Cardiovascular Disease

Cardiovascular disease is a broad term used to refer to any and all diseases related to the vascular system or the cardiac muscle. These include diseases include coronary artery disease, cerebrovascular disease (CVD), Hypertension, rheumatic disease of the heart, congenital diseases, congestive cardiac failure etc. “Atherosclerosis are the root cause of the biggest killer of the 21st century.” According to the WHO estimates of 2003, more than 16 million people died from cardiovascular diseases. (www.who.int). In the UK alone, more than 200,000 deaths were related to cardiovascular diseases. (British heart foundation- coronary artery disease statistics, 2006 edition).

 In England, according to the 2006 health survey, more than 13.6% males and more than 13% females are suffering from some sort of cardiovascular disease and more than 24% of males as well as females are currently classified as obese. (Health Survey for England 2006: CVD and risk factors adults, obesity and risk factors children, 2008).
Most of the cardiovascular diseases originate from the same underlying anomaly and that is atherosclerosis. It is the deposition of fat and related compounds in the walls of the vessels which eventually get occluded.

“Mechanisms contributing to atherogenesis are multiple and complex. A number of theories—including the role of dyslipidemia, hypercoagulability, oxidative stress, endothelial dysfunction, and inflammation and infection by certain pathogens—have been propounded from time to time explain this complex phenomenon. Recently it has been suggested that atherosclerosis is a multi-factorial, multi-step disease that involves chronic inflammation at every step, from initiation to progression, and that all the risk factors contribute to pathogenesis by aggravating the underlying inflammatory process. A better understanding of the pathogenesis of atherosclerosis will aid in devising pharmaceutical and lifestyle modifications for reducing mortality resulting from coronary artery disease (CAD)” (Mallika V, 2007).

Pathophysiology

All the vessels in the human body are made up of three distinct layers, according to their placement. These are the intimal layer (inner most), the mucosal layer and the serosal layer (outer most). Atherosclerosis is characterised by lesions in the intimal layer of the vessels. These are known as atheroma. The affected arteries are usually medium to large in size. These include the carotids, the aorta the coronary arteries etc. the most frequently, the lesions or atherosclerotic plaques are formed in arteries which have turbulent or non laminar blood flowing through them. This provides ample opportunity for plaque formation and the initiation of the pathology. (Plaques are lesions sub-endothelial in nature, and contain phospholipids and cholesterol. The turbulent blood flow in the arteries causes the cells in the blood to create adhesion molecules and get attached to the walls of the artery as well as create an environment to “bind inflammatory cells” (Merck, 2008).

Major risk factors for this disease include, obesity, smoking, raised blood pressure in the form of hypertension, dyslipidemia and diabetes. Diet plays a big role in the causation of the disease (Patho-physiology of Atherosclerosis, 2008). Chemicals causing oxidative stress can lead to inhibition of nitric oxide, which plays a large role in the prevention of adhesion molecules formation. Once the levels of nitric oxide diminish, “it stimulates inflammatory response initiation which ultimately leads to migration of monocyte across the endothelium and into the sub-endothelium space.” (Merck, 2008). Lipids of low and very low density also move into the space. It is here that the macrophages start taking up the lipids and transform into lipid laden foam cells. The end result of all this is the formation of fatty streaks, which are visible from the endothelium. These streaks can grow into plaques, if the process of LDL and VLDL uptake continues. These can lead to damage of the passing erythrocytes, or to rupturing of the membranes or of vasa vasorum.

Inflammatory growth factors stimulate growth of connective tissue in the lesion are eventually end up creating is “a sub-endothelial fibrous plaque with a fibrous cap, made of intimal smooth muscle cells surrounded by connective tissue and intracellular and extra-cellular lipids. A process similar to bone formation causes calcification within the plaque” (Merck, 2008).

“Atherosclerotic plaques may be stable or unstable. Stable plaques regress, remain static, or grow slowly over several decades until they may cause stenosis or occlusion. Unstable plaques are vulnerable to spontaneous erosion, fissure, or rupture, causing acute thrombosis, occlusion, and infarction long before they cause stenosis. Most clinical events result from unstable plaques, which do not appear severe on angiography; thus, plaque stabilization may be a way to reduce morbidity and mortality” (Merck, 2008).

