis and associates,347 the authors
noted that between 1973 and 1987, CAD mortality decreased by 42% in
Americans less than 54 years of age, and decreased by 33% in Americans aged 55
to 84 years. This decline has been variously attributed to changes in smoking
habits,320 lifestyle,321,725,819,820, 821,822 the environment,322 dietary habits,323 gradual
improvements in diagnosis over time,62 and shifts in mortality from other
diseases.324
Figure 9: Percent of State Economic Areas with Late Onset (Occurring After
1968) of Decline in Cardiovascular Mortality.
Page 24
_________________________________________________________
From: Wing et al.399
The actual cause of this decline may be a combination of many of these factors.
Indeed, Stallones63 argued in 1980 that no single one of these factors could
account for the early rise, then fall of CAD mortality in the United States.
Although reductions in CAD mortality were recorded for affluent Americans in
the mid 1960s, epidemiologic studies have shown that decreases in CAD mortality
among American blacks and the poor occurred much later and have been
significantly less.37,43 In 1970, the life expectancy of blacks in the United States
was a significant 7.6 years less than that of whites.216 By 1988, the gap had
narrowed slightly to 6.4 years.214,216 It is possible that the adoption of beneficial
changes in diet, lifestyle and environment occurs more quickly among affluent
populations who have more formal education, and greater access to health-related
information and guidance. This may explain the lag in CAD mortality reduction
among indigent population groups.
Population Studies which Examined Acute versus Chronic CAD: The 20th
Century Epidemic
A recent analysis by Slater and associates325 of acute (predominantly thrombotic
or arrhythmic) and chronic (predominantly atherosclerotic) CAD death rates
between 1931 and 1980 indicated that an epidemic of acute ischemic heart disease
occurred with dramatic rises in acute CAD deaths among (predominantly white)
males between 1931 and 1968, with a rapid decline thereafter [see Fig. 10].
Figure 10: Life Table Proportions of Men Dying From Acute and Chronic
CAD
1931-1980.
Page 25
_______________________________________________________________________________
From: Slater et al.325
A similar trend in acute CAD mortality was seen throughout this 50-year period
among women, but to a lesser degree than men. Compared to men, females
enjoyed an increasing margin of benefit from 1931 through 1950, and a narrowing
margin since 1960. In contrast, these investigators noted fairly stable and
comparable rates for chronic CAD mortality for both men and women during this
period. Robertson884 found that the incidence of chronic CAD (atherosclerosis)
was as extensive in inhabitants of Jamaica as in urban American inhabitants of
New Orleans, but that the incidence of acute CAD (acute myocardial infarction, or
AMI) was 2.4% in Jamaica versus 16.1% in New Orleans. This differential
suggests factors present in, or common to urbanized and Westernized population
groups which increase the probability of thrombosis or vasospasm when
superimposed upon fixed atherogenic plaques in population groups with similar
levels of atherosclerotic disease. These factors may have been more common to
whites and members of upper SES prior to the 1960s, but currently are more
common to blacks and members of lower SES (at least until the 6th or 7th decade
of life). This hypothesis is supported by current U.S. census data on mortality
from all forms of heart disease which shows that black males and females (who are
significantly more likely than whites to reside in major urban inner-city areas)
Page 26
have higher death rates from acute CAD for most of their adult lives. Black males
and females consistently demonstrate a higher mortality rate per 100,000
population than whites for all forms of heart disease (both acute and chronic) from
birth through age 84 (but not after age 85). Similarly, black males and females die
more frequently per 100,000 of population from all forms of ischemic heart
disease from birth through age 64 (but not from age 65 and beyond); of acute
myocardial infarction from birth through age 54 in males (but not after age 54);
and of acute myocardial infarction from birth through age 84 in females (but not
after age 85).216
Historical Events Effecting Populations and Their Impact on CAD Risk
The Surgeon General, the Heart Association, and the 1960 CAD Risk Shift
Since early 1964, there has been a documented decline in the American per
capita consumption of tobacco, animal fats and oils, butter, milk, cream and
eggs.375 Historically, two significant forces for change can be identified which
occurred during the early 1960s and which were probably responsible for this
decline. In January, 1964, the Surgeon General of the United States Public Health
Service warned of the health hazards of tobacco consumption, with a particular
emphasis on cigarette smoking.370 Several months later, the American Heart
Association recommended a change in the American diet, with the goal of
reducing heart attacks and strokes by limiting the intake of saturated fat and
cholesterol.371 A decline in mortality from CAD began the same year these
warnings were issued.318,319,372 A possible explanation for the narrowing margin
of acute CAD mortality between women and men since 1960 which was
documented by Slater et al325 is the significant reduction in smoking among men
beginning in the early 1960s and the increase in smoking among women
subsequent to the aggressive tobacco advertising campaigns for women's cigarette
brands during the same decade. This increase in smoking among women may
Page 27
have offset any potential benefits from reduction of dietary fat and cholesterol
consumption, and may have been more predominant among members of lower
SES. Similarly, the greater prevalence of smoking and higher saturated fat
consumption among blacks since the 1960s may have contributed to rapid
increases in acute CAD seen among this group beginning in the 1960s and
subsequently.
Wartime Dietary Restrictions and CAD Risk
Populations which are subject to dietary restrictions which invariably include
reduced intake of fat, have been shown to have reduced blood cholesterol levels.
During the World War II, extremely low serum cholesterol values were observed
among the inmates of numerous European concentration camps.442,452,453,454
During war-time, it is common for diets of entire populations to fall in energy
value, animal protein content, and in fat and cholesterol content while
simultaneously increasing in carbohydrate and crude fiber (high-residue) content.
The consumption of meat, milk and dairy foods, eggs, animal fat, highly processed
low-residue carbohydrates, and sugar usually decreases during war-time, while
significantly more cereals, cereal products, whole grain breads, vegetables, and
legumes are consumed.442 A decline in CAD mortality was reported in several
Scandinavian countries after comparable changes in dietary habits which were the
result of such deprivation (including shortages of tobacco and sources of dietary
saturated fats), rather than the voluntary adoption of a healthy lifestyle, during
World War II.373,374,442 Conversely, a significant rise in mean blood cholesterol
levels and an increase in CAD risk occurred in German subjects who experienced
profound "improvements" in their diet, including increased intake of fat, between
1947 to 1949 following the war.455
Other Population Studies on Demographic Change, Effects on Diet, and CAD Risk
Nationwide reductions in the intake of animal fat and cholesterol, 1,2,36 and a
Page 28
concomitant reduction in the percentage of male smokers,2,99,102,103 during the last
three decades clearly have been primary contributors to the substantial decline in
American CAD morbidity and mortality since 1964.3,33,99,100,371 Epidemiologic
studies among populations of other developed countries experiencing a decline in
the rate of CAD, [see Fig. 11], have partially attributed these improvements to
increased popular awareness of the benefits of the adoption of a healthier
lifestyle.273,725,819,820,821,822
Figure 11: Death Rates From CAD by Country
in 35 to 74 Year-Old Males
_____________________________________________________________
_
From: Levy RI. Atherosclerosis 1981;1:312.
Conversely, other industrialized nations, including Russia, Bulgaria, Poland,
Romania,Yugoslavia, Crete, and Italy, have adopted poor dietary habits with
increased consumption of animal fat, and have increased their use of tobacco
Page 29
products. These increasingly urbanized populations have demonstrated
escalations in cardiovascular disease and associated cardiovascular mortality
during this same period, thereby further verifying the positive association between
these risk factors and CAD [see Fig. 11].6,273
Case-control studies have verified epidemiologic findings among population
groups. In both the Western Electric Study,205 and the Ireland-Boston Diet Heart
Study,554 dietary cholesterol consumption and saturated animal fat intake
significantly predicted 20-year CAD mortality. In a 20-year follow-up of Seventh
Day Adventists by Snowdon and Associates,555 it was observed that meat
consumption was associated with an increased risk of CAD for both men and
women, and risk increased as the frequency of meat consumption increased.
Animal protein consumption, and its associated high levels of saturated fat, is
probably highest among lower SES populations in contemporary America. A
nutritional study conducted among blacks, Hispanics, and other lower SES
minorities and whites in East Harlem, found nutritional deficiencies in many
categories, with the exception of animal protein.969 Increased saturated animal fat
intake by the indigent may increase the risk of CAD morbidity and mortality in
this population.
Historical Changes in Infant Mortality, Human Lifespan and SES
Lifespan has increased greatly for children in the twentieth century. A white
male infant born in 1900 had a life expectancy of 48 years. By 1988, the life
expectancy of a similar infant increased to over 72 years.216 Increases in infant
and early childhood life-expectancy realized during the last nine decades were
primarily due to significant reductions in infant and early childhood deaths from
infectious disease and other causes.3,5,7,8,216,371 However, research suggests that
these declines may be occurring predominantly in white versus minority sub-
groups. Data published by Grossman et al302 demonstrates that while urban white
Page 30
infant mortality rates in the northwest Unites States declined between 1981 and
1990, the infant mortality rates of urban blacks and other minority groups rose
alarmingly during the same 10-year period. Alexander and colleagues404 recently
published a study which indicates that, similar to the trends seen with CAD
mortality among the urban poor, the increased infant mortality among the indigent
is probably due to certain environmentally-associated risks, and not due to risk
factors associated with race. The researchers examined the pregnancy outcomes of
married adult black, Filipino, or non-Hispanic white women who all were
residents of Hawaii, whose spouses were on active duty in the military, and who
had similar availability and access to comparable prenatal care and hospital
delivery services. Despite persistent ethnic differences in birth weight, no
significant ethnic differences were seen in neonatal or post-neonatal infant
mortality rates.
Race and Historical Changes in Human Life Expectancy Among Adults
The average life-expectancy of a 65-year old white male increased by only 3.39
years from 1900 to 1988 (lifespan, or the age at which he would expect to die
increased from 76.51 years to 79.9 years),3,7,8,216 with virtually no increase (0.39
years) in the decade between 1979 and 1988.216 The average life expectancy for a
65-year old black male has increased by only 3.02 years from 1900 to 1988 (from
75.38 years to 78.4 years); with virtually no increase (0.11 years) between 1979
and 1988.216 Average life expectancy data for blacks during this period is more
limited and was not consistently stratified by race, was combined into a broad
category as "all other," or in some cases was not even tabulated for blacks in
certain years prior to 1970.216
Since birth and one year life expectancies have increased markedly by 25.7 and
19.5 years respectively between 1900 and 1988, (24 and 17.4 years respectively
for white males; 32.4 and 22.7 years respectively for black males) and because
Page 31
most of these gains occurred between 1900 and 1959,216 which was prior to the
wide availability of antibiotics and vaccines, this gain probably reflects
improvements in pediatric care, reductions in childbirth mortality, and
improvements in infectious disease control rather than advancements in the
treatment of CAD. Because the current life expectancy of a black male is 7.4
years less than that of a white male at birth but differs only by 1.5 years at age
65,216 this suggests that early mortality from causes other than CAD (such as
higher infant mortality due to lack of prenatal care, prenatal drug, alcohol or
tobacco abuse, drug related childhood deaths, and increased adolescent deaths due
to urban violence) may also be compounding the factors resulting in shorter
lifespan among blacks.
A History of Pharmacologic Secondary Intervention Trials: Their Effect upon
Lifespan
The emphasis of traditional medicine has typically been upon secondary
prevention, which is the treatment of manifest coronary heart disease (CHD),
rather that upon primary prevention, which is the method of disease prevention
directed towards changing lifestyle or habits among presently healthy patients.
Within the last decade, however, this emphasis appears to be slowly changing.
Figure 12: Mortality in Secondary Prevention Trials
Trials With Objectives of Serum Cholesterol Reduction and Their Effect on Mortality
Treatment versus control all-cause mortality differences are not significant (p=ns)
_________________________________________________________
From: LaRosa JC. Cholesterol lowering, low cholesterol, and mortality. Am J Cardiol 1993;72:778
Page 32
Diagnosis and treatment of heart disease in the United States has significantly
improved during the last three decades. These advancements have led to
pharmaceutical and medical interventions which have demonstrated benefits when
they have been evaluated using disease-specific endpoints (i.e. coronary events,
cardiac death, progression of atherosclerosis) in secondary prevention trials when
disease is manifested [see Fig. 12].904 In patients without evidence of CHD,
however, pharmacologic treatment of established risk factors such as
hypertension, coronary atherosclerosis, or elevated blood cholesterol has not
significantly influenced CAD morbidity or mortality, 5,18,22,23,24,25,26,27,28,29,30,31,33,65,76,
77,78,92,93,94,98,99,100,101,902,903,905 and in some trials has even resulted in increased risk
of death or morbidity among patients receiving treatment versus those who
remained untreated, [see Fig. 13].74,75,76,77,78,98,906,908
Figure 13: Mortality in Primary Prevention Trials
Increased mortality from non-cardiovascular causes (NON-CVD);
All-cause mortality not significantly different between control and treatment groups (p=ns)
________________________________________________________________
From: LaRosa JC. Cholesterol lowering, low cholesterol, and mortality. Am J Cardiol 1993;72:778
There is no data which indicates that reduction, or eradication of CAD would
necessarily increase lifespan or life-expectancy. To the contrary, there is evidence
that another major degenerative or infectious disease might supplant CAD, if it
were eliminated, as the major cause of death. Most pharmacologic intervention
trials have not succeeded in extending lifespan, and many have only modified the
Page 33
ultimate cause of death (i.e. fatal arrythmia or cancer as a mortality end-point
versus infarction, stroke, or heart failure).5,74,75,76,77,78,98,99,349,677,908 The results of
these intervention trials may reflect the potential long-term toxicity of the
pharmacologic therapies which have been studied to date, and do not necessarily
exclude benefits that might be associated with newer classes of agents for CAD
risk factor reduction, or benefits which might be associated with aggressive
lifestyle and dietary interventions. In a secondary prevention trial of aggressive
lifestyle and dietary interventions by Ornish et al,909 41 patients with significant
CAD were followed for one year. Patients who were placed on an austere fat-
restricted diet, and who were enrolled in an exercise and stress modification
program experienced significant regressions of angiographically-evident coronary
atherosclerosis. This trial was too small and too short in duration to detect
significant differences in total mortality, but the results of larger and longer diet
and lifestyle trials have shown trends toward reduced all-cause mortality.
Life expectancy is not necessarily inversely proportionate to CAD mortality. It
is interesting that Sweden, Denmark, Canada, and the United States, which boast
some of the highest life expectancies, are among the countries with the highest
CAD mortality rates. Japan, France, and Italy are notable exceptions with low
CAD mortality rates and high life expectancies,62 although the Japanese have a
high incidence of hypertension,476 and hemorrhagic stroke, and the French have a
high incidence of smoking-associated cancers and alcoholic cirrhosis.
Some minimal gains in over-all mortality rates in the United States, and the
modest increase in life expectancy of an older adult over the last several decades
may have been due to significant reductions of in-hospital mortality (e.g. those
reductions resulting from new treatment approaches including coronary bypass
surgery, angioplasty, and thrombolysis) occurring within the last two decades
among patients suffering from acute myocardial infarction.33,72,73,99 Declines in
Page 34
CAD death rates within the United States, however, are primarily related to
prevention, or the reduction in the percentage of people who are at risk for
developing the disease.3,99,100,371 Clearly, changes in diet, exercise patterns, and
the reduction of smoking and stress are among the best methods of reducing this
risk. In fact, the disparate results in stroke and CAD mortality reduction in
numerous hypertension trials may be due to confounding factors which may be
reducing cardiovascular risk within the control groups of these studies. These
factors include a reduction in tobacco use,102,103 increased exercise, greater
potassium and anti-oxidant vitamin intake resulting from increased fruit and
vegetable consumption67,68,69,105,106 improved blood pressure control,183 resolution
of Type II diabetes80,115,253,271 (secondary to weight loss or dietary fat reduction),
reduction in dietary sodium intake,99,105,184,185,186,187,188,189 and improvements in
maternal health (the health of the mother is the most important determinant of
stroke risk among offspring).107 These improvements in cardiovascular morbidity
and mortality manifested by heterogeneous populations may not exist to the same
degree within specific sub-populations, and particularly those sub-groups largely
comprised of members of the lower socioeconomic class.
Primary Intervention and Human Lifespan
Although data from both primary and secondary intervention trials of
pharmacologic treatments (aimed at reducing known risk factors such as
hypertension or hyperlipidemia) are suggestive of reduced coronary events and
cardiac death [see Figures 12 and 13], neither have demonstrated consistent and
significant reductions in all-cause mortality,5,75,76,77,902,903,904 certain
pharmacologic primary prevention trials have demonstrated increased mortality
when performed in subjects without clinical manifestations of coronary artery
disease,5,14,18,65,75,76,77,348,904,906 and no trial has demonstrated an ability to increase
human lifespan. For these reasons, most researchers use improved quality of life,
Page 35
or various cardiac endpoints as markers of successful outcome in these trials.
In 1988, the United States Public Health Service estimated that the average
length of life for a male was 71.5 years, and for a female, 75.6 years.216 It is
interesting to note that Psalm 90, written between 1450 and 1410 BC, quotes a
similar statistic: "As for the days of our life, they contain 70 years, or if due to
strength, eighty years." The patriarchal statistician quoting the latter figures
however, probably did not adjust for early infant mortality.
Population Studies Which Examined Racial Differences in CAD
Surveys conducted in the United States in the first six decades of this century
(primarily from the rural South), in the Caribbean, and from the African medical
literature report an extremely low incidence of CAD, including morbidity and
mortality resulting from ischemic heart disease and coronary atherosclerotic
disease,44,416,419,420,421,422,425,427,428,429,430,431,433,434,438,439,440,441,443,444,445,446,450,451,817,954,95
5,956, thrombosis and myocardial
infarction,44,388,416,417,418,419,420,423,427,430,434,435,436,437,441,443,444,
445,446,451,456,953,955,958,959,960,961,962,963,964 and
angina,44,388,416,418,419,421,422,423,425,427,432,434,451, 953,955,958,959,960,961,962,963,964 in blacks as
compared to whites [see Table 2].
Table 2: Death Rate per Hundred Thousand from CAD
1940 and 1945
Year White Black
1940............................... 81.8 ............................ 34.6
1945................................ 106.5 .......................... 41.3
_______________________________________________________
Adapted from: Federal Security Agency, United States Public Health Service,
Office of Vital Statistics: Vital Statistics, in Special Report 1948;27:295.
In a study of rural Southern blacks published in 1924, Woody506 became one of
the first researchers to document a difference in the incidence of heart disease
Page 36
between blacks and whites. Brock and Bronte-Stewart spoke of "the remarkable
immunity of the [African] Bantu people to myocardial infarction,"444 and studies
conducted among rural Africans in the early decades of this century consistently
reported a lower incidence of CAD416,417,442,443,444,445,446 and hypertensive heart
disease in blacks as compared to whites.412,413,414,415,424,425,426 In 1927, Stone and
Vanzant434 concluded that the incidence of coronary atherosclerosis was between
two to four times more common among whites than among blacks, and in 1950,
Blanche and Handler427 in a pathological comparison of the coronary arteries of
47 black patients to white controls, reported "that coronary artery disease and
coronary thrombosis occur with considerable less frequency" in the black versus
the white population, and that the rate of development of coronary atherosclerosis
was slower in blacks than in whites by approximately a decade. Blanche and
Handler found evidence of coronary thrombosis in 16% to 23% of 1,961
necropsies performed upon whites, versus 1% to 2% of 2,963 necropsies
performed on blacks. In an analysis of the 1960-1962 Evans County, Georgia
heart study database, Bartel et al965 determined that electrocardiographic (ECG)
abnormalities were significantly less common among blacks as compared to
whites in this rural population study, and that abnormal ECG manifestations were
less predictive of the subsequent development or presence of CAD in blacks.
