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Running head: DIRECT CAUSAL REALATIONS 1

Direct Causal Relations Between Cholesterol And Heart Disease

Eunhye Kim

Madonna University

ESL 4230 Argumentative Paper (D3)

April 24, 2017


DIRECT CAUSAL REALATIONS BETWEEN CHOLESTEROL AND HEART DISEASE 2

Direct Causal Relations Between Cholesterol And Heart Disease

Cholesterol and animal saturated fat have been major sources of nutrition for mankind,

but these days they are also well known as major causing factor leading to the death. According

to American Heart Association (AHA 2014), High cholesterol is one of the major controllable

risk factors for coronary heart disease, heart attack and stroke. The more blood cholesterol rises ,

the more risk of coronary heart disease is involved. American Heart Association also defines

high cholesterol as one of the many causes of heart disease and warns of its dangers. However,

many studies have been conducted to learn the actual effect of cholesterol on general wellness of

public. Schwab (2014) investigated the effects of dietary fat on body weight, diabetes type 2,

cardiovascular disease, and cancer in a meta-study. He analyzed 607 studies and found that

dietary fat intake did not affect cardiovascular disease as well as metabolic diseases such as

diabetes type 2. This result is a complete contradiction to very common knowledge that high

level of cholesterol will cause to serious medical conditions. Therefore, it is essential to look into

science based studies regarding co-relationship between the high cholesterol level and

cardiovascular diseases. In fact, many studies have shown that the incidence of type 2 diabetes,

including cardiovascular disease, in high-risk patients is not as high as in the normal range. In a

few more studies, I will explain why there is no direct correlation between fat and cardiovascular

disease.

When considering the co-relationships between heart disease and high cholesterol, it is

important to note that the presence of many wrong studies about relationships between

cholesterol and heart disease. After World War II, In 1954, Ancel Keys published a study entitled

"Study of the Seven Countries" by investigating the relationship between dietary cholesterol

intake by country and heart disease. He argued in this study that the incidence of heart disease is
DIRECT CAUSAL REALATIONS BETWEEN CHOLESTEROL AND HEART DISEASE 3

higher in countries that consume large amounts of animal saturated fats. However, this study was

originally a study of the intake of saturated fats and the incidence of heart disease in 22 countries

around the world, and there was no correlation between these two factors. However, Ancel Keys

made a bold claim that he chose only the seven countries he wanted among the 22 countries and

that there was a correlation between the two (Peturssin as cited in Schwab, 2012). Scientific

research should be conducted through the selection of samples and the methodologies that are

systematically established through the samples. Using only specific samples to obtain the

research results that a researcher wants is not a scientific study and its reliability and validity are

low.

Table 1: This shows that Ancel Keys chose only the seven countries he wanted among the 22

countries and that there was a correlation between the two, Saturated fat and cholesterol, 2016

Lee, H, Healthy Viewpoints. n.p. Retrieved from

http://www.meconomynews.com/news/article.html?no=17867
DIRECT CAUSAL REALATIONS BETWEEN CHOLESTEROL AND HEART DISEASE 4

Despite these manipulations, however, the hypothesis was accepted because at that time

there was not enough time to verify these claims. Later, in 1961, a team of researchers from the

Framingham Health Research Center in the United States, made a hasty announcement that

cholesterol was the most obvious risk of heart disease. The manipulation of research is the study

of the most invaluable form that undermines the reliability and validity of scientific research. If a

researcher manipulates a study as intended, the study loses its value as a scientific study. Thirty

years later, it turns out that there is a problem with this method. The researcher of this study and

the institution that handles this study should disclose this fact and correct the facts.

However, after 30 years of researching the data, it turned out that there was a problem

with the design of the study. Before these erroneous studies could be validated, the American

Heart Association's Nutrition Committee was encouraged to take vegetable oil instead, along

with recommendations to reduce animal saturated fat and cholesterol intake. This fact shows how

large the wavelengths of erroneous studies can be. Before the judgments of whether the results of

the research were reliable or not, government agencies issued false information based on the

findings. In particular, governments and institutions play an important role in empowering the

people through institutions and policies. However, when they use the information with

unconfirmed information on them, it is unreasonable to spread the unfounded fact that high fat is

the leading cause of other diseases, including heart disease. Thirty years later, Castelli (2014),

who participated in this study, found no correlation between reperfusion of cholesterol and heart

disease. However, he could not make the official announcement of the results, and he mentioned

a few words in another article. For instance, according to Castelli (2014), "The more saturated fat

you eat, the higher your cholesterol intake, the lower your blood cholesterol level, even though

the calorie intake increases (p. 610). Despite this lack of correlation between cholesterol levels
DIRECT CAUSAL REALATIONS BETWEEN CHOLESTEROL AND HEART DISEASE 5

and heart disease, it was accepted without any doubt due to erroneous findings. Although the

researcher acknowledges and acknowledges that there has been an error in the research process,

the already widespread misinformation is being accepted as fact. Therefore, the direct causal

relationship between high fat and heart disease should be considered once more.

