Are Dietary Saturated Fats Associated with Cardiovascular Disease - Literature review Example

ARE DIETARY SATURATED FATS ASSOCIATED WITH CARDIOVASCULAR DISEASE? due: Table of Contents Table of Contents 2 Abstract 3 Volk, Altern Med Rev 2007; 12(3):228-245 19 Conclusion 19 Problems in Research Methodology 19 Sample Selection 20 Determining Cause of Death 20 Dietary Assessment 21 Bibliography 23 Abstract Intake of saturated fats is restricted by dietary guidelines because they are claimed to be associated with increased risk of cardiovascular diseases; which are the leading cause of death worldwide, accounting for about 30% of total deaths in 2008. The lipid hypothesis was established in the 1950s, linking intake of saturated fats with increased risk for cardiovascular diseases. However, scientists opposed this hypothesis based on certain irregularities in data collection and interpretation. Regardless of the strength of alternative hypotheses, national dietary guidelines proceeded to adopt the recommendations of the lipid hypothesis. Current dietary guidelines in most countries encourage intake of foods rich in carbohydrates and hydrogenated fats instead of saturated fats, to reduce the risk of cardiovascular diseases. Even after the change in dietary recommendations, cardiovascular diseases are still the leading cause of death worldwide. Recent studies have found flaws in the association of saturated fats and risk of cardiovascular diseases. Meta-analyses, observational studies, random controlled trials and systematic reviews report scientific evidence against the hypothesis. Recommendations for a review of dietary guidelines is, therefore, been called for, to reflect the actual scientific evidence. After a careful scrutiny of the available evidence, it was found that there is a lack of concrete evidence that increased intake of dietary saturated fats is linked to increased risk of cardiovascular diseases. However, substitution of polyunsaturated fats shows a reduction while simple carbohydrates increase the risk of cardiovascular diseases. Replacement with monounsaturated and omega-6 fatty acids has been found to have no significant effect. Word count: 250 Introduction Cardiovascular disease (CVD) defines a class of conditions that affect the circulatory system; that is the heart and blood vessels. Examples of these ailments are cerebrovascular disease, high blood pressure and coronary heart condition among many others. Cardiovascular conditions are the principal cause of loss of lives universally, accounting for up to 30% in 2008, and middle and low-income countries contributing 80% of all CVD deaths (Alwan, 2011). Furthermore, the number of deaths is also predicted to increase to 23.3 million annually by 2030 (p.11). Apart from the fatal health effects, cardiovascular diseases also have serious economic effects. For instance, in poor countries where the prevalence is highest, the poorest households are trapped in a vicious cycle where CVDs and poverty reinforce each other. CVDs increase household poverty through massive spending on treatment while poverty limits the ability of the family members to access preventative healthcare. The governments of these developing countries also spend much of the country’s revenue in treating CVDs, accounting for 6.77% of the GDP (Alwan, 2011). There are various causes of these diseases, ranging from dietary intake to genetics. The World Health Organization identifies risk factors of CVDs such as tobacco use, insufficient physical exercise and poor dietary intake as some of the major ones. There are several types of cardiovascular diseases that are not caused by behaviour. Examples include congenital heart failure, which is a birth disorder characterised by defective heart structure, and rheumatic heart disease, caused by a streptococcal bacteria. Increased intake of saturated fats has traditionally been linked to a higher risk of cardiovascular diseases. As a result, most dietary guidelines recommend limited intake of saturated fats to reduce the risk of getting cardiovascular diseases. Fats have been at the centre of this debate from the beginning. Fats are essential nutrients that have got several roles in the body, including structural, functional and sources of energy. Fats are essential components of cell membranes, brain cells and other important body components such as hormones. They are also used in various processes such as gene expression, transfer of signals in the nervous system and protection of major organs in the body (Dutchen, 2012). They are also a source of energy for the body. They provide the highest amount of calories per gram (9 calories) compared to other macronutrients such as carbohydrates and proteins (4 calories/gram). Additionally, the body stores energy in the form of fats since they pack more energy per unit (in adipocytes) compared to glycogen, the storage form of glucose. Metabolism of fats in