Prevention of Coronary Heart Disease: Diet, Lifestyle and Risk Factors in the Seven Countries Study
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Although these efforts represent a major challenge, such a task must be faced in order to halt the atherosclerosis epidemic that threatens the world. Cardiovascular disease CVD is the main cause of death in Brazil, as well as in the world, including rich and poor countries. Of note is the increase in the number of elderly individuals, especially over 80 years of age. Such group accounted for 0. In Brazil, this group represented 0. As the Brazilian population gets older, non-communicable diseases will burden the health care system, and the costs associated with such diseases already account for half the costs of all hospital admissions.
This rate of non-communicable diseases is not necessarily an inevitable result of modern society, but rather a problem that can be avoided. The main factors behind most of these diseases, i.
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Atherosclerosis in particular is responsible for most cardiovascular events. Atherosclerosis is a chronic inflammatory and proliferative disease, which may cause obstructions of the coronary, cerebral and peripheral arteries. Atherosclerosis tends to be a progressive process that begins early in life, probably in childhood. It is typically multifactorial in origin, most often dependent on risk factors such as hypercholesterolemia, diabetes, smoking, hypertension, sedentarism, and obesity.
Atherosclerosis results from a complex interaction of hemodynamic and biochemical factors and is determined by circulating blood cells, endothelial cells, smooth muscle cells, blood lipids, and connective tissue of the arterial wall. Once considered to be the result of fat deposition in the arterial wall, it is now viewed as an inflammatory and proliferative process that can lead to arterial wall thickening and eventual complete obstruction that hampers myocardial blood flow, thus causing the clinical syndromes of angina or infarction 3.
These mechanisms, however, are not the subject of this paper.
Seven Countries Study
As far as clinical evolution is concerned, coronary atherosclerosis has two distinct phases Figure 1 : the asymptomatic phase that may begin at birth and proceed until mid-life when symptoms occur. This phase is usually associated with non-obstructive lesions. However, some of these lesions may suffer acute instabilization due to plaque rupture, with partial or total occlusions, causing acute coronary syndromes or infarction. The symptomatic phase is characterized by flow limiting, advanced lesions and is associated with classical clinical manifestations such as effort angina, heart failure or myocardial infarction MI.
Hence, this is the phase that more commonly causes complications. Until recently, most medical efforts were directed towards the symptomatic phase, including diagnostic procedures and treatments. Lately, more emphasis has been placed on identifying patients in the early, asymptomatic phase. Thus, several biomarkers and noninvasive imaging techniques have been developed whose main goal is to identify individuals in the early stages of atherosclerosis, in order to avoid its progression or even to prevent its development.
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CAD is responsible for most clinical complications of atherosclerosis. Its treatment is basically covered by four types of interventions: 1 coronary surgery; 2 percutaneous coronary interventions; 3 drug treatment; 4 lifestyle modification. The first two focus on CAD complications, such as angina or infarction, do not interfere with the biochemical nature of the disease. Drugs and healthy lifestyle, on the other hand, not only can prevent disease development but can also prevent complications, reduce or abolish progression and even induce plaque regression.
The choice of either approach or of a combination of the two has major implications, including effectiveness, costs, adherence, and side effects. The purpose of this article is to compare these two latter approaches, drug treatment and lifestyle modification, highlighting the peculiarities of each one and offering practical suggestions for physicians. Ancel Keys, in his landmark Seven Countries Study published in 4 , observed that cardiac mortality was directly associated with fat consumption in different countries; the more fat people ate, the greater was coronary mortality.
In , Kannel et al. These two fundamental clinical observations followed the original discoveries of the Russian investigators Anichkov, Ignatowski and Chalatov 6 who, in the early 's, fed rabbits with milk and eggs and demonstrated that atherosclerosis was produced only by egg cholesterol. Although it took about 50 years for these basic discoveries to reach the clinical arena, when they finally did, their impact was immense and changed medical research and practice forever. Several epidemiological studies subsequently confirmed these relationships, which covered a wide range of cholesterol concentrations, including those considered to be normal or mildly elevated.
