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METHODOLOGY RESEARCH THE RELATIONSHIP OF DRINKING BEER AND CORONARY ARTERY DISEASE IN MEN AGED 30 TO 40 YEARS OLD. (Spira Penta Orbis – 9 th Nov 2011) GROUP 1 NAME NIM Fawza Nabila Faudzi C11110858 Ahmad Farhan Hasbi C11110869 Mohamad Luqman Hadi bin Ismail C11110880 Mohamad Fareez Hairi Mohd Saupi C11110846 Gadis M.P Randa C11110801 Luke Michael C11110835 Miftah Farid Asmaun C11110812 Ahmad NurFakhri C11110823
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Page 1: Spira Penta Orbis

METHODOLOGY RESEARCH

THE RELATIONSHIP OF DRINKING BEERAND CORONARY ARTERY DISEASE

IN MEN AGED 30 TO 40 YEARS OLD. (Spira Penta Orbis – 9th Nov 2011)

GROUP 1

NAME NIMFawza Nabila Faudzi C11110858Ahmad Farhan Hasbi C11110869

Mohamad Luqman Hadi bin Ismail C11110880Mohamad Fareez Hairi Mohd Saupi C11110846

Gadis M.P Randa C11110801Luke Michael C11110835

Miftah Farid Asmaun C11110812Ahmad NurFakhri C11110823

METHODOLOGY RESEARCH, DEPT OF PATHOLOGY ANATOMYFACULTY OF MEDICINE

UNIVERSITY OF HASANUDDIN2011

Page 2: Spira Penta Orbis

RESEARCH TITLE: THE RELATIONSHIP OF DRINKING BEER AND CORONARY ARTERY DISEASE

IN MEN AGED 30 TO 40 YEARS OLD.

RESEARCH QUESTIONS:1. What is the importance of this research study?2. What is the effect of drinking beer to coronary artery disease?3. Is there any difference between low/moderate beer drinker and high beer drinker towards

risk of coronary artery disease?4. What are the contents of beer that can cause coronary artery disease?5. What is coronary artery disease?6. Is there any scientific evidence to prove this research study?

FOX – LION PHENOMENON:The “fox”: Amount of beer consumed per dayThe “lion”: Hypertension, Diabetes, Dyslipidemia, Smoking In our research study, the “lion” will be ‘chased out’ as this will affect the final results of our research study.

VARIABLES:a) Independent variable : Amount of beer consumed per dayb) Dependent variable : Risk of coronary artery disease (CAD)c) Controlled variable : Hypertension, Diabetes, Dyslipidemia, Smoking (EXCLUDE)

EXCLUSION AND INCLUSION CRITERIA:a) Inclusion criteria : We only include samples that are men and their age is between 30 to

40 years old. b) Exclusion criteria : Exclusion criteria is the confounding factor. In this case, the confounding

factor or the thing that should be exclude are samples that smoking, samples that have diabetes, samples that have dyslipidemia and

samples that have hypertension. The major risk factors of CAD are high level LDL in blood, hypertension, smoking and others.1 So, if we do not exclude these factors, it will affect the final results of this research study.

1 S.GORINSTEIN et al. Moderate beer consumption and the blood coagulation in patients with coronary artery disease. Journal of Internal Medicine 241: 47-51, 1997

Page 3: Spira Penta Orbis

OPERATIONAL DEFINITIONa) Heavy beer drinker Heavy drinking indicates usual intake of more than 3 drinks per day of wine, liquor or beer. In absolute terms, amount of pure alcohol consumed >30g/day are considered as heavy drinking 2

b) Moderate beer drinker The recommended daily limits for moderate alcohol consumption are no more than two drinks for men or one drink for women per day 3

c) Coronary artery disease (CAD)Risk of coronary artery disease is measured using exercise cardiac stress test (ECST).A positivetest was defined as horizontal and segmental ST depression or elevation of 0.1 mV .4