the body is a complex process which is dependent on the type of fat. After digestion in the small intestine, transport is facilitated by carrier proteins called lipoproteins. Lipoproteins vary in the amount of cholesterol in their structure and have got different functional roles. Cholesterol, a product of digestion and also synthesized in the liver is essential for various body functions. However, excess cholesterol accumulates in the blood vessels and may lead to narrowing of the blood vessels or formation of plaques, which leads to heart diseases. High-density lipoproteins (HDL) are responsible for removing the excess cholesterol from the circulation back to the liver for further metabolism. Low-density lipoproteins (LDL), deliver cholesterol to the cells. The amount of either HDL or LDL in blood circulation will, therefore, determine if a person is at risk of getting cardiovascular diseases or not. Not all types of fatty acids have been linked to cardiovascular diseases. There are two major classes of fatty acids i.e. saturated and unsaturated. Saturated fatty acids consist of single bonds between carbon atoms in their structures while unsaturated fatty acids contain at least one double-bonded carbon atom in their structure. Sources of saturated fats include most animal fats such as butter, lard and cheese, and others such as coconut oil and cocoa butter. Saturated fats are used as sources of energy, during gene expression and cell messaging and immune function. Unsaturated fat sources include fish oils, most vegetable oils, and olive oil and are important structural components of brain cells, among other uses. Saturated fats have been previously shown to increase the chance of cardiovascular disease by elevating the levels of LDL in the blood circulation. These conclusions are grounded on the findings of several observational studies done in the 1950s and 1970s. Ancel Keys, a biochemist, conducted studies in a number of countries and reported that the higher the fat consumption in a country, the higher the deaths caused by heart disease (Keys, 1970). Several government agencies, especially those that are responsible for health and nutrition, adopted this hypothesis and recommended guidelines that restricted saturated fat intake and promoted intake of carbohydrates and unsaturated fatty acids instead. The recommended intake of saturated fats, according to the National Health Service, is 30g for men and 20g for women (NHS Choices, 2013). Studies have also been conducted on the same hypothesis, and the results suggest that the metabolism of saturated fats increases the level of Low Density Lipoprotein (LDL) cholesterol in the blood (Mattson & Grundy, 1985; Nicolosi et al., 1985; Shepherd et al., 1980). LDL cholesterol is the cause of cardiovascular diseases. Thus, these studies support an increased intake of unsaturated fats and restrict intake of saturated fats to reduce LDL cholesterol and subsequently, risk of heart disease. They also recommend substitution of saturated fats with carbohydrates to keep the levels of LDL cholesterol low. However, more recently, there has been debate on the validity of the claims that saturated fatty acids are the main cause of cardiovascular diseases. Several studies and reviews have been conducted and the findings do not point any specific relation between fatty acids and heart disease (Mozaffarain et al., 2004; Siri-Tarino, 2010; Gillman et al., 1997; Yamagishi et al., 2010). These studies include both observational and meta-analyses. In the observational studies, a cohort, consisting of subjects whose diets are typically high in saturated fats, was selected and followed up for a period. Incidences of heart disease were then monitored. The meta-analyses searched journals for publications on the relationship between high intake of saturated fats and occurrence of heart disease. Both of these failed to find any causal relationship between saturated fats and heart disease. The media has also contributed to the debate involving these claims. Most of them report the findings but fail to mention that the topic is still under discussion. Statements such as “Everyone was wrong: saturated fats are good for you” (English, 2013) may be misleading. The relationship that has been supposedly identified by past research pertains only to heart disease and the presence of debate clearly indicates that the issue has not been conclusively settled. Excessive intake of fats has its health problems, not related to cardiovascular diseases. For instance, taking too much energy and taking little physical activity predisposes one to overweight and obesity, which also increase chances of getting type 2 diabetes mellitus. Controversy Of course, claims refuting practices that have been in use for more than four decades have not gone unopposed. These findings have been strongly opposed by several scholars who claim that there are errors in the study designs