Both drug therapy and diets began to be tested to ascertain whether they could change the natural history of atherosclerosis. Definitive assessment of whether LDL reduction would be beneficial was facilitated by the development of potent cholesterol-lowering drugs, the 3-hydroxymethylglutaryl coenzyme A HMG-CoA reductase inhibitors, termed statins. Since then a series of studies have demonstrated their efficacy in preventing major cardiovascular events. Patients who had already experienced coronary events, those at particularly high risk for events, namely diabetics and patients with peripheral artery disease, were the initial natural focus.
Some of the most important trials are summarized here. The authors concluded that adding simvastatin to existing treatments safely produced substantial additional benefits for a wide range of high-risk patients, irrespective of their initial cholesterol concentrations. The secondary endpoint, analyzed by time of first event, was "major coronary events", which comprised coronary deaths, definite or probable hospital-verified non-fatal acute MI, resuscitated cardiac arrest, and definite silent MI verified by electrocardiogram.
Simvastatin produced highly significant reductions in the risk of death and morbidity for patients with coronary heart disease CHD followed for a median tie of 5. The 4S study also provided evidence for a beneficial effect of simvastatin on fatal plus nonfatal cerebrovascular events. The magnitude of the risk reduction was consistent for the major end points of myocardial infarction, i. However, there was no significant reduction in overall mortality. In addition, the CARE Trial showed that patients 60 years old or older, women and those with impaired left ventricular ejection fraction, in all of whom the efficacy of lowering cholesterol levels had been questioned, also experienced a similar risk reduction.
This agreed with the reduction in cerebrovascular endpoints found in post hoc analyses of data from several previous trials conducted in hypercholesterolemic populations. The long-term intervention with pravastatin in ischemic disease LIPID Study 7 was another study with pravastatin, which provided evidence that lowering cholesterol levels with statin in patients with a broad range of initial cholesterol levels and a history of MI or unstable angina reduced the risk of death from CAD, CVD, and all causes combined.
In addition, the risk of MI or stroke was significantly reduced. By implication, this result suggests that these agents may work by additional mechanisms that are unrelated to lipid lowering. Some investigators have suggested that statins also have pleiotropic properties, such as modulation of inflammation within the arterial wall, that may contribute to their beneficial effect.
In the Anglo-Scandinavian Cardiac Outcomes Trial Ascot 7 , 19, subjects aged 40 to 79 years, with hypertension and at least three other cardiovascular risk factors were randomized to one of two antihypertensive regimens. The lipid-lowering arm included 10, subjects with TC of 6. The primary endpoints were death from CHD and nonfatal heart attack.
Additional benefits were reduced risk of stroke, total cardiovascular events, and total coronary events. These and other well-conducted studies firmly established that cholesterol lowering, independently of baseline values, reduced cardiovascular events in a broad population spectrum, including those who suffered previous events and those at high risk as well. The primary endpoint was the incidence of first acute major coronary events, fatal or nonfatal acute MI AMI , unstable angina, or sudden cardiac death.
The differences between the two treatment groups appeared as early as after one year. A total of subjects underwent randomization. There were no such changes with placebo.
Reductions in all-cause and CAD mortality were not significant; noncardiovascular death, including death from cancer, trauma or suicide, did not differ between groups. These two major trials lend support to the concept that hypercholesterolemia alone, even in the absence of overt CAD, deserves treatment both in men and women. Patients suffer the highest rate of death and recurrent ischemic events during the early period after an acute coronary syndrome ACS , but when the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering Trial Miracle 7 was designed it was not clear whether early initiation of treatment with a statin could reduce the occurrence of early events.
Thus, Miracle sought to determine whether treatment initiated 24 to 96 h after an ACS reduces death and nonfatal ischemic events. Atorvastatin reduced recurrent ischemic events over a week period of treatment. There was a 2. Although the study was not powered to assess mortality, it did show beneficial effects of atorvastatin on ACS. The more intensive regimen resulted in a lower risk of death from any cause or major cardiac events than did a more moderate degree of lipid lowering.
