Health Effects of Fats: Vascular Disease

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Effects of Diet on Cardiovascular System
It could also cause health complications. Examples include oxygen, digested foods, waste materials and hormones. For example, endothelial function is blunted in patients with a number of traditional cardiovascular risk factors, and treatment of those risk factors tends to improve or restore endothelial function. This is an indication of good health and efficient cardiovascular system. Schematic diagram of the interactions proposed in this paper In the endurance exercise-trained state or with high levels of physical activity, endothelial function and parasympathetic tone augmented heart rate variability are enhanced.

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Diabetes and Its Effects on the Cardiovascular System

Some of these compounds are chemically active and trigger damaging changes in the body. Tobacco smoke contains over 60 known cancer-causing chemicals. Smoking harms almost every organ in the body, causing many diseases and reducing health in general. Dangerous chemicals in Tobacco smoke include: Raised blood pressure and heart rate. Tightening of blood vessels in the skin, resulting in drop in skin temperature.

Less oxygen carried by the blood during exercise causing fitness to deteriorate. Stickier blood which is more prone to clotting Damage to the lining of the arteries, which is thought to be a contributing factor to atherosclerosis the build-up of fatty deposits on the artery walls Atherosclerosis Reduced blood flow to extremities fingers and toes Increased risk of stroke and heart attack due to blockages of the blood supply.

There are also more serious effects associated with smoking. Cancer of the lung, mouth, nose, larynx, tongue, nasal sinus, oesophagus, throat, pancreas, bone marrow, kidney, cervix, ovary, ureter, liver, bladder, bowel and stomach. All of which are connected to the circulatory system through blood vessels and so bear the risk of spreading to the heart and other essential organs of the circulatory system. Heart diseases including coronary artery disease and heart attack.

Both of which are directly linked As well as Poor blood circulation in feet and hands, which can lead to pain and, in severe cases, gangrene and amputation.

Normal Circulation Poor Circulation The effect of Diet on the Circulatory System Diet also has a significant effect upon the overall health and wellness of your circulatory system. Your diet affects the health of your blood vessels.

Some of the foods you eat cause cholesterol plaques to build up in your arteries. If these vessels become clogged by plaques, you can't deliver blood as efficiently. Similarly, if vessels harden, they're susceptible to tearing, which can lead to clot formation and clogging of the vessels.

Vascular Health Foods with large quantities of saturated and trans fats impact your vascular health negatively. Your body makes cholesterol from saturated and trans fats. Eating large quantities of saturated and trans fat-containing foods increases your risk of vascular disease.

Unhealthy Foods Most common in animal products Saturated Fat Trans Fats Occur in processed foods If vessels become clogged, your heart health is also affected. The heart is a muscle, and like other body muscles, it depends upon a steady supply of blood. Clogging of the arteries that feed the heart leads to heart attack. Limiting unhealthy fats to maintain heart health and minimize your risk of heart attack.

Heart Health Some foods benefit the circulatory system. For instance, unsaturated fats which occur mostly as plant-based oils. They are heart healthy and improve your cholesterol levels, preventing buildup of plaques in the arteries. Eating plenty of dietary fibre also helps, particularly soluble fibre, which absorbs cholesterol in the digestive tract and helps prevent your blood cholesterol levels from rising as high. Good sources of fibre include fruits, vegetables, whole grains and beans.

Healthy Food Diet and Cardiovascular Disease The role of diet is crucial in the development and prevention of cardiovascular disease. Diet is one of the key things you can change that will impact all other cardiovascular risk factors. Fat Research shows that fat levels have a strong correlation with the risk of coronary artery disease, Sodium High blood pressure is a major risk factor for cardiovascular disease.

If you have a diet high in sodium you risk high blood pressure. Fruit and Vegetables Eating a diet high in fresh fruits and vegetables protects your heart. Fruit and vegetables contain components that protect against heart disease and stroke. Wholegrain Cereals Whole grains are unrefined and do not have the bran or germ removed. They contain folic acid, B vitamins and fiber, all of which are important protectors against heart disease.

Fish In countries where fish consumption is high there is a reduced risk of death from cardiovascular mortality. Nuts Eating nuts regularly is associated with decreased risk of coronary heart disease. Soy There is evidence that soy has a beneficial effect on blood lipid levels.

Alcohol If you have the occasional drink you may protect your heart, but only if you drink in moderation. In conclusion both smoking and diet effect the circulatory system. Harriet Tubman - A woman of Great Moral In this context, we do not cite any studies where the primary intervention has been strength training. As is the case for exercise, there have been hundreds, if not thousands, of interventional trials mostly with drugs or diet that have attempted to control or modify one or more risk factors for cardiovascular disease.

One recent notable example investigated the effects of moderate to high doses of statin treatment in a large cohort of patients who were judged at high risk for cardiovascular disease. They used a high dose of rosuvastatin to treat these patients.