and other details (Willet et al., 2014). Errors have been identified regarding their selection of data, some claiming that the data was biased or wrongly interpreted. Another issue that is still under discussion is the nutrient that is recommended as a replacement for saturated fats. According to Willet et al. (2014), replacing saturated with polyunsaturated fats results to a decrease in heart disease risk (para 3). Replacement with carbohydrates, however, does not cause any significant change (para 3). However, the current dietary guidelines suggest otherwise, as is evident from proposed models of healthy diets such as the USDA Food Pyramid and Plate Model. The claims are, therefore, contradictory to some extent. Dietary guidelines encourage replacement of saturated fats with carbohydrates or polyunsaturated fats, since dietary saturated fats and cholesterol are claimed to increase the serum cholesterol and subsequently the risk of heart diseases. This theory of saturated fat metabolism is based on observed association rather than established causation. Recent studies have also found contradicting evidence (Volek et al., 2008); yet national health bodies and other institutions still remain reluctant to adopt the new evidence. The controversy is actually not new and has been around for more than four decades. There is substantial scientific evidence against the hypothesis that saturated fats are directly linked to heart disease risk. The intent of this study, consequently, is to assess the evidence for and against the claim that saturated fats have a relationship with heart disease. Conclusions will be based on a critical analysis of the study designs, reliability and validity, and other crucial indicators that support the statements of recent studies that propose an alternative hypothesis. The paper will also analyse previous studies in the same manner, taking into consideration the strengths and weaknesses of their arguments. Critical analysis The relationship between intake of saturated fats and risk of heart disease is still unclear. Most of the studies conducted in the past years did not succeed in establishing a clear association and acknowledged that the metabolism of fats in the body is a multifaceted process that is yet to be understood (Shepherd et al., 1990). Conclusions made in this topic were majorly based on observational studies and several clinical trials involving both humans and animals, but the exact mechanism remains elusive. An observational study employs a study design where the researcher simply observes a correlation between two variables, without establishing causation. A randomized controlled trial, on the other hand, establishes causation between two variables and usually involves invasive methods. Thus, it is more reliable than an observational study. The same case applies today. The claims being recently made by the scientists are based on observational studies carried out for a certain period and meta-analyses of existing literature (including a variety of study designs) on the subject. Nevertheless, this does not infer that the results are not reliable. Observational studies have been proven over the years to provide valid results and also as a guide for further research. Seven Countries Study by Ancel Keys Two studies are widely considered to have contributed important information in the development of the lipid hypothesis: the Seven Countries Study conducted by Ancel Keys and the Framingham Heart Study. Ancel Keys was the main advocate for the reduction of dietary saturated fat (specifically cholesterol), to reduce coronary heart disease risk. He made this deduction based on his research in 1952 (and later in 1970) where he reported a strong link between high dietary cholesterol intake and high coronary disease mortality in a survey of six countries (Keys, 1952). Figure 1: The relationship between high dietary fat intake and coronary heart mortality in six countries as presented by Keys (1953). However, his original database actually consisted of data from 22 countries, and the strength of association was greatly reduced by the widespread of the data when all of them were considered. Unfortunately, he selected only the combination of countries whose data supported his hypothesis, excluding the rest of the conflicting data (Scherstén et al. 2011). Unless the researcher justifies the reasons for exclusion of certain data, such actions are against the rules of scientific research and, therefore, any conclusions based on such research should not be considered valid. In the scenario of the Seven Countries Study, no rationale for exclusion of data was given. However, the data shows a correlation, only that the interpretation by Keys was not exactly accurate. Figure 2: The original database from which Keys selected his six countries (Yerushalmy & Hilleboe, 1957) Keys also derived his data from unreliable sources. In his original study, the