Hypertensive Heart Disease and Race
Many of these early researchers, however, noted that the incidence of
hypertension or hypertensive heart disease was more common among Eastern and
Southern American blacks and among American Virgin Island blacks than among
rural African blacks or among whites.411,413,419,424,425,426 In 1937, Nye811 reported
that blood pressures among Australian Aboriginals were characteristically normal
or subnormal by European standards, and a large study among native South
African blacks by Donnison415 showed that until the age of 40, blood pressures of
Page 37
native blacks and Europeans were similar, but between the ages of 40 and 60, the
average blood pressure of the native declined, whereas the pressure of the
European rose steadily. Saunders and Bancroft413 postulated that the difference
observed in the prevalence of hypertension between American Virgin Island
blacks and African blacks may have been due to the poorer diet of the American
Virgin Island black as compared to his African counterpart, citing the
unavailability of "agricultural products in any quantity," and that the general
Virgin Island diet was found to be "inadequate," with deficiency diseases
occurring on a relatively common basis. The researchers concluded that among
the study participants, "poverty, with its associated vitamin deficiencies, may tend
to raise blood pressure." Supporting these early observations of an association
between hypertension and reduced vegetable intake, Melby et al,931 in a study of
blood pressure and blood lipids among 167 black vegetarians, semi-vegetarians,
and non-vegetarians, found serum cholesterol levels to be 13% lower among
vegetarians than among non-vegetarians, and that the incidence of hypertension
among black vegetarians was half that of the non-vegetarians (16% versus 31.1%),
despite significantly greater use of antihypertensives among the non-vegetarians.
Urbanization, Migration, Race, and CAD Risk.
Kesilman411 in a study of 2,230 blacks, concluded that transplantation of blacks
from rural environments and the subsequent stress associated with urbanization
was responsible for disparate results seen among higher blood pressures of eastern
black males versus those recorded previously among primitive blacks, among rural
black agricultural workers, or among whites. In support of this hypothesis,
Kesilman cited statistics from the Metropolitan Life Insurance Company for 1936
which showed that the lowest mortality for cardiovascular-renal disease among
blacks occurred among agricultural workers, and the highest death rate occurred in
the densely populated urban centers. Similarly, Dahl941 stated in 1958 that
Page 38
hypertensive disease was rare among primitive populations, and Schwab and
Schulze hypothesized in 1932 that "stress and strain" incidental to urbanization
and "acculturation" were responsible for the development of hypertension among
urban blacks. Examining indexes of deprivation among 18,930 subjects living in
rural, small town, and urban areas in 1993, Reading et al940 concluded that there
was a "substantial disadvantage to living in urban areas compared with rural
areas". This disadvantage was the consequence of poorer health that resulted from
certain social or environmental factors which were unrelated to the subjects'
current level of material deprivation. The authors further concluded that "there is
a consistent association between increasingly urban environments and poorer
measures...of child and adult health."
In a report based on observations made in the early 1960s, Kuller957 determined
that sudden death in patients with atherosclerotic disease occurred less frequently
in black males than in whites, however studies of predominantly urban
populations in Nashville,966 New Orleans,967 and in South Carolina968 which were
published in the following two decades, reported higher rates of cardiac arrest in
blacks than in whites. A large urban population study by Becker and
associates,178 which examined 6,451 patients experiencing out-of-hospital cardiac
arrest between 1987 and 1988, found that blacks were at significantly higher risk
for cardiac arrest and sudden death than whites, and were significantly less likely
to survive the event. The survival rate of blacks was less than one third that of
whites, (p80% V
FIBER 19gr/d 33gr/d 11gr/d 19g/d
*A=animal V=vegetable; S= saturated
____________________________________________________________________________________________________________________
Adapted from: Connor et al538 de Lorgeril et al,270,534,850,970and Campbell et al.855
Total carbohydrate consumption, consisting almost exclusively of unprocessed
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complex carbohydrates and starches, was 75-80% of total calories. In contrast,
grains, fruits, and vegetables comprised approximately 50% of American daily caloric
intake between 1909 and 1913, when significantly more Americans lived in rural
areas. Paralleling swift trends in urbanization, grain, fruit, and vegetable
consumption fell to only 30% of daily caloric intake in the United States by 1959, and
remained approximately at that level through 1980.2 Currently, consumption of these
foods is increasing (primarily among the upper socioeconomic class).
It is interesting to note, however, that population groups such as the rural
Chinese and the Mexican Tarahumara Indians who consume diets high in
carbohydrate and low in fats generally have lower HDL cholesterol levels and
higher triglycerides than populations that eat diets high in saturated fat.538,742 In
several clinical studies, low fat diets were consistently associated with a mild
reduction of HDL cholesterol.549,891 This suggests that diets which lower LDL
cholesterol or increase its resistance to oxidation may be preferable to dietary,
lifestyle, or pharmacologic interventions which primarily increase plasma HDL
levels without reducing the potential for oxidative stress and the oxidation of
LDL.
There are numerous similarities between the rural Chinese diet, the Pacific Rim
diet of Japan,212,540,541 the rural Eastern European diet of Poland, Romania and
Yugoslavia,392 the diet of the Tarahumara Indians of Mexico,538 the diet of the
Ugandans of East Africa,539 and the Mediterranean diet of southern Italy, Greece,
Crete, and other Mediterranean islands.270 These diets are primarily based on the
liberal consumption of fruits, whole grains, vegetables, beans, cereals, legumes,
other complex carbohydrates, and dairy products with little use of red meat, and
moderate use of fish or poultry, and have consistently been associated with low
plasma cholesterol levels.476,855 According to Ansel Keys: "Fruits and vegetables
other than roots and tubers are much more prominent in the average diets in Italy
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and Greece than in those of Finland, the Netherlands, and the United States.526"
The greatest similarity is the fact that all six of these dietary regimens offer
significant protection against the risk of developing CAD in these
populations.212,269,270,392,476
Saturated Fat and Sugar Intake of Populations
Examining the increases in serum cholesterol associated with changes in the
United States civilian diet between 1909 and 1965, Khan attributed a significant
part of the historical increase in blood lipids to changes in diet which occurred
during this period, which included a 5% increase in meat consumption, a 132%
increase in poultry consumption, a 7% increase in egg consumption, and a 34%
increase in dairy product consumption (excluding butter). 36 The author stated that
"beef in 1909 was leaner than the average beef referred to in the current handbook
of nutrient values." Examining the relationship between diet and CAD mortality
in Europe, Lopez-S and associates similarly noted increases in animal fat
consumption between 1934 and 1959, stating that the profile of the high risk
coronary patient involves, (in addition to hypertension, obesity, and elevated
blood lipids), "the luxurious consumption of high fat foods rich in cholesterol,
reduced exercise and activity patterns, and certain psychological and emotional
stresses associated with continued striving for success." 376 These authors further
stated that increases in CAD morbidity and mortality observed
during the twenty-five year period were manifested to a greater degree in
technically advanced countries, and may be "the price of affluence and
advancement."
Armstrong and associates61 examined the effect of certain dietary practices on
CAD mortality in England and Wales from 1950 to 1967 and compared these
results to those of thirty other countries. These authors found that total green
vegetable consumption consistently was inversely correlated with CAD mortality
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in both men and women. Per capita sugar (refined carbohydrate) consumption
however was directly proportional to the incidence of CAD in England and Wales
and in the 30 country comparison populations [see Fig. 15]. This may be due in
part to the effect of hyperglycemia on increased lipoprotein oxidation, 823,834,835,836
increases in plasma triglycerides,742 and decreases in plasma HDL cholesterol that
may accompany high carbohydrate diets,742 and the lack of sufficient antioxidant
vitamins and other nutrients in these urban diets due to processing and refining.
Figure 15: Incidence of CAD in Males and Females Plotted Against
Sugar Consumption in 30 Countries.
____________________________________________________
From: Amrstrong et al.61
Several other researchers518,519,520 previously noted a strong association between
increased consumption of sugar and refined carbohydrates and the increased
consumption of saturated fats in study populations. In his review of research
related to CAD risk factors in twenty countries, Stamler35 cited sociocultural,
dietary, and lifestyle factors and argued against a population genetic susceptibility
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in the etiology of CAD.
Figure 16: Per Capita Calories Available From Principal Animal Sources
and Age-Standardized CAD Mortality For 20 Countries in 1973.
________________________________________________________________________________________
From: Stamler35
Stamler stated that per capita saturated fat and cholesterol consumption (Dairy,
eggs, meat and poultry consumption as a percent of total calories consumed) was
directly proportional to CAD mortality per 100,000 in 20 countries [see Fig. 16].
Artaud-Wild and associates476 examined milk intake (in addition to saturated fat
and cholesterol intake) in 40 countries to explain the French and Finnish
deviations from expected CAD mortality rates and postulated that higher milk and
butterfat consumption in Finland and greater vegetable consumption in France
may be the cause of the apparent paradox [see Fig. 17]. Similarly, Turpeinen532
documented a correlation between dairy fat consumption and CAD mortality rates
for 22 industrialized countries, and Renaud and de Lorgeril533,534 found a strong
correlation between CAD mortality rates and the consumption of dairy fat
(excluding fat from cheese) in 19 countries. Interestingly, Renaud and de Lorgeril
found no increased risk of CAD associated with cheese consumption, and this was
similar to the earlier finding of Ansel Keys in his pioneering Seven countries
Study,522,526,527,534,546 and to the subsequent findings of the Adventist Health Study,
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which showed that the highest tertile of cheese intake (3 times per week or greater)
among a cohort of 26,473 non-diabetic white men and women was associated with
a decreased risk (p=ns) of fatal coronary events.851,891
Figure 17: Death Rate from CAD Correlated With Daily Dietary Intake of
Saturated Fat/Cholesterol and Milk Products in 40 Countries, 1976-1978.
__________________________________________________________________________________
From: Artaud-Wild et al.476
Both de Lorgeril and Keys postulated that the fermentation process of cheese, and
possibly other fermented milk products, may modify and render the milk fat less
bioavailable.534
Joossems and colleagues535 found significantly higher CAD mortality in
northern Belgium than in southern Belgium. These researchers noted that butterfat
consumption was far greater in northern Belgium. Even France has a contrasting
pattern of cultures regarding diet. Butterfat consumption is high in the north
where the incidence of CAD is higher.533
Monounsaturated fat
In southern France, which enjoys low CAD incidence rates, olive oil is the
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primary dietary fat.536 It is noteworthy that in the Seven Countries Study, Keys
and colleagues546 demonstrated that the CAD death rate was inversely
proportional to the percentage of dietary calories derived from monounsaturated
fats such as olive oil. Barradas et al895 fed 21 healthy volunteers 21g of olive oil
daily for eight weeks and found a pronounced decrease in platelet aggregation
when platelet rich plasma and whole blood samples of these volunteers were
stimulated by adenosine diphosphate (ADP) or adrenalin, which suggests a
protective effect of olive oil during conditions of stress. In metabolic studies,
monounsaturated fatty acids possess a beneficial low density lipoprotein-lowering
effect without significantly lowering desirable high density lipoprotein
cholesterol levels,476,547,548,549,550,742,891 and in-vitro studies have demonstrated that
diets rich in monounsaturated fatty acids reduce the oxidation of LDL
cholesterol.742,891
The associations noted in these population studies are complex and must be
interpreted with care. Many of these population cohorts are and have traditionally
been industrialized and highly urbanized in their demographics, and Westernized
in their dietary practices. Others are less urbanized and are predominantly rural in
demographics. Interestingly, Armstrong and associates presented an example
which emphasizes the need for interpretive caution when dealing with
demographics of large populations. These authors noted a strong association
"between ischemic heart disease mortality and the number of telephones in a
population, which in turn is related to dietary saturated fat..." 61
Addressing epidemiological studies linking CAD to sugar consumption,
Keys522,523,524 noted that dietary sucrose is probably not a major factor for the
development of CAD because the association between dietary fat and CAD is not
markedly reduced when controlling for sucrose intake. However, Antar and
coworkers,277 examining dietary changes between 1889 and 1961 in relation to the
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incidence of CAD, found the principal change to be decreased consumption of
total carbohydrates with a greater progressive decline in the intake of complex
carbohydrates and a concurrent increase in refined simple sugars. A subsequent
analysis of this and other data by Armstrong et al61 noted that the
hypocholesterolemic properties of fiber in unrefined complex carbohydrates may
be partially responsible for the strong negative association between increased
complex carbohydrate consumption in selected populations and CAD. The lack
of fiber, vitamins, and antioxidants in a refined high carbohydrate diet, however,
might result in adverse lipid changes including decreases of serum HDL and
increases in plasma triglycerides, and the hyperglycemic effect of refined sugars in
conjunction with a low-fiber diet may increase susceptibility of LDL to
oxidation.834,835,836 Artaud Wild and co-workers,476 in their epidemiologic study
of CAD mortality in 40 countries, similarly suggested that soluble fiber, as well as
saponins and antioxidants, might be the factors present in unrefined complex
carbohydrates and other natural antioxidant compounds which confer a CAD-
protective effect through their inherent hypocholesterolemic properties and by the
prevention of LDL oxidation.. Both the Boston Irish Diet Heart Study554 and the
Western Electric Company Study205 demonstrated that certain components of, or
dietary properties common to vegetables which were not related to their effects on
serum cholesterol, were associated with reduced CAD risk.891 Antar and
associates277 suggested that a 75% reduction in apple consumption over the 70-
year period of their study may have been partially responsible for the increase in
CAD mortality due to a loss of dietary pectin, a significant source of soluble
dietary fiber. Additionally, these authors cited previous scholarship demonstrating
that ingestion of large quantities of sugar increased serum lipids, and that high
intakes of starch and grain products had the opposite effect.355,356,357 These effects
may be due to the differential effect of fiber versus dietary sucrose on insulin
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sensitivity.
Slattery and coworkers2 examined trends in CAD mortality and food
consumption in the United States between 1909 and 1980, and found that national
dietary changes preceded CAD mortality changes in the American population by
10 to 20 years. These authors further noted that in the years between 1909 and
1913, three times more calories were consumed in the form of grain products
(38% of total calories) than calories consumed of animal products (12% of total
calories). By 1957 through 1959, the consumption of grain products and animal
products (meat, poultry, fish) were equal, with each supplying approximately 20%
of calories. Consumption of fats and oils increased from 12% of calories in 1909-
1913 to 17% of calories in 1957-1959. By the mid 1960s, consumption of meat
products and dairy products began to decline, and by 1975, the consumption of
grain products began to increase.
There has been one consistent theme in each of the major population studies
(especially those conducted prior to 1960) which have been reviewed: As the
standard of living of these study populations increased, a concomitant increase in
the consumption of animal fat and refined carbohydrates and a reduction in the
consumption of complex carbohydrates generally occurred, with increases in CAD
mortality following shortly thereafter.
VI. Physiology and CAD Risk
Resting Heart Rate, Blood Pressure, Vasospasm, Left Ventricular Mass and
Function, Platelet Aggregation, Plasma Fibrinogen, and Serum
Catecholamines and Their Relationship to Stress, Diet, Smoking, Exercise,
and SES.
The revolutionary fields of neurobiology and neurocardiology seek to define the
complex manner in which the brain communicates with the heart and various other
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organs of the body, and how the brain plays an active role in physical
disease.10,225,494,761 The physiological effects of the brain's interaction with the
sympathoadrenal and pituitary-adrenal response systems, include effects on heart
rate, blood pressure, hemostasis, vascular reactivity, left ventricular mass, immune
function, and possibly atherogenesis.10,225,351,492,494,496,699,701,709,734,740
Heart Rate and CAD Risk
The effects of acute and chronic stress on heart rate are well
documented.10,225,493,736,740 Elevated heart rate may be an independent risk factor
for cardiovascular death, especially in persons with hypertension. 110 Numerous
epidemiologic studies have demonstrated that elevated resting heart rate is
associated with increased incidence of CAD and death from all causes, and a
recent analysis of the Framingham database of 5,209 men and women followed for
36 years has supported this negative association of increased heart rate with
cardiovascular mortality and death from all causes.110
Exercise and CAD Risk
Over 66% of the approximately 2 million Americans who died in 1986 were
reported to have exercised rarely,214 and this lack of aerobic exercise may be
responsible, in part, for elevated resting heart rates frequently seen among the
sedentary. Physical training and regular exercise, which is more prevalent among
members of upper socioeconomic groups, has been shown to reduce levels of
plasma fibrinogen, (an essential protein for the clotting of blood), 719 and resting
heart rate and blood pressure,253,259 and these reductions may be associated with
beneficial changes in plasma lipids,3,111 a reduction in the incidence of
atherosclerosis,225, 239 and reduced CAD risk.3,111,225,724 Research conducted with
50 sedentary hypertensive men259 suggested that regular aerobic exercise may be
as effective as drug therapy in controlling mild hypertension. A recent study by
Massie260 indicated that the higher the baseline blood pressure and hypertension,
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the greater the likelihood that exercise would be effective in reducing blood
pressure.
Fibrinogen Levels, Platelet Aggregation and CAD Risk
French researchers de Lorgeril and Renaud872 reported that numerous hemostatic
factors including fibrinogen, factor VII, leukocytes and platelets have been
demonstrated by epidemiology to be closely related to thrombosis and acute
coronary events. Kimura and colleagues610 demonstrated that smoking was
associated with significant (p240mg/dL) showed no significant differences in
all-cause mortality. In both men and women, cholesterol levels below 160mg/dL
were associated with increased mortality from all causes, including multiple-site
cancers, hemorrhagic stroke, COPD, chronic liver disease, and death by violence,
[see Fig. 28].5 In a study of a representative sample of the U.S. population, low
cholesterol levels were strongly associated with non-cardiovascular mortality in
people aged >70 years,5,911 and two studies have indicated that this relationship is
strongest among people of low SES, and among those who are sedentary, and
abuse alcohol or tobacco.911,912
Figure 28: Relative Risk of Total Mortality Plotted Against Total Cholesterol
Page 118
A Pooled Population Study
______________________________________________________________
From: LaRosa5
The increase in cancer and all-cause mortality seen in meta-analyses of primary
prevention trials is largely due to the negative results of the World Health
Organization trial of clofibrate,5,908 and to the mildly negative or neutral results of
other pharmaceutical trials, rather than due to any adverse effect associated with
dietary and lifestyle interventions.
Hypercholesterolemia is prevalent in urbanized, high-income countries, and less
common in Third World countries.279 People in developed countries tend to
consume significantly more dietary saturated animal fat than do people in third
world countries whose fat consumption is typically half of the amount consumed
in the United States.442 It has been demonstrated that in Third World urban areas
of increasing affluence, lower levels of HDL cholesterol and higher levels of
atherogenic LDL cholesterol are found. In third World countries which are
undergoing rapid development and urbanization, such as Malaysia, CAD mortality
is rapidly accelerating as tobacco use is increasing, and the average Malaysian
urban diet is incorporating increased amounts of fat.279
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Research by Wilder et al,852 which was conducted among 912 urban residents of
lower-income, inner-city Baltimore, showed that there was a significant trend
(p70 3.2 3.1 0.92
___________________________________________________________________________________________________
From: Wilder et al852
Evidence based on actual dietary intake from a compilation of 171 clinical and
epidemiologic studies suggests that consumption of total dietary fat has decreased
in the United States between 1950 and 1984,853 however, between 1960 and 1971,
blacks appeared to have increased their consumption of fat, which was
accompanied by a 322% increased mortality from prostate cancer in addition to
significant increases in cardiovascular mortality among blacks during this
period.854
Changes in Carbohydrate Consumption.
Antar and associates277 reviewed data for per capita food supplies in the United
States between 1889 and 1961, and concluded that two significant changes had
occurred in the American diet over the previous seventy years. There were slight
increases in the consumption of dietary fat, including saturated fat from both
animal sources and hydrogenated oils, and significant decreases in the
consumption of complex carbohydrates and starches such as cereal grains, apples,
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potatoes, and whole grain flours which were replaced by increased consumption of
heavily processed simple sugars and syrups. The authors noted an increase in
animal sources of protein in the last decade of their study (1951-1961), and a
decrease in vegetable sources of protein. They concluded that changes in
carbohydrate consumption may have been a contributing factor to the increase of
ischemic heart disease in America. Lopez-S, et al,376 similarly noted an increase in
consumption of simple carbohydrate with a concurrent decrease in the
consumption of complex carbohydrates in a study of European food consumption
between 1934 and 1959.