We chose this trial as an example because of the very large number of subjects and because the reduction in risk approximates, but does not exceed, that reported for exercise and physical activity studies. When these data are compared with Fig.

However, it is interesting to note that various forms of exercise intervention typically cause only modest reductions in LDL or increases in high-density lipoproteins HDL; Halverstadt et al. This means that exercise is much less effective than statins in lowering LDL. Thus, it would seem that the beneficial effects of exercise on cardiovascular risk are not dependent on changes in blood lipids.

The data are a little bit better for type 2 diabetes. There have been a number of recent intervention trials showing, for example, that min per week of moderate or vigorous walking can reduce by about half the number of high-risk middle-aged subjects who develop full-blown type 2 diabetes over a 5—10 year period of follow-up Lindstrom et al. Additionally, exercise seems better than drug-based interventions for the prevention of diabetes in high-risk patients Tuomilehto et al. However, less than half of the improvement in the risk for coronary heart disease could be attributed to improvements in traditional risk factors Fig.

The filled bars show the risk reduction due to high levels of physical activity for all traditional risk factors in combination and for specific individual risk factors. Data from Mora et al. Over the last 25—30 years, the vascular endothelium has emerged as a key site of cardiovascular control. In this context, blunted endothelial function is emerging as a risk factor for cardiovascular disease, and normal or enhanced endothelial function appears to be protective against cardiovascular disease Green et al.

For example, endothelial function is blunted in patients with a number of traditional cardiovascular risk factors, and treatment of those risk factors tends to improve or restore endothelial function.

Importantly, so does exercise training DeSouza et al. There are numerous examples of the beneficial effects of exercise on endothelial function. For example, DeSouza and colleagues showed that young sedentary subjects had much better endothelial function as measured by acetylcholine-mediated forearm vasodilatation than older sedentary subjects. By contrast, there was no difference between young endurance-trained and older endurance-trained subjects. There are various indices of autonomic function; however, none of them is perfect, and none is as simple as obtaining a blood test for cholesterol or glucose or simply measuring blood pressure with a cuff.

Additionally, many widely studied or used markers of autonomic function are subject to some debate regarding their underlying mechanisms Eckberg, ; Karemaker, For example, renal noradrenaline spillover correlates well with muscle sympathetic nerve activity in resting humans Wallin et al. In spite of some of these limitations, we believe that enough information is available to begin to ask whether autonomic dysfunction is in fact the missing risk factor that is altered by exercise, and how it might interact with other risk factors.

This shows that reduced heart rate variability is a marker of poor outcomes in middle-aged patients at risk for cardiovascular disease. In subsequent sections, we will argue that poor heart rate variability is related to increased vascular stiffness as a result of poor endothelial function and reduced baroreflex function. A, B, C and D reflect specific outcomes as follows: A, coronary heart disease; B, myocardial infarction; C, fatal coronary heart disease; and D, total mortality.

Diabetic subjects with any marker of reduced heart rate variability had increased morbidity and mortality. Data from Liao et al. In the Studies of left ventricular dysfunction SOLVD trial of asymptomatic subjects with left ventricular dysfunction, individuals with resting noradrenaline levels above the median had double or triple the all-cause mortality, cardiovascular mortality, hospitalization for development of congestive heart failure and development of myocardial infarction or angina Benedict et al.

Thus, evidence of sympathetic activation in these patients appeared to be at best a poor prognostic sign and was probably a major contributor to their poor outcomes. In the Coronary artery risk development in young adults CARDIA study, young healthy subjects were followed for 15 years in an effort to understand factors that might predispose some individuals to develop hypertension.

One of the most powerful predictors of who became hypertensive was the blood pressure response to acute sympathoexcitatory stress at baseline Matthews et al. Individuals in the quartile with the largest increase in blood pressure developed hypertension at about five times the rate of individuals in the lowest quartile. This again suggests that there is an important link between the autonomic nervous system and cardiovascular risk factors in humans.

Less is known about how baseline levels of sympathetic activity interact with lipid and metabolic risk factors. Given the potent vasoconstricting effects of increased sympathetic traffic, how is normotension maintained in subjects with high sympathetic activity?

These two factors limit the blood pressure-raising effects of the high sympathetic activity in these subjects. In terms of hypertensive subjects, there is evidence both for and against a relationship between sympathetic activity and blood pressure.

By contrast, blood pressure typically rises with age and becomes more closely linked to sympathetic activity after the age of 40 Narkiewicz et al. Therefore, we have at best a modest relationship between increased baseline sympathetic activity and blood pressure along with limited data on how the sympathetic nervous system interacts with metabolic risk factors such as lipids and diabetes.

However, there is at least a hint of what might be happening during ageing, especially in female subjects. In an effort to understand how reduced endothelial function in combination with high MSNA might influence the cardiovascular system, we performed a systemic infusion of the nitric oxide synthase inhibitor N G -monomethyl- l -arginine l -NMMA and measured the effects on blood pressure and systemic haemodynamics in a group of healthy young men with widely varying baseline MSNA Charkoudian et al.

