The lifestyle factors are the way of living ol'an inclividual ant1 con~prisc of the diet,smoking, alcohol, physical ac~ivity :ind stress. Thcsc arc vety importanl components in the risk profile of an individual and all of them can be modified or eliminated for pi-evention of Cardio-vascular diseases.
Diet
Diet is an important deteiminant of Cardio-vascular risk. The effect of diet is mediated through the influence of biological risk factors, such as lipids, glucose level, blood pressure and obesity. A diet high in calories and rich in saturated fat and cholesterol is a major risk factor for atherosclerosis and CAD. Saturated fatty acids increase low-density lipoprotein (LDL) cholesterol (also called 'bad' cholesterol) levels, the most important component promoting atherosclerosis.Poly-unsaturated fatty acids are good as they lower LDL-cholesterol. However they have an undesirable effect of reducing the high-density lipoprotein (HDL) cholesterol - also called 'good' cholesterol. Mono-unsaturated fatty acids lower LDL cholesterol without affecting HDL cholesterol. Hydrogenation of vegetable oils converts some polyunsaturated fats to trans-saturated fats. Trans-fats have more atherogenic i-isk than the saturated fats because they not only increase LDL cholesterol but also decrease HDL cholesterol. Additionally they raise triglyceride level and promote platelet aggregation and thrombosis.
While the amount and type of fat in the food is considered very important, the role of other components cannot be ignored. Aniinal proteiil increases the homocystiene level in the blood and may contribute to atherosclerosis. Energy dense refined cabohydrates like sugar increases the caloric intake and excess consu~nption may lead to obesity and high blood sugar. Even in absence of overt diabetes, a raised blood sugar may cause endothelial darnage because of formation of advanced glycated end products. Excess salt in the diet contribute to development of Hypertension, a major risk factor for CAD.
Cigarette Smoking
Smoking is the single most important preventable risk factor for CAD. There is strong evidence that smoking can significantly increase CAD morbidity and mortality, an adverse effect, which is related to the amount of tobacco smoked daily and the duration of smoking. Approximately 50-150 microgram of nicotine is absorbed through the lung with each puff of smoke. Nicotine is a potent agonist of sympathetic nervous system and causes release of nor-epinephrine whichin turn increases coronary tone and provokes vasoconstriction.Many studies have shown that smokers have approximately twice the risk of CAD as non-smokers. Smoking causes endothelial injuiy, increases heart rate and blood pressure, decreases oxygen level in the blood because of production of carbon mo~loxide, lowers HDL cholestmol, causes coronary spasm, increases platelet aggregation and promotes blood clotting - all of which aggravates the atherosclerotic and ischaemic process.
Passive smoking or so-called 'second-hand' smoking has also been found to increase CAD risk, Non-smokers exposed to cigarette smoke have increased iisk of Cardio-vascular diseases. Different forms of non-smoke tobacco are also harmfulSmoking cessation is rapidly followed by a significant decrease in Cardio-vascular morbidity and mortality. The benefits of smoking cessation are seen regardless of how long and how much the patient previously smoked.
Excess Alcohol Consumption
Excessive alcohol consumption is, an established preventable cause of morbidity and mortality. The effects of alcohol on the Cardio-vascular system are highly complex. Moderate alcohol intake has been thought to have a protective effect on CAD mediated mostly by an elevation in serum HDL cholesterol as well as by the effects of alcohol on platelets and fibrinolysis. Howevel; excess alcohol consumption is associated with an increased risk of Cardio-vascular disease due to Hypertension and haeinorrhagic stroke or to sudden atshythmic death. It can also dan;age the myocardiuin and other organs like liver, brain and muscle.
Physical Inactivity
Prospective epidemiological studies have shown that a sedeiitary lifestyle is associated with an adverse effect on the risk of death from all causes and CAD.Relative risk .of Cardio-vascular diseases conferred by physical inactivity appears to parallel in magnitude that conferred by Hypertension, dyslipidaernia or use of tobacco products. Physical inactivity and sedentary habits are associated with at least two-fold increase in the iisk of CAD. Lack of physical exercise has several har~nf~il effects to promote atherosclerosis. There is a tendency for increase in body weight, decrease in cardiac reserve: and decrease in insulin sensitivity with impaired glucose tolerance, increase in blood lipids and a rise in blood pressure.