index of fat as a proportion of total consumed calories was based on the quantity of available fat for consumption i.e. the total fat produced in the country plus imports, minus food not used for human consumption (Yerushalmy & Hilleboe, 1957). The data, therefore, was not for actual food consumption. His other variable, mortality from cardiovascular diseases, was also not reliable. It was derived from death certificates and population estimates. The data was marred by differences in diagnostic habits, reporting patterns and standards of the medical profession in the countries studied. To validate his hypothesis on dietary fat, Keys conducted another study involving seven countries, where cohorts were followed up for 15 years, and cardiovascular diseases monitored (Keys et al., 1984). The study design employed could not establish an actual causation, apart from the general population-specific association. Furthermore, the results on survival rates in participants with low serum cholesterol were contradictory; cholesterol levels among survivors were significantly high. For instance, in the Serbian cohort, the cholesterol levels of survivors ranged between 15-45% higher than the participants who had died. The research, therefore, neither confirmed nor invalidated his hypothesis. His choice of sample was also not representative enough. It mainly represented the white population so the results could not be extended to other populations such as Hispanics and Africans. Following the conclusions made by Keys, several other scientists conducted further research to prove that saturated fat obtained from animal origins was the chief cause of cardiovascular diseases. For instance, Dr Norman Jolliffe, of the Nutrition Bureau, New York Health Department, formed the Anti-Coronary Club in 1957, consisting of 814 males in the experimental group and 463 in the control group. They were aged between 40 and 59 years. The experimental group was supposed to take the “Prudent Diet” which was claimed to reduce instances of heart disease. The diet consisted of margarine and corn oil instead of butter, cold breakfast cereals in the place of eggs and instead of meat, chicken and fish. Their matched counterparts took the opposite – eggs every morning and meat three times a day (Enig & Fallon, 2008). In 1966, the outcomes of the investigation were published in the Journal of the American Medical Association. The participants in the Anti-Coronary Club group were found to have average serum cholesterol of 220mg percent while the control group had a slightly higher average of 250mg percent (Christakis et al., 1966). Also, in the duration of the study, there were eight cardiovascular disease-related deaths in the Anti-Coronary Club group and none in the control group (p.600). Despite these results, they proceeded to state that the difference was not significant and asserted it was because of the higher prevalence of overweight in the experimental group. Dr. Jolliffe, the pioneer of the Anti-Coronary Club, was dead by the time the results were out. He had succumbed to a vascular thrombosis in 1961, although the obituaries listed a different cause of death (Enig & Fallon, 2008) The Framingham Heart Study The Framingham Heart Study was conducted in 1948 with the aim of identifying causative factors of coronary heart disease by following up the participants for a long period. The study consisted of about two-thirds of the adult population between 30 and 62 years, living in Framingham, Massachusetts, in 1948 (Volk, 2007). The first limitation presents itself in the representativeness of the sample. Results from this study are applicable particularly to a white, middle-class suburban population. Therefore, generalization to other populations is questionable. The European Society of Cardiology endorsed the employment of the Coronary Risk Chart, which is based on data from the Framingham Heart Study but faced opposition from researchers. They cited the big regional difference between the two populations and incidence of coronary heart disease (Thomsen et al., 2002). They noted that use of the risk chart would specifically lead to an overestimation of coronary risk in a Danish population (p.817). The same applies to many populations around the world which are significantly different from the Framingham sample. The results from the study also face other challenges. They neither support nor invalidate the hypothesis, similar to the case of the Seven Countries Study. Before the age of 50, the data suggests that very low serum cholesterol levels increase longevity. The level of cholesterol is directly associated with overall and CVD-related mortality; for each 10mg/dL increase in serum cholesterol, overall mortality increases by 5% and CVD mortality by 9%. However, after 50 years, neither high nor low serum cholesterol levels increases overall mortality (Anderson et al. 1987). The study does not explain the