If the collagen and other extra-cellular matrix covering the plaque are not strong enough then, the plaque has the potential to rupture. Rupture of the plaque leads to exposure of plaque contents to the circulating blood and its constituents. This leads to thrombosis of the site of rupture. In the end, the rupture of an unstable plaque can lead to:

Organisation and infusion of the thrombus itself into the plaque, leading to rapid plaque growth. Rapid growth of plaque and thrombus can lead to occlusion of the vessel, leading to ischemia of the organ it supplies. The thrombus may dislodge and detach itself from the vessel wall. This creates an emboli and it can get lodged in the lung or in the other vessels and obstruct blood flow to organs. Unstable plaques, after rupturing may lead to filling of the site with blood, leading to ballooning and eventual rupture of the vessel walls.

Risk factors

Dyslipidemia: this means that the blood has either high LDL content or low HDL content. LDL promotes deposition of fat in the sub-endothelial sites and hence increases risk of atherosclerosis. HDL on the other hand can protect the body form plaque formation as it transports antioxidants which prevent LDL oxidation and deposition into the sub-endothelial spaces.

Hypertension: this leads to vascular inflammation through Angiotensin II related processes. The inflammation stimulates mediators and other chemicals to be released which promote thrombosis and oxidation of LDLs.

Diabetes, tobacco use, high lipoproteins all can increase the risk of atherosclerosis. (Beckman J A, 2002)

Atherosclerosis as a disease is usually an asymptomatic until the lesions become so big as to prevent or hinder the smooth blood flow through the arteries where they are present. When the disease becomes symptomatic, it usually presents itself as symptoms leading to unstable angina, stoke, infarction etc. it can also cause occlusion of a vessel through emboli formation and lead to ischemia of the area it supplies. Cases of Sudden death, arterial dissection and rupture have also been associated with atherosclerosis (Pathophysiology of Atherosclerosis, 2001).

The treatment of patients suffering from atherosclerosis is usually multi-directional. It includes life style modification, drugs, Antiplatelets along with ACE inhibitors as well as beta blockers. It is well known that diet plays a large role in the prevention of atherosclerosis and associated diseases. Therefore careful balancing of diet is an important aspect of preventing atherosclerosis.

The Potential Role of Diet in Reducing the Incidence of CVD

Much has been talked about and debated over the decades concerning the importance of the role that diet plays in determining the incidence of cardiovascular diseases in general as well as atherosclerotic disease in specific. Initially the theory was that all fat and related products were harmful to health when it came to cardiovascular situation. Therefore it was advised that they replace their fat in diets with carbohydrates sources. Since our staple foods are potatoes, rice and maize etc increase usage and dependence on these has led to a generation of obese people like we have never before encountered in the history of the disease. Moreover the prevalence of the disease has been climbing since. Later on it was realised that certain types of fat groups were in fact useful, necessary and even beneficial for the avoidance of the disease. The medical literature then started studies in this aspect and found that unsaturated fats were in fact beneficial.

Current studies show that there is more benefit to be achieved from increased the levels of High density lipoproteins (HDL) in the blood than there is, by reducing the levels of Low density lipoproteins (LDL) in the blood. A problem which was recently discover in studied, was that it has been shown that children as young as 5 or 7 years of age have been known to have fatty streaks in the walls of their vessels. This means that the pathology of the disease starts from a very young age. And the resultant pathology that we see in people with coronary artery disease is the result of plaque formation over a period spanning decades of accumulation. Therefore it must be kept in mind that dietary modification which is initiated only after the patient has been diagnosed with the disease is usually too late to reverse the pathological changes that have already occurred. Where the diet can play an important role is in preventing the pathology to start with. Healthy dietary habits from a young age can help prevent the development of the fatty streak lesions and therefore prevent the coronary artery disease in the future.