Most studies of the relationship between cholesterol levels and heart disease have not

found that correlation. First, look at the findings of the Japanese atheroscerosis society (JAS).

This study compared cholesterol and total mortality with the lowest cholesterol level (> 240 mg /

dL) and the lowest mortality rate (<160 mg / dL). A study in a small city in Japan, Acehara,

compared LDL lipoprotein levels, not total cholesterol, with mortality. As a result, both men and

women had the highest mortality rate in the lowest LDL group. Although men have a high rate of

death from heart disease in the high LDL-level group, women die of heart disease in the high

LDL-level group. For this reason, LDL levels alone should not be correlated with the risk of

developing heart disease (Oqushi, 2009). A similar study was conducted in Norway. A 10-year

prospective study found that the group with a blood cholesterol level greater than 270 mg / dL

had a mortality rate of 28% lower than the group with a serum cholesterol level below 183 mg /

dL. In particular, women with higher cholesterol levels are more likely to benefit from it

(Petursson 2012). To sum up, although men with the highest level of LDL group has the highest

mortality rate, LDL level itself should not be account for developing heart diseases.

In 1980, the US Department of Agriculture announced the Food Pyramid and Meal

Guides line, encouraging the public to eat grains, vegetables, and fruits. This is part of a

recommendation by the American Heart Association's Nutrition Council in 1961 to recommend

replacing vegetable fats with a recommendation to reduce animal fat and cholesterol intake. The

animal saturated fat ingested increased blood cholesterol levels and caused heart disease. Of
DIRECT CAUSAL REALATIONS BETWEEN CHOLESTEROL AND HEART DISEASE 6

course, intake of animal saturated fat demonstrates a slight increase in cholesterol levels after

eating. For example, a study conducted by Pedurssin(2012),who recited Tecumsh Study(Nichols

1976) and County Study(Stulb, 1965), 70% of the subjects showed a slight increase and the

remaining 30% showed a remarkable synergy effect. However, this is a transient short-term

phenomenon after the meal, and there is no dose-response proportional relationship between

them and the cholesterol is self-regulating in the body. It has already been shown in many studies

that this increased level of cholesterol does not affect the development of heart disease. A meta-

analysis of 76 studies involving more than 650,000 people published in 2014 also suggests that

they did not find any association between saturated fat intake and heart disease or death from

heart disease (Chowdhury 2014). In a study published in 2010, a meta-analysis of 21 articles

covering a total of 347,747 patients found that heart disease or stroke occurred in about 3%

(11,006) of follow-up periods for 5 to 25 years, Analysis shows that no correlation has been

found. Even in the group with the highest intake of saturated fats, there is no correlation with the

onset of cardiovascular disease (heart attack, stroke)(Siri Tarino, 2010). Thus, there is no

specific correlation between cholesterol levels and the incidence of heart disease due to the

intake of animal saturated fats.

Nevertheless, there are still many studies showing that cholesterol causes heart disease

(Najafi 2013; Cristina 2012; & Mahmoud 2009). The main evidence supporting this claim is the

fact that cholesterol is concentrated in the atherosclerotic plaque. Because of the presence of

cholesterol in the field, cholesterol has been identified as a cause of atherosclerotic plaque and is

believed to be the cause of heart disease. However, as mentioned earlier, there is a new

relationship between cholesterol levels and heart disease, which is known to being related to

inflammation of the blood vessel wall. In other words, damage to the inner wall of the blood
DIRECT CAUSAL REALATIONS BETWEEN CHOLESTEROL AND HEART DISEASE 7

vessel occurred before the atherosclerotic plaque, and to prevent further blood vessel rupture and

bursting, structural material such as cholesterol is needed, and Low Density Lipoprotin (LDL)

lipoproteins are loaded with cholesterol and are brought to the inflammation site. In the

meantime, lipoproteins collected in the field were oxidized due to inflammation, and the

cholesterol contained in them was exposed to secondary oxidative damage, which further

contributed to aggravating inflammatory damage to the blood vessel wall. In other words, it is

not high-fat cholesterol that causes plaque accumulation on the wall of the blood vessel to

narrow the wall of the blood vessel. In fact, as inflammation causes damage to the blood vessel

wall, plaque accumulates to protect the wound, and these plaques block blood vessels, resulting

in cardiovascular disease.