Subsequent research has shown that ingestion of large amounts of refined simple
sugar is associated with increases in all major fractions of serum lipids, while
intake of complex carbohydrates, grain products, and starches have the opposite
effect, possibly due to different fiber contents of the dietary regimens. 277,355,356,357
The indigent, and specifically the urban poor, consume significantly more refined
sugars and carbohydrates than do the affluent.
Trans-fats and Hydrogenated Oils.
Prior to 1990, there was a dearth of reports in the clinical literature on the
pathophysiologic effects of trans-fatty acids in the human diet. Trans-fatty acids
are created by the hydrogenation of vegetable oils. They are also formed naturally
in the rumen of cattle and comprise approximately 5% of dairy and beef fat.306,915
The seminal article by Mensink and Katan907 suggested deleterious effects upon
both HDL and LDL cholesterol subfractions in healthy subjects consuming diets
containing 10% of energy as trans-fat. Similarly, the research of Zock and
Katan,916 showed that a diet containing 7.7% of energy as trans-fat increased LDL
and decreased HDL cholesterol even when compared to a diet containing saturated
fat.916,306 Additionally, the consumption of hydrogenated oils and trans-fatty acids
has been associated with increased incidences of chronic degenerative diseases,
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including CAD306 and cancer.604
Hydrogenated oils are created by the bubbling of hydrogen gas through liquid
vegetable oil, adding hydrogen atoms to the double chemical bonds of these
unsaturated fats, and causing them to act like a saturated fat, solidifying at room
temperature. This process increases the shelf-life of the oil, and of the food
products made with the oil. Trans-fatty acids, mostly derived from the full or
partial hydrogenation of vegetable oils and supplied primarily in the form of
margarine, constituted about 6% of the dietary fat in the average American diet in
1985, and considerably more in the diets of individuals who consume large
quantities of fried foods, margarine, cookies, crackers, white breads and
pastries.307 Margarine is one of the primary sources of trans-fat in the human diet,
and recent U. S. Department of agriculture statistics show that margarine is now
the leading contributor of total fat in the American diet, and may currently
account for over 7% of all dietary fat consumed in the United States.560,603 The
trans-fatty acid content of typical margarines sold in the United States is high, and
ranges from 10 to 30% of total fat content, however levels as high as 60% have
been reported.306 The consumption of trans-fats increased progressively in the
United States in the first half of this century and paralleled the increases in CAD
observed during this period, however consumption has remained relatively stable
at around 6-7% of total dietary fat consumption in the past few decades. Increased
consumption of trans-fats, however, is associated with lower levels of education,
and with lower SES,306 which may contribute to the increased risk of CAD, and
acute cardiovascular events associated with the indigent.
Trans-fat consumption has been associated with increases in atherogenic low
density lipoprotein, decreases in protective high density lipoprotein, adverse
effects upon hemostatic factors including increases in platelet aggregation, and
decreases in the normal production of prostaglandins, which act as free radical
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scavengers, and regulate the blood clotting process.306,307,603,907,916 Theoretically,
trans-fats could precipitate acute coronary events by accelerating the
atherosclerotic process through adverse lipid effects, while simultaneously
increasing the potential for thrombosis through adverse effects on prostaglandins
and platelet aggregation. In fact, trans-fats have been associated with an increased
risk of acute coronary events in at least one major clinical study. In a recent study
of 521 people by Ascherio and co-workers,306 it was determined that 239 patients
who recently had suffered a myocardial infarction were significantly more likely
to have consumed greater amounts of trans-fatty acids (in the form of partially
hydrogenated vegetable oils or margarines) than the 282 healthy control subjects.
In addition to acute events, trans-fats have also been associated with chronic CHD.
A British case-control study by Thomas et al918 determined that persons dying of
CHD had a higher proportion of trans-fatty acids (in this population largely
derived from the partial hydrogenation of marine oils rather than vegetable oils) in
their adipose tissue than did persons who died from other causes. Willett,
Stampfer, and co-workers917 found an increased risk of CHD which was associated
with increased trans-fatty acid intake in a large prospective study of women.
Trans-fats have also been associated with other degenerative, free radical-
mediated diseases. Australian researchers found that melanoma patients
consumed twice the amount of hydrogenated polyunsaturated fats as compared to
healthy controls.604
Exposure to dietary trans-fatty acids is "almost universal" in industrialized
countries.306 Because the indigent in the United States tend to consume more fried
foods, margarine, crackers, pastries, french fries, and other refined and highly-
processed baked-goods (which frequently contain more that 10% of their total fat
as trans-fat306) than do the affluent, they have a higher per-capita consumption of
the artificially produced trans-fats. Because members of lower SES tend to
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consume more animal fat from beef and dairy sources, the American poor also
have a higher per-capita consumption of naturally occurring trans-fats. These
combined factors may increase the risk for acute and chronic coronary events
among the indigent.
Polyunsaturated Fats and Oils.
Although polyunsaturated fatty acids (PUFAs) have been associated with
decreases in blood cholesterol, research has demonstrated that the non-linolenic
acid members of this class of fatty acids can produce an increase in platelet
aggregation,859,970 PUFAs serve as a major source of lipid peroxides which may
accelerate the pathological oxidative modification of lipoproteins. 970
Obesity and Dietary Fat Consumption
Obesity is clearly and significantly related to dietary fat consumption, and is
caused by an imbalance between calories consumed and calories expended
through metabolic or physical activity.3, 115, 253, 294 Because foods which are high in
fat supply as much as 2.25 times as many calories per ounce,3 less of these foods
need to be consumed to reach an imbalance between caloric intake and
expenditure. Furthermore, 27% of the calories contained in carbohydrates are
used and lost in the metabolic process of digestion and assimilation, whereas only
3-6% of fat calories are similarly required for internal processing. Americans
consume as much as 40% of their dietary intake in the form of fats,602,855 and it is
not surprising that the incidence of obesity among adults in the United States is
high: Approximately 19% of men and 28% of women are considered
overweight.294
Obesity, Race, SES and Mortality
Some data suggests that obesity may predispose individuals to lower
socioeconomic status and increase the risk of developing hypertension and
diabetes-related CAD. Gortmaker and co-workers332 found that obese young
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women were less likely to marry, had lower incomes, and had less education than
non-obese women, and that obese young men were less likely to marry than non-
obese men of the same age. In two studies of almost 70,000 women, Rimm and
associates demonstrated a strong association between low SES and obesity.264,265
The Charleston Heart Study266 examined the influence of obesity on mortality, and
found that it was predictive of all cause and CAD mortality in black men, but not
in white men.
Weight reduction had the greatest effect, and was more effective than dietary
sodium reduction or stress management in a study which examined lifestyle and
dietary modifications, and their effect on blood pressure. Sodium restriction and
stress management were of intermediate effect and were more effective than
calcium, magnesium, potassium or fish oil supplementation. 913
The First National Health and Nutrition Examination Survey demonstrated that
black women had age-adjusted weights which were 9 to 16 pounds higher than
those of white women, regardless of SES.4 That this racial predisposition to
obesity is probably environmental rather than genetic is validated by two studies
by Garn et al,267,268 which found that girls in low SES (predominantly black)
families are similar to, or slightly less obese than female children in high income
families, however low SES women are more likely to be obese after adolescence
than their high-income counterparts.
Obesity has not consistently been associated with increased risk of death from
CAD or all-cause mortality in several clinical studies. This has often confounded
the results, especially when these studies were structured to determine excess
mortality among the obese. Epidemiologists examining the data from the Harvard
Alumni Health Study181 have determined that cigarette smokers tended to be
thinner and less healthy than non-smokers. The death rate among smokers was
elevated in both the very thin and the very heavy. Among non-smokers, however,
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increased risk of death was directly associated with increased body weight. Low
SES blacks tend to be more obese than affluent blacks, and the indigent tend to be
more obese than the wealthy, regardless of race.
Diabetes, Fat Consumption and SES
Epidemiologic Studies and Diabetes
The incidence of adult onset, non insulin-dependent diabetes mellitus (NIDDM),
a significant independent risk factor for CAD, is greatest among members of
lower socioeconomic groups,42,383 who tend to be more obese.383 Similar to
observations concerning the association of CAD and SES, the association of
diabetes and low SES has not always remained constant. Interestingly, Grover407
noted in a 1948 public health report that mortality per 100,000 from diabetes
mellitus was from 55 to 120% higher among whites than among non-whites
between the years 1919 and 1941. This risk factor shift may reflect the greater
consumption of dietary fat, sedentary lifestyles, and greater tendency toward
obesity among whites versus blacks during this period. In support of this
hypothesis, Kesilman411 noted that obesity was a rarity among 2,230 American
black males examined between 1937 and 1941, and numerous researchers have
documented the infrequent occurrence of diabetes among rural African blacks who
consume little dietary fat, and are rarely sedentary or obese.812,813,814
Recently, Grossman et al302 found that the ten-year adjusted death rate from
diabetes was almost four times higher among urban blacks than among urban
whites, and Knapp et al42 reported in 1985 that low SES Mexican-Americans have
a greater prevalence of diabetes than whites. Kelley and co-workers383 reported in
1993 that diabetic patients from the socially and economically deprived inner city
were less likely to use insulin, had a shorter duration of diabetes, were older and
tended to live alone, and were more likely to smoke and to have cardiovascular
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disease than were patients from more prosperous areas.
Pathophysiology and Prevention of Diabetes.
Diabetes is one of the major risk factors for the development of CAD, and
significantly increases the risk of CAD morbidity and mortality. 14,17,21,32,34,80,81,82
Diabetes causes metabolic, hemostatic, coagulation and lipid abnormalities, and
has been associated with increased plasma fibrinogen.729 Adult onset (Type II)
diabetes is characterized by insulin resistance of the body's cells due to increased
body fat. Approximately 90% of U.S. adults with adult-onset diabetes are
obese,253,279 and between 50 and 80% of Type-II diabetes, and 30% of diabetes
deaths are estimated to be preventable by control of obesity.115
Diabetes and Diet.
Recent research has determined that the amount of fat a person consumes is
directly proportional to the risk of developing adult-onset diabetes. In a three-
year study of 123 non-diabetic patients with impaired glucose tolerance,271
researchers determined that study participants who subsequently developed
diabetes had the highest mean consumption of fat (43.4% of total calories). Those
individuals who remained glucose intolerant but did not develop diabetes
consumed an intermediate amount of fat, and those who converted to normal
glucose tolerance consumed the least fat. Because adult-onset diabetes is more
prevalent among obese individuals, dietary counseling is the foundation of
diabetes treatment.80,279 The presence of abdominal fat (expressed as high waist-
to-hip ratios) is predictive of the subsequent development of diabetes. 52,253 The
use of weight control, reduced saturated fat intake, increased consumption of
complex carbohydrates, increased consumption of fiber, and the even distribution
of daily caloric intake (through multiple small meals) are effective methods of risk
reduction in diabetics.
Dietary antioxidants may be beneficial in the treatment of Type I and Type II
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diabetes, because oxygen free radicals have been implicated in the pathogenesis of
the disease.486 Furthermore, tissue antioxidant status may be compromised under
conditions of dietary restriction for weight loss,486 (frequently recommended in the
treatment of diabetes), and dietary supplementation may address this deficit. It is
important to note that iron overload may promote diabetes by increasing
production of free radicals, and vitamin C may enhance iron absorption in patients
with high iron intakes (especially from animal sources), thereby potentially acting
as a pro-oxidant in diabetics with a positive blood iron balance.668
Pancreatic beta cells, which are responsible for the production of insulin, are
vulnerable to destruction by free radicals generated by the body's own immune
system in Type I diabetes. Antioxidants have proven effective in preventing
diabetes in animal models subjected to active oxygen species,485 however
controversy exists concerning the risk of vitamin E supplementation in
autoimmune disorders including Type I (Juvenile Onset) diabetes and lupus
because of the immune-enhancing properties of the vitamin.668
Pediatric Nutrition Education Efforts, Obesity, and Diabetes.
The best hope for prevention of obesity and its associated diseases is through
programs of nutritional education directed toward school children, teenagers and
mothers which emphasize dietary counseling for reduction of fat and total caloric
intake, good dietary sources of antioxidants and fiber (including fresh fruits and
vegetables), and a program of regular physical exercise.294 These programs are of
urgent necessity among the indigent who are at greater risk of pediatric and adult
obesity, and of adult-onset diabetes.
Dietary Fiber Consumption, Socioeconomic Status and CAD risk.
Fiber is provided exclusively by vegetable sources, and is well known to lower
serum cholesterol without changing serum triglycerides or HDL cholesterol. 891
Fiber is not found in fats, sugars, meat, fish, milk or dairy products, and in most
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beverages. The foods highest in fiber are complex carbohydrates, and include
unprocessed whole grains, wheat bran, brown rice, legumes, seeds and nuts, and
fruits and vegetables.247,294 Most edible plants contain large amounts of vitamins
and minerals, and are also are an excellent source of pectins, gums and soluble
fibers which have all been shown to lower serum cholesterol,226,294,875,877,891
prevent CAD,875,878 hypertension,875,879 certain forms of cancer,875,880,881
gastrointestinal disorders,875,882 diabetes,875,883 and aid in weight loss.668,875,880
Dietary fiber is the structural part of plant foods, and includes polysaccharides
(cellulose, hemicellulose, pectin, mucilage and gums from vegetables and fruits),
and lignin (from fruits with seeds, and grains) that are not able to be digested by
enzymes within the human gastrointestinal tract. Dietary fiber is divided into two
basic classifications (soluble and insoluble) based on hydrophilicity and solubility.
Soluble fiber, consisting of pectins, mucilages and gums, dissolves and thickens
in water forming a hydrophilic gel. These fibers are found in a variety of whole
grains, legumes, the pulp and rind of fruits, seeds, and in seaweed. Soluble
pectins, mucilages and gums chelate, or bind with, intestinal bile acids and steroid
materials. This chelating effect is responsible for the reduction of blood
cholesterol by preventing the intestinal absorption of bile acids and steroid
materials, the building blocks of cholesterol.278,294 Soluble fiber also keeps blood
glucose levels more constant, and may be especially beneficial in diabetes by
providing tight glycemic control, and reducing the post-prandial insulin demand.
By forming a gel in the gastrointestinal tract, soluble fiber slows and modulates
the absorption of nutrients into the bloodstream, avoiding hyperglycemic
elevations, and hypoglycemic troughs in blood glucose levels. 226
Insoluble fiber, often called roughage, consists of cellulose, hemicellulose and
lignin. It is supplied by the woody, structural parts of plants including fruit and
vegetable skins, seeds, husks, hulls, and bran--most of which are typically
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removed by the modern process of refining. The bulking effect that the insoluble
fibers have on the stool allows more water to be drawn in to dilute the toxic
contents of the stool, and speeds transit time through the gastrointestinal
tract.247,294 This increased motility may also decrease the absorption of fats
contained within the gastrointestinal contents, and may reduce the amount of bile
salt acids which are potentially reabsorbed in the small intestine, ultimately
reducing blood cholesterol levels. Additionally, speeding intestinal transit may
limit exposure of the intestinal wall to toxic or carcinogenic compounds in the
stool, reducing the risk of colon cancer, diverticular disease, and irritable bowel
syndrome.875 Both soluble and insoluble fiber may have value in weight control
by adding bulk to the meal and enhancing feelings of post-prandial satiety.226
Phytosterols, Tocotrienols and their Association with Fiber and Serum Cholesterol
Extraction and processing of fiber from plant products to create a concentrated
fiber supplement may not provide the same degree of hypocholesterolemic benefit
that may be received from the consumption of the whole food. Plants are
nutritionally dense complex carbohydrates which supply other substances in
addition to fiber which can also effect serum cholesterol levels. These substances
include phytosterols and tocotrienols. Phytosterols are plant sterols which have
the ability to limit absorption of both endogenous and exogenous cholesterol, and
subsequently lower serum cholesterol in moderate doses.891 Sources of
phytosterols include seeds, nuts, whole wheat, corn, soybeans, and many vegetable
oils. Soy protein is rich in nonsteroidal estrogens, or phytoestrogens of the
isoflavone class, which suppress tumor growth in vitro and may be partly
responsible for the low breast cancer incidence among Chinese and Japanese
women who have a high soy intake.900
Tocotrienols are chemically related to tocopherol, or vitamin E. These
substances have been shown to have 3-hydroxy-3-methylglutaryl coenzyme A
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(HMG co-A) reductase inhibition activity, and subsequently lower serum
cholesterol.891 Tocotrienols are found in cereal seeds and palm oil, however the
saturated C16 palmitic acid found in palm oil may antagonize the
hypocholesterolemic effects of the tocotrienols supplied by the oil.
Epidemiological and Clinical Studies.
As early as 1961, Antar and associates277 postulated that significant reductions
in the consumption of whole flour and grains, an important source of fiber,
between 1889 and 1961 may have been a factor in the CAD increases during this
same period. These researchers also theorized that the four-fold decrease of apple
consumption during this seventy-year period, and the concomitant increase in
citrus consumption may also have been partially responsible for CAD increases
during this period since dietary pectin is found in the flesh of the apple, but only in
the uneaten rind of citrus fruit. In 1962, Adelson and Keys355 found that men with
high levels of serum cholesterol had statistically significantly lower intakes of
grain products, than did men with lower levels of serum lipids, and in the early
1970s, Burkitt and Trowell876 linked low intake of dietary fiber with several
Western diseases.
People in developed countries tend to consume significantly less dietary fiber
(about 10-20 grams per day) than do people in third world countries who typically
consume 30 to 50 grams of fiber daily.247,442 The current recommended dietary
fiber intake for healthy American adults is 20 to 35 g/d,875 however average
consumption in the United States is about 11 grams per day. Among the American
poor, consumption is even less.
Epidemiologic studies by two groups of British clinicians in the early 1970s
demonstrated that rural Africans with high fiber intakes had lower incidences of
numerous chronic degenerative diseases including CAD, obesity, diabetes,
diverticulitis, irritable colon, hiatus hernia, hemorrhoids, colon cancer, gallstones,
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and dental caries.304,305 Similarly, epidemiologic studies of rural Africans in the
early decades of this century demonstrated that diabetes, gallstones, peptic ulcer
disease, kidney stones, endocrine disorders of the pituitary and thyroid, and
prostatic hypertrophy were a rarity among these population groups. 812,813,814,815
These degenerative diseases are endemic to urbanized societies which tend to
consume less fiber, and they are frequently associated with increasing affluence
[See Table 5]. It is difficult, however, to isolate the effect of fiber alone since
most people who consume less fiber may also consume more calories from fat;
exercise less; consume fewer dietary sources of antioxidant vitamins (including
beta carotene, vitamin E, and vitamin C); consume less protective vegetable
substances (including phytoestrogens, phytochemicals, flavonoids, isoflavones,
phytosterols, tocotrienols and arginine); and may be more likely to smoke, and be
of lower SES.306,900
Dietary fiber may confer additional benefits in the reduction of CAD risk.
Recent evidence suggests that vegetarians and individuals with high fiber intakes
are less likely to be hypertensive than those individuals who have low-fiber
intakes,303 possibly because high-fiber foods are an excellent source of potassium.
Short-term studies utilizing high-fiber diets have shown beneficial reductions in
post-prandial glucose, serum cholesterol, and insulin requirements in persons with
Type II (adult onset) diabetes.294 Extreme excesses in fiber consumption,
however, can lead to decreased absorption of minerals including calcium, zinc,
iron, copper, magnesium, and chromium.247,668
Prevalence of Smoking, Attitudes to Smoking, and the Access to Tobacco
Products by Adolescents.