Dietary Fats (Saturated Fat, MUFA, PUFA, Trans-Fats)

Fats are one of the three groups of foods classified as macronutrients. This group has the highest capacity to release high metabolic energy when the human body needs it. Apart from, this, they help in dissolving the fat soluble vitamins, namely A, D, E, and K. The also help in adding flavors to our foods and more importantly they play crucial role in forming certain cell structures. If consumed in excess, it usually ends up functioning as a storage compound in the body. It has been long established that certain types of fats are unhealthy for human consumption and can lead to the risk of developing cardiovascular illnesses.

There are four main groups of fats which include Saturated Fats (SFA), Monounsaturated (MUFA), polyunsaturated fats (PUFA) and Trans fats. The differences between them structurally come from the variable numbers of double bonds available in the compound. (Lam, 2002)

Saturated fats (SFA): these compounds contain no double bonds, are usually found in animal foods like poultry, meat and milk and milk products like butter etc. other sources include, kernel oils, coconut and palm oils. According to an American survey, diet in that nation contains more that 14% fat. (Lam, 2002).

Many studies have significantly shown the link between the consumption of SFA and the increased incidence of cardiovascular diseases.  Even though the exact mechanism of the biochemical events is not known, we do know that SFA also raise the levels of Low density lipoproteins (LDL) also known as bad cholesterol. If the ratio of high density cholesterol to low density cholesterol remains the same, then SFA levels independently are not known to cause any increased risk of a cardiovascular incident. Therefore keeping this relationship in mind, it is best not to eliminate SFA from diet but to obtain it in required amounts.

Monounsaturated Fatty Acids (MUFA)

The biochemical structure of MUFA contains a single double bond. The best sources for obtaining MUFA are olive oil, canola oil and peanut extracted oils.  MUFA is the type of fat which the scientists refer to as the good fat.  Several studies show that consuming MUFA regularly in diet can reduce the risk of breast cancer many folds. The consumption of oil oils is greatest in the Mediterranean region. This is to say that people in that region have a regular source of MUFA It has been noticed the incidence and prevalence of cardiovascular diseases in that region is considerably lower than that of countries having a western diet pattern. (Forman D, 2006 & Lam, 2002)

There are three ways in which the MUFA help prevent cardiovascular diseases.

The first way in which by which his can be done is by decreasing and slowing the oxidation process of low density lipoproteins as well as that of cholesterol. This in effect decreases the rate of atherosclerosis. The second way in which this is done is by decreasing the levels of TGL, which is a form of fat compound present inside the plaque. The third and last way known by which the risk of heart disease an be reduced is by increasing the intake of high density lipids of HDLs. Research shows that HDL increase in diet has the greatest effect in reducing risk of coronary artery diseases.  Saturated fats increase the risk of heart disease whereas unsaturated fats decrease the risk for the disease. Therefore a diet which encourages the reduction of saturated fat use as well as encourages increased usage of unsaturated fats increases the chances of a cardiovascular disease free life many folds. (Lam, 2002).

Therefore, in order for to prevent cardiovascular diseases like atherosclerosis one must start substituting butter with olive oils in daily routine as this has a high MUFA content. Nuts including hazelnuts and peanuts have a higher MUFA content. So their consumption should be encouraged.

Polyunsaturated Fat (PUFA)

These fat compounds made up of multiple double bonds in their structure. Fatty acid chains are a common presentation. Usually found in fish oils and vegetable oils, they are seen as liquid oils at room temperature. Soy oils and sunflower oils are rich in PUFA. Research has shown that although naturally occurring PUFA is healthy for our body and can even reduce the risks of cardiovascular disease. Hu FB, (2002) has suggested that if we fulfill part of energy requirement from MUFA and PUFA, rather than carbohydrates, we can reduce the risk of a cardiovascular event by 19% and 38% accordingly. “Sunflower oil, with its higher PUFA content, has been shown to yield greater lipid-lowering effects than olive oil.” (Putting dietary fat into proportion: Striking a balance between saturated and unsaturated fats, n.d.).

Unfortunately as most of the oils we consume are processed, they structures of the PUFA are greatly altered in the process and they lose their beneficial effects in the process. Therefore the market available sources which include sunflower oil and other vegetable oils are not healthy for consumption and do not reduce the risks of cardiovascular diseases. Good sources for naturally occurring PUFA include, wild salmon fish, nuts and seeds.