difference in the cardiovascular risk among people under 50 years and those above. Such results show that there were certain confounding factors that were not considered, and further investigation is necessitated to deduct clear indications of causation. Multiple Risk Factor Intervention In 1970, another study was conducted by the National Heart, Lung and Blood Institute, focusing on the effect of several risk factors on coronary heart disease deaths. The factors investigated were cigarette smoking, elevated serum cholesterol levels and hypertension, and if their modification would subsequently lead to a reduction in coronary heart deaths. The study design included 12,000 men between 35 and 57 years who were at increased risk of death by coronary heart disease but no clinical evidence of any heart disease at the beginning of the study. High levels of serum cholesterol, cigarette smoking and blood pressure were considered the inclusion criteria for the participants. Three screenings were carried out, eventually remaining with a sample of 12,866 men (Volk, 2007). The men were then separated into two groups of almost the same size. In the first group, “usual care” (UC), they were referred to their usual physician for medical care for the risk factors as appropriate. The second group, “special intervention” (SI), received a program aimed at the termination of cigarette smoking and decrease of blood pressure and serum cholesterol levels. The SI group were monitored by a group of health professionals including nutritionists, nurses, general health counsellors and physicians. Their blood pressure was screened, and they were advised to maintain a healthy weight. To control their blood pressure, medication was offered, and salt intake restricted. Their diet consisted of less than 300mg/day of cholesterol and was later reduced to 250mg/day following a change in the national nutrition guidelines. The group reported their method of obtaining mortality data i.e. through the approval of a Mortality Review Committee (Volk, 2007). This study, so far, was relatively the most reliable as far as methodology and choice of study sample is concerned. The reduction of risk factor levels occurred in both clusters, but to a greater degree for men in the SI group (Multiple Risk Factor Intervention Trial, 1982) Similar to previous studies, the overall results of the study were unexpected. After a six-year follow-up period, 260 deaths were reported in the UC group, of which 124 were attributed to coronary heart disease, and 145 to cardiovascular diseases (including coronary heart disease). In the SI group, 265 deaths occurred, of which 115 were classified as coronary heart disease and 138 as CVD (inclusive of coronary heart disease). The death rate for all causes was reported as 2.1 percent higher for the SI group (Volk, 2007). According to the study, two important conclusions were made. First, the intervention did not affect coronary heart disease, at least, under those circumstances. Second, they noted improvement in the UC group despite lack of intervention, but the expected benefits of the intervention were not realized in the SI group (Multiple Risk Factor Intervention Trial, 1982). Studies Providing Evidence against the Lipid Hypothesis Several studies have provided reliable evidence against the lipid hypothesis. The supposed relationship between saturated fats and risk of cardiovascular diseases has been challenged based on several reasons. These include the unclear understanding of the metabolism process, unreliable source of data on which the hypothesis is based and the existing contradicting evidence provided in current literature. Even after the adoption of the hypothesis by dietary guidelines, the majority of deaths are currently as a result of obesity and coronary heart disease in most developed and developing nations. A lot of domestic and national resources have also been invested in the treatment of cardiovascular diseases more than ever before while cholesterol-reducing drugs continue to be the highest selling drugs around the world. Below are some studies that provide evidence contradicting the lipid hypothesis. Chowdhury et al., Ann Intern Med 2014;160 (6):398-406 The study is a meta-analysis of 32 observational studies of dietary fatty acids intake, 17 observational studies of biomarkers of fatty acids, and 27 randomized controlled trials of supplementation with fatty acids. The results from the observational studies showed that the difference between the relative risks for coronary heart disease in diets high in saturated fats and those high in omega-6 polyunsaturated fats was trivial. Increased consumption of saturated fat showed no effect on coronary disease (relative risk of 1.03 in 20 studies). Elevated intake of omega-3 fatty acids was associated with a reduction (RR 0.87 in 16 studies) while trans-fatty acids increased the risk of coronary disease (RR 1.16 in five