Smoking is clearly related to heart disease, and cessation of smoking may have a
greater effect in reducing the long-term risk of CAD than changes in any other risk
factor,496 with the possible exception of diet.5,914 Smoking may increase exposure
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to psychological stress by increasing a smoker's tolerance of a stressor, 496,790 and
may interact synergistically with psychological stress to increase CAD
risk.496,786,787 Smoking has been described as a habit as addictive as the use of
heroin or cocaine,223, 295 is well recognized to have a marked negative impact on
life expectancy, may double the risk for CAD morbidity and mortality after
controlling for all other known risk factors,496 is the single greatest cause of death
in the United States,115 and is significantly more prevalent among blacks,497 the
young,497 the poor,497 individuals with limited control over their jobs or lives,709
and those reporting higher levels of stress.496,497 Because blacks tend to be
concentrated at the lower end of the socioeconomic spectrum and frequently report
experiencing more life stress than whites, they are significantly more likely to
report being a smoker than are whites. Stress differences, however, are more
potent than race in determining smoking status.497
Historical Background of Smoking.
The deleterious effects of smoking may take as long as 20 to 35 years after
smoking initiation to manifest as chronic degenerative disease.343,344,345 The use of
tobacco products in the United States remained relatively low for the first four
decades of this century, however at the onset the second World War, cigarette use
increased dramatically from about 2,000 per annum in 1940 to almost 3,500
cigarettes per adult smoker per year by 1945.296 This phenomena, which occurred
predominantly among men, was undoubtedly due to the inclusion of four packs of
cigarettes in each of the military field rations, or K-rations, which were distributed
to American GIs during World War II,337,475 and certainly was responsible in part
for the dramatic increases in CAD among American males following the war.
Cigarette use began to slowly decline from its highest point in 1963 around the
time of the publication of the first Surgeon General's report, and is currently at its
lowest level since World War II.222,341,342 In 1965, 60% of black males and 51% of
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white males were smokers. In 1985, those numbers fell to 41% and 32%
respectively.497 The recent focus of tobacco advertising has been women, children
and minorities,223,336,338 and consequently tobacco use has declined less rapidly
among these groups. Pierce and co-workers336 found that in girls younger than
18 years, smoking initiation increased abruptly around 1967, when women's
cigarette brands and their aggressive advertising campaigns were introduced. This
increase was highest in those females who had never attended college. Feigelman
and Gorman497 reported that 35% of adult white females were smoking in 1965,
with only 28% still continuing to smoke in 1985. For black women, the
consumption of cigarettes remained virtually unchanged over the same 20-year
period: 33% were smoking in 1965, and 32% were still smoking in 1985.
It is estimated that 58% of teenage smokers purchase cigarettes illegally, 339 and
these illegal sales occur more than twice as frequently in black as in white
neighborhoods.340 A 1994 population-based study by Grossman and co-
workers302 indicated that over 67% more urban black mothers smoke than urban
white mothers, and other national studies have documented excessive rates of
smoking among black men.
Demographics and Epidemiology of Smoking.
In a recent review article on the human costs of tobacco use, MacKenzie and
associates223 noted that even the three life insurance firms which are owned by
tobacco companies charge smokers nearly double for term life insurance because
smokers are almost twice as likely as non-smokers to die at any given age.
Smoking causes disease and aggravates existing disease. The risk of developing
CAD is greatly increased among men and women with diabetes who smoke, and is
much higher in smokers than non-smokers with or without diabetes.220 According
to a report of the Surgeon General,221,222 smokers have as much as a four-fold
greater incidence of CAD, a 70% greater CAD death rate, and a four-fold greater
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risk of sudden death than non-smokers. In a review of articles published between
1977 and 1993, (which identified factors contributing to death in the United
States), CAD was identified as the most common cause, and the use of tobacco
products was identified as the greatest contributor to mortality. 115 Heart disease,
lung cancer, stroke, and hypertension are all smoking- related diseases which are
more prevalent among the poor and among black Americans [see Table10].
Table 10: Smoking Related Illnesses by Race and Sex
Disease White Males Black Males White Females Black Females
Lung Cancer 79.3 125.3 33.5 33.9
Oral Cancer 17.2 22.5 --- ---
Heart Disease 257.8 308.2 126.7 191.5
Stroke 35.2 64.2 29.6 53.8
Hypertension 21.2 28.3 20.0 39.8
__________________________________________________________________________________________________________________
Adapted from: Feigelman W, and Gorman B.497 Heart disease and stroke figures were collected by the National Vital Statistics System on
age-adjusted death rates for selected causes of death per 100,000 population for 1983, National Center for Health Statistics (1986:Table 21).
Cancer statistics are age-adjusted cancer incidence rates per 100,000 population reported to the National Cancer institute, National Center for
Health Statistics (1986:Table 36); Hypertension statistics are age-adjusted rates per 100,000 adults aged 25 to 74 for 1976-1980, National Center
for Health Statistics (1985:Table 8, p.125).
An increased rate of death observed among the very thin in several clinical
studies has often confounded the results especially when these studies were
structured to determine excess mortality among the obese. Epidemiologists
examining the data from the Harvard Alumni Health Study,181 a study following
predominantly white, high SES men enrolled as Harvard undergraduates between
1916 and 1950, have determined that cigarette smokers were thinner than non-
smokers and that the mortality rate among smokers was 82% higher than among
non-smokers. Furthermore, among smokers (who comprised half the study
population), the death rate was elevated in both the very thin and the very heavy.
Among non-smokers, however, increased risk of death was directly associated
with increasing weight. The heaviest non-smoking men had a 67% higher
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adjusted mortality than subjects who weighed 20% below the United States norm.
These data suggest that obesity is a risk factor for CAD among non-smokers, that
obesity potentiates the deleterious effects of smoking (by increasing the rate of
death from CAD among obese smokers), and that smoking increases the risk of
death from cancer or other degenerative diseases (which often manifest themselves
as weight loss associated with smoking). These findings further demonstrate that
the risk of death from smoking is probably greater that the risk of death from
obesity alone.
Of the 2 million American adults who died in 1986, 76% of those reported to
have died at a relatively young age (45 to 64 years) had been smokers. 214 There is
a strong inverse relationship between the level of education and current smoking
status.4,219 Currently, higher rates of smoking are prevalent among blue-collar
workers, blacks, the unemployed, and among those of low income and lower
socioeconomic status, however data suggests that this trend has not been
consistent over time. In the United States, smoking was more prevalent in the
early decades of the twentieth century among the affluent who were able to more
easily afford the habit, than among the rural indigent whites and blacks. Between
1916 and 1950, the rate of smoking among high-SES Harvard undergraduztes was
over 50%,181 and in 1954, nearly twice as many medium income Europeans were
identified as heavy smokers as compared with low income Europeans. 444
Currently, this situation has been reversed among those of high-SES, both in
Europe and in the United States. This reversal took place within the decade of the
1960s, and undoubtedly contributed to the CAD risk factor reversal between the
socioeconomic classes in America.
The Pathophysiology of Smoking.
The adverse effects of smoking on the cardiovascular system involve numerous
mechanisms610 including a direct toxic and vasoconstrictive effect on the vessel
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wall,496,611 alterations in serum lipids,612 increases in low density lipoprotein
oxidation,837 increases in vascular hydraulic stress and myocardial oxygen
consumption (secondary to smoking-associated increases in heart rate),610
increases in blood pressure,496,788 circulating catecholamines,496,613,614,788 platelet
hyperactivity,615,616,625,872 thrombosis and thrombin generation,610,615,625,872
erythrocyte peroxidation,899 plasma fibrinogen,719,730,731,732,872 increased indices of
oxidative stress and lipid peroxidation,899 and decreased production of tissue
plasminogen activator (TPA), a beneficial endogenous thrombolytic.617,618 The
effect of smoking on serum catacholamines can further increase platelet
hyperactivity and adhesiveness, leading to potential thrombosis and cardiovascular
events.610,619 Kannel and co-workers732 attributed one-quarter to one-half of the
increased risk of atherothrombotic cardiovascular disease associated with smoking
to the effect of smoking on plasma fibrinogen concentrations, and subsequent
hemostatic abnormalities. Ascherio et al,823 in a 4-year follow-up study of the
dietary iron intake and the incidence of CAD among almost 45,000 men, noted
that increased intake of heme iron, (supplied in the diet predominantly by meat),
was associated with a significantly increased risk of myocardial infarction in
smokers. These authors postulated that excess heme iron potentiated the oxidation
of LDL, (especially in the absence of sufficient dietary antioxidants, and in the
presence of oxidative stresses such as smoking), and noted that smoking was
associated with increased heme iron and dietary fat intake, and reduced
consumption of fiber and antioxidant vitamins.
Tobacco smoke generates highly reactive phenoxy free radicals by itself, and
interacts within the body to create a cascade of other destructive free radicals 281,899
which have been implicated in the pathogenesis of myocardial ischemia and
infarction.479,480,481
Research indicates that smoking may interfere with vitamin C absorption, while
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increasing vitamin C requirements.469,640 Recent data published by Margetts and
Jackson282 at the University of Southhampton indicates that smokers, who have
the highest metabolic demand for antioxidant protection, are less likely to
consume adequate quantities of foods which are high in antioxidant nutrients, than
are non-smokers. This study examined the dietary habits of 618 smokers and
compared their diets to those of 1,224 non-smokers. The researchers concluded
that the smokers were at increased risk of developing chronic disease not only due
to the physiopathologic effects of smoking, but also due to the fact that their diets
were higher in fat and seriously inadequate in specific anti-oxidant nutrients.
Smokers ate significantly more white bread, sugar, cooked meat dishes, butter, and
whole milk, while consuming less whole meal bread, high fiber cereals, fruits, and
carrots. The frequent selection of white breads in lieu of whole grain varieties by
smokers is significant in light of the results of one major population study 851,891
which found that this choice was associated with a 37% increased risk of coronary
events (p=0.006). Margetts and Jackson further stated that smokers consumed
more fat, and had lower intakes of fiber, protein, vegetables, beta carotene, and
vitamin C. This nutritional deficit, according to the researchers, was likely to
further exacerbate the damage caused by smoking. These findings are similar to
those reported in other studies which examined the relationship between diet and
smoking.283,284,285,286,287,469,571,572,595,596,641
Pacht and colleagues498 found deficient levels of vitamin E in chronic cigarette
smokers. Similarly, Riemersma and associates469 found low vitamin E levels
among angina patients who were smokers, and Brown et al899 found that smokers
sustained an increased free radical load (characterized by increased indices of lipid
peroxidation) because of their exposure to large quantities of reactive free radicals
in the gas and tar phases of cigarette smoke. The researchers determined that this
increased lipid peroxidation was reduced in vitro following vitamin E
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supplementation. These findings are in accordance with other clinical research
which suggests that smoking reduces plasma vitamin E levels, and increases
oxidative stress.590,591
Numerous researchers have reported lower antioxidant levels of plasma carotene
among smokers.282,469,471,571,572,595,596,642 A recent report from the American Journal
of Clinical Nutrition demonstrated that non-smokers who regularly encounter
second-hand cigarette smoke (approximately 20 hours per week or more) had
significantly lower levels of vitamin C than non-smokers who were not exposed to
smoke, although their dietary intakes of the vitamin were comparable. Similarly,
Rimersma et al,469 in a recent clinical study evaluating the protective effect of
antioxidant vitamins against angina pectoris and CAD, noted that smokers were
found to have lower vitamin C levels than non-smokers. The National Health and
Nutrition Examination Survey,639 found plasma vitamin C levels to be lowest in
those who smoked the most cigarettes. The Health Professionals Follow-up Study
of over 50,000 male health professionals revealed that high serum levels of
vitamin C reduced the risk of non-fatal myocardial infarction or death in cigarette
smokers.471
Cigarette Smoking and Alcohol Consumption.
Cigarette smoking is linked with increased alcohol consumption. Excessive
alcohol consumption, (and especially concentrated forms of alcohol devoid of
antioxidant flavonoids like those found in red wine), can further increase the
oxidative stress on the body by increased production of free radicals during the
metabolism of ethanol.484 Examining data from the Physicians' Health Study,
Robbins and co-workers625 reported that over twice as many smokers among the
22,071 American male physicians studied reported daily drinking as compared
with never-smokers.
Smoking, Oxygen-Free Radical Damage, and Atherogenesis.
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Smokers have significantly higher serum concentrations of atherogenic low
density lipoprotein (LDL) cholesterol,288,612 and decreased levels of beneficial high
density lipoprotein cholesterol (HDL).625 The increased oxidative stress brought
on by smoking (and reduced levels of cardioprotective HDL secondary to
smoking), renders LDL more susceptible to atherogenic modification by
oxidation,471,589,590,591,609 and may simultaneously predispose the vasculature to
vasospasm.482 Additionally, serum LDL in smokers has a greater potential for
oxidation due to high ratios of phenoxy and other free radicals and reactive
oxygen species to antioxidant vitamins in smokers.281,282 These deficits are caused
by lower dietary intakes of antioxidants, and greater metabolic demand in
smokers.282 Oxidized LDL is more likely to be taken up by monocytes and
macrophages (a chemotactically activated monocyte) to form foam cells which
become the foundation of atherosclerotic plaque and atheroma, leading to CAD. 281,
289,333,471,573,574,578,891 Research shows that scavenger receptors located upon the
monocyte are responsible for stimulating and activating the monocyte to become a
macrophage. These scavenger receptors are sensitive to oxidized LDL (LDLOX),
but are insensitive to unaltered LDL particles.891 Furthermore, oxidized LDL may
contribute to atherogenesis by reducing macrophage motility in the arterial
intima,577 increasing monocyte accumulation,578 and increasing cytotoxicity.579 In
vitro studies have demonstrated that flavonoids, one of the many forms of dietary
antioxidants which most smokers consume in lesser quantities, 282,283,284,285,286,287,288
may prevent the cytotoxicity of oxidized LDL.566
The Nicotine Paradox.
Demographic data indicates that the indigent497,719 and those who are
experiencing significant life stress are more likely to smoke,496,497 while
concomitantly engaging in lifestyles and dietary practices which are more likely to
exacerbate the biochemically-adverse effects of smoking. Furthermore, data
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suggests that smoking may adversely effect an individual's ability to cope with
stressful life situations. Epstein and Perkins496 stated that smoking reduces anxiety
and sensitivity to unpleasant situations which may lead to "increased and extended
attempts to actively cope with ongoing stressful tasks to the point where coping
becomes physiologically maladaptive." Experiencing psychological stress
frequently leads to increased smoking for subjective stress reduction, 496,791
however smoking exacerbates stress-induced increases in autonomic nervous
system activity, and increases serum catecholamines.496,699,788 Gilbert789 called this
differential effect of smoking on specific psychological and subjective responses
the "nicotine paradox".
In the setting of cardiovascular disease, it has been hypothesized that the
increased dietary or supplemental consumption of antioxidant vitamins and
flavonoids by smokers might inhibit the oxidation of LDL cholesterol into its
atherogenic form333,537,565,570,587 while preserving normal endothelial function,334
however the benefits of smoking cessation probably exceed those conferred by
nutritional supplementation or improved diet in established smokers. 335
In summary, smoking is associated with significant increases in oxidative stress,
and with reductions in the intake of dietary antioxidant nutrients, thus causing an
imbalance between these destructive and protective processes in the human body.
Smoking is more prevalent among the lower socioeconomic class, 497 and its
detrimental effects are therefore most likely experienced by the indigent. Stress
counseling, and instruction in coping skills and techniques may be of benefit when
combined with smoking cessation counseling, especially among members of lower
socioeconomic status.
Alcohol Consumption, the French Paradox, and Socioeconomic Status.
The associations between alcohol consumption and cardiovascular disease are
complex. Studies indicate that regular moderate use of alcohol is associated with
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a lower risk of major coronary events.197,198,202,280,402,403,476,543,544,545 Beneficial
increases in high density lipoprotein (HDL) levels subsequent to moderate alcohol
consumption have been suggested as a possible mediating factor for this protective
effect.202 However, heavy alcohol consumption and problem drinking are
associated with an increased incidence of hypertension,
arrhythmias, alcoholic cardiomyopathies, and an increased mortality from all
causes, including cardiovascular disease, coronary heart disease, liver disease, and
cancer.190,191,197,198,199,201,202,203,476,543 Excessive alcohol consumption is frequently
associated with smoking,625 inadequate diet,901 malnutrition and nutritional
deficiencies,889,901 malabsorption,901 low plasma antioxidant status,889 increased
indices of oxidative stress (increased serum MDA),889 low socioeconomic
status,552 and high psychological stress.552 These factors have been suggested as
potential major confounders in the determination of associations between alcohol
consumption and CAD.552,625 In a review by McGinnis and associates115 of
articles published between 1977 and 1993 which identified factors contributing to
death in the United States, the abuse of alcohol was identified as the third most
prominent contributor to mortality, after use of tobacco and inadequate diet and
exercise. In a 1994 population-based study of 1.5 million northwestern whites,
blacks, urban American Indians, and Alaskan natives who were followed for ten
years, Grossman and co-workers302 demonstrated that age-adjusted alcohol-related
deaths per hundred thousand were 28% higher among urban blacks than among
urban whites.
According to the National Mortality Follow-back Survey, of the approximately
two million Americans who died in 1986, 84.5% of those who died at the youngest
age were reported to have consumed 12 or more alcoholic drinks per day. 214
Alcohol abuse is estimated to have been a major contributing factor in 60 to 90
percent of cirrhosis deaths,115 and black adults are 60% more likely to have died of
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cirrhosis of the liver than whites.214
Alcohol consumption is greatest among individuals of lower socioeconomic
status, among men, and among young adults. Respondents in clinical surveys who
are obese, who smoke, and who do not use seat-belts are more likely to be among
the 9% of all adults who identify themselves as chronic heavy alcohol
consumers.190, 200, 204 It is estimated that this small group of heavy drinkers may
consume 40-50% of all alcoholic beverages.200
Excessive alcohol consumption may have an adverse effect on serum antioxidant
levels which is independent of nutritional status. Excessive consumption of
alcohol has been associated with low serum vitamin E levels,499,889
malondialdehyde (MDA) markers of oxidative stress and free radical activity, 889
and with significant losses of serum magnesium. This "magnesium wasting" may
account for the vasopressor effect and arrhythmias which have been associated
with the excess consumption of alcohol. Numerous studies have shown that
alcoholics have lower serum beta carotene,901 alpha tocopherol,889 selenium,889 and
ascorbic acid889 concentrations than control subjects who drink moderately.
Excessive alcohol ingestion is one of the foremost factors which is known to
aggravate hypertension, and has been strongly associated with the development of
hypertensive disease in urbanized populations in the Third World.279
Alcohol is metabolized into the double free radical acetaldehyde, which can
attack and cause protein cross-linking damage to hepatic and cardiac tissues.281,484
This may account for alcohol-induced cardiomyopathies and fibrotic cirrhosis
which commonly occur in chronic heavy drinkers. These deleterious effects of
alcohol may be magnified in low SES populations, and among smokers 282 whose
diets tend to be deficient in many basic nutrients, including anti-oxidant vitamins,
selenium, and magnesium.
Epidemiology of Alcohol Consumption and the French Paradox.
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The French and Italians, who lead the world in per capita consumption of wine
(147 and 153 liters per person per year respectively)661 are among the lowest in the
incidence of, and mortality from CAD,61,392 although their fat intake, LDL, and
HDL cholesterol levels are similar to higher risk populations such as the United
States. Epidemiological studies suggest that consumption of alcohol at the level
of 20-30 grams per day, (similar to the level of intake in France), can reduce the
risk of CHD by at least 40%.873 The French consume 18 times as much wine per
capita as do Americans, and 30 times more than the Fins. Alcohol is commonly
believed to protect from CAD by preventing atherosclerosis through the action of
increasing HDL cholesterol. Theoretically, this effect would increase hepatic
uptake of LDL, and reduce the potential of LDL oxidation. Small clinical and in
vitro studies have suggested that alcohol may raise HDL in some individuals, but
large-scale epidemiological studies have shown that serum concentrations of this
factor are no higher in France than in other higher-risk countries,873 shedding some
doubt on the alcohol-HDL hypothesis. The antioxidant flavonoid compounds
present in red wine, however, may be partly responsible for the reduced risk of
CAD among wine drinkers, since the French consume more of these polyphenolic
flavonoids than do most other populations.467,570 Additionally, alcohol is may
protect from CHD by its effects on hemostatic mechanisms. Data from a study
conducted in Caerphilly, Wales, suggests that platelet aggregation, which is
directly related to CAD, is significantly inhibited by alcohol consumption at those
levels of intake which have traditionally been associated with reduced risk of
CAD. Research conducted by Folts et al at the University of Wisconsin, Madison
demonstrated that red wine possessed twice the anti-platelet activity of beer or
white wine. The researchers postulated that unlike white wine, the process of
creating red wine allows the crushed grape skins, stems and seeds to remain in
contact with the juice during fermentation. This solid material, which is later
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filtered and removed, contains antioxidant flavonoids which have been shown to
possess anti-platelet activity. Additionally, red grapes which are grown in a cool,
moist climate contain an antioxidant and antifungal agent called resveratrol, which
is also an inhibitor of platelet activity.