2 DHARAM PA. Cardioprotective Effects of Light – Moderate Consumption of Alcohol: A Review of Putative Mechanisms. Alcohol & Alcoholism 37: 409-415, 20023 U.S. Department of Health & Human Services National Institutes of Health National Institute on Alcohol Abuse and Alcoholism, 2006. Young Adult Drinking. 4 ALAN GB, VICTOR SB, ROBERT HP, EDWARD SO, YIHONG K: Graded Exercise Stress Tests in Angiographically Documented Coronary Artery Disease. Circulation 49: 348-356, 1974

Page 4: Spira Penta Orbis

SPIRAL PENTA ORBIS APPROACH

1. Construct Conceptual Writing Framework

2. Explore the Dynamic Potential of Each Variable

Beera) Beer contains alcohol

Whenever available, we extracted information on amount of alcohol consumed, using grams of alcohol per day as the common unit of measure. When a study did not specifically report the grams of alcohol per unit, we used 12.5 g/drink for analysis. We standardized portions as a 12 oz (355ml) bottle or can of beer, a 5 oz (148 ml) glass of wine, and 1.5 oz (44 ml) glass of 80 proof (40% alcohol) distilled spirits. Volume of intake was categorized as <2.5 g/day (<0.5 drink), 2.5–14.9 g/day (about 0.5–1 drink), 15–29.9 g/day (about 1–2.5 drinks), 30–60 g/day (about 2.5–5 drinks), and >60 g/day (≥5 drinks).5

Alcohol content of different beer styles6

Description Amount Alcohol (g) Amount containing 80g alcohol (approx)

Draught bitter ½ pint 8.7 5 pintsDraught ale, mild ½ pint 7.4 5 pints

b) Beer contains maltose

Data from Buckee and Hargitt state that beer contains maltose (0.02% w/v as glucose). In general, though, because beer has the sugar maltose in it, it is by far the most fattening of all alcoholic beverages. Most alcoholic beverages when consumed with a meal help delay digestion and thereby have a favorable effect on the glycaemic index of the meal. The maltose in beer is digested more rapidly than any other food and causes large swings in blood sugar and

5 PAUL ER, SUSAN EB, BARBARA JT, KENNETH JM, WILLIAM AG. Association of alcohol consumption with selectedcardiovascular disease outcomes: a systematic review and meta-analysis. British Medical Journal 2011;342:d671.6 MICHAEL GM: Alcohol and coronary heart disease. International Journal of Epidemiology 30: 724-729, 2001

High beer drinking(>3 glass/day)

Coronary Artery Disease(CAD)

Page 5: Spira Penta Orbis

insulin levels. This is the origin of a beer belly. We do not get wine bellies because wine does not contain maltose. Light beers with lower carbohydrate content are better than regular beers.7

Table IV. Sugar content of a range of beers.Beer MaltoseLager 0.008

Light lager 0.01Pale ale 0.0003

All values in % (w/v) and derived from Thomas et al

Brewer’s wort (to make beer, brewers use water and barley to create a sweetened liquid called the wort, which they flavor with hops, then ferment with yeast) contains the sugars sucrose, fructose, glucose, maltose, maltotriose, dextrin material, and a complex mixture of amino acids, peptides, proteins, vitamins, ions, nucleic acids and other constituents.8

c) Beer contains barley

Good brewing practices from barley to beer are important for the production of a high quality beverage. Water is added to barley to trigger the germination of the barley during the steeping step of the malting process. Germinating barley can be held under anaerobic conditions for 24 hours or more, until it becomes acidic due to the action of naturally present LAB. Alternatively, malt can be sprayed with a suspension of Lb. delbrueckii and then incubated at approximately 50°C for a period of 24–36 hours before kilning17. A third method is that the kilned malt is steeped in water at 45–50°C until the LAB in the malt have formed about 1% lactic acid. The malt is carefully dried, thus concentrating the lactic acid to between 2 and 4%.9

Fig. 2c. Basic schematic representation of the brewing process.10

7 C.W. BAMFORTH: Beer, Carbohydrates and Diet. Journal of The Institute of Brewing.8 Sandra HdC, Eduardo MC, José RE: Structural Complexity on the Nitrogen Source and Influence on Yeast Growth and Fermentation. J. Inst. Brew. 108(1):54–61, 20029 Anne V, Tadhg O’S, Douwe VS. Enhancing the Microbiological Stability of Malt and Beer : A Review. J. Inst. Brew. 111(4), 355–371, 2005