Trans Fats

Trans-fat has the worst effects on the health and increases the risk for the cardiovascular diseases. Formally known as hydrogenated polyunsaturated fats, they become unhealthy during the process of hydrogenation in the manufacturing process. The resulting fat, can easily cross the cell membrane barrier and make the cell membrane weak. (Lam, 2002).

Like saturated fat, Trans-fat also is associated with the increase in LDL cholesterol levels. Even ore importantly, Trans aft is known to decrease the levels of the good cholesterol, i.e. HDL levels. The reduction in HDL and the increase in LDL levels compound their effects and are associated with a 93% increase in the risk elevation of cardiovascular diseases. Since trans-fats do not occur naturally and are only available through processed foods, there is no available form which might be healthy for consumption.

Carbohydrates

It is known that in ancient times, when men survived on hunted food as well as what ever grew naturally, had a diet which consisted of carbohydrates greater than 50%. In Australia, the native population used to consume an indigestible plant which fermented in the colon. Yet no case of cardiovascular disease had been known to exist and the population average age was greater than 60 years. Carbohydrate diet forms the staple diet in most regions of the world. It ranges form rice to maize and potatoes. Generally carbohydrate consumption is thought to play a role in the prevention of coronary artery disease as well as stroke. Not all the forms of carbohydrates are healthy for consumption in excessive amounts. Proper combination of complex carbohydrate diet along with digestible ones does reduce the risk of cardiovascular diseases. “There are a variety of ways in which a high carbohydrate diet might be protective of cardiovascular disease risk.

Firstly, this occurs by way of maintenance of insulin sensitivity, especially in the basal state. High carbohydrate diets tend to lower basal (fasting) glucose and insulin over several days. In turn, this decreases risk factors (hyperglycemia and hyperinsulinaemia) for cardiovascular disease. Secondly fermentable carbohydrate in the colon produces absorbable SCFA (short chain fatty acids), with potential regulation of hepatic gluconeogenesis and insulin handling. Effects on lipoprotein metabolism are also in evidence. Increasing satiety and decreasing the energy density of the diet, making obesity less likely.” (Carbohydrates in human nutrition, 1998).

Specific carbohydrate foods are beneficial at different levels and against different carbohydrate groups. There is broad consensus that overall all carbohydrate derived from plant source is beneficial and reduces the risk for cardiovascular diseases. Research although has shown that relying on a single type of source for carbohydrate is not beneficial and a wide variety of sources must be consumed to derive the optimal benefit.

Dietary Fiber

 A study by Ludwig et al in 1999 showed that dietary fiber has an inverse relationship with CVD, blood pressure as well as LDL and HDL ratios. Their study suggested that fiber may play a greater role in role in protecting against weight gain and CVD than fat does in causing them. It is suggested that fiber decreases the rate of insulin secretion after a meal and hence it takes a longer time for food to be digested therefore decreasing the net food intake over a period of time.

A study by Bagger M (1996) showed that increase in fiber content in diet as well as decrease in fat intake has the net effect of lowering the systolic blood pressure thereby reducing the CVD risk. Lairon D et, al in (2003) also made similar findings in his study and concluded that dietary fiber assisted in maintaining low levels of triglycerides as well as kept blood pressure levels in check.

“Several large randomized trials of primary and secondary prevention to date have demonstrated the efficacy of diets based on an abundance of plant foods and, therefore, high carbohydrate quality. The recommendations to follow a diet including an abundance of fiber-rich foods in order to prevent CVD and diabetes are based on a wealth of consistent scientific evidence” (Pereira MA, 2003)