Inhibition of platelet reactivity and adhesiveness by wine may be one
explanation for the paradoxically low rates of coronary heart disease in France,
since pilot studies have confirmed that platelet reactivity is lower in France than in
Scotland.873
Because French per capita absolute alcohol consumption is 50% higher than the
Italians, twice that of Americans and four times that of the Fins, this may account
for the much higher morbidity and mortality from alcoholism among the French.661
Alcohol consumption versus CAD risk forms a "U-shaped" curve, with the
greatest benefits conferred upon moderate drinkers, and the least benefits
bestowed upon non-drinkers and excessive drinkers.280,543 Meade and
associates733 showed that non-drinkers had higher plasma fibrinogen levels than
drinkers, which additionally may be partly responsible for the slightly increased
risk of CAD among abstainers. It is feasible that members of upper SES may be
more likely to moderate their drinking, and may tend to choose wine as a beverage
of choice more frequently than the indigent, thereby reducing their CAD
risk.402,476,543,544,545,569,570
Destructive Personal Behaviors and Their Relationship to SES
There is evidence that socioeconomic status effects behavioral styles, as well as
coping styles.4 It is also conceivable that behavior and coping styles may effect
socioeconomic status. Stephen Covey108 defines habits which are present in
successful people, or those who have attained high socioeconomic status. They
include self-discipline, independence, teamwork, cooperation, empathy,
unselfishness, personal integrity, responsibility, prioritization, goal-setting,
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communication, and striving for excellence. Bennett, in his "Book of Virtues"
similarly defines principles of life-success including self-discipline, compassion,
personal responsibility, courage, work ethic, loyalty, faith, and honesty.
According to the Report of the National Commission on America's Urban
Families,224 the traditional family is the institution which has historically been
responsible for teaching these constructive personality traits which cannot be
enforced by laws but which are essential to both personal happiness and societal
success. Because single parent and dysfunctional families are more prevalent
among the impoverished, destructive personal behavior is associated with lower
SES; because the American social welfare system encourages and rewards single
motherhood, weakens the traditional family, and disproportionately impacts upon
the families of the poor, destructive personal behavior is associated with lower
SES; and because of increasing tendencies among many Americans to abdicate to
institutions other than the family the responsibility for instilling a belief system
and the establishment of moral guidelines for our children, these positive
personality traits may not be taught as thoroughly, or received as enthusiastically
as in previous generations of Americans.
Hope is a strong motivating factor, and the possession of a personal dream
allows men and women to press forward toward the attainment of that goal.
Dependency upon a social system or upon society for long-term support and
subsistence ultimately robs individuals of their independence and dignity,
quenches their ambition, and steals their dream of hope.
VIII. Dietary Electrolyte Mineral, Mineral, and Antioxidant
Vitamin and Flavonoid Consumption and CAD.
Dietary Antioxidants, Recommended Daily Allowance, and SES
Certain lifestyle modifications may be reducing cardiovascular risk factors
within certain upper socioeconomic population groups. These modifications
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include a reduction in tobacco use,102,103 increased intake of potassium, fiber, anti-
oxidant vitamins, and flavonoids (due to increased fruit and vegetable
consumption),67,68,69,105,106,467 blood pressure control secondary to weight loss,183
reduction in dietary sodium intake,99,105,156,184,185,186,187,188,189 and improvements in
maternal health.107 These lifestyle modifications are less likely to be undertaken
by the indigent. Furthermore, the poor may require even higher levels of dietary
antioxidant nutrients due to exposure to significantly greater amounts of free
radicals generated daily by environmental pollutants including radiation,
insecticides, herbicides, cigarette smoke, automotive exhaust, water pollution, and
smog, which are all characteristic elements of the modern urban environment more
common to members of the lower socioeconomic class.487,491
The Recommended Daily Allowance, or RDA, is the arbitrary level of intake of
a given essential nutrient which has been set by the Food and Nutrition Board of
the National Research Council (NRC),487,489 and is defined by the NRC as "the
level of intake of an essential nutrient considered...to be adequate to meet the
known nutritional needs of practically all healthy persons." 665 Many nutrition
scientists believe that the RDA are too low,487,489,491,804 and represent nutrient
intakes sufficient to prevent deficiency disease or symptoms in healthy individuals
rather than to ensure optimal health or therapeutic effect.487,489 The first RDAs
were developed in 1943 to facilitate dietary planning and the procuring of food
supplies for the armed forces,487 however they are currently being used as
guidelines for public assistance food programs and may therefore exert more
considerable influence over the diets and vitamin intake of the poor, 491,664 than
over the diets of the affluent, who are more likely to take nutritional supplements.
According to Smith and Turner: "Through the past four decades, the RDA have
been increasingly used in statutory and regulatory food programs. They serve...as
the indirect basis for the definition of poverty."664
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The Ratio of Dietary Sodium to Magnesium and Potassium in Hypertension.
Sodium and potassium are essential electrolyte minerals which are involved in
the regulation of muscle contractile force and relaxation, bio-electrical functions
including nerve stimulation and generation of bio-electrical impulses, and the
regulation of cellular water balance and the intra-cellular distribution of fluids.
Magnesium, an essential mineral which helps promote the absorption and
storage of sodium and potassium, is involved in carbohydrate and amino acid
metabolism, and is essential for the conversion of blood sugar into energy. Proper
magnesium levels are critical for the normal functioning of nerves and muscles
(including the heart), and Magnesium is involved in the regulation of
neuromuscular contractions by countering the stimulating effect of calcium.
Magnesium may reduce blood cholesterol levels and possibly reduce the risk of
atherosclerosis. The dietary need for magnesium increases when blood
cholesterol levels are elevated, and when consumption of calcium and protein is
high.844,845
Sodium is supplied by seafood, poultry, red meat, and in many refined and
processes foods. Food sources of potassium include all vegetables, especially
green leafy vegetables, whole grains, fruits, potatoes, and seeds. Magnesium is
found chiefly in fresh green vegetables, raw unmilled wheat germ, soybeans,
whole grains, figs, corn, apples, oil-rich seeds and nuts, seafood, and milk.844,845,846
The typical American diet is deficient in magnesium and potassium,151 but high in
sodium.145 These mineral and electrolyte imbalances may be further exaggerated
in the diets of the poor. A low dietary sodium to magnesium and potassium ratio is
more important to the normalization of blood pressure than simple reduction of
sodium intake alone. Increased sodium intake secondary to the consumption of
refined and processed foods has been associated with the risk of hypertension. 279
Ohambo and co-workers330 emphasized that increased salt intake was a major
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factor in the increased incidence and prevalence of hypertension in urbanized
Africans, and particularly those within the middle-class. A decreased intake of
potassium associated with a decline in the intake of vegetables has been suggested
as playing an etiological role in the development of hypertension in peoples
moving from rural to urban areas,279,327 and an increased intake of calories,
coupled with decreased activity levels and resulting obesity has been linked to the
occurrence of hypertension in the Third World.279,331
Low magnesium concentrations have been linked to hypertension occurring
both at rest and during stress, and to vasospasms in the coronary
arteries.152,153,154,155 Conditions which have been associated with reduction of
blood magnesium levels include psychological stress, alcoholism, and diabetes,
and these are frequently associated with elevated blood pressure.145,247,844,845,846
Magnesium supplementation has been shown to decelerate hypertensive response
and abnormal cardiovascular reactions to stress.145 Potassium supplementation
and sodium restriction have been shown to be beneficial as a nutritional approach
to antihypertensive therapy.14,156,157,158,159,184,185,186,187,188,189,844,845,846 A potassium
depleted diet was associated with increased blood pressure in both
normotensive255 and hypertensive individuals.256
Dietary Calcium Intake, Hypertension, and CAD.
Calcium is an essential element which is involved in the blood-clotting process,
and in the regulation of heart rate and blood pressure through its bioelectrical
effects on nerve stimulation and through its cellular effects upon vascular smooth
muscle contraction.472,844,845,846 Milk and dairy products are the major sources of
calcium.247,844,845,846
Clinical and Epidemiologic Studies
The observation that regions with hard water high in calcium content
experienced lower cardiovascular mortality initiated the original epidemiologic
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interest in the relationship between calcium and cardiovascular disease. Studies of
populations which are at high risk of developing hypertension show that a low
dietary calcium intake correlates with increased prevalence of hypertension. 253,257
Serum ionized calcium has been reported to be lower in hypertensive persons than
normotensive persons,208, 209 and increasing dietary calcium intake has been shown
to reduce elevated blood pressure in several population groups. 190-192,209 Recent
clinical evidence suggests a beneficial hypotensive effect of calcium
supplementation in some hypertensive persons.210,211,258 Several dietary surveys
suggest that hypertensives as a group consume less calcium than normotensive
persons,200 and that individuals of low SES tend to consume less calcium than the
affluent. Watson and co-workers194 report that rural black hypertensive women
consume diets very low in calcium, and in studies assessing dietary intakes, it was
determined that hypertensives consumed less (and in one study, an average of 25%
less) calcium than normotensives.195,196 Knapp and co-workers,42 in a study of
low-SES Mexican-Americans in the San Antonio Heart Study, reported that
calcium intake was very low, and constituted only 55% to 67% of the RDA.
These researchers commented that calcium intake increased with increasing SES.
Dietary Iron Intake and CAD.
Iron is a mineral concentrate in the blood which is also present in every living
cell. All iron in the human body exists as a chelate, and is bound to protein. The
major function of iron is to combine with protein and copper to make hemoglobin,
the material which gives red blood cells their color and serves as a transport for
oxygen between the lungs and tissues.844 Iron is supplied in the American diet
primarily from animal sources including organ meats and red meats such as beef,
pork, or lamb.823,844,845,846 This form of iron, which exists in the form of
hemoglobin, is designated "heme iron", and is more completely absorbed than is
non-heme iron.823,841,844,855 Plant sources of iron supply the mineral in the form of
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non-heme iron, and include leafy green vegetables, whole grains, dried fruits,
legumes, and molasses. In men with replete iron stores, 26% of dietary heme iron
is absorbed, compared with only 2.5% of non-heme iron. In iron deficiency,
absorption of heme iron increases moderately, whereas the absorption of non-
heme iron increases approximately nine-fold.841 These data suggest that although
both animal and plant sources of iron are equally capable of replenishing iron
stores in anemic deficiency, the consumption of heme iron as a primary dietary
source of iron is more likely to lead to an iron overload situation in individuals
with normal or positive iron balances.
Clinical and Epidemiologic Studies
Several clinical studies have indicated that high iron stores may increase the risk
of acute cardiovascular events. Most of these studies have suggested that high
iron intake (particularly from animal sources), is associated with an increased risk
of acute thrombotic events, but not with an increased risk of atherosclerosis.823 In
a recent prospective study among 1,932 Finnish men by Salonen and co-
workers,827 dietary intake of iron and serum ferritin (predominantly supplied in the
Finnish diet by meat828) was strongly associated with acute myocardial infarction.
Similarly, in a 4-year follow-up study of almost 45,000 men with no previous
history of CAD, Ascherio et al823 found that dietary intake of heme iron,
(primarily supplied by red meat), but not non-heme iron, was associated with an
increased risk of acute cardiovascular events including AMI. These researchers
noted that intake of non-heme iron was directly associated with an increased
dietary intake of vitamins and fiber, and inversely associated with smoking and
risk of myocardial infarction.
Consistent with a positive association between heme iron intake and increased
coronary risk is the 20-year follow-up observation by Snowdon, Phillips and
Fraser,555 who reported a 60% increased risk of fatal coronary disease among both
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male and female Seventh Day Adventists consuming meat at least six times per
week as compared with those consuming meat less than once per week. In a
subsequent analysis of this same Adventist Health Study data base ten years later
by Fraser et al,851 beef consumption was related to definite fatal CHD in men
(p28.2 μM/L), [See Fig. 32].
Figure 32: Risk of Angina Pectoris and Plasma Concentrations of Vitamin E
___________________________________________________________________________________________________________
From: Riemersma et al.469
Similarly, Byers870 reported that an increased dietary intake of vitamin E reduced
death from myocardial infarction.
A prospective study of antioxidant vitamins and the incidence of CAD in
women, which was conducted by Manson et al,805 used food frequency
questionnaires to estimate dietary intake of vitamin E, and found that the
incidence of CAD was lowest among women with the highest intake of alpha
tocopherol.
Page 162
Laboratory and Clinical Studies of Vitamin C:
Vitamin C, or ascorbic acid, is an essential water-soluble antioxidant vitamin
and reducing agent which neutralizes various oxygen free radicals, detoxifies
carcinogenic organic radicals, converts nitroso compounds into less carcinogenic
products, and prevents nitrosamine formation in the intestinal tract. 490 Vitamin C
is the least stable of vitamins, and rapidly looses potency through exposure to
light, heat, and air, which stimulate the activity of oxidative enzymes. Stress
increases the body's need for Vitamin C, which is used up more rapidly under the
increased oxidative conditions of stress. Vitamin C enhances the intestinal
absorption of iron by reducing ferric iron to the more easily absorbed ferrous form,
enhances the absorption of magnesium and calcium, and prevents the oxidation of
vitamin E.844,845,846 Good sources of this vitamin include most fresh fruits and
vegetables.844,845,846
The current RDA for vitamin C, 60mg for adults, is an amount easily met by
most American diets, however numerous researchers recommend significant
increases in the RDA.489,491,673,674,804 At very high intakes, vitamin C has been
reported to reduce spontaneous tumors in mice, increase anti-inflammatory and
antimicrobial activity, enhance immunity, and prolong the survival of cancer
patients relative to historical controls.490,673,675,676 High concentrations in vitro of
ascorbate can inhibit LDL oxidation, and reduce uptake of oxidized LDL by
macrophages. Furthermore, ascorbate has been shown to be as potent an
antioxidant as probucol, while also protecting endogenous LDL antioxidants alpha
tocopherol and beta carotene by serving as a sacrificial antioxidant. 804 The in vivo
effects of ascorbate in the prevention of LDL oxidation have not been fully
delineated.
Calculated ascorbic acid intake from fresh green vegetables was inversely
correlated with standardized mortality from CAD and cerebrovascular
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accident,105,650,667 and low plasma levels of vitamin C have been associated with
high incidence of cancer, as well as deaths due to non-malignant causes.669,670,671
Earlier concern by some scientists over proposed adverse effects of large doses of
vitamin C, (dependency, renal calculi, and destruction of vitamin B 12 ), have been
allayed by subsequent research.490 Free radical scientists have known that
although ascorbic acid typically acts as an antioxidant in model systems, under
some conditions it can act as a pro-oxidant.488 Vitamin C can increase absorption
of dietary iron (particularly iron supplied by red meat and in the more reactive
form of heme iron) which acts as a catalyst in free radical formation. Extremely
high doses of vitamin C in patients with high positive heme iron balances may
further increase tissue iron stores, and increase the potential for free radical tissue
damage.488,668
Clinical and Epidemiologic Studies
Vitamin C did not demonstrate a significant protective effect against the risk of
developing CAD in women in the Nurses' Health Study,69,470 and was found to be
less protective than vitamin E or beta carotene, however other epidemiologic
evidence does suggest protective cardiovascular benefits for vitamin C. 580,581,804
The Health Professionals Follow-up Study471 revealed a cardiovascular protective
role for vitamin C in male smokers, however the benefit of vitamin C
supplementation among non-smoking men was not statistically significant.
Ramirez and Flowers659 found that men with angiographically-evident coronary
atherosclerosis and regional wall kinetic abnormalities had lower serum vitamin C
levels (leucocyte ascorbic acid levels) than those with normal angiograms,
irrespective of smoking status. Rimersma and associates469 evaluated the
protective effect of vitamin C in the reduction of the risk of angina pectoris.
Although not as strong as the protective relationship for vitamin E, vitamin C did
demonstrate benefit. In this study, the quintile with the highest vitamin C levels
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(>57.4 μM/L) had an 80% lower risk for angina when compared to subjects with
the lowest dietary vitamin C intakes (19,034 IU/day) had
a 29% lower risk of coronary artery disease (multivariate relative risk of 0.71, p
value for trend=0.02) than patients with the lowest intake (<3,969 IU/day), [See
Fig. 34].
Figure 34: Beta Carotene Consumption and the Risk of CAD in Men
___________________________________________________________________________________________________________
From: Rimm et al,471
Other epidemiological studies have suggested an inverse relationship between
beta carotene intake and risk of CAD, and acute myocardial infarction. In a
preliminary analysis of the extensive US Physicians' Health Study, Gaziano et
al588 showed that beta carotene supplementation was associated with a statistically
significant 44% reduction in major cardiovascular events, (including myocardial
infarction, stroke, and death from cardiovascular disease), among a subgroup of
physicians with chronic stable angina who had been taking 50mg of beta carotene
(83,300 IU, or the equivalent of consuming ten carrots) on alternate days.
A subsequent study by Gaziano and co-workers,808,894 of 1,299 elderly
Massachusetts residents, demonstrated that those individuals who were in the
highest quartile for dietary beta carotene intake had the lowest risk of myocardial
infarction and fatal cardiovascular disease. The age and sex adjusted relative risk
for fatal cardiovascular disease during five years of follow-up was 0.54 (95% CI;
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0.34-0.87), and relative risk of fatal myocardial infarction was 0.25 (95% CI; 0.09-
0.67). Adjustment for smoking and alcohol consumption did not significantly
change these results.
Antioxidants and Effect upon Serum Lipids
Although vitamin E has been shown to prevent the oxidative modification of
LDL in vitro, in three clinical studies of vitamin supplementation471,597,598,599 no
significant alteration of serum lipid ratios in vivo was detected. Rimersma and co-
workers469 found that vitamin E did not alter LDL or HDL levels, possibly
indicating that vitamin E's cardiovascular benefit is related to its antioxidant and
anti-platelet effects. Increased serum levels of vitamin C, however, have been
associated with beneficial blood lipid effects including increased HDL and
decreased LDL subfractions.68,651
Free Radical Theory
In the late 1950s, Denham Harman first formulated the free radical theory of
disease and tissue damage, and recommended the use of antioxidant vitamins to
reduce this damage. Subsequently, free radicals have been implicated in over one
hundred human degenerative diseases.871
All cells in the body use oxygen to break down nutrients and to generate energy
within the mitochondria of the cells. During the process of breathing, oxygen is
inhaled into the lungs and is bound to carrier molecules of hemoglobin and
transported by the blood to all other body tissues. Stable oxygen atoms contain a
nucleus and eight pairs of electrons which orbit about that nucleus. Oxygen
usually arrives at the tissue sites in this stable form, but occasionally it looses an
electron in transit and arrives in the form of an unstable oxygen free radical. All
free radicals exist for an infinitesimally brief moment in the form of atoms or
molecules possessing one or more unpaired electrons. Typically an electron (or
multiple electrons) is missing from one or more of the outermost (and most
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vulnerable) atomic orbits of a free radical. The resulting electrical imbalance
causes a free radical to be highly reactive and unstable, as it immediately seeks to
abduct nearby electrons to resolve its own internal imbalance.281,869 This process is
accomplished within nanoseconds, and the theft of an electron from a neighboring
fat or protein molecule often results in a chain reaction in which one molecule
after another in a cell steals an electron from its neighbor. In the process, proteins
are denatured, and fats are peroxidized, permanently damaging them and changing
their character and structure. Because of their highly vulnerable outer electron
orbitals, cellular proteins and lipids are the primary free radical targets.