On the other hand regular exercise has salutary bio-chemical and metabolic effect.It decreases LDL cholesterol and triglyceiides, increases IlDL cholesterol,improves insulin sensitivity and Ilelps in maintaining ideal body weight. It also stimulates collateral circulation in the heart and improves blood supply to the heart muscle. The Framingham Offspring study found that patients who participated in at least one hour of physical activities per week had an improved cardiac risk profile and decreased presence of associated risk factors would be predicted to reduce CAD mortality. The US Railroad Study, with mortality follow-up for 17-20 years, showed that the age-adjusted risk estimate for CAD death was increased to 1.39 for sedentary nlen who expended less than 40 kcal /week. The relationship for physical activity was independent and statistically significant when looked into in multivariate analysis.
Stress/Psychosocial Tension
Stress and psychosocial tension are other lifestyle factors in initiating coronary artery disease and precipitating 'heart attacks'. Many prospective and case-control studies have assessed for correlation oS depression, anxiety and neuroticism with CAD and almost all the studies consistently reported that emotional distress precedes the developnlent of syinpto~ns of coronay artery disease. Chronic stressful situations in jobs, family and social arcas inay aggravate the disease anlong women with established CAD has been shown to
process. ~ & i t a stress predict a poorer prognosis. Job related factors that appear to influence the induction or exacerbation of CAD include perceived job stress, role ambiguity, job autonomy, high demand and low decision latitude, change of assignment,unemployment and retire~nent etc.
The effect of stress is mediated through the sympathetic ncrvous system and hormones - the stress hormones like adrenaline and nor-adrenaline; the steroid hon~lones such as cortisols and other hormolles like renin and aldosterone, These hornlones increase heart rate and blood pressure, cause endothelial dainage and dysfunction, promote atherosclerosis and thrombosis, and cause coronay spasm.
Diet
Diet is an important deteiminant of Cardio-vascular risk. The effect of diet is mediated through the influence of biological risk factors, such as lipids, glucose level, blood pressure and obesity. A diet high in calories and rich in saturated fat and cholesterol is a major risk factor for atherosclerosis and CAD. Saturated fatty acids increase low-density lipoprotein (LDL) cholesterol (also called 'bad' cholesterol) levels, the most important component promoting atherosclerosis.Poly-unsaturated fatty acids are good as they lower LDL-cholesterol. However they have an undesirable effect of reducing the high-density lipoprotein (HDL) cholesterol - also called 'good' cholesterol. Mono-unsaturated fatty acids lower LDL cholesterol without affecting HDL cholesterol. Hydrogenation of vegetable oils converts some polyunsaturated fats to trans-saturated fats. Trans-fats have more atherogenic i-isk than the saturated fats because they not only increase LDL cholesterol but also decrease HDL cholesterol. Additionally they raise triglyceride level and promote platelet aggregation and thrombosis.
While the amount and type of fat in the food is considered very important, the role of other components cannot be ignored. Aniinal proteiil increases the homocystiene level in the blood and may contribute to atherosclerosis. Energy dense refined cabohydrates like sugar increases the caloric intake and excess consu~nption may lead to obesity and high blood sugar. Even in absence of overt diabetes, a raised blood sugar may cause endothelial darnage because of formation of advanced glycated end products. Excess salt in the diet contribute to development of Hypertension, a major risk factor for CAD.
Cigarette Smoking
Smoking is the single most important preventable risk factor for CAD. There is strong evidence that smoking can significantly increase CAD morbidity and mortality, an adverse effect, which is related to the amount of tobacco smoked daily and the duration of smoking. Approximately 50-150 microgram of nicotine is absorbed through the lung with each puff of smoke. Nicotine is a potent agonist of sympathetic nervous system and causes release of nor-epinephrine whichin turn increases coronary tone and provokes vasoconstriction.Many studies have shown that smokers have approximately twice the risk of CAD as non-smokers. Smoking causes endothelial injuiy, increases heart rate and blood pressure, decreases oxygen level in the blood because of production of carbon mo~loxide, lowers HDL cholestmol, causes coronary spasm, increases platelet aggregation and promotes blood clotting - all of which aggravates the atherosclerotic and ischaemic process.
Passive smoking or so-called 'second-hand' smoking has also been found to increase CAD risk, Non-smokers exposed to cigarette smoke have increased iisk of Cardio-vascular diseases. Different forms of non-smoke tobacco are also harmfulSmoking cessation is rapidly followed by a significant decrease in Cardio-vascular morbidity and mortality. The benefits of smoking cessation are seen regardless of how long and how much the patient previously smoked.
