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Article Excerpt
KEY POINTS
* Lean Australian red meat cuts are low in fat and have a ratio of cholesterol-raising saturated fatty acids (SFA) to cis-monounsaturated fatty acids (MUFA) to cis-polyunsaturated fatty acids (PUFA) of around 24:40:14. This is less cholesterol-raising than was earlier estimated, because cuts are now leaner and part of the SFA is stearic acid (that does not raise plasma cholesterol). and there are several other (cholesterol-lowering) PUFA as well as linoleic acid present. Low-fat, predominantly monounsaturated lean meat cuts have been shown to be acceptable in cholesterol-lowering diets. This does not mean that meat eaten with the fat on will not raise plasma cholesterol.
* Meat is low in sodium, high in potassium and has been shown in human dietary experiments not to raise the blood pressure.
* Meat is high in protein and contributes to weight reduction by increasing satiety and helping reduce intake in ad-lib weight-reducing diets. Overweight increases the risk of increased plasma cholesterol, increased blood pressure and diabetes.
* Meat is a good source of bioavailable iron. The hypothesis that people with high iron stores have increased risk of heart disease has not been confirmed in a number of epidemiological studies.
* Human studies suggest that dietary long-chain omega-3 PUFAs are protective against sudden cardiac death, consistent with lower risk of ventricular fibrillation.
INTRODUCTION
Most fat in the human diet is a mixture of triglycerides. The pattern of fatty acids attached to the glycerol has been known since 1956 to affect the plasma cholesterol concentration. (1) The hardest evidence comes from strictly controlled metabolic ward experiments with metabolically normal human subjects. Saturated fatty acids (SFAs) raise the plasma cholesterol, polyunsaturated fatty acids (PUFAs) lower it, and monounsaturated fatty acids (MUFAs) have an intermediate, neutral effect. (1,2) The cholesterol-raising effect of SFAs is about twice as potent as the lowering effect of PUFAs. This is expressed in Ancel Keys classic equation: (2) [DELTA]cholesterol = 2.74 [DELTA]SFAs - 1.3 [DELTA]PUFAs (where [DELTA] = change; plasma cholesterol is in mg/100 mL and fatty acids are estimated as percentage of total daily calories). Hundreds of human experiments have since been conducted, many papers published, and we now have meta-analyses which strongly confirm the original findings. (3,4)
This is still the main message for public health education, but for health professionals, there are further modifications.
* Serum cholesterols nowadays are usually expressed in SI units, as mmol/L, so the numbers in the original Keys equation need to be divided by 38.6.
* Beyond serum total cholesterol, a knowledge of LDL-cholesterol (increases risk) and HDL-cholesterol (decreases risk) and triglycerides can better predict risk of coronary heart disease (CHD).
* Individual SFAs differ in their cholesterol-raising effect. PUFAs have different physiological effects if they belong to the omega-6 or omega-3 series. And different plant-derived oils, which contain predominantly MUFAs, do not all have the same effect on serum cholesterol, presumably because of the other lipids they contain (phytosterols, squalene). (5)
This paper outlines the effect of dietary components on risk of cardiovascular disease and considers the role of red meat in this context.
DIETARY FATTY ACIDS
Of the SFAs, only lauric (12:0), myristic (14:0) and palmitic (16:0) raise plasma cholesterol levels. Myristic is the most potent in this regard, (6) and palmitic is the most abundant of all three in foods. SFAs with 10 or fewer carbon atoms (in medium chain triglycerides) do not appear to raise serum cholesterol. (7) At the other end of the series, it has been repeatedly found that stearic acid (18:0) has little or no cholesterol-raising effect. (8,9) It is rapidly converted to oleic acid in vivo. To estimate the effect of fatty acid pattern on serum cholesterol, it is better to refer to fatty acids with carbon chains of 12:0 + 14:0 + 16:0, rather than total SFA.
Among the PUFAs, by far the most abundant in foods and oils is linoleic acid, cis 18:2, n-6. Hence, any effect on cholesterol attributed to PUFAs is due very largely to linoleic acid. The intake of PUFAs from food reported in the Australian 1995 National Nutrition Survey of 12.5 g/day (10) was around 10 times greater than that reported for the linolenic acid (18:3), and about 100 times greater than that reported for eicosapentaenoic acid (EPA 20:5) + docosapentaenoic acid (DPA 22:5) + docosahexaenoic acid (DHA 22:6)--of about 130 mg/day. (11)
Linoleic acid is the only fatty acid known to lower plasma and LDL-cholesterol levels even when it is added to the diet, increasing fat and energy intakes. (1,12) Other common PUFAs, linolenic (18:3, omega-3) (7) and arachidonic (13) (20:4, n-6), do lower plasma cholesterol, but this is of little practical importance because of their low levels in most foods. High-dose fish oils may raise plasma LDL-cholesterol a little. This is perhaps due to SFA in the fish oil, together with EPA and DHA, but they raise HDL-cholesterol too. (7) Beneficial effects of fatty fish and fish oils on cardiovascular disease are not from plasma cholesterol lowering, but from effects that include reducing the risk of ventricular arrhythmias and the tendency to thrombosis.
All that has been written above assumes that the fatty acids have double bonds in the usual, natural CIS configuration. But if the MUFA or PUFA is in the TRANS configuration, the effect on serum cholesterol is similar to that of SFA (14) and, with high intakes, HDL-cholesterol may be lowered as well. (15) Most human experiments have been conducted with trans 9, 18:1, called elaidic acid. Trans-unsaturated fatty acids occur naturally in small percentages in...
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