Phospholipids comprise the outer cellular membrane, and the semi-rigid fibrils of
the cytoskeleton and nuclear matrix are composed primarily of proteins. These
proteins and lipids can be irreparably damaged by oxidative free radical attack,
leading to degenerative disease of body organ systems. Living cells attempt to
repair damaged components, but cumulative damage occurs over decades, and this
cumulative damage is thought to be responsible for the process of aging. The
"cumulative damage theory" was tested in 1993 when researchers from Southern
Methodist University in Dallas demonstrated that fruit flies which were genetically
engineered to resist free radical damage lived 30% longer. This is the first direct
evidence that free radical damage does cause aging. Indirect evidence, however,
has been available for decades.
The superoxide free radical is an unstable form of oxygen with a powerful
electron hunger. Living cells produce a protective enzyme, superoxide dismutase
(SOD), in response to the presence of the superoxide free radical. SOD is capable
of quenching and neutralizing superoxide. Research has shown that the longevity
of an organism is directly proportional to the amount of SOD that it contains.
Studies have also shown that lifespan is inversely proportional to metabolic rate.
Animals with the highest lifespan have the highest levels of SOD when expressed
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as a function of their metabolic rate. This may explain why fruit flies, which
produce very little SOD in relation to their size and metabolic rate, have a life span
which is measured in days, and why long-term caloric restriction, which reduces
the metabolic rate, has been shown to extend lifespan in certain species. The
bacterium radiodurans contains the highest level of SOD, and the greatest
concentration of the antioxidant enzymes peroxidase and catalase of all living
creatures, enabling it to resist the damaging effects of radiation, and to thrive
within nuclear reactors.
The hydroxy radical, a "fearsomely reactive radical,"869 attacks whatever atoms
or molecules are nearby, leaving behind a legacy in the form of self-propagating
free-radical chain reactions which result in the damage and destruction of living
tissues. If hydroxy radicals are generated in close proximity to membranes or
lipoproteins, lipid peroxidation occurs, which is implicated in the development of
atherosclerosis. If these radicals are generated in proximity to DNA, they can
attack the purine and pyrimidine bases and cause potentially carcinogenic
mutations.869 A significantly less reactive radical is the oxygen free radical,
superoxide, which is created by the addition of one electron to the oxygen
molecule during molecular accidents during which molecules within living tissue
react directly with free oxygen. An example of this is the oxidation of
catecholamines which occurs subsequent to stress reactions. Consequently,
superoxide can react with free iron and copper ions to form the more damaging
hydroxy radical.869 Free iron and copper ions are both contained in heme iron
(supplied primarily by red meat) and are more readily available, and therefore
potentially more reactive than is elemental iron contained in non-heme iron
derived from plant sources. Stress, therefore, may generate catecholamines which
react with oxygen to form the superoxide radical which, in the presence of high
iron stores from animal sources, can react to form the most atherogenic form of
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free radicals, the hydroxy radical. This series of events may explain the increased
atherogenic risk associated with stress, and the interaction of stress and diet,
especially among individuals consuming the substantial quantities of red meat and
the more limited quantities of antioxidant nutrients typically found in the
traditional Western diet.
All free radicals are produced by metabolic processes occurring within the body
or through interaction with the environment, [See Table 11].281,486
Table 11: The Sources of Free Radicals Within the Body
1. Natural cellular energy processes.
2. The immune system (monocytes, including neutrophils and macrophages generate
free radicals to destroy invading bacteria and viruses), and inflammatory response.
3. Environmental pollution, and various toxins.
4. Alcohol, (the double free radical acetaldehyde is a metabolic end-product).
5. Tobacco smoke.
6. All forms of electromagnetic radiation (including sunlight, radon, cosmic
radiation).
7. Stress.
8. Catecholamines (react with oxygen to form the superoxide free radical).
9. Side effects of certain drugs, (i.e. adriamycin).
10. The process of respiration (1 to 3% of the oxygen we breathe is used to make the
free radical superoxide.
_____________________________________________________________________________________
Adapted from: Sharma281 and Halliwell869
Free Radicals and the "Western Diseases"
Subsequent research has confirmed the role of free radicals in the etiology of
both CAD and cancer, which are the principal Western nation killer
diseases.67,486,489,491,580,662,663 The diseases associated with free radicals are
degenerative in nature and include cancer, CAD, senile cataracts, atherosclerosis,
adult-onset diabetes, rheumatoid arthritis, ulcerative colitis, Crohn's disease,
ischemic stroke, Reynaud's disease, Behcet's disease, ulcers, and
emphysema.281,486,491 By one estimate, more than 85% of all chronic and
degenerative diseases are the result of oxidative damage.666
During ischemic re-perfusion, oxygen free radicals are produced which may lead
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to further tissue damage and re-perfusion injury,652,655,656,657 the development of
arrhythmias,653 and the depression of myocardial contractility.654 Grech and co-
workers656 postulated that activated neutrophils may be the source of re-perfusion
associated free radical generation during the progressive neutrophil leucocyte
infiltration of damaged myocardium.
It is necessary that free radicals be contained to prevent wide-spread tissue
damage. Containment clearly depends upon sophisticated systems that involve
vitamins E and C, and trace elements selenium, manganese, copper and zinc, and
probably involves both beta carotene and vitamin A.489
Antioxidants and Prevention of Oxidative Modification of LDL
Antioxidant molecules are stable electron donors which are able to neutralize
reactive and unstable free radicals by fulfilling the free radical's electron hunger,
yet without becoming a reactive free radical themselves. Antioxidant molecules
are complex, and possess such large numbers of electron orbitals that the loss of a
single electron, while temporarily resulting in the formation of a free radical, does
not result in a reactive molecule. When vitamin E, (found within membranes and
lipoproteins), blocks the chain reaction of lipid peroxidation by scavenging the
intermediate peroxy radical, the resulting tocopherol radical is predominantly non-
reactive, and is easily converted back into alpha tocopherol by vitamin C. 869
Vitamins E, C, and A, beta carotene, and the flavonoid compounds are all potent
antioxidants,281,471,562,563,564,571,572,830,831,832,833,869 and are supplied in the human diet
primarily by plant sources. Dietary antioxidants are easily destroyed during
cooking, food processing and storage,487,658 and individuals who consume
significant quantities of heavily refined and processed foods may have
significantly lower intakes of antioxidants. Recent clinical studies provide
persuasive evidence that poor plasma status of these antioxidant nutrients does
occur in Westernized nations, and that this deficiency is associated with an
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increased risk of CAD and cancer.67,489,580,663 Numerous epidemiological case-
control studies have shown a strong inverse correlation between CAD and stroke
mortality and the consumption of fresh green vegetables, (from which antioxidant
vitamin intake could retrospectively be calculated).105,489,554,650,667 The incidence
of, and mortality from cancer has also been found to be negatively associated with
plasma antioxidants, including vitamins A and C, and beta carotene in studies
conducted in Hawaii,669 Washington,670 and Boston.671
Antioxidant levels may effect longevity in the human. Epidemiologic evidence
suggests that vitamin C may increase human life-span,646 and animal studies have
shown that vitamin E intake is proportional to longevity in mammals. 647
Antioxidants inhibit the oxidative modification of LDL, and may significantly
reduce the risk of CAD according to several epidemiological and clinical
studies.67,69,469,470,471,580,581,582,588 The susceptibility of LDL to oxidation has been
correlated with the severity of atherosclerosis,621 and this susceptibility is
dependent on tissue and serum antioxidant status.830 The resistance of LDL to
oxidation is directly proportional to the level of antioxidants such as beta carotene
and lipid soluble vitamin E contained within the LDL
particle,281,468,470,488,571,572,573,574,810,830,831,832,833,869 and vitamin C has been shown to
stabilize and protect these endogenous antioxidants contained within the LDL
particle, [See Fig. 35].592,869
Figure 35: Antioxidant Levels within Serum LDL
and the Onset and Degree of Lipid Peroxidation
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___________________________________________________________________________________________________________
From: Esterbauer et al,468
Vitamin E may possess greater inhibitory effect on LDL oxidation than either
beta carotene or vitamin C.595,624 Oxidized LDL is chemotactic for circulating
monocytes,281,578,891 and may be selectively taken up by the monocytes or
macrophages, processed by the scavenger receptor mechanism, and incorporated
into the cholesterol esters that become fatty streaks and plaque in the arterial wall,
(forming pathologically-modified, relatively immobile monocytes, or "foam cells")
initiating the atherosclerotic process.281,471,573,574,809,891 Oxidized LDL may also
contribute to atherogenicity by the reduction of macrophage motility in the arterial
intima,577 increasing sub-intimal monocyte accumulation,578 and by increasing
cytotoxicity in vascular smooth muscle and endothelial cells. 579 Oxidized LDL
may exacerbate existing coronary lesions by increasing vasoconstriction in the
arteries.620 Interestingly, the scavenger receptors on activated monocytes are
insensitive to unaltered LDL, suggesting that only the oxidatively modified
LDLOX and not LDL itself is inherently atherogenic.891 Apparently, increased
HDL levels may reduce atherogenic risk by reducing the potential for LDL
oxidation, or by removal and disposal of the oxidized portions of the LDL
particles prior to their incorporation in the arterial wall as atheromatous streaks. 891
Dietary Fats and LDLOX
Certain dietary fats are more resistant to oxidative modification. Oleic Acid, an
omega-9 C18:1 monounsaturated fatty acid supplied primarily by olive oil, is one of
the most resistant fatty acids, and is more resistant to oxidation than is linoleic
acid.891 Because dietary fat intake determines the type of fat which is incorporated
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into the phospholipids and triglycerides contained in the LDL particle, dietary fat
consumption can directly effect the potential for LDL oxidation. This may explain
the protective effect associated with the olive oil-rich Mediterranean diet.
Vitamins and LDLOX
Sufficient quantities of water-soluble antioxidants (such as vitamin C) are
required in the hydrophilic environment of intracellular spaces, 593 and sufficient
lipid-soluble antioxidants (such as vitamin E, or carotene) are required in the
blood, within the LDL particle,832,833 and in the sub-endothelial space, (a
hydrophobic environment in which much of the oxidation of LDL particles occurs,
and which favors the protective effect of the fat-soluble antioxidant vitamins over
water-soluble vitamins) to neutralize free radical oxidative attack on arterial
intima and on LDL subfractions which results in atherogenesis. 537,594 Indeed,
intracellular antioxidant levels may be more important than serum levels in the
inhibition of cell-mediated oxidation of LDL.471,586 Lipid soluble antioxidants are
transported within the LDL molecules in the serum, preventing or reducing the
process of toxic lipid peroxidation of these molecules by free radicals, 483,832
reducing the formation of vessel wall irritants which can damage arterial intima,
and preventing the suppression of the synthesis of prostacyclin (PGI 2), a natural
antioxidant hormonal compound which helps to prevent the formation of abnormal
blood clots.392 In addition, data suggests that the flavonoid antioxidants and other
plant phenolic compounds can inhibit lipid peroxidation in vitro, 869 and inhibit
cyclo-oxygenases, which may reduce the risk of acute myocardial infarction by
reducing the potential for thrombosis.568
Laboratory and Clinical Studies of Folate and the B Vitamins.
Folic acid (Folate, or Folacin) is part of the water-soluble vitamin B-complex and
functions as a coenzyme, together with vitamins B12 and C, in the metabolism of
proteins. One of the primary roles of folic acid is the formation of heme, the iron-
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containing protein found in hemoglobin which is necessary for the formation of
red blood cells. Folic acid is produced primarily by plants, and is supplied in the
diet by whole grain cereals and breads, fresh green leafy vegetables, fruits,
oranges, cantaloupe, beans, broccoli, spinach, cabbage, cauliflower, peas, sweet
potatoes, beets, greens, sprouts, and yeast.844,845 Processing and refining destroy
folate. Folate levels are 50% higher respectively in whole grain breads than in
white bread.253 Folic acid is also destroyed by exposure to heat, light, air, and
during storage.844,845 There is some evidence which suggests that folic acid may
be beneficial in the treatment of atherosclerosis,472,844 and reduced levels of folate
have been associated with an increased risk for early-onset CAD.925 Excessive
alcohol consumption increases the need for folic acid either through malabsorption
of the vitamin, or by inadequate diet (which is common among alcoholics).
Vitamin B6
Vitamin B6 is an essential, water-soluble vitamin which plays a crucial role in
both cardiovascular and immune function. It assists in the normal function of
linoleic acid, in the release of glycogen for energy, and helps maintain the balance
between sodium and potassium.844,845 Leafy green vegetables, whole grain cereals,
potatoes, legumes, fruits, spinach, lentils, and soybeans are some of the primary
sources of vitamin B6 in the human diet.844,845,846 Processing, refining, and light
destroy vitamin B6. Vitamin B6 levels are 400% higher in whole grain breads than
in white bread.253
In numerous clinical studies, Vitamin B6 status has been shown to be negatively
correlated with aging in humans,921 and a deficiency status has been shown to
increase plasma levels of homocysteine,622,925 a marker for increased risk of CAD,
stroke, and vascular disease.622,923,924,925,926,927,928 Clinical research suggests that
the bioavailability of piroxidine supplementation does not change with age, and
that the risks associated with vitamin B6 deficiency may be reduced by
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supplementation with pyridoxine.622,920,921 Because of dietary inadequacies,
vitamin B6 deficiency is more prevalent among members of lower Socioeconomic
status.
Vitamin B12
Vitamin B12 (or cobalamin) is a water soluble essential vitamin which is unique
in that it is the only naturally occurring organic compound containing cobalt as
part of its structure, and is the most structurally complex of the vitamins. Vitamin
B12 cannot be synthesized by the human body, and animal protein is essentially the
only substantial natural source of the vitamin in the diet.844 Because vitamin B12 is
supplied by animal sources including eggs, dairy products, poultry, and fish, 253,472
supplementation may be required by vegetarians, and by older individuals who
may tend to consume less animal protein. Conditions of increased oxidative
stress, fatigue, or recovery from illness may also warrant increases in vitamin B 12
intake,472 and supplementation among the elderly may also be prudent. Numerous
investigators have reported serum cobalamin deficiency among the elderly, and a
recent examination of the extensive Framingham database by Lindenbaum and co-
workers919 showed that deficient serum cobalamin levels were found among over
40% of 548 elderly surviving members of the original Framingham cohort.
Deficient levels were found in only 18% of younger control subjects. Vitamin B 12
deficiency is associated with increased levels of homocysteine. The risks
associated with vitamin B12 deficiency may be reduced by supplementation with
cobalamin, especially among the elderly.919
Clinical and Epidemiologic Studies
A prospective study by Stampfer et al, 622 the Physicians' Health Study
investigation which was published in 1992, demonstrated an increased risk of
myocardial infarction among American physicians with elevated levels of plasma
homocysteine. Physicians with the highest levels of homocysteine were three
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times more likely to suffer a myocardial infarction than those with the lowest
levels. Folate and vitamin B6 were shown to reduce otherwise elevated levels of
homocysteine in a subgroup, and reduce the risk of acute myocardial infarction.
This research confirms previous scholarship published in 1991 in the New
England Journal of Medicine923 by researchers in Ireland and Great Britain, who
found that 28 to 42% of patients with CAD, cerebral vascular disease, or
peripheral vascular disease had elevated levels of homocysteine. Similarly, Boers
et al,926 Malinow et al,927 and Genest et al928 showed that elevated levels of
homocysteine predicted premature onset of CAD, PVD, and stroke in both men
and women. In December 1993, an association between B-vitamin intake and
homocysteine levels was confirmed by an analysis of the extensive Framingham
database of 1,160 elderly men and women age 67 to 96, and published in the
Journal of the American Medical Association. This report clearly demonstrated an
association between plasma homocysteine levels and B6, B12, and folate
consumption. Nearly 30% of the 1,100 Framingham patients examined had
elevated levels of homocysteine, and two-thirds of those with elevated levels also
had sub-therapeutic plasma levels of B6, B12, and folate.
Similarly, Clarke and co-workers923 demonstrated that patients with high serum
levels of homocysteine were nearly 28 times more likely to develop premature
vascular disease than those with normal levels. A case-control study examining
early onset CAD among 101 white male patients, and 108 white male controls
conducted by Pancharuniti et al925 demonstrated an inverse correlation between
plasma levels of homocysteine and those of both vitamin B12 and folate, and found
that elevated plasma homocysteine was an independent risk factor for early-onset
CAD.
Although the American poor typically consume adequate amounts of animal
protein, and therefore are not likely to be deficient in vitamin B12, the indigent
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consume less foods which are high in the other B vitamins and folate than do the
affluent, rendering the poor more susceptible to deficiencies of these vitamins,
potential increases in homocysteine levels, and increased risk of CAD.
Laboratory and Clinical Studies of Flavonoids.
Flavonoids (or bioflavonoids) are a large group of polyphenolic antioxidants
which occur as natural compounds found in fruits, vegetables, nuts, seeds, leaves,
flowers, bark (tea), and wine.281,467,561,562 Flavonoids represent an important class
of antioxidants which may have a stronger scavenging effect upon oxygen free
radicals than the antioxidant vitamins.623 The most important flavonoids in human
nutrition are anthrocyanins, flavonols, flavones, catechins, and flavanones. 467 In
food plants, they impart color to flowers, stems, the skin of fruits, and leaves.
Many of the medicinally active substances in herbs are bioflavonoid compounds.
Bioflavonoids were first isolated as an "impurity" in a preparation of vitamin C
by Hungarian researcher Albert Szent-Gyorgi who named the substance "vitamin
P." Szent-Gyorgi, who subsequently won the Nobel Prize in medicine for the
discovery of vitamin C, determined that the flavonoid compounds had biological
activity which was distinct from that of vitamin C, and were beneficial in
protecting the capillaries.472 Subsequent research has demonstrated that they
possess powerful antioxidant activity, and may reduce atherogenesis and inhibit
the formation of blood clots.467,472,473,474,542 Flavonols are scavengers of free
radicals such as superoxide anions,563 singlet oxygen,564 and lipid peroxy
radicals,575 and have the ability to protectively sequester metal ions through
liganding.576 This process of free radical scavenging interrupts radical chain
reactions, stabilizes cellular processes, preserves cellular integrity, and reduces
intracellular oxidative damage, and the oxidation of serum LDL. Oxidized LDL is
atherogenic and may be important in the pathogenesis of atherosclerotic
disease.467,567 Research has demonstrated that Quercitin, a major flavonol,
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inhibits the oxidation and cytotoxicity of LDL in vitro.565,566 Additionally,
Flavonoids inhibit lipid peroxidation and cyclo-oxygenases,568,869 resulting in
reduced platelet aggregation. This may reduce the potential for thrombosis, and
coronary artery disease.568,869
Although not classified as vitamins, both animal and clinical studies have
demonstrated that flavonoids possess vitamin activity, and some researchers
consider them to be essential for humans.472 They are synergistic with other
antioxidant compounds such as vitamin C, and exert a beneficial effect on
capillary stability and permeability.294 High serum iron status, and particularly
iron from animal sources, may compromise the potentially protective effects of the
phenolic flavonoid compounds. Similar to ascorbate and to many of the other
antioxidant vitamins and nutrients, phenolic compounds have shown pro-oxidant
effects when mixed with high concentrations of iron ions in vitro. 568 This suggests
that the less tightly bound and more reactive elemental iron contained in heme iron
(supplied by red meat) may, in the situation of a positive heme iron balance, cause
dietary phenolic compounds to paradoxically react as pro-oxidants. High heme
iron status is a condition which is more common to members of the lower
socioeconomic class in America who tend to have high animal protein intakes, and
equivalent iron intakes to those of higher SES.42 Because the indigent are less
likely to obtain iron (in its non-heme form) from plant sources, this may place the
American poor at greater risk for acute thrombotic events.