Reduction of clinical events with more intensive lipid-lowering therapy was apparent as early as 30 days after the beginning of therapy. This reduction was similar to that reported with statin treatment in the placebo-controlled Miracle Trial. These data corroborated previous observations that patients with ACS can particularly benefit from early and intensive lipid-lowering therapy with statins.
Acute LDL lowering by statins and simultaneous improvement in endothelial function have also been demonstrated. Based on these observations, it is now generally accepted that statin therapy should be used in ACS, provided LDL is elevated. Whether regression of established coronary lesions can be achieved by any means is a key question. Earlier studies 10 relied on coronary angiography and assessed effects of various interventions including diets, exercise, surgical ileal shunt, as well as not so potent lipid-reducing drugs such as colestipol, colestiramine, niacin, and lovastatin.
In the last decade, when imaging techniques for plaque evaluation were developed and more potent anti-lipidemic drugs became available, investigations of this issue regained impetus. Figure 2 shows the results of the Meteor study. In these circumstances, all investigators observed that major lipid lowering induced slower lesion progression or even plaque regression.
The most significant finding seemed to be plaque stabilization in the treatment groups while lesion progression occurred uniformly among untreated controls. An alternative strategy to modify atherosclerotic evolution was tested by Nissen et al. Indeed, plaque volume as assessed by intracoronary ultrasound was reduced compared to controls.
This strategy, however, is cumbersome, but the study's contribution must be taken as a proof of concept. These impressive observations indicating that major lipid reductions by statins may indeed impact the nature of the atherosclerotic process, leading to plaque stabilization or even regression, have major significance for medical practice. The phenomenon of regression has been convincingly demonstrated for the first time in the history of atherosclerosis. These studies lend support to the notion that medical treatment is in fact extremely efficacious; indeed it is the only way by which the biochemical atherosclerotic process can be slowed.
Whether it could be interrupted on a long-term basis, or even totally prevented, will depend on future investigations. In the TNT Trial, a total of 10, patients underwent randomization and received double-blind treatment with either 10 or 80 mg atorvastatin. Both atorvastatin groups had low rates of CAD events. The rate for the group given 10 mg atorvastatin was lower than the rates reported with statin treatment in placebo-controlled, secondary prevention trials of populations with a baseline risk similar to that of TNT patients.
Cholesterol Treatment Trialists 7 also examined this question and their results showed an approximately linear relationship between the absolute reductions in LDL cholesterol and proportional reductions in the incidence of coronary and other major vascular events. This finding is reinforced by those of some direct randomized comparisons of different statin regimens, which also indicate that larger LDL cholesterol reductions produce larger reductions in vascular disease risk. Reductions were similar irrespective of pretreatment cholesterol concentrations or other characteristics - age, gender, or pre-existing disease - of the study participants.
A recent meta-analysis 16 involving , patients in 26 trials also demonstrated that lower LDL levels are indeed associated with greater reductions in CVD events. Current practice, therefore, holds that LDL should be lowered to about 70 or even less, at least for secondary prevention. Since atherosclerosis is an inflammatory disease and elevated inflammatory markers such as high-sensitivity C-reactive protein hsCRP indicate a poor prognosis, a question has been raised regarding the possible value of reducing hsCRP in patients without overt hypercholesterolemia.
Accordingly, Ridker et al. However, the issue of how important isolated high CRP is remains controversial and further studies are needed until a definitive answer is obtained. A concern about statin treatment is their long-term effects. Most clinical trials have only a duration of years, which is too short an observational period, considering the life-long duration of atherosclerosis.
A recent observation has shed some light on this question. Men prescribed statin therapy for 5 years during the clinical trial had fewer cardiovascular events a decade later, although a majority of the study cohort stopped taking their cholesterol-lowering medication. Over the post-trial period, when treatment was under the control of the patients and their physicians, a statistically significant reduction in death from CHD or nonfatal AMI remained among treated patients compared to placebo-treated individuals.