studies). In terms of circulating fatty acid composition, saturated fatty acids were also not associated with coronary disease risk (RR 1.06 in eight studies). Similarly, no association was established with monounsaturated, alpha-linoleic, long-chain omega-3, trans, and omega-6 fatty acids. The authors noted that in the randomised controlled trials, there lacked statistically significant evidence that supplementation with alpha-linoleic and long-chain omega-3 fatty acids reduced the risk of coronary disease. The largest reduction in risk was observed in omega-6 supplementation, although it was not statistically significant (RR 0.85 in eight studies). In conclusion, the authors stated that “the current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats” (Chowdhury et al. 2014, p.328). Schwab et al., Food Nutr Res 2014; 58 The study is also a meta-analysis that investigated the effect of the type and amount of dietary fat on cardio-metabolic factors and the risk of getting type 2 diabetes mellitus, cardiovascular diseases and various types of cancer. As far as cardiovascular diseases are related, a systematic review of the randomized controlled trials showed that total fat intake between saturated fat intake and risk of cardiovascular diseases. After ten years of follow-up, saturated fat intake was inversely associated with danger of developing cardiovascular diseases. A different study (Howard et al., 2006) supports these findings; it found that specifically lower intake of saturated fats was not associated with a low risk of coronary heart disease among postmenopausal women. According to the results, a reduction in the amount of dietary saturated fats was not found to have any association with risk of cardiovascular disease. Figure 3: Relative Risk of Coronary Heart Disease adopted from Mozaffarian et al. (2010) Other studies investigated the effect of substitution of saturated fats with other macronutrients (Mozaffarian et al., 2010). Replacement of saturated fats with carbohydrates was associated with increased risk for cardiovascular diseases. It was, however, dependent on the type of carbohydrate, with increased risk found in simple carbohydrates, but no significant effect with complex carbohydrates. Substitution with polyunsaturated fatty acids resulted to a decreased risk of between 14 and 20%. Some randomised controlled trials showed that a replacement of saturated fatty acids with an increased amount of unsaturated fatty acids (PUFA and MUFA) reduced the risk significantly. Increasing PUFAs to account for 5% of total energy intake resulted to a 10% decrease in risk for CVD, while increasing to 15% resulted to a decrease of 19%. Studies taking longer durations reported greater benefits had no significant effect on the risk of any cardiovascular disease outcomes. The same applied for saturated fatty acids, whereby most of the investigations did not find any direct connection Volk, Altern Med Rev 2007; 12(3):228-245 The research assesses the studies on which the current assumptions of a causal relationship between cardiovascular diseases and dietary fat consumption are based. The author analyses the flaws in methodology in the early studies and also the research studies in support of a contrary hypothesis. It also explores alternative views on the use of statins as a remedy for coronary heart disease. The author notes that a review of the early studies produced significant methodological errors especially in sample selection, data collection methods and measurement of outcome indicators (Volk, 2007). After a review of the methodological quality of the early studies in comparison with current literature, the author concludes by saying that: “The lipid hypothesis of atherosclerosis is based on false premises, including linear causation, fallacious national mortality statistics, biased age and subject selection, and methodological inaccuracies” (Volk 2007, p.243) Conclusion The following are some of the shortcomings of most of the studies on which the lipid hypothesis is based. Problems in Research Methodology Epidemiological studies involved in establishing the relationship between nutritional intake and disease incidence are limited by several factors. The ability of their study designs to identify and account for confounding factors, and establishing precise measurements of dietary intake and mortality are some of the major limitations. Problems in selecting a representative sample, measuring outcome indicators and adequate dietary assessment significantly limit the reliability and validity of the results (Volk, 2007). Sample Selection Important to consider is the modification of results caused by genetic factors. The Framingham Study, for instance, included groups of family in their sample or whole communities. Large numbers of people with hypercholesterolemia may lead to the interpretation that the problem of high cholesterol affects the total population when