Page 6: Spira Penta Orbis

Coronary Artery Diseases (CAD)a) CAD is caused by atherosclerosis

Atherosclerosis begins as deposits of cholesterol and its esters, referred to as fatty streaks, in the intima of large muscular arteries. In some persons and at certain arterial sites, more lipid accumulates and is covered by a fibromuscular cap to form a fibrous plaque. Further changes in fibrous plaques render them vulnerable to rupture, an event that precipitates occlusive thrombosis and clinically manifest disease (sudden cardiac death, myocardial infarction, stroke, or peripheral arterial disease).

The extent of both fatty streaks and raised lesions (fibrous plaques and other advanced lesions) in the right coronary artery and in the abdominal aorta was associated positively with non-HDL cholesterol concentration, hypertension, impaired glucose tolerance, and obesity and associated negatively with HDL-cholesterol concentration.

There has been little or no doubt for many years that the raised lesions of atherosclerosis (a collective term for fibrous plaques and the associated complications) determine the risk of clinically manifest coronary artery disease (CAD), both for populations and for individuals. CAD events become frequent in a population when the average extent of coronary artery raised lesions in middle-aged persons approaches 30% of the coronary intimal surface; individuals with CAD have on average 60% of the coronary intimal surface involved with raised lesions. Recent studies by angiography, ultrasonography, and histochemistry show that the qualities of raised lesions also predict risk of an occlusive event.

The relation of fatty streaks to more advanced lesions is different in the coronary arteries than in the aorta. Fatty streaks begin to appear in the coronary arteries 5–10 y later than in the aorta. Comparisons of the localization of lesions in the coronary arteries show a close correspondence between the localization of fatty streaks in young persons and that of raised lesions in older persons. In nonblack populations, the extent of coronary artery fatty streaks in young persons predicts the extent of raised lesions in older persons. However, although women have about the same extent of or more coronary artery fatty streaks than do men, they have only half the extent of raised lesions at older ages10

10 Henry CMGJ, C Alex MM, Edward EH, Gray TM, Richard ET, Jack PS: Origin of atherosclerosis in childhood and adolescence. The American Journal of Clinical Nutrition. 2000;72(suppl):1307S–15S

Page 7: Spira Penta Orbis

3. Conduct the Correlation among Factor

a) Alcohol - Atherosclerosis

Total homocysteine (tHcy) is recognized as a CVD risk factor. It is elevated in patients with chronic alcoholism and falls following alcohol withdrawal; therefore, alcohol may have a deleterious effect on health by raising tHcy levels.11

It was shown that chronic alcohol intake among alcohol dependent patients redounds to markedly elevated homocysteine plasma concentrations; the data indicated that actively drinking alcoholics had twice the level of homocysteine in their plasma than did the healthy controls. In another study, plasma homocysteine levels were found to be significantly correlated with the extent of alcoholisation assessed with the blood-alcohol concentration among alcoholic subjects at admission. The mean value of plasma homocysteine levels fell after cessation of drinking from 33.6mol/l to 13.9mol/l on day 3 after admission. Several mechanisms contributing to the hyperhomocysteinemia have been discussed. A direct inhibition of MS by acetaldehyde, which is an alcohol breakdown product, might cause an elevation of homocysteine levels. Homocysteine is metabolized via remethylation and transsulphuration, for reactions, folate, vitamin B6 as well as vitamin B12 are essential co-factors. Reduced availability of folate, vitamin B6 and vitamin B12 cause an impairment of homocysteine metabolism. Low folate intake, poor absorption, decreased hepatic uptake and retention, increased urinary excretion of folate account for the folate deficiency observed among alcohol dependent patients. Genetic factors involved in homocysteine and folate metabolism also may contribute to the association between elevated homocysteine plasma concentrations and alcohol dependence. An excess of MTHFR 677T-allele found among alcohol dependent patients compared to healthy control subjects potentially affects homocysteine plasma levels.12