At the same time, these inflammatory processes lead to immune cells such as

macrophages infiltrating into the blood vessel wall from the blood, which leads to the formation

of flakes while forming foam cells by predosing the oxidized cholesterol. It was found that LDL

lipoproteins with lower particle sizes were better oxidized and penetrated more into the

inflammatory site of the vascular wall. Therefore, LDL lipoprotein and cholesterol in it is a

rescue team to prevent damage and rupture of blood vessel wall, not a direct cause of heart

disease. For this reason, it is necessary not to lower the cholesterol level, but to find the cause of

inflammation in the blood vessel wall and eliminate it.

There are more interesting studies done by Schwab in 2014 related to the co-relationship

between high cholesterol level and developing diseases. According to several studies (Schwab

2014), bacteria, tobacco, cariogenic waste, oxidized fats, trans-fats, blood pressure, and other

stresses are the direct causes of damage to the vessel wall. They can cause inflammation of the

vascular wall through a variety of mechanisms including bacterial toxin release, inflammatory
DIRECT CAUSAL REALATIONS BETWEEN CHOLESTEROL AND HEART DISEASE 8

cytokine release, free radical generation, excessive acid formation, vortex formation, and heavy

metal inflow. As a result of the inflammation, cholesterol is gathered to prevent vascular damage

and prevents the progression of inflammation.

In conclusion, high cholesterol is well known as major causing factor leading to the

death; however, in fact, cholesterol level does not have any co-relationship with cardiovascular

diseases. The reason why many people still believe cholesterols will cause cardiovascular

diseases is because there was a conducted experiment insisting high cholesterol levels will lead

to cardio diseases. Nevertheless, the experiment was conducted objectively. That is, they only

selected samples that had their desired outcomes, so that they could manipulate their result. After

that, many other studies have done based on that outcome, which leads to misjudgment upon the

concept of cholesterols, in fact, there is none causing relationship. The accumulation of

cholesterols caused by inflammation, which is a real cause of cardiovascular diseases, is only

compensated reaction to minimize inflammation.


DIRECT CAUSAL REALATIONS BETWEEN CHOLESTEROL AND HEART DISEASE 9

References

Castelli, W. P.(2014). A conversation with the editor[interview by William Clifford Roberts]. Am

Jani Cardiol, 94(5), 609-622

Chowdhury R, et al. (2014). Association of dietary, circulating, and supplement fatty acids with

coronary risk: A systematic review and meta-analysis. Annal Intern Med. 160(6), 398-

406

De Souza, RJ, et al.(2015). Intake of saturated and trans unsaturated fatty acids and risk of all

cause mortality, cardiovascular disease, and type 2 diabetes: Systematic review and

meta-analysis of observational studies. Br Med J. 11(351), 3978

Japan Atherosclerosis Society (2007). Guidelines for prevention of atherosclerotic cardiovascular

diseases. J Atheroscler Thromb, 5-57

Oqushi, Y., Hamazaki, T., & Kirihara ,Y. (2009). Blood cholesterol as a good marker of health in

Japan, World Rev Nutr Diet, 100. 63-70

Petursson H, et al. (2012). Is the use of cholesterol in mortality risk algorhythm in clinical

guidelines valid? Ten years prospective data from the Norwegian HUNT 2 study. J Eval

Clin Pract, 18(4), 927-928

Schwab, U. et al.(2014). Effect of the amount and type of dietary fat on risk factors for

cardiovascular diseases, and risk of developing type 2 diabetes, cardiovascular diseases,

and cancer: A systematic review. Food NutriRes, 58

Siri-Tarino PW, et al.(2010). Meta-analysis of prospective cohort studies evaluating the

association of saturated fat with cardiovascular disease. Am J Clin Nutr, 91(3), 535-546
DIRECT CAUSAL REALATIONS BETWEEN CHOLESTEROL AND HEART DISEASE 10

American Heart Association (2016), Why Cholesterol Matters?. Retrieved from

http://www.heart.org/HEARTORG/Conditions/Cholesterol/WhyCholesterolMatters/Why

-Cholesterol-Matters_UCM_001212_Article.jsp#.WN5OORiqFhA

American Heart Association (2016), Understand Your Risk for High Cholesterol. Retrieve from

http://www.heart.org/HEARTORG/Conditions/Cholesterol/UnderstandYourRiskforHigh

Cholesterol/Understand-Your-Risk-for-High-Cholesterol_UCM_001213_Article. jsp#.

WN5JwxiqFhA

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