There are many micronutrients and trace elements and other chemicals which we consume through fruits and vegetables, that are thought to have beneficial effects against cardiovascular diseases. “Polyphenols have antioxidant, anti-inflammatory, and cell-cycle regulatory effects” (Napoli, 2007). “This is thought to prevent the initiation of the atherosclerotic pathology. It is thought to prevent endothelial damage and maintain vascular functionality. These compounds are found in Concord grape juice and in pomegranate-derived juices. The dietary flavonoid quercetin exerts systemic and coronary vasodilator effects in experimental models, and its consumption is associated with reduced CVD in epidemiological studies” (Napoli, 2007). Phytochemicals which are usually found in the green leafy vegetables are thought to have beneficial against cardiovascular diseases. They can be also found in tea and red wine. Studies show that by consuming extra 3 cups of tea, people can have a reduced cardio vascular risk of up to 10 percent. Other studies have not been able to make a clear recognition of benefits of these compounds and have encouraged further studies. (Erdman JW, et al, 2007)

Apples contain large quantities of phytochemicals. Since they work as antioxidants, their consumption reduces the oxidative stress and hence reduces the risk of developing endothelial injury which can lead to atherosclerosis (Boyer J, 2004).

During deficiency states or incases of imbalanced diets, an amino acid called homocysteine gets involved in the metabolism of methoinine. There seems to be a rise in the levels of homocysteine during deficiency states of vitamin B6 and 12 and folic acid for that matter. Research has shown that raised levels of this compound are directly linked with damage to endothelium, platelet aggregation and other cellular activities that occur during the process of inflammation and therefore aid the atherosclerotic lesion formation. It is imperative that as well as trying to avoid nutrients which may be harmful in the process of atherosclerotic formation, care must be taken not to consume insufficient amounts of useful nutrients. Therefore a balanced and a healthy diet encompassing all vital nutrients and food groups is a must for avoidance of the disease.

“Numerous epidemiologic and intervention studies have been conducted to help provide dietary recommendations for optimal cardiovascular health. The most compelling data appear to come from trials that tested intervention diets rich in fruits, vegetables, MUFA, and PUFA, particularly the n-3 PUFA. In addition, some degree of balance among various food groups appears to be a more sustainable behavioral practice than extreme restriction of a particular food group” (Napoli C, et. al, 2007).

Therefore it is recommended that rather than restricting oneself to one type of food, one should consume all kinds of food. Increase the quantities of foods which are considered beneficial and limiting or maintaining the quantities of foods which are deemed hazardous. Studies show that high levels HDL are more beneficial in preventing a fatal incident of coronary artery disease than does lowering the LDL levels. More over numerous studies have time and again shown the link between salt intake and hypertension. Hypertension led to turbulent blood flow and can lead to several fatal consequences. Studies which compared the role of diet only on the incidence of cardiovascular incidents were not promising. They showed that even though diet modification does decrease the incidents of CVD, the results are not drastic.

Therefore they advise that diet can play a greater preventive role from a young age in hindering the development of the atherosclerotic pathology.  As for its role after the diagnosis of the disease, to prevent a fatal incident, diet modification although imperative, is not sufficient enough to influence the outcome of the patients. Therefore, a carefully planned dietary habits as instructed by the dietitian along with other life style changes like less  stress, less fatigue, avoidance of smoking, along with medical therapy is the best way to prevent fatal CVD accidents as well as prevent the progression of the disease.

Conclusion

 Cardiovascular disease has become widespread and is currently the greatest health hazard in the developed countries. As the developing countries are also acquiring the dietary habits of the developed, CVD is also spreading in those regions. It is imperative that people drastically alter their dietary habits and modifies their life style in order to prevent the occurrence of CVD.  Diets which include healthy fats like MUFA and PUFA, and proteins along with “whole grains as the main form of carbohydrate, with an abundance of fruit and vegetables, and adequate n-3 fatty acids. Such diets, which also have many other health benefits, deserve more emphasis in dietary recommendations to prevent chronic diseases” (Napoli C, et. al, 2007).

Changes in dietary habits are generally cost-effective, and the means are widely available. Through heightened attention of health professionals and the public to current data on appropriate nutritional practices, better measures can be adopted to help reduce CVD risk at the public health level, both for youths and adults. The association between nutritional and genetic factors will be clarified, as well as the forecast that in the future it may be possible to tailor dietary and physical exercise advice on preventing CVD more precisely to the individual’s particular risk profile.” Napoli C, et. al, 2007)

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