Elevated homocysteine levels (also called hyperhomocysteinemia) may cause irritation of the blood vessels. Elevated levels of homocysteine show an increased risk for (1) hardening of the arteries (atherosclerosis), which could eventually result in a heart attack and/or stroke, and (2) blood clots in the veins, referred to as venous thrombosis. An elevated homocysteine level is associated with an increased risk for developing atherosclerosis, which can in turn lead to coronary artery disease (CAD), heart attack, and stroke. The magnitude of risk for CAD is not well defined. Generally, it seems that people with an elevated homocysteine level may have about twice the risk of CAD compared with those without a high homocysteine level. However, the risk is dependent on the homocysteine level. For example, in one study, researchers found that for every 10% elevation in homocysteine, there was nearly the same rise in the risk of CAD. The risk may also be related to how long someone has had an elevated homocysteine level.13

11 A. GIBSON, et al. Alcohol increases homocysteine and reduces B vitamin concentration in healthy male volunteers—a randomized, crossover intervention study. Q J Med 2008; 101:881–88712 Ulrich C.L: Alterations in Homocysteine Metabolism Among Alcohol Dependent Patients – Clinical, Pathobiochemical and Genetic Aspects. Current Drug Abuse Reviews, 2008, 1, 47-55

Page 8: Spira Penta Orbis

b) Maltose – Atherosclerosis

The maltose in beer is digested more rapidly than any other food and causes large swings in blood sugar and insulin levels.

Metabolic syndrome is strongly associated with endothelial dysfunction and increased atherosclerosis risk. Insulin resistance and adaptive hyperinsulinemia are thought to cause endothelial dysfunction and exert mitogenic influences on vascular smooth muscle cells, in contrast to insulin’s vasodilatory effect by promoting NO release under normal physiological conditions.

Circulating adipokine levels are elevated in obese and insulin resistant states in animals and humans, and intra-abdominal fat appears to produce several of the adipokines in greater amounts than other fat depots.

A large number of adipokines also affect insulin action, blood sugar, and fat metabolism and consequently insulin resistance, which ultimately leads to Type 2 diabetes. Hence, they exert direct as well as indirect influences on the process of atherosclerosis.

Furthermore, leptin increases platelet aggregation and arterial thrombosis via a leptin receptor-dependent pathway, has a direct action on macrophages by increasing the release of monocyte colony-stimulating factor, promotes cholesterol accumulation in macrophages under high glucose conditions, and stimulates angiogenesis. 14

Fig. 2. Effects of metabolic syndrome of insulin resistance on endothelial dysfunction. Insulin resistance and adaptive hyperinsulinemia are thought to cause endothelial dysfunction by promoting endothelial activation and a proatherogenic

environment. The adipokines reinforce these detrimental effects. The molecular links between obesity and atherosclerosis are

explored through the effects of fat-derived adipokines on endothelial function and vascular health.15

13 Elizabeth A.V, Amy C.S, Caron P.M, Stephan M : Homocysteine and MTHFR Mutations : Relation to Thrombosis and Coronary Artery Diseases. Journal of The American Heart Association. Circulation 2005, 111:e289-e29314 David C. W. Lau, et al. Adipokines: molecular links between obesity and atherosclerosis. Am J Physiol Heart Circ Physiol 288:H2031-H2041, 2005. First published 14 January 2005

Page 9: Spira Penta Orbis

c) Barley – Atherosclerosis

Barley is the source of carbohydrates and is largely found in beer drink. Barley is one of the main components in malting process. So it shows that barley contains high carbohydrates.

TABLE C : TOTAL CARBOHYDRATE CONTENT OF BEVERAGES15

Food Carbohydrate (g) per servingBeer 10 -20

Light and low carb beer 2.5 - 10

Based on the table above, it shows that beer have high contents of carbohydrate. Consuming large amount of carbohydrates, will eventually lead to obesity.