Excess Alcohol Consumption
Excessive alcohol consumption is, an established preventable cause of morbidity and mortality. The effects of alcohol on the Cardio-vascular system are highly complex. Moderate alcohol intake has been thought to have a protective effect on CAD mediated mostly by an elevation in serum HDL cholesterol as well as by the effects of alcohol on platelets and fibrinolysis. Howevel; excess alcohol consumption is associated with an increased risk of Cardio-vascular disease due to Hypertension and haeinorrhagic stroke or to sudden atshythmic death. It can also dan;age the myocardiuin and other organs like liver, brain and muscle.
Physical Inactivity
Prospective epidemiological studies have shown that a sedeiitary lifestyle is associated with an adverse effect on the risk of death from all causes and CAD.Relative risk .of Cardio-vascular diseases conferred by physical inactivity appears to parallel in magnitude that conferred by Hypertension, dyslipidaernia or use of tobacco products. Physical inactivity and sedentary habits are associated with at least two-fold increase in the iisk of CAD. Lack of physical exercise has several har~nf~il effects to promote atherosclerosis. There is a tendency for increase in body weight, decrease in cardiac reserve: and decrease in insulin sensitivity with impaired glucose tolerance, increase in blood lipids and a rise in blood pressure.
On the other hand regular exercise has salutary bio-chemical and metabolic effect.It decreases LDL cholesterol and triglyceiides, increases IlDL cholesterol,improves insulin sensitivity and Ilelps in maintaining ideal body weight. It also stimulates collateral circulation in the heart and improves blood supply to the heart muscle. The Framingham Offspring study found that patients who participated in at least one hour of physical activities per week had an improved cardiac risk profile and decreased presence of associated risk factors would be predicted to reduce CAD mortality. The US Railroad Study, with mortality follow-up for 17-20 years, showed that the age-adjusted risk estimate for CAD death was increased to 1.39 for sedentary nlen who expended less than 40 kcal /week. The relationship for physical activity was independent and statistically significant when looked into in multivariate analysis.
Stress/Psychosocial Tension
Stress and psychosocial tension are other lifestyle factors in initiating coronary artery disease and precipitating 'heart attacks'. Many prospective and case-control studies have assessed for correlation oS depression, anxiety and neuroticism with CAD and almost all the studies consistently reported that emotional distress precedes the developnlent of syinpto~ns of coronay artery disease. Chronic stressful situations in jobs, family and social arcas inay aggravate the disease anlong women with established CAD has been shown to
process. ~ & i t a stress predict a poorer prognosis. Job related factors that appear to influence the induction or exacerbation of CAD include perceived job stress, role ambiguity, job autonomy, high demand and low decision latitude, change of assignment,unemployment and retire~nent etc.
The effect of stress is mediated through the sympathetic ncrvous system and hormones - the stress hormones like adrenaline and nor-adrenaline; the steroid hon~lones such as cortisols and other hormolles like renin and aldosterone, These hornlones increase heart rate and blood pressure, cause endothelial dainage and dysfunction, promote atherosclerosis and thrombosis, and cause coronay spasm.
In the predisposition to CAD the role of personality especially the Q p e A has also been considered to be of soine importance. TypeA people are characterised as highly ambitious, competitive, exacting in attitude, impatient, deadline oriented and in a constant struggle with the environment. In contradistinction, Q p e B people are more passive, not in a hurry, take time to relax, pursue hobbies and other recreations and less disturbed by environmental stress. The Western collaborative Sludy Group showed that Type A men had more than twice the prevalence of CAD as Type B men. In the Framingham Heart Study Type A behaviour patterns were associated with a two-fold increase in the developlnent of angina pectoris and also a high rate of silent myocardial infarction. The mechanism by which Type A personality traits could influence atherogenesis is not clear. But it could be related to increase in the risk imparted by stress and the whole process modulated by the persolla1 response.
Studies have shown increased adrenergic receptor density in the healthy offspring of parents with documented premature CAD and Type A personality and this increased receptor density is compatible with increased peripheral alpha-receptor activity,rise in blood pressure and coronary vasoconstriction. However Type A people react differently even in non-stressful situations and so stress cannot be talcen as the sole mechanism of increased risk in such type of persons. Not all the elements inm behaviour of Type A personality have significant coronay risk; it is mostly the negative elements like hostility, cynicism etc., that confer the increased risk in such persons.
Studies have shown increased adrenergic receptor density in the healthy offspring of parents with documented premature CAD and Type A personality and this increased receptor density is compatible with increased peripheral alpha-receptor activity,rise in blood pressure and coronary vasoconstriction. However Type A people react differently even in non-stressful situations and so stress cannot be talcen as the sole mechanism of increased risk in such type of persons. Not all the elements inm behaviour of Type A personality have significant coronay risk; it is mostly the negative elements like hostility, cynicism etc., that confer the increased risk in such persons.
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