The results, according to the authors, were presumably due to the stabilization of existing plaque and a slowing of the progression of CAD. However, the problem concerning the long-term effects of statins remains largely unresolved and is especially pertinent to young patients who need long-lasting treatments. Treatment of abnormally low HDL levels is more difficult but potentially very significant as the role of HDL as target for therapy is being increasingly recognized. A trial conducted on post-infarction patients has demonstrated that an increase in HDL-C levels obtained with gemfibrozil mg twice daily in patients with relatively low LDL-C levels prolongs reinfarction-free survival We 21 also gave niacin to patients with low HDL and measured endothelial function after three months.
Although niacin did not increase total HDL during this short period, endothelial function was improved in every patient, suggesting that niacin improved HDL function. In summary, statin therapy has definitive beneficial effects both in terms of secondary and primary prevention: it reduces overall cardiovascular events, including cardiac death, fatal and nonfatal AMI, stroke and the need for revascularization. These benefits were shown in men and women alike and irrespective of hypertension, diabetes, smoking habits, and also in the elderly.
No increase of cancer was documented. Therefore, statin is the most valuable drug for the treatment of atherosclerosis. Unresolved issues in statin therapy. As shown in Figure 3 , there are many unresolved issues regarding statins. This means that, although highly significant from a statistical point of view and biologically meaningful as well, total cardiovascular risk is far from eliminated.
Ideally, a treatment should eradicate a disease as done, for instance, with antibiotics when pneumonia is successfully treated. Hence, there is considerable room for improvement in atherosclerosis treatment. Possibly, adequate measures to correct lifestyle behavior are indicated. Another major problem is the long-term use of statins in young individuals; neither long-term effects nor side-effects have been adequately assessed.
Lifestyle Changes for Heart Attack Prevention
Similarly, the issue of costs is fundamental giving the prevalence of atherosclerosis in poor countries. Remaining unresolved issues are self-evident as shown in Figure 3. Renin-angiotensin system blockade by angiotensin-converting enzyme ACE inhibitors or by an angiotensin II Ang II subtype 1 receptor antagonist has been expanded beyond patients with heart failure or left ventricular systolic dysfunction.
In another study of the anti-inflammatory effects of Ang II subtype 1 receptor blockade in hypertensive patients with microinflammation EUTOPIA 23 , the Ang II subtype 1 receptor antagonist olmesartan significantly reduced vascular microinflammation in patients with essential hypertension. This was reflected by a rather high level of microinflammation and a mean baseline serum hsCRP concentration of 4.
Thus, the beneficial cardiovascular effects documented for inhibitors of the renin-angiotensin system e. Antiplatelet therapy is another very effective preventive measure.
For instance, aspirin reduces the incidence of MI in males over the age of 50 years. Whether this approach should be employed in the general population or only in patients at high risk is unclear, and the optimal dosage is not known. A prudent approach would be to administer mg daily to men with multiple coronary risk factors.
Fibrates can increase HDL and are especially effective in hypertriglycidemia.
Low HDL-C associated with elevated TG-rich lipoproteins and their remnants represents an important therapeutic target. Obesity, metabolic syndrome, and type 2 diabetes are intimately associated with an atherogenic phenotype featuring low HDL-C combined with elevated TG-rich lipoproteins and small dense LDL. Hence, there is great interest in treatment strategies involving niacin, fibrates or their association to treat dyslipidemia. Niacin is also effective in lowering lipoprotein levels. An unhealthy lifestyle has devastating effects on survival, as shown by Peto et al. The authors noticed that both conditions severely reduced life expectancy, reaching an incredible year span among smokers.
In the Whitehall Study 26 , 19, male civil servants were followed for 38 years in London. A to year shorter life expectancy was observed among high-risk individuals, i. Similar reductions occurred with other risk factors such as diabetes. Unfortunately, most lay people as well as many doctors are not aware of these impressive figures! Several studies have compared the effects of lifestyle interventions to those obtained with drug treatment in coronary disease.