it actually is a risk for a selected few. Several of the major studies supporting the lipid hypothesis also failed to give any information on the exclusion criteria or dropouts. Such information is important to consider because people who agree to invitations to participate in cohort studies may be more interested in health and, therefore, may not reflect the normal dietary intake of the population (Volk, 2007). Determining Cause of Death Most studies relied on death certificates as proof of cause of death. Death certificates usually give very inaccurate data, as a certain study indicates (Lozano et al., 2001). This predisposition is because of the variations in codes used to denote death from cardiovascular diseases in different countries. Wide variations in coding among different countries have resulted to widespread misinterpretation of data (p.3). The adjustment of mortality rates would change the results of most of these studies significantly, including those on which the lipid hypothesis is based. Errors may also be introduced through other ways such as low autopsy rate, presence of other illnesses and lack of understanding of the complex disease process (Lauer et al., 1999). Death from coronary heart disease may be difficult to establish because in certain cases, coronary heart disease may not be the initial cause of death, although it may be present and significant at the time of death (p.618). To prove this, a report from the Framingham Study was prepared to compare the reported causes of death among 2,863 deceased subjects from the study as identified by death certificates and by a panel of physicians (Lloyd-Jones, et al., 1998). The findings indicated that only 67% of the certificates that listed cause of death as coronary heart disease were confirmed by the physicians. In the case of stroke, only 59% were confirmed to be valid. The error increased significantly with age, whereby death due to coronary heart disease among participants’ ages 65-74, 75-84 and above 85 were 18, 31 and 109% respectively (p.1020). Changes in the International Classification of Disease codes also contribute to further errors. Dietary Assessment In nutritional epidemiology, measures of association such as relative risk are mostly used instead of biological constants. The investigation of one risk factor and its association with a chronic disease is complicated by the inter-correlation of many other dietary, environmental and genetic factors. Volk (2007) suggests that coronary heart disease is also influenced by lack of antioxidants, high homocysteine levels, and a deficiency of other essential micronutrients and trace elements (p.240). Nourishment that is elevated in fat may also contain high levels of sugar, low fibre and other micronutrients, thus producing errors in interpretation. High variations in the daily diets of a population also introduce errors, in addition to the complex interactions and structures of processed foods (Freudemheim, 1999). Research involving fatty acids is mostly biased by assumptions based on previous research. Consequently, most of the research is inclined towards the influence of saturated fatty acids on lipoprotein metabolism and cholesterol in the blood. Studies can only analyse a small proportion of the wide variety of foods available today. An attempt to analyse the interrelationships between all available foods is a near impossibility, coupled with the large uncertainty caused by the loss of nutrients during food processing. Nutritional epidemiology includes studies that base their data on 24-hour recalls and food frequency questionnaires, followed by an analysis in comparison to a food composition table. Given the variability of dietary components and the long follow-up periods the studies take, interpretive comparison among such studies is rendered speculative (Volk, 2007). The lipid hypothesis may not be sustainable any longer. So many studies, including observational studies, randomized controlled trials, systematic reviews and meta-analyses have proven that the theory is based on very little and conflicting evidence and, therefore, should not continue being supported. A review of guidelines based on the hypothesis is required since cardiovascular diseases are still the leading cause of death today. Furthermore, other effects associated with coronary heart disease such as increased poverty and waste of resources in the management of coronary heart disease is detrimental to the development. Evidence from the literature has also shown that replacing saturated fats with carbohydrates (as dietary guidelines recommend) increases the jeopardy of coronary heart disease. Polyunsaturated fatty acids have been proven to be beneficial and should be encouraged. In conclusion, we can say that, presently, there is a lack of definite proof that a diet low in saturated fats has positive health effects. 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