TNF-α, an inflammatory cytokine released in greater quantities by obese humans and patients with insulin resistance, not only initiates but also propagates atherosclerotic lesion formation. TNF- α activates the transcription factor nuclear factor-ĸB (NF-ĸB), which accelerates experimental atherogenesis, in part by inducing the expression of VCAM-1, ICAM-1, MCP-1, and E-selectin in aortic endothelial and vascular smooth muscle cells. TNF- α reduces NO bioavailability in endothelial cells and impairs endothelium-dependent vasodilatation, promoting endothelial dysfunction. TNF- α may also promote apoptosis in endothelial cells by dephosphorylating protein kinase B, or Akt, and thereby contribute to endothelial injury, an effect counteracted by insulin.16

15 C.W. BAMFORTH: Beer, Carbohydrates and Diet. Journal of The Institute of Brewing.16 AAFJE SIERKSMA, et al. Effect of Moderate Alcohol Consumption on Adiponectin, Tumor Necrosis Factor-Alpha, and Insulin Sensitivity. DIABETES CARE, VOLUME 27, NUMBER 1, JANUARY 2004

Page 10: Spira Penta Orbis

4. Explore the Surrounding Factors

Metabolic syndrome has big influence on atherosclerosis

CAD risk can be calculated from risk factors and the presence of clinical signs and biochemical abnormalities. The Framingham risk score is often used as an initial evaluation parameter of CAD risk in individuals with countless risk factors, including those with Metabolic Syndrome (MS).

The MS is a multiple risk factor for cardiovascular disease and is characterized by increased waist circumference, raised triglycerides, reduced HDL cholesterol, elevated blood pressure, and raised plasma glucose. From these, reduced HDL-c and elevated blood pressureare common components of both CAD risk and MS.

Some factors related to MS such as dyslipidemia, hyperglycemia, hypertension, obesity and other risk factors like low levels of physical activity and smoking have already been well established as CAD risk factors.

Diagnosis of Metabolic Syndrome was made according to the criteria of NCEP-ATP III. The 5 components used were plasma levels of triglyceride, HDL-C and, fasting plasma glucose, systolic and diastolic blood pressure and WC measurements. Metabolic syndrome was diagnosed when 3 or more of these components were abnormal.

The association between MS and CAD risk found in this study was similar the one observed in studies conducted in the United States and Europe, where they found a 2 to 3 times greater probability for an increase in CAD risk in individuals with MS. A positive correlation was observed of CAD risk score and the number of MS components, that is, the greater the number of MS components the higher the risk of developing CAD.

In this study, recommended intake of saturated fats and dietary fiber are, together with greater muscle mass, inversely associated with CAD risk score. On the other hand, the presence of MS and high plasma uric acid are associated with CAD risk score.17

So, in our study we shall exclude maltose and barley as the component that cause atherosclerosis, because it is not both maltose and barley that cause atherosclerosis, but consumption of both maltose and barley cause metabolic syndrome. Insulin resistance is caused by high intake of maltose while obesity is caused by high intake of barley that eventually caused the incidence of atherosclerosis formation.

So, to make our experiment more reliable and accurate, we just take alcohol as the component in beer that causes CAD.

17 Mauro MT,et al. Metabolic syndrome & dietary components are associated with coronary artery disease risk score in free-living adults:a cross-sectional study. Diabetology & Metabolic Syndrome 2011, 3:7

Page 11: Spira Penta Orbis

THEORITICAL FRAMEWORK

High beer drinking

(>3 glass/day) [3]

High amount of ALCOHOL

High amount of MALTOSE

High amount of BARLEY

Elevated homocysteine plasma

concentrations

Irritation of blood vessel

Venous thrombosis

Atherosclerosis

Insulin resistance Circulating adipokine level elevated

Increased source of carbohydrate

Obese TNF- α is released in

greater quantities

Coronary Artery Disease

(CAD)[5]

HypertensionSmoking

Dyslipidemia

Diabetes Mellitus

[6], [7]

[9]

10 [8]

8 15

1114

14

14

12,13

18, 19, 20

21

17

22

23

24

25

Dependent & Independent variable

The correct experimental pathway

Confounding factor

Relationship linkage


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