Ford et al. It can be seen that interventions on risk factors were more effective in reducing mortality than all drugs and invasive procedures in the USA as well as in different European countries. Of particular note are the studies in Finland where a national and meticulous program was implemented see ahead. Countless studies on diets have been published 28 and the Mediterranean diet has been especially analyzed.
It is traditional in Mediterranean countries, especially Spain. Several studies were designed to test its efficacy. The Mediterranean diet significantly reduced the combined endpoint of cardiac death, nonfatal AMI and noncardiac death. The effects of the Mediterranean diet on mortality were analyzed according to adherence to the diet using a well-defined score. Trichopoulou et al. The effects were dose related and different nuts had similar effects on blood lipids. Interestingly, effects were greatest in people with high baseline LDL and low body mass index BMI and among those on Western-type diets.
As mentioned earlier, high-fat diets are notoriously detrimental. In North Karelia, Finland, a program was launched aimed at the adoption of a healthy diet and progressively extended to the entire country Universities and several entities were involved in this program. Although Finland is a peculiar country because of its small size and highly educated citizens, this study is a proof of concept showing that major population lifestyle changes can be achieved.
High carbohydrate consumption is also a major source of calories and is presently recognized as a significant, if not the most important cause of inadequate diets worldwide. Effects of glucose overload have been meticulously investigated. O'Keefe et al. They documented that variation in plasma glucose correlated directly with oxidative stress, increased CRP and decreased arterial endothelium dilation. But they also documented that the glucose increase could be substantially reduced by simultaneous ingestion of red wine, almonds, vinegar, and whey protein but was not affected by beer and gin, suggesting that this postprandial glucose increment is amenable to simple dietary interventions.
Regarding the efficiency of different types of diet, Sacks et al. The data indicate that reduction in caloric intake is the dominant factor regardless of how it is achieved. Based on these findings, there is general consensus that the Mediterranean diet is indeed effective and possibly the most adequate for CVD prevention. Initiatives to correct unhealthy dietary habits, both at the individual and population levels, are generally frustrating. Initial gains in weight reductions for instance, are frequently overcome by weight regain over the next 1 to 2 years.
Salt is another fundamental component of the Western diet and is responsible in part for one major risk factor, i. Even small increases in blood pressure cause a considerable increase in cardiovascular events in both women and men Tuomilehto et al. In the Intersalt Study, Perry and Beevers 38 observed that, in different countries, mortality due to stroke, is directly proportional to salt excretion in urine, which reflects salt ingestion. Joossens and Kesteloot 39 , in a single epidemiological investigation, observed that systolic blood pressure increased steadily as people aged among populations that added salt to their diet, such as Americans and Europeans; on the contrary, among primitive populations such as the Yanomani and Carajas Indians of Brazil, who did not add salt to their diets, blood pressure remained the same through ages 20 to The impact of dietary salt reduction has been a constant preoccupation.
Bibbins-Domingo et al. In this interesting simulation, the authors investigated the implications of a 3. There were significant reductions in all parameters and a huge saving in money expenditure. In heart failure patients, even smaller amounts may be needed. TFAs result from hydrogenation of fish and vegetable fats for industrial purpose, or else from natural digestion in ruminant animals.
Usually they are measured in adipose tissue, whole blood or red blood cell membranes. They induce expression of inflammatory markers, increase insulin resistance and cause endothelial dysfunction Hence, the metabolic milieu, which favors the development of atherosclerosis is induced and this is strong evidence of biological plausibility of an association between TFA intake and CVD.
On the other hand, the direct relationship between TFAs and CAD is less robust and has been deemed as "probable" in evidence-based guidelines From our point of view, the evidence regarding lipids is unquestionable. However, as mentioned earlier, its biological plausibility is clear. Under these circumstances, we would favor the removal of TFAs from the food supply. About three decades ago, Bang et al. Kromann and Green 44 further reported that acute MI rates in this same population were markedly lower than those in Denmark. Sekikawa et al. Japanese men had the lowest levels of atherosclerosis, whereas whites and Japanese Americans had similar levels.