Clinical and Epidemiologic Studies
A recent epidemiologic study from the Netherlands, the Zutphen Elderly
Study,467 an extension of the Dutch cohort of the pioneering seven-country study
by Keys,522,526,527,546,600 assessed patients' intake of certain flavonoids found in
fruits, vegetables, tea, and wine. Researchers measured the concentration of
flavonoids in various foods, and used dietary surveys to estimate the quantity of
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flavonoids consumed by 805 men (aged 65 to 84 years) between 1985 and 1990.
The primary sources of flavonoids for these men were black tea (which accounted
for 61% of their intake), onions (13%), and apples (10%). During the five-year
period there were 43 deaths. Even after adjusting for other factors known to be
protective against heart disease, the risk of dying was three times higher in the
men with the lowest flavonoid intake.
There is a significant body of additional research verifying the beneficial effects
of the flavonoid compounds. Frankel and associates542 reported that antioxidant
phenolic substances in red wine (which contains 10 to 20 mg/L of combined
flavonoids569) inhibited the oxidation of human LDL in vitro. Cold pressed olive
oil also contains antioxidant phenolic substances which have shown the ability to
completely stop the in vitro oxidation of LDL. The flavonoid compounds present
in red wine may be partly responsible for the reduced risk of CAD among wine
drinkers (the "French Paradox").467,570
Because members of lower SES tend to consume significantly fewer vegetables
and fruits than the affluent, they may consume less than the 20 to 30 milligrams of
bioflavonoids that the average American consumes on a daily basis, and may be at
greater risk of developing CAD or death. Additionally, research indicates that low
dietary intake of flavonoids is associated with increased lifetime cigarette
smoking, which further potentiates the risk of CAD in this population. 467
IX. Summary, Conclusions and Recommendations
The Legacy of the Welfare State.
Since 1960, the population of the United States increased by 41%, and the
Gross Domestic Product has nearly tripled. During this period, however, total
social spending by all levels of government (measured in constant 1990 dollars)
has risen from $143.73 billion to $787.0 billion--more than a five-fold increase.405
The legacy of this social welfare spending is enormous. Following World War II
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and prior to 1960, the gross federal debt remained stable, at around $250 billion.
Since the institution of the federal welfare programs in the mid 1960s, and their
proliferation in the 1970s, the gross federal deficit has grown exponentially [see
Fig. 36].
Figure 36: Gross Federal Debt, 1945 to 1992
_________________________________________________________________________________
Source: The Cato Institute
Inflation-adjusted spending has increased by 630% on welfare and by 225% on
education, yet during this same thirty-year period, there has been almost a 600%
increase in violent crime; more than a 400% increase in illegitimate births; a 300%
increase in the rate of divorce; a tripling of the number of American children
living in single-parent homes; more than a tripling of the teenage suicide rate; and
a precipitous drop of almost 80 points on the Scholastic Aptitude Test (SAT)
scores. 405 States spending the most tax dollars per pupil on public education
frequently have the worst students in academic performance. Although the
District of Columbia's per pupil expenditures are among the highest in the nation,
its public schools are last in the nation in academic testing scores.
Crime is increasing exponentially in American cities despite a hemorrhaging of
federal and state tax dollars into prevention and rehabilitation programs. Despite
police and prison spending which is four times the national average, and despite
one of the strictest gun laws in the nation, Washington, D.C. remains the murder
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capitol of the United States.
When the great Society social welfare spending programs were first established
in the early 1960s, approximately 12.3% of the American people were living at or
below the poverty level. After thirty years and an expenditure of over $2.3 trillion
on welfare programs, the percentage of Americans living at or below the poverty
level is currently unchanged or worsened; and is now estimated to be between
12.3% and 15%, depending on the type of measurement used to determine the
level of poverty.109,160 According to the most recent census data, the number of
American poor increased in 1992 by 3.4% to 36.8 million persons. This represents
an increase of three times the rate of population growth, and the highest level
achieved since 1962, which was prior to the creation of most federally funded
social welfare programs.160 Black and Hispanic Americans were three times more
likely to be poor than whites, and 1992 census data indicated that one third of all
blacks lived in poverty and 29.3% of all Hispanics were poor,160 although these
population groups receive a disproportionately higher per capita share of federal
social welfare dollars.
The food stamp program has experienced exponential growth within the last
decade, increasing in cost to the American taxpayers by 55% to $22 billion
between 1990 and 1993 alone. During this same period, there was a 35% increase
in the number of food stamp recipients to 27 million Americans.
Although the percentage of Americans below the poverty level appears to be
slightly increasing despite the exponential increase in welfare spending, and
although this expansion in American poverty has paralleled the explosion of crime
in America, poverty has almost nothing to do with crime. In a recent review of the
social science literature on violence and delinquency, Heritage Foundation scholar
Patrick Fagan demonstrates that it is changing family structure and dynamics, and
not poverty which effects crime in the United States. If the poverty-causes-crime
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hypothesis were correct, one would expect to see crime rates fall as incomes rise,
and vice versa. History clearly negates this view. Crime in America rose
gradually from 1905 to 1933, a period of economic growth and rising personal
incomes, however when the Great Depression hit, the crime rate fell dramatically
as families were pulled together for their survival.
Conversely, data from all 50 states show a direct correlation between the rise of
single-parent families and the increase in juvenile crime. In fact, a 10-point
increase in the percentage of children living in single-parent homes accompanies a
17 percent increase in juvenile crime. Even in high-crime, inner-city
neighborhoods, well over 90 percent of children from intact, stable families never
commit crimes, while only 30 percent of children from broken homes in these
same neighborhoods avoid criminal behavior.
The statistical data seems to implicate dysfunctional single parent families and
not single parent families arising from the death of a spouse. As important as two
parents are, it is not the number of parents who raise a child that effects his
inclination towards criminality and aggression; it is also the quality of his
relationship with his family. Single-parent families of illegitimate children led by
never-married welfare-dependent women are radically different from families led
by widows raising legitimate children. In the latter family, the memory of the
father is present, even if he is not, lending the mother a measure of necessary
moral authority. Children of such families demonstrate none of the pathology
associated with children of never-married parents. Families dependent upon
welfare are significantly more likely to be headed by never-married mothers, and
are therefore vastly more susceptible to these pathological behaviors.
The expansion of the social welfare state has negatively impacted upon both the
non-working recipients of welfare and upon working Americans. Due in large
part to decades of escalating social welfare spending, the current American tax
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structure is confiscatory by comparison with four decades ago, and frequently
forces wives and mothers of young children into the work place to maintain a
standard of living.809 Since 1950, prior to the establishment of all federally funded
social welfare programs, the income tax burden on an average American family of
four has increased over 6-fold from 4% of income in 1950 to 24% of income in
1980.405 In the 1990s, the tax burden of an average family with children has
increased by a factor of over nine times the rate imposed in 1950, and currently
this average family pays 37.6% of their gross earnings for federal, state and local
taxes, Social Security, and Medicare.809 The current average family tax burden
totals over 45% if the "employer contribution" to Social Security tax, which
actually represents a hidden portion of employee compensation, is taken into
account. The amount of this tax burden exceeds the current annual cost of the
average home mortgage.809 In Sweden, Norway, and Eastern Europe, the tragic
legacies of their social welfare programs have literally devastated national
economies and crippled their middle class,109 yet these programs have not
significantly alleviated poverty in those countries.
Among Americans of lower socioeconomic status, the social welfare program
and federal taxation policies have been responsible for a number of detrimental
effects including:
1) Causing the loss of independence and personal initiative by the creation of
multi-generational wards of the state. Family fragmentation generates a
particularly debilitating form of poverty: welfare dependency. This is especially
true for unmarried adolescent mothers, nearly 80% of whom receive welfare
within 5 years of becoming a parent. More than 40% of long-term and lifetime
welfare recipients had their first child at age 17 or younger.224 Because the under-
class of non-productive citizens is experiencing slow growth across the United
States, and rapid acceleration in major urban areas, this poses a significant
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economic threat to certain communities whose pool of productive tax-paying
citizens remains stable, and constitutes a crisis to communities whose productive
working population is shrinking.
2) Causing or facilitating the breakup of the family, by selectively rewarding
single parenthood, while removing benefits for traditional two-parent households.
According to the Report of the National Commission on America's Urban
Families, "The current welfare system, through it's misguided incentives, keeps
families apart. For example, for a woman on [Aid to Families with Dependent
Children (AFDC)], it is better for her to collect AFDC than to marry the father of
her children if the father is not holding a high wage job." 224 For those families not
receiving federal assistance, current federal tax policies will increase the tax
burden on 52% of married couples. A "marriage penalty" is written into the new
IRS tax code requiring husbands and wives to pay $1,244 more in federal tax than
they would if they were divorced or living together out of wedlock. 810
3) Placing incentives on illegitimate birth by providing increasing monthly
stipends for the birth of each successive child, or otherwise helping to facilitate
illegitimate births. In fact, although the poor constitute between 12.3 to 15 percent
of the American population,160 one third of all U.S. births in 1993 were to mothers
on Medicaid,312 a government program providing hospitalization and medical care
to the poor or to persons of limited income, ninety percent of which is financed
through federal tax dollars, and ten percent of which is financed through state and
local funds. In 1993, two hundred and sixty Medicaid patients in twelve States,
58% of whom were additionally receiving assistance through Aid to Families with
Dependent Children (AFDC) which covers primarily single mothers, received
fertility drugs which were paid for by Medicaid.312 Sixty three percent of these
women already had children and two women already had eight children each, all
of whom were currently on public assistance. The state of New Jersey alone spent
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almost a quarter of a million dollars on fertility assistance to Medicaid recipients
in 1993 alone, even in light of the fact that most private health insurance plans do
not cover infertility services.
4) Causing or facilitating the abdication of personal, family, and community
responsibilities by the appearance that the state will fulfill those responsibilities
for the individual, and by placing economic dis-incentives upon the fulfillment of
those responsibilities. In 1961, John Kennedy challenged and inspired the
American people with, "Ask not what your country can do for you--ask what you
can do for your country." Richard Nixon wrote that by the end of the decade of
the 1960s, however, "many people were asking why the federal government had
not done all the things it had promised and undertaken to do for them." 888
5) The establishment of an "entitlement mentality" by convincing members of
lower SES that society is responsible for their support and sustenance. By
defining social welfare programs as "entitlement programs," the American
government has delivered a dangerous and misleading message to the economic
under-class it should rather seek to motivate and "lift by its bootstraps." Certain
members of the American under-class perceive these programs as payment of a
debt owed, rather than as governmentally-sponsored charity. Senator Robert
Byrd406 recently criticized the Supplemental Security Income (SSI) federal
disability program for making disability cash payments to individuals solely on the
basis of their claim to be drug addicts or alcoholics. He further stated concern that
this well-intentioned entitlement program was being misused by parents who were
coaching children to fail tests or misbehave in school in order to be classified with
a behavioral disorder and qualify for monthly SSI disability payments of up to
$446.00. Byrd stated that he was concerned about "the damage that is being done
to our children, in teaching them that their future lies not in hard work, but in
ripping off the federal government."406
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6) Increasing Hopelessness and Despair among the working poor by placing
negative incentives on the American work ethic, and among welfare recipients by
the bureaucratic stripping of their dignity and by the establishment of an almost
inescapable cycle of dependency. Concerning the social welfare programs
established in the early 1960s under Lyndon Johnson's "Great Society", Richard
Nixon wrote: "The problems were real and the intention worthy, but the method
was foredoomed. By the end of the decade its costs had become almost
prohibitively high in terms of the way it had undermined fundamental
relationships within our federal system, created confusion about our national
values, and corroded American belief in ourselves as a people and as a nation."
The former President further stated, "From 1960 to 1969, the cost of welfare
benefits for families with dependent children nearly tripled. More than a quarter
of a trillion federal dollars was spent between 1964 and 1969 in an attempt to
eradicate poverty and inequality. But instead of solving problems, these programs
themselves became part of the problem, by raising hopes they proved unable to
fulfill...Perhaps most demoralizing of all, the working poor watched while the
non-working poor made as much money--and in some cases even more money--by
collecting welfare payments and other unemployment benefits. This began a bitter
cycle of frustration, anger, and hostility."888
7) Ethnic polarization, by convincing the poor that society is responsible for their
problems, and by demoralizing the productive working poor by granting economic
perks to the non-working poor equal to or greater than those capable of being
earned by the working poor. Congress is currently considering legislation which
will further establish the dependence of the indigent upon the social welfare
system, and further polarize the working poor and middle class by granting
welfare recipients a short-cut to the lifestyle of the self-reliant upper middle class.
Housing and Urban Development (HUD) assistant secretary for fair housing
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Roberta Achtenberg has called the current administration's $60 billion Housing
Choice and Community Reinvestment Act "the largest investment in civil rights
that the federal government [has] made in the past fifteen years." An additional
$149 million is being sought by HUD for the "Moving to Independence" program,
which will provide rental vouchers to indigent people in inner-city public housing
projects to move into surrounding middle class and affluent suburbs. HUD is
using the Section 8 program, passed by congress in 1974, to provide $7 billion this
year, and $14 billion per year by 1996 in direct rent subsidies to approximately
two million low-income families. These rent subsidy vouchers will entitle welfare
recipients and their families to live in apartments with rents as high as $1,657 per
month, ($19,884 per year), for a four bedroom apartment in some well-to-do areas,
a higher rent than the vast majority of American upper middle-class renters are
currently paying.887
In addition to these programs which increase resentment among the working
poor, there is an increasing national tendency to shift blame on American society
for both the socioeconomic status and criminal behavior of the poor. This attitude
grants "psychological absolution" to criminal activity if the perpetrator is poor,
and may encourage criminal behavior among the indigent.
The Probable Cause of the Paradoxical Shift of SES associated Risk.
The paradoxical shift in SES-associated cardiovascular disease risk may be
explained by differential changes which occurred between high and low
socioeconomic classes in the decade of the sixties. These changes involved
modifications in lifestyle and diet, and either placed individuals at greater or at
lesser risk of oxidative modification of LDL cholesterol [see Table 12 and 13], or
degenerative tissue injury. Changes which were instituted by higher SES
Americans were predominantly influenced by the recommendations of both the
American Heart Association and the Surgeon General of the United States in early
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1964. Changes which were instituted by lower SES Americans were primarily
influenced by popular advertising, peer influence, and the American social welfare
system, and began within the same decade. While the affluent lived in stable
neighborhoods, had greater access to health education, eschewed saturated fat,
cholesterol, and tobacco, and began to embrace an active lifestyle, the American
poor migrated to the unstable and stressful environment of the inner city. Here the
under-class increased consumption of highly processed foods rich in saturated fat
and cholesterol, and were increasingly exposed to radio, print media, and
television advertising which encouraged the use of tobacco and alcohol. The poor
abandoned their "indigent" diet of vegetables, fruits and cereal grains in favor of a
highly processed, high-fat, "urbanized" diet high in sugar and salt. Availability of
federal welfare dollars allowed greater affordability of high fat foods, or presented
opportunities for diversion of money to purchase tobacco products, and the non-
productivity and demoralization of a dependent welfare existence encouraged an
increasingly sedentary lifestyle.
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TABLE 12: Factors Effecting the Oxidation of LDL Cholesterol and Their
Prevalence among Individuals of Low or High SES in the United States, 1900
to 1964.
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TABLE 13: Factors Effecting the Oxidation of LDL Cholesterol and Their
Prevalence among Individuals of Low or High SES in the United States since 1964.
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Working Hypothesis
1. Factors causing the rise in CAD mortality which was documented primarily
among the upper socioeconomic class between 1900 and 1940:
During the white majority migration from the farms to the cities, urbanization
resulted in the fragmentation of the nuclear and the extended family, decreased
social support, and increased stress. Technological advances, which were more
accessible in urban areas, resulted in more sedentary lifestyles, and increasing
affluence was associated with the adoption of popular, although deleterious,
dietary and lifestyle changes. These included the abandonment of the traditional
"rural diet" of vegetables, fruits and grains; the adoption of an "urban diet" rich in
saturated animal fat and highly processed and refined foods; and the increased
affordability and availability of tobacco products among the upper socioeconomic
class. These factors contributed to the rise in CAD incidence, acute coronary
events, and coronary death rates observed among the affluent during this period.
2. Factors causing greater CAD mortality among members of low SES after 1960:
The establishment of the social welfare "Great Society" programs of the early
1960s accelerated the migration of the rural poor to the cities, subjecting the
indigent to significantly greater stress than was experienced in the rural areas.
The decade of the 1960s saw a marked trend toward the disintegration of the
traditional supportive nuclear family which accelerated in the vacuum created by
an American moral decline, and the abandonment of the Judeo-Christian basis for
a "national ethic." A federal tax structure placing increasing burdens upon the
American working family, driving mothers of young children into the work-force,
and a national social welfare policy preferentially rewarding fatherless families
further contributed to the disintegration of the supportive nuclear family unit, and
the increase of despair, dependency, and hopelessness among the American
indigent. The family has historically been the bastion of this support, and its
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weakening in the moral vacuum of the 1960s left in its wake dysfunctional
members who were more vulnerable to the ravages of psychological stress, and
who were at increased risk of acute, catecholamine-mediated coronary events.
Into these dysfunctional households were born increasing numbers of children
whose unwed mothers were destined to remain single due to destructive incentives
built into the American social welfare system, further establishing the
abandonment of responsibility and cycle of despair. The feeling of powerlessness
among those entrapped within the social welfare system increased the life stress of
those consigned to the system, and drove others to regain that lost power and self-
determination through violent criminal activity which primarily impacted the
urban poor, and further increased the stress and the cycle of hopelessness of their
seemingly inescapable condition.
Additionally, the urban indigent experienced a shift from an active rural lifestyle
and a healthy agrarian diet (high in fiber, indoles, flavonoids, cruciferous
vegetables, phytochemicals, and natural dietary sources of antioxidant vitamins
and minerals) to a subsidized and more expensive urban diet which was higher in
fat, lower in fiber, and consisted largely of highly refined and vitamin-depleted
foodstuffs. Prior to 1960, the poor had a lower risk for sudden coronary death and
CAD mortality than did the rich because the poor could not afford the luxurious
indulgences of the affluent of that era, including a leisurely lifestyle, and a diet
rich in saturated fat. The poor were less able to afford tobacco products than were
the wealthy. In the first half of this century, blacks, and the rural poor consumed
diets out of economic necessity. These healthy foods cost less than the more
"prestigious" highly processed or prepared foods. The rural poor led significantly
more active lifestyles associated with the demands of a farming economy, and
frequently were members of stable family groups characterized by the presence of
both parents, and of the extended family members. Following 1960, an abrupt
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change occurred. Changes in lifestyle, environment, dietary habits, or other
factors known to contribute to CAD could not individually account for increases
in CAD mortality observed among the poor, but collective changes in many or all
of these risk factors could acount for the magnitude of the observed increases.
Increases in refined sugar intake, tobacco consumption, alcohol abuse, sedentary
lifestyle, and decreases in the consumption of high-fiber complex carbohydrates
all served to increase the risk of CAD among the indigent. These dietary and
lifestyle changes are consistent with populations experiencing increasing affluence
while not having access to, or choosing to ignore a model of preventive dietary
and lifestyle changes [see Fig. 37].
Figure 37: Income among Rural Bantu, Urban Blacks, and White Europeans
and Corresponding Animal Fat and Vegetable Fat Intake, and Serum
Cholesterol
with Superimposed Rates of Electrocardiographically Evident AMI
______________________________________________________________________________________________
Adapted from: Brock and Bronte-Stewart444
A documented nine-year decline in physical activity occurred primarily among
members of lower SES in the late 1960s, and continued into the decade of the
1970s. Transition from the higher daily exercise and intense activity levels
associated with a rural self-sufficient lifestyle, to a more sedentary lifestyle
associated with non-productive social welfare dependency, resulted in an
increased risk of CAD among the poor.
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The poor abandoned a rural lifestyle rarely associated with the use of tobacco
products due to monetary, social, and religious restrictions. In the cities, the use
of tobacco products increased considerably due to greater affordability, relaxation
of social and moral restrictions, and increased access and advertising exposure to
tobacco products.