The idea was that there was at least some evidence that NO levels are higher in individuals with high baseline MSNA and that this NO buffers the blood pressure-raising effects of the high sympathetic activity. While the 2—7 mmHg differences noted in the dose—response curves in Fig.

Low- and moderate-dose nitric oxide synthase inhibition causes larger increases in blood pressure in the subset of subjects with high baseline levels of MSNA. Data from Charkoudian et al. Based on epidemiological evidence, and observations similar to those outlined above, we propose that high levels of sympathetic activity will interact negatively with traditional risk factors in middle-aged subjects.

This is likely to be made worse by weight gain, which has been shown to dramatically increase baseline levels of MSNA Fig.

This means that as individuals enter their 40s and 50s, those with high MSNA or who those gain weight especially visceral fat may be at increased risk.

These individuals will also be likely to have reduced vasodilator function as a result of endothelial dysfunction associated with the metabolic syndrome, sedentary lifestyle and high levels of oxidative stress that limit the ability of NO to cause vasodilatation. As noted previously, almost all of the major cardiovascular risk factors are associated with reduced endothelial function. In addition to reduced endothelial function, there might be increased circulating vasoconstrictor substances and increased vasoconstrictor responsiveness that will further contribute to vascular dysfunction as middle-aged individuals drift into the cardiovascular disease phenotype Nielsen et al.

Data from Gentile et al. All of these factors together then contribute to a vicious cycle of high sympathetic outflow, reduced vasodilator function and cardiovascular disease that would self amplify over time Fig.

In the endurance exercise-trained state or with high levels of physical activity, endothelial function and parasympathetic tone augmented heart rate variability are enhanced. Large conducting vessels remain compliant, and the effects of high sympathetic outflow, when present, are buffered. These positive interactions may account for observations showing that exercise is more protective against cardiovascular risk than predicted by its effects on traditional risk factors.

With physical inactivity, there is a loss of endothelial function during middle age, a potential accumulation of risk factors, and increased vessel stiffness.

These effects of physical inactivity permit the effects of high sympathetic tone to be more fully expressed while parasympathetic tone is progressively lost.

These negative interactions may account for observations showing that physical inactivity is a more potent cardiovascular risk factor than widely appreciated. There is strong evidence to suggest that exercise training can keep the autonomic nervous system healthy. For example, exercise is protective against age-related reductions in baroreflex function in humans Monahan et al.

In this context, endurance-trained older subjects have baroreflex function that is similar to moderately active young subjects. This improvement in baroreflex function, which on a population basis is likely to manifest as improved heart rate variability, could be the result of both greater blood vessel distensibility and better signal transduction in barosensitive areas of the carotid sinus and aortic arch, or it could also represent improved or maintained central integration in the brainstem cardiovascular centres.

However, the key point is that moderate exercise, endurance training and high levels of physical activity are highly protective against age-associated baroreflex dysfunction. Finally, exercise training can clearly reduce muscle sympathetic nerve activity in patients with congestive heart failure Fraga et al. Since exercise is also protective against weight gain and visceral obesity, it is likely to blunt the age-associated rise in MSNA. There are also important confirmatory and mechanistic data from animal studies to show that exercise training limits sympathoexcitation and favours sympathoinhibition in the brainstem cardiovascular centres.

For example, Mueller has shown that the increases in arterial pressure and lumbar sympathetic nerve activity are blunted when bicuculline is injected into the rostral ventrolateral medulla. Additionally, the reductions in heart rate during the pressor response are greater in exercise-trained animals.

These data imply strong central nervous system effects of exercise on the autonomic nervous system that favour sympathoinhibition and enhanced vagal outflow. In summary, we have tried to be provocative in this paper and used an impressionistic approach to integrate key data about exercise and the risk factor gap in cardiovascular disease.

In this context, autonomic dysfunction is clearly a marker of poor outcomes in large populations of middle-aged humans. Autonomic dysfunction, including sympathetic activation, is also a marker of bad outcomes in patients with various risk factors for cardiovascular disease. We also argue that any negative effects of autonomic dysfunction are amplified by concurrent endothelial dysfunction and, indeed, there is some evidence for direct and deleterious interactions between elevated sympathetic nervous system activity and NO function Hijmering et al.

In the context of the above ideas, we believe there is a vicious cycle between autonomic dysfunction and endothelial dysfunction that can largely be prevented or ameliorated by exercise training. We also believe that this vicious cycle explains why exercise is more protective than it should be based on its effects on traditional risk factors for cardiovascular disease.

Therefore, our global hypothesis is that the risk factor gap can be explained by the following effects of exercise and physical activity on the cardiovascular system. National Center for Biotechnology Information , U. Journal List J Physiol v.

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