Japanese had 2-fold higher levels of serum marine-derived n-3 fatty acids than whites and Japanese Americans living in the USA. Very high levels of marine-derived n-3 fatty acids have antiatherogenic properties that are independent of traditional cardiovascular risk factors and may contribute to reducing the burden of atherosclerosis in the Japanese, a lower burden that is unlikely to be the result of genetic factors.
Similar results were obtained in two recent studies in Japan Once or twice weekly consumption of fish i. Increasing fish intake above this level is of little additional benefit. In contrast, Japanese men consume more than g fish every day on average from early in life. Interestingly, omega-3 intakes in Japan are only one quarter of those among Eskimos, the population that gave origin to the omega-3 hypothesis.
Intriguing observations have been recently made in Alaska Although some investigators continue to report that Inuit consuming traditional diets have lower CHD rates, others are questioning this dogma. At least part of the problem in Alaska appears to be not a lack of omega-3 but the introduction of massive amounts of shortenings and other saturated fats into their Westernizing diet.
This difference may be critical. The Japanese experience, when contrasted to that of the Inuit and the Norwegians, suggests that the cardioprotective punch of the long-chain omega-3 fatty acids may be no match for diets high in fat, particularly saturated fat. Alcohol, red wine, polyphenols, resveratrol. All clinical studies are concordant in that abstainers and heavy drinkers have higher mortality rates than individuals who drink moderately. For instance, Mukamal et al.
The effect was present in men, women, whites and non-whites and included coronary and stroke mortality; however, risk reduction tended to be stronger for CHD than for cerebrovascular disease. Also, Ronksley et al. Alcohol increases HDL, which is protective against atherosclerosis, and polyphenols in red wine have many protective effects including vasodilation, anti-oxidation and anti-platelet effects. Non-cardiovascular diseases have also been reported to be favorably influenced by moderate drinking.
However, these clinical studies are observational and no controlled investigation has ever been performed; uncertainties also remain regarding drinking frequency, quantity, binge drinking, and sources of alcohol, i. More recently, major interest has emerged regarding the possible beneficial effect of resveratrol - a polyphenol encountered in red wine, plants and fruits - on aging.
So far the only intervention that effectively increases cell proliferation in culture and living organisms such as Saccharomyces cerevisae , fish and worms, is caloric restriction Since resveratrol follows the same metabolic pathway as caloric restriction, including structural DNA preservation and P53 reduction, the hypothesis was raised that it could prolong life.
Indeed, in experiments with hypercholesterolemic mice, Baur et al. Nevertheless, we did find preservation of vascular function, increased aerobic capacity, P53 reduction, and telomere length preservation, all of which suggest protective actions of both red wine and small doses of resveratrol on vascular function. Both these experimental and clinical observation studies show a potential benefit of moderate alcohol consumption, especially red wine.
However, direct controlled studies on men are still locking. Regular exercise reduces cardiovascular events 52 through a number of physiological mechanisms. The most striking metabolic effect of exercise is to reduce plasma TG; but exercise also reduces insulin resistance and therefore contributes to diabetes control; regular exercise decreases blood pressure and increases HDL but has no effect on LDL.
It improves mood, body weight, and inflammatory and hemostatic variables. Physical training improves exercise capacity, increases collaterals in CAD patients and improves endothelial function. Hence, it is now considered to be part of recovery programs following these interventions. In the long term it reduces sudden coronary death; however, sudden death is more frequent during intense exercise than during moderate exercise. In our group, Casella-Filho et al. They interpreted the data as evidence that exercise can functionally improve HDL even if its total value does not change, probably by interference with its sub-fractions.
