The Dietary Analysis Helped Me Become More - amazonia.fiocruz.br

Glen D. Although Analyxis studies showed that saturated fat diets with very low levels of PUFAs increase serum cholesterol, whereas other studies showed high serum cholesterol increased the risk of coronary artery disease CADthe evidence of dietary saturated fats increasing CAD or causing premature death was weak. Over the years, data revealed that dietary saturated fatty acids SFAs are not associated with CAD and other adverse health effects or at worst are weakly associated in some analyses when other contributing factors may be overlooked.

Several recent analyses indicate that SFAs, particularly in dairy products and coconut oil, can improve health. The replacement of saturated fats in the diet with carbohydrates, especially sugars, has resulted in increased obesity and its associated health complications. Well-established mechanisms have been proposed for the adverse health effects of some alternative or replacement nutrients, such as simple carbohydrates and PUFAs.

The focus on dietary manipulation of serum cholesterol may be moot in view of numerous other factors that increase the risk of heart disease.

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The adverse health effects that have been associated with saturated fats in the past are most likely due to factors other read article SFAs, which are discussed here. This review calls for a rational reevaluation of existing dietary recommendations that focus on minimizing dietary SFAs, for which mechanisms for adverse health effects are lacking.

Since the Framingham Heart Study reported that high serum cholesterol was a major risk factor for coronary heart disease 1there has been an aggressive campaign in the medical community to decrease serum cholesterol. It has been a widely accepted belief that dietary saturated fats and dietary cholesterol cause an increase in Tne total cholesterol, as well as LDL-cholesterol LDL-C 2 and thereby increase the risk of heart disease if consumed 2. Over the years, it became clear that high levels of LDL circulating in the blood are susceptible to lipid peroxidation, which results in the oxidized LDL being scavenged by macrophages lining certain arteries, particularly around the heart, leading to atherosclerosis 3. Although this mechanism provides a The Dietary Analysis Helped Me Become More for high serum LDL-C causing atherosclerosis, evidence of the involvement of saturated fats is Dietsry, even though it is well established that a diet high in saturated fat increases serum cholesterol and a diet high in polyunsaturated oil decreases serum cholesterol 45.

In fact, PUFAs are the components that are oxidized and generate antigenic substances that are recognized by immune cells for clearance of oxidized LDL in atherogenesis 6 — 8. Numerous reports and reviews in recent years have begun to call the perceived pernicious effects of dietary saturated fatty acids SFAs into question. The purpose of this review is to summarize the scientific understanding as it relates to dietary fats in health and disease, particularly with regard to the innocuous nature of SFAs and the physiological effects that have implicated PUFAs in numerous disorders and diseases.

The role of dietary fats in cardiovascular disease CVD and many other BBecome is complex, yet there is a powerful inertia that has allowed the saturated fat doctrine to endure.

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Dietary fat studies in the midth century stressed the relationship of dietary SFAs and PUFAs to serum cholesterol levels with an aim toward decreasing the likelihood of the development of coronary artery disease CAD and premature The Dietary Analysis Helped Me Become More 45. Once lipoprotein fractions were separated in the blood, it became evident that LDL and VLDL were the carriers of cholesterol that were most closely associated with risk of heart disease 9. Later it was found that the ratio of total serum cholesterol to HDL-C was a better indicator of heart disease risk By the s, the mechanisms by which dietary fats and specific types of fatty acids were regulating serum cholesterol and lipoproteins were beginning to be revealed.

A family of proteins known as sterol regulatory element binding proteins SREBPs were discovered in the early s. These proteins move to the nucleus in cholesterol-depleted cells to alter transcription of several genes involved in lipid metabolism When intracellular cholesterol levels are low, SREBP-1 promotes expression of genes for synthesis of cholesterol and LDL receptors that remove cholesterol from the circulation.

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When intracellular cholesterol levels are high, SREBP-1 is not activated by protease cleavage, and the genes for cholesterol production and LDL receptors are downregulated. SREBP-1 also activates promoters for genes involved in fatty acid synthesis and lipid storage In this way, PUFAs can stimulate fatty acid oxidation in the Thee to minimize their potential for free radical oxidation in the body when their levels are high in the diet.

Analysus One must keep in mind that this complex array for regulation of expression of a wide range of genes is also subject to an even more complex array of responses to dietary PUFAs and other dietary factors. Single nucleotide polymorphisms in genes for many of the above factors, as well as in genes for several apolipoproteins, TNFs, glutathione peroxidases, and other proteins result in a wide range of individual responses to dietary constituents. The consequences of such genetic variation Helper be either little change or very large changes in serum lipids and lipoproteins in response to diet, depending on an individual's genetic makeup However, one should not lose sight of the fact that levels of many other proteins are being altered in the process, which can give rise to a wide array of physiological responses that influence susceptibility to many unhealthy conditions, such as CVD and cancer.

Short-chain SFAs, such as those in dairy fat and coconut oil, can also influence gene expression via interactions with various G protein—coupled receptors that are linked to several hormonal The Dietary Analysis Helped Me Become More, including insulin and leptin, that regulate overall energy metabolism in the body They identified several mutations that produce nonfunctional LDL receptors, resulting in death from atherosclerosis and heart disease at an early age. Goldstein and Brown 22 also identified several genes that code for other proteins involved in cholesterol transport and metabolism, such as apolipoprotein B apo Bwhich is a component of LDL that binds to LDL receptors. There are other proteins involved in LDL synthesis, Becomee, and clearance that can result in a genetic predisposition to increased serum LDL cholesterol and FH 23 — In the early s, it was discovered that men with CVD tended to have smaller HDL particles than healthy controls A prospective, population-based cohort study also found an increased risk of Continue reading in middle-aged men with smaller, dense LDL particles than in men with larger LDL particles, although the relationship did not show a linear dependence on particle size It later became evident that LDL particle size was influenced by several factors and was not necessarily a useful predictor of Becoke disease risk; the nature of LDL is influenced by both dietary and genetic factors Lipoprotein a [Lp a ] is a complex lipoprotein that has several properties in common with LDL.

Like LDL and VLDL, The Dietary Analysis Helped Me Become More a contains apo B, but also contains highly variable forms of apolipoprotein a that strongly influence its atherogenicity and propensity to promote heart disease ]