Non-communicable diseases
Liam J. Donaldson, Paul D. Rutter in Donaldsons' Essential Public Health, 2017
Subsequent research has collected data to enable distinctions to be made and has shown that monounsaturated and polyunsaturated fats, derived from plant sources, are generally good, reducing the risk of heart disease and diabetes. The other two tend to promote the occurrence of non-communicable diseases, particularly the trans fats (created by industrial hydrogenation processes). The foods of a Mediterranean diet are high in ‘good’ fats – olives, fish, nuts, seeds and fish – while many UK diets are too high in ‘bad’ fats – red meat, butter and cheese. There is a common public misconception that a low-fat diet is a good diet. This can cause health-conscious people to reduce their intake of good fats as well as bad. Also, choosing low-fat foods as the healthy option is not always best since many contain large amounts of harmful simple carbohydrates to enhance taste in the absence of fat. The body can make most of the fats that it requires by reconstituting other fats, but not omega-3 fatty acids. They are vital for cellular function and, eaten in sufficient quantities, reduce the risk of heart disease and stroke, and possibly some cancers. Oily fish, such as salmon and tuna, is a great source of omega-3 fatty acids. There are two major types of cholesterol in the bloodstream: low-density lipoproteins (LDLs), which carry cholesterol from the gut to the rest of the body; and high-density lipoproteins (HDLs), which carry it from the rest of the body to the gut for disposal. LDL is therefore ‘bad’ cholesterol, because it results in cholesterol being deposited in cells and arteries. But HDL is ‘good’ cholesterol, because it clears cholesterol away from cells and arteries. A person’s level of LDL cholesterol is affected by dietary intake of fat and carbohydrate more than the type or amount of cholesterol consumed. This is counterintuitive and a difficult health message, but the approach on cholesterol is to follow the advice on fats and carbohydrates, choosing the good versions of each. Dietary protein is the major building block of muscle, and is broken down into energy and amino acids, 20 in all, 10 of which are essential. From amino acids, many other proteins – vital for cellular processes – are built. Fish, poultry and beans are healthier sources of protein than red meat (beef, lamb and pork). This is not because of the proteins themselves (there is little difference, in health effect, between them). It is because of what comes with the protein. For example, red meat typically contains fat as well as protein, much of it saturated fat. Processed meat also often contains substantial amounts of sodium.
‘I just want a normal life': the impact of obesity
Jenny Radcliffe in Cut Down to Size, 2013
Dyslipidaemia is the medical term for high levels of certain fats (lipids), called cholesterol and triglycerides, in the blood. There are two types of cholesterol:High density lipoprotein (HDL) cholesterol – sometimes called good cholesterol.Low-density lipoprotein (LDL) cholesterol – sometimes called bad cholesterol.Too much LDL cholesterol in the blood increases atherosclerosis– the build-up of fatty deposits in the arteries – and so increases your risk of heart disease, stroke and high blood pressure. Good HDL cholesterol, on the other hand, seems to clean up excess cholesterol from the blood and protects against atherosclerosis. People are particularly at risk if they have high levels of LDL and low levels of HDL cholesterol. Triglycerides are fats present in the blood which, together with cholesterol, form the blood lipids. They come from the fat eaten in foods, such as meat and dairy products, and are also made by the body from other sources of energy, like carbohydrates. Calories from a meal that are not used to produce energy are converted to triglycerides and transported to fat cells to be stored. Like LDL cholesterol, high levels of triglycerides in the blood increase the risk of coronary heart disease. Around a fifth of weight loss surgery patients have dyslipidaemia.
The Science of Longevity
Robert Fried, Lynn Nezin in Evidence-Based Proactive Nutrition to Slow Cellular Aging, 2017
Cholesterol is one of the lipids found throughout the body in all tissues including blood. It is an important component of living cells. Together with carbohydrates and proteins, lipids are the main constituents of plant and animal cells. Cholesterol plays a central role in the formation of cell membranes, and is required for the formation of bile acid in the liver and the production of hormones, such as steroid hormones in the adrenal glands. The blood and liver make all the cholesterol needed and circulate it through the blood. Serum LDL cholesterol and HDL cholesterol first rise progressively with age in men and women. Then they both decline with age (Ferrara et al. 1997). The rate of decline is affected by cardiorespiratory fitness (Park et al. 2015). Furthermore, while serum cholesterol progressively rises with age, the rise is steepest in those men and women with cardiovascular heart disease (Gertler et al. 1950). In the early 1980s, the Lipid Research Clinics Program Prevalence Study sponsored by the NHLBI also reported that plasma lipid and lipoprotein concentrations in men and women rise with age. Higher total cholesterol values in men, compared with those in women, appear between the ages of 20 and 50 years, and higher LDL cholesterol levels were observed in the same age span.