Thus, even short periods of exercise can substantially ameliorate endothelial function while increasing resistance to LDL oxidation. The molecular mechanisms underlying the beneficial effects of exercise were examined by Werner et al. In normal mice, short-term voluntary running up-regulated cardiac telomerase activity, reduced the expression of proapoptotic mediators such as cell-cycle-checkpoint kinase 2, p16 and p53, compared to sedentary controls. Running also prevented doxorubicin-induced apoptotic cell death. In eNOS and TERT knockout mice, running had no effect, thus indicating the pivotal role of these enzymes as mediators of the effects of exercise.
Further characterization permitted these investigators to establish that these salutary effects of running were also mediated by insulin growth factor These effects persisted for at least 6 months. This is an important, novel contribution to our understanding of the mechanisms underlying the benefits of exercise. These lines of evidence justify why cardiologists recommend regular exercise programs for CVD prevention and treatment.
Tolerance to exercise through stress testing, however, should be assessed before entering such programs.
Seven Countries Study « Heart Attack Prevention
Performing exercise within safe ranges of submaximum tolerance rather than at extenuating levels is a salutary practice, since excessive strain may induce sudden death in people with CAD. A comparison of mortality by lung cancer in people who never smoked, those who quit smoking at age 30 or age 50, and those who continued to smoke is very revealing 1. People who never smoked had almost no mortality by age 75 due to cancer; people who continued to smoke, had a death rate about 12 times higher; quitting at age 30 was better than at 50, but in both cases it was significantly better than continuing to smoke.
In heart disease, many studies have shown the benefits of not smoking or quitting smoking. Iestra et al. This greater benefit in the general population is largely attributable to cancer prevention. Although quitting smoking has been a formal cardiologist recommendation for many years, its implementation remains a considerable challenge.
Obesity is one of the most prevalent risk factors, not only in Brazil but also all over the world. Even children and adolescents are suffering, which is a unique phenomenon in the history of humanity. A BMI above 30 is considered obesity while the normal index ranges from 23 to Causes of obesity are essentially two: 1 excessive caloric ingestion mainly through foods rich in fats and carbohydrates and 2 lack of exercise.
Both situations are frequently associated with psychological factors including anxiety, stress and depression. Obesity is frequently associated with diabetes and metabolic syndrome, which in turn predispose to CAD. As shown above 25 , obesity reduces life expectancy and greatly impairs quality of life. In principle, obesity can be avoided or treated. Several measures are required for this purpose: a diet with no excessive calories, principally restricting saturated fats and carbohydrates; regular exercise; medications to control excessive anger, and, most recently, bariatric surgery.
But all require major changes in lifestyle. Cognitive behavioral therapy 56 is of particular value in this respect, as well as counseling by a nutritionist. Unfortunately, the long-term efficacy of weight reducing programs is disappointing, as shown by the Diabetes Prevention Program Research Group 57 ; although patients respond well initially, they regain weight over the next years.
Alcohol and coronary heart disease in the Seven Countries Study; D. Physical activity, physical fitness and coronary heart disease in the Seven Countries Study; A. Part III: Biological risk factors and coronary heart disease. Serum cholesterol and coronary heart disease in the Seven Countries Study; D. Blood pressure and cardiovascular diseases in the Seven Countries Study; A. Body fatness, coronary heart disease and all-causes mortality in the Seven Countries Study; D. Type 2 diabetes, glucose tolerance and cardiovascular diseases in the Seven Countries Study; D. Kromhout, E.
Electrocardiographic predictors of coronary heart disease in the Seven Countries Study; A. Menotti, H. Multivariate analysis of major risk factors and coronary risk in the Seven Countries Study; A. Risk factors for global coronary risk in preventive and clinical cardiology; A. Menotti, D. Diet, lifestyle and prevention of coronary heart disease The integration of observational and experimental evidence; D. Kromhout, et al. Epilogue for the Seven Countries Study; H. Springer Book Archives Fakta. Ta kontakt med Kundesenteret. Avbryt Send e-post.
Les mer. Om boka Prevention of Coronary Heart Disease: Diet, Lifestyle and Risk Factors in the Seven Countries Study In the s I was struck by reports about many apparently healthy middle-aged men who dropped dead instantly from heart attacks. The causes of these sudden deaths were unknown.