The urban poor, and specifically the blacks, benefited less from, or had less
access to patient and consumer preventive education concerning the advisability of
reducing of animal fat and cholesterol intake, and smoking cessation. Both the
Surgeon General's and the American Heart Association's 1964 recommendations
on smoking and dietary changes were largely unheard or unheeded by the lower
socioeconomic class.
3. Factors causing an early decline in CAD death rates primarily among members
of higher SES, first seen in California in the early 1960s, and seen nationally by
the end of the decade:
California led the nation in the quest for a healthier lifestyle, including smoking
cessation and dietary improvements. A significant reduction in the percentage of
smokers occurred primarily among those of upper SES in the mid to late 1960s,
and the acceptance of the importance of reduced fat and cholesterol diets
contributed directly to this national trend of reduced CAD mortality which
occurred primarily among the affluent. Data from several long- term population
studies suggests that reductions in mean serum cholesterol were more significant,
and were achieved more rapidly by the highly educated.35
Additional research suggests that reduction in milk and butterfat intake, and
increased consumption or substitution of monounsaturated fats and vegetables
(which are dietary practices more common among members of higher SES), may
have been responsible for significant reductions in CAD risk. 476,891 In the Seven
Countries Study, Keys et al546 demonstrated that the CAD death rate was
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negatively correlated with the percentage of dietary calories from
monounsaturated fats such as olive oil. Consumption of monounsaturated fat is
highest among the affluent in the United States.
In addition to changes in diet and smoking habits which were adopted by
Americans in the decade of the sixties and subsequently, data indicates that
millions of Americans have become more active in their leisure time, and that
members of higher SES tend to be more active than the indigent or less educated.35
Californians have also led the nation in the adoption of more active lifestyles.
This may also have contributed to early CAD reductions there.xxx
4. Factors causing greater CAD incidence among younger members of lower SES;
the increases in acute CAD among both the indigent young and among women;
and the narrowing of the CAD margin between women and men:
The environment common to the urban poor is conducive to stress-associated
disorders. There is a high prevalence of hypertension and an increased potential
for psychosocial effects on blood pressure and hemostatic factors among blacks
and the indigent. Living in an unstable urban environment increases cortisol
levels. This, in conjunction with drug and alcohol abuse, tobacco use, a sedentary
lifestyle, and dietary insufficiencies associated with poverty, increases the risk of
acute thrombotic events. The young urban poor have greater exposure to these
risks.
Tobacco advertisers target (or have targeted) blacks, the young, and women.
Alcohol and high-fat food advertisers frequently target urban blacks. These
advertising campaigns have been responsible for increases in smoking initiation
and fat consumption among younger blacks, and for increases in smoking
initiation among women (and particularly younger women of lower SES). They
have contributed to the narrowing margin of CAD incidence between blacks and
whites, and have reduced the margin between men and women.
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Differences in rates of acute CAD between men and women parallel changes in
smoking behavior over time, with the margin of men's use of tobacco versus
women increasing from 1931 through 1950, and narrowing since 1960.
Concomitant increases in female smokers following aggressive advertising
campaigns directed at women in the late 1960s and early 1970s were probably
responsible for the narrowing of the gap between female and male CAD deaths in
the last two decades.
Increased caffeine, tobacco and salt consumption is more prevalent among those
of lower SES, and among the urban young. Drug abuse is more prevalent among
the urban poor, and is most prevalent among the youthful poor. These behaviors
increase serum catecholamines, heighten the effects of stress, and may precipitate
acute coronary events among the younger urban poor.
Mortality data by race and sex for 1960 through 1975 indicated that
improvements in CAD mortality occurred for white males but not black males,
which is consistent with differences in smoking behavior between the two races
during this period, and presently. Currently, younger members of lower SES are
significantly more likely to engage in CAD risk behavior, have poorer coping
skills, and demonstrate significantly more aggressive behavior.
Social support appears to have a protective effect against CAD. This may
explain why women, who tend to have stronger social relationships and intimate
ties than men, experience lower CAD rates, however the greater trend toward non-
traditional or dysfunctional families among the indigent may be reversing this
protective trend more exclusively among poor women. Social isolation,
depression due to lack of social support, deterioration of the family unit, poor
stress coping styles, job stress or the stresses associated with joblessness, and
unresolved anger and hostility are among the psychosocial factors which may link
low SES to increased CAD. Frustration and perceived loss of control over one's
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life due to repeated non-achievement and social failure, conditions more common
to young members of lower SES, may result in a fatalistic attitude which increases
psychological pressure and coronary risk.4,10,279,328,328
5. Factors causing reduced incidence of CAD among older blacks and older
members of lower SES:
This phenomenon may be due to an unmasking of a true genetic resistance to
CAD among blacks who predominate the lower SES. This resistance is suggested
by the reduced rates of CAD consistently seen in clinical studies of blacks in the
first half of this century, and is validated by recent angiographic studies showing a
decreased prevalence of coronary atherosclerotic plaques in blacks, by
epidemiologic studies showing lower incidence of CAD among upper SES blacks
than among whites of lower or higher SES, and by census data showing
consistently lower mortality from CVD among older blacks versus whites.
According to U.S. Census data,217 major cardiovascular diseases accounted for
37.7% of deaths reported due to all causes in 1989 among blacks and for 44.3% of
those deaths reported among whites. From birth through age 69, black mortality
from major CVD (16.1% of all deaths) consistently exceeds that of whites
(10.65% of all deaths) as a percentage of total deaths, however by age seventy
(and consistently thereafter), whites succumb to CVD at a significantly higher
rate.217
The reduction of certain at-risk behaviors (drug abuse, stressful lifestyle related
to urban violence, hostile behavior, smoking, alcohol abuse, and dietary abuses)
which are more common to youthful members of lower socioeconomic status may
occur less frequently among elderly blacks, resulting in a statistical shifting of
increased CAD risk, (and especially an increased risk of acute events), to younger
members of low SES, [see Fig. 38].
Figure 38: Relative Risk of Cardiac Arrest in Blacks as Compared to Whites
According to Age
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Bars are 95% Confidence Intervals.
A relative risk of 1 would represent an equal risk for both blacks and whites.
____________________________________________________________________________________________
From: Becker et al.178
Many of the at-risk behaviors described above could explain the significant
increases in acute (thrombotic or arrhythmic) deaths among younger blacks which
account for most of the increased risk prior to age 70. At age 70 and beyond,
increases in CAD deaths among older whites are primarily due to chronic
(atherosclerotic) disease. Research has shown that of the known risk factors for
CAD, stress has the greatest potential for rapidly increasing the incidence of acute
CAD in a younger population. Because acute CAD was relatively uncommon
among blacks and among the indigent prior to the decade of the 1960s, and
because significant increases have occurred among blacks and among the indigent
since the establishment of the Great Society social welfare programs, the welfare
system itself may be responsible for these deleterious effects by adversely
effecting life stress, lifestyle or diet among those who have subjected themselves
to, and have become dependent upon the system. If the welfare system were
examined as though it constituted a risk factor for CAD, exposure to this "risk
factor" would be greatest among younger members of low SES. Exposure to this
"risk factor" results in significantly increased risk of CAD versus similarly aged
individuals of higher SES who were not exposed.
Page 201
Since blacks who have lived to a older age have survived the higher risk of acute
CAD which strikes younger blacks at a greater frequency, a possible resistance to
chronic CAD (which becomes evident at advanced age among blacks) may benefit
blacks more greatly than similarly aged whites.
Other research701 has demonstrated that older employed subjects are more
likely to be in jobs with greater decision latitude--in part due to advancements and
promotions--and therefore may be subjected to lower levels of occupational stress
that their younger counterparts.
Older members of lower SES may benefit from the formation of more stable
social relationships which may be lacking in many younger indigent non-
traditional families. In one study, the major difference between the minority high
and low CAD risk groups was the degree of social support.237 The group with the
higher rate of CAD maintained fewer close family and social ties. The low risk
group had strong nuclear families, and maintained close social ties with other
members of the ethnic group. Social networks, religion and a stable marriage
reduces stress and associated CAD risk, and the young urban poor are more poorly
represented in these areas than their older counterparts. The elderly have a greater
commitment to religion, more stable social connections, and are more likely to be
in a stable marriage.
6. Factors causing reduced CAD risks among high SES blacks:
High SES blacks are more likely to be older, and less likely to be currently
exposed to the social welfare system than are their younger counterparts. They are
more likely to have greater autonomy over, and less stress associated with their
daily lives. Reduced CAD risk in these individuals may be due to migration from
stressful inner city environments to the more secure suburban areas, which
together with improved diet, increased exercise, smoking cessation, and other
beneficial lifestyle variables (more consistently and more rapidly adopted by the
Page 202
affluent, the more mature, and the more educated) certainly play a large role in this
differential.
Blacks with the lowest incidence of CAD are rural African blacks who consume
very little or no meat and dairy products,442,444,448,460 and who observe a low-fat
diet similar to the Mediterranean dietary regimen described by de Lorgeril, [see
Fig. 39], consisting largely of vegetables and unrefined cereals high in thiamine,
antioxidant vitamins, and fiber.451,461 Highly educated blacks are more likely to
institute such a diet, or to remain compliant on an austere saturated animal-fat
limiting diet, than those who are less educated.
Figure 39: The Mediterranean Food Pyramid and the USDA Food Pyramid
__________________________________________________________________________________________________________________
__
Source: DeLorgeril,270,850 The U.S. Department of Agriculture; Harvard School of Public Health
7. Factors causing increased CAD among older members of upper SES:
This phenomenon may possibly be due either to an age-related unmasking of
increased genetic resistance to CAD among blacks who predominate the lower
SES, or to concomitant increases in risk behaviors among members of higher SES
to a greater extent than their lower SES counterparts. Because this CAD risk factor
shift typically occurs after age 65, this may reflect the stress of retirement which
may weigh more heavily upon members of upper SES whose lifestyles may
Page 203
change more radically, and who may have their personal identities more closely
tied to their occupations. Frustration and perceived loss of control over one's life
due to abdication of personal responsibility for day-to-day decisions is prevalent
in nursing facilities631 which are more affordable to older members of upper SES.
Additionally, life changes which disrupt relationships (such as retirement
involving residential moves) have the greatest effect on CAD risk,225,236 and
members of upper SES are more likely to experience, or are more able to afford
these types of sweeping changes at retirement.
Recommendations to Reduce CAD Risk Associated with Lower SES.
1. Redesign the welfare system.
a. Change public policy to counter dependency social factors by stopping tax-
subsidization of behaviors which virtually guarantee high rates of illegitimacy.
b. Encourage responsible behavior by requiring all able recipients of welfare to
work in exchange for their benefits, and by requiring AFDC mothers with older
children to contribute community service in exchange for benefits received.
c. Reverse the destructive incentives for single parenthood built into the welfare
system by reduction of economic penalties on marriage for single mothers.
d. Limit both the monetary value and duration of social welfare benefits to the
non-working poor to prevent demoralizing the productive working poor.
e. Encourage the church, community, and extended family to reassume many of
the responsibilities of caring for the poor currently shouldered by the federal
government.
2. Change federal tax codes which place additional economic penalties on married
working couples, families, and the working poor .
a. This could be accomplished by the adoption of the 17% flat tax reform
proposed in U.S. Representative Richard Armey's Freedom and Fairness
Restoration Act. This act provides substantial marriage and per-child deductions
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which would essentially remove the working poor and the lower middle class from
the tax roles.
3. Reform the judicial system to establish significant penalties to deter criminal
activity while expediting and limiting the appeals process.
a. Special emphasis should be given to the establishment of swift and strong
penalties for criminal activity most likely to impact the urban poor, with minimal
or limited opportunities for appelate delay.
4. Remove the economic barriers that keep the under-class in poverty, and weaken
the family.
a. Provide tax incentives for businesses to locate in urban enterprise zones,
incentives for tenant ownership, and responsible investment in low-income
housing.
b. Remove both economic and healthcare incentives for poor women to raise
children without fathers, and strengthen social taboos discouraging elective single
parenthood.
c. Improve efforts to collect child-support payments by requiring parents to
report child-support obligations to the IRS which is empowered to deduct
delinquent payments from tax refunds.
d. Require fathers to take responsibility for their children and obtain gainful
employment through the elimination, limitation, or rapid reduction of social
welfare benefits for non-working, absent, or non-supportive fathers with children,
and the requirement of special courses in responsible fatherhood as a condition for
any interim welfare benefits.
e. Provide job placement assistance and effective employment counseling, and
after a minimum period, require recipients of welfare to obtain gainful
employment, or to constructively contribute or serve the state in some capacity.
5. Reform public education to include instruction on an ethical system of values,
Page 205
encouragement of individual responsibility, parental involvement, and instruction
on CAD risk factors, exercise, beneficial lifestyle modifications, and nutrition.
a. Reestablish the fundamental purpose of education, providing for both
intellectual and moral education of the young.
b. Establish inner-city community-based or church-based public education
programs on lifestyle modifications, nutritional and dietary interventions, exercise,
hypertension, weight and obesity counseling.
c. Establish programs of psychosocial intervention, including stress and coping
skills, counseling, and support groups for anger resolution.
d. Establish instruction on general health guidelines to include risk factors for
CAD, and patient information concerning heart attack symptoms, smoking
cessation, alcohol abuse counseling, medication compliance, regular medical
follow-up, dietary interventions, exercise, lifestyle modification counseling,
reduction in fat and sodium, maternal health counseling, treatment and control of
hypertension, and bood glucose and diabetes control.
6. Establish national guidelines to improve access and quality of health care for
the poor.
a. Require health care cost sharing at a fixed level for both those on welfare and
the working poor.
7. Establish smoking cessation support and counseling programs, especially within
the inner city.
8. Establish effective and accessible community-based screening for known and
suspected CAD risk factors within the inner city to include drug use, obesity,
stress, inadequate diet, hypertension, hyperlipidemia, adult-onset diabetes, chronic
welfare dependency, and other risk factors.
9. Establish and facilitate programs of psychological counseling, stress coping
skills, and depression counseling within major urban areas:
Page 206
a. Review assertive, healthy ways to express anger, along with relaxation
techniques to foster tranquility, and to reduce hostilities.
b. Instruction on active, healthy coping styles.
c. Strengthen the role of churches, synagogues, and religious organizations.
10. Establish national policies, or grass roots community efforts to rebuild and
preserve the traditional two-parent family, and support and preserve the role of the
extended family.
a. Legislatively reverse the destructive incentives for single parenthood built
into the welfare system, and reduce the CAD risk factor of social isolation through
community and church efforts.
b. Modify tax law to encourage the proliferation and preservation of traditional
two-parent families.
c. Establish methods to successfully integrate married couples, (who currently
are under-represented), in federally-subsidized housing projects. Much of the
crime problem confronting residents in public housing stems from the absence of
stable married couples, and married adult males who can function as good role
models for adolescents.
d. Rescind no-fault divorce laws for parents with children.
e. Remove major obstacles to adoption.
f. Encourage and support the establishment of extended family groups.
11. Improve opportunities for productive employment, and require healthy
recipients of social welfare to contribute by working for their benefits.
a. This program can be patterned after the Houston, Texas model which was
challenged by the ACLU and ruled an unfair requirement due to the fact that it
existed in no other state.
12. Facilitate indigent patient programs for antihypertensive or cardiovascular
disease therapy through coordination with pharmaceutical concerns.
Page 207
a. Improved tax incentives could be offered to pharmaceutical concerns for the
institution of such programs, however this should be managed by private
enterprise, or by the local community to remain effective.
13. Help to establish or encourage proper youth role models who advocate
acceptance of individual responsibility, and eschew blame-shifting.
a. This program should be managed by private enterprise, or by the local
community to ensure its effectiveness.
b. Identify risk taking behavior more common among those of lower SES, and
determine ways to discourage it or channel it in a positive direction.
14. Return to religious and moral codes of ethical standards.
a. Remove federal and legislative prohibitions against the free establishment of
religion-based moral or ethical programs within the public sector.
15. Establish programs to improve environmental factors, especially urban
conditions more common to members of the lower socioeconomic class:
a. Address urban environmental hazards and pollutants.
16. Design a widely acceptable, easily-adopted diet based on the Mediterranean,
European, or Pacific Rim Model [see Fig 39].
Page 208
APPENDIX A
List of Figures
Figure Title Page
1. Death Rate Due to CAD 1900 through 1988 4
2. Decline in Age-Adjusted Mortality From All Causes Since 1972 5
3 Prevalence of CAD 1960-62 by Race and Social Class 6
4. All-Cause Mortality by Education and Race 11
5. All-Cause Adult Mortality by Income 12
6. All-Cause Adult Mortality by Employment Status 14
7. A Graph of the Paradoxical 1964 Risk Factor Shift 17
8. Incidence of CAD by age and SES, 1960-62 and 1967-69 19
9. State Economic Areas With Late CAD Mortality Decline 24
10. Males Dying From Acute and Chronic CAD 1931-1980 26
11. Death Rates From CAD by Country in Adult Males 30
12. Mortality in Secondary Prevention Trials 34
13. Mortality in Primary Prevention Trials 35
14. Poverty Rates of Families With Children by Race 51
15. Incidence of CAD versus Sugar Consumption in 30 Countries 83
16. Fat Consumption Versus CAD Mortality in 20 Countries in 1973 84
17. Fat and Milk Product intake versus CAD Deaths in 40 Countries 85
18. Household Composition, 1960-1990 106
19. Married Couple Families with Working Wives 1960-1990 107
APPENDIX A (Continued)
Figure Title Page
20. Percentage of Children Wishing More Time With Their Mothers 109
21. Single Mother Families and Poverty 110
22. Percentage of Unmarried Teenage Mothers, 1970 and 1990 111
Page 209
23. Poverty Rates of Families With Children By Race: 1959-1990 114
24. Premarital Births By Race: 1960-1964 and 1985-1989 115
25. Incidence of Hypertension by Level of Tension in Men aged 45-59 125
26. The Control Hypothesis in Hypertension, CAD and Sudden Death 134
27. CAD Mortality In Men (1968-78) Versus Infant Mortality 141
28. Relative Risk of Mortality Plotted Against Cholesterol Level 146
29. Serum Selenium Levels in CAD Patients Versus Controls 194
30. Dietary Vitamin E Consumption and CAD in Men and Women 199
31. Inverse Correlation Between Vitamin E and CAD 201
32. Plasma Vitamin E and Risk of Angina Pectoris 202
33. Plasma Vitamin C and Risk of Angina 206
34. Beta Carotene and Risk of CAD in Men 210
35. Antioxidant Levels Within Serum LDL 218
36. Gross Federal Debt, 1945-1992 229
37. Income vs. Fat Intake among Rural Bantu, Urban Blacks, Whites 246
38. Relative Risk of Cardiac Arrest in Blacks versus Whites by Age 252
39. The Mediterranean Food Pyramid versus the USDA Food Pyramid 255
APPENDIX B
List of Tables
Table Title Page
1. Risk Factors For Atherosclerosis...................................................... 3
2. Death rate per 100,000 from CAD, 1940 and 1945.......................... 39
3. Reported Exercise by Americans, 1977............................................. 57
4. Mortality and Cardiovascular Events on Mediterranean
Versus American Heart Association Diet.......................................... 72
5. Diseases of Wealth and Poverty........................................................ 75
6. Composition of Three Low CAD Risk Diets vs American Diet........ 79
7. Characteristics of Strong Families...................................................... 105
8. The Process of Atherosclerosis......................................................... 137
Page 210
9. Average Daily Frequency of High Fat Food Consumption............... 147
10. Smoking Related Illnesses by Race and Sex....................................... 167
11. Sources of Free Radicals Within the Body........................................ 215
12. Factors Effecting the Oxidation of LDL and Their Prevalence
Among Low or High SES in the United States, 1900 to 1964........... 241
13. Factors Effecting the Oxidation of LDL and Their Prevalence
Among Low or High SES in the United States, since 1964............... 242
Page 211
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