The Role of Dietary Cholesterol in Lipoprotein Metabolism and Related Metabolic Abnormalities: A Mini-review
Published in Critical Reviews in Food Science and Nutrition, 2016
Fatemeh Ramezani Kapourchali, Gangadaran Surendiran, Amy Goulet, Mohammed H. Moghadasian
Cholesterol plays a vital role in cell biology. Dietary cholesterol or “exogenous” cholesterol accounts for approximately one-third of the pooled body cholesterol, and the remaining 70% is synthesized in the body (endogenous cholesterol). Increased dietary cholesterol intake may result in increased serum cholesterol in some individuals, while other subjects may not respond to dietary cholesterol. However, diet-increased serum cholesterol levels do not increase the low-density lipoprotein/high-density lipoprotein (LDL/HDL) cholesterol ratio, nor do they decrease the size of LDL particles or HDL cholesterol levels. Elevated levels of LDL cholesterol, reduced HDL cholesterol levels, and small, dense LDL particles are independent risk factors for coronary artery disease. Dietary cholesterol is the primary approach for treatment of conditions such as the Smith–Lemli–Opitz syndrome. Recent studies have highlighted mechanisms for absorption of dietary cholesterol. These studies have help understand how dietary and/or pharmaceutical agents inhibit cholesterol absorption and thereby reduce LDL cholesterol concentrations. In this article, various aspects of cholesterol metabolism, including dietary sources, absorption, and abnormalities in cholesterol metabolism, have been summarized and discussed.
The Impact of Egg Limitations on Coronary Heart Disease Risk: Do the Numbers Add Up?
Published in Journal of the American College of Nutrition, 2000
For over 25 years eggs have been the icon for the fat, cholesterol and caloric excesses in the American diet, and the message to limit eggs to lower heart disease risk has been widely circulated. The “dietary cholesterol equals blood cholesterol” view is a standard of dietary recommendations, yet few consider whether the evidence justifies such restrictions. Over 50 years of cholesterol-feeding studies show that dietary cholesterol does have a small effect on plasma cholesterol concentrations. The 167 cholesterol feeding studies in over 3,500 subjects in the literature indicate that a 100 mg change in dietary cholesterol changes plasma total cholesterol by 2.2 mg/dL. Today we recognize that dietary effects on plasma cholesterol must be viewed from effects on the atherogenic LDL cholesterol as well as anti-atherogenic HDL cholesterol since the ratio of LDL:HDL cholesterol is a major determinant of heart disease risk. Cholesterol feeding studies demonstrate that dietary cholesterol increases both LDL and HDL cholesterol with little change in the LDL:HDL ratio. Addition of 100 mg cholesterol per day to the diet increases total cholesterol with a 1.9 mg/dL increase in LDL cholesterol and a 0.4 mg/dL increase in HDL cholesterol. On average, the LDL:HDL ratio change per 100 mg/day change in dietary cholesterol is from 2.60 to 2.61, which would be predicted to have little effect on heart disease risk. These data help explain the epidemiological studies showing that dietary cholesterol is not related to coronary heart disease incidence or mortality across or within populations.
Dietary cholesterol inhibits the development of aberrant crypt foci in the colon
Published in Nutrition and Cancer, 1996
Ahmed El‐Sohemy, Cyril Kendall, A. Venket Rao, Michael Archer, W. Robert Bruce
We evaluated the effect of dietary cholesterol and oxidized cholesterol on the promotion of aberrant crypt foci (ACF), which are putative precancerous lesions in the colon. Sixty female C57BL/6J mice were given four weekly injections (ip) of azoxymethane (AOM) then fed either a control AIN‐76 diet or the control diet supplemented with 0.3% cholesterol or 0.3% oxidized cholesterol for 100 days. The oxidized cholesterol was prepared by heating cholesterol at 110°C for 48 hours. Gas chromatographic analysis of the oxidized cholesterol showed that 96% of the cholesterol was unchanged and less than 2% of the cholesterol was oxidized. The remaining 2% impurities were unidentified and present in both the cholesterol and heated cholesterol. The number of ACF in the group fed cholesterol was significantly lower than the control group (7.9 ± 1.0 vs. 12.5 ± 1.2, p < 0.01). The number of ACF in the group fed oxidized cholesterol (10.1 ± 1.1) was not different from the control or cholesterol groups. The size of the ACF (no. of crypts per focus) did not differ between the three dietary groups. Serum low‐density lipoprotein (LDL) cholesterol was greater in the cholesterol‐fed group than the control group (40.5 ± 4.6 vs. 24.3 ± 3.6 mg/dl, p < 0.05). LDL cholesterol from the animals fed oxidized cholesterol (37.7 + 4.7 mg/dl) was not different from the control or cholesterol‐fed animals. Total and high‐density lipoprotein (HDL) cholesterol did not differ between the groups. The results show that dietary cholesterol significantly inhibits the promotion of ACF in the colon. The elevated LDL cholesterol may inhibit de novo cholesterol synthesis in the preneoplastic colonic epithelial cells, thereby inhibiting DNA synthesis and cell proliferation.