Fatty Acid Intake and Bladder Cancer Risk: A Multicenter Case-Control Study in Iran

This report summarizes our current understanding of how monounsaturated fatty acids (MUFAs) affect risk for cardiovascular disease (CVD). This is a topic that has attracted considerable scientific interest,1 2 3 in large part because of uncertainty regarding whether MUFA or carbohydrate should be substituted for saturated fatty acids (SFAs) and the desirable quantity of MUFA to include in the diet. MUFAs are distinguished from the other fatty acid classes on the basis of having only 1 double bond. In contrast, polyunsaturated fatty acids (PUFAs) have 2 or more double bonds, and SFAs have none. The position of the hydrogen atoms around the double bond determines the geometric configuration of the MUFA and hence whether it is a cis or trans isomer. In a cis MUFA, the hydrogen atoms are present on the same side of the double bond, whereas in the trans configuration, they are on opposite sides. The American Heart Association Nutrition Committee recently published a scientific statement regarding the relationship of trans MUFA to CVD risk,4 and the present statement, therefore, will be limited to a discussion of dietary cis MUFAs, of which oleic acid ( cis C18:1) comprises ≈92% of cis MUFAs. In the United States, average total MUFA intake is 13% to 14% of total energy intake, an amount that is comparable to (or slightly greater than) SFA intake. In contrast, PUFAs contribute less (ie, 7% of energy). The major emphasis of current dietary guidelines involves replacing SFAs with complex carbohydrates to achieve a total fat intake of ≤30% of calories. There is evidence suggesting that the substitution of MUFA instead of carbohydrate for SFA calories may favorably affect CVD risk.5 6 7 The American Heart Association dietary guidelines for healthy American adults recommend a diet that provides <10% of calories from SFA, up …

To assess the intake of trans fatty acids (TFA) and other fatty acids in 14 Western European countries. A maximum of 100 foods per country were sampled and centrally analysed. Each country calculated the intake of individual trans and other fatty acids, clusters of fatty acids and total fat in adults and/or the total population using the best available national food consumption data set. A wide variation was observed in the intake of total fat and (clusters) of fatty acids in absolute amounts. The variation in proportion of energy derived from total fat and from clusters of fatty acids was less. Only in Finland, Italy, Norway and Portugal total fat did provide on average less than 35% of energy intake. Saturated fatty acids (SFA) provided on average between 10% and 19% of total energy intake, with the lowest contribution in most Mediterranean countries. TFA intake ranged from 0.5% (Greece, Italy) to 2.1% (Iceland) of energy intake among men and from 0.8% (Greece) to 1.9% among women (Iceland) (1.2-6.7 g/d and 1.7-4.1 g/d, respectively). The TFA intake was lowest in Mediterranean countries (0.5-0.8 en%) but was also below 1% of energy in Finland and Germany. Moderate intakes were seen in Belgium, The Netherlands, Norway and UK and highest intake in Iceland. Trans isomers of C18:1 were the most TFA in the diet. Monounsaturated fatty acids contributed 9-12% of mean daily energy intake (except for Greece, nearly 18%) and polyunsaturated fatty acids 3-7%. The current intake of TFA in most Western European countries does not appear to be a reason for major concern. In several countries a considerable proportion of energy was derived from SFA. It would therefore be prudent to reduce intake of all cholesterol-raising fatty acids, TFA included.

BackgroundWe prospectively examined the associations of total fat and fatty acid intake with type 2 diabetes (T2D) among Japanese adults.MethodsThis study was conducted using data from the Japan Collaborative Cohort Study for Evaluation of Cancer Risk (JACC). A validated food frequency questionnaire evaluated the intake of total fat and fatty acids. Diabetes was assessed using self-reported data. Multivariable logistic regression analysis was performed to calculate the odds ratios (ORs) and 95% confidence intervals (CIs) of incident T2D across quintiles of total fat and fatty acid intake after adjusting for potential confounders.ResultsA total of 19,088 non-diabetic participants (age range, 40–79 years) enrolled in the JACC between 1988 and 1990 were included in this study. During the 5-year study period, 494 the participants developed T2D. The OR of T2D for the highest versus lowest quintiles was 0.58 (95% CI, 0.37–0.90) for total fat, 0.78 (95% CI, 0.51–1.20) for saturated fatty acid (SFA), 0.55 (95% CI, 0.35–0.86) for monounsaturated fatty acids (MUFA), 0.61 (95% CI, 0.39–0.96) for polyunsaturated fatty acids (PUFA), 0.64 (95% CI, 0.42–0.99) for n-3 PUFA, and 0.70 (95% CI, 0.45–1.09) for n-6 PUFA. Total fat and fatty acid (except SFA and n-6 PUFA) intake were inversely associated with T2D in men. Total fat and fatty acid intake were not associated with T2D in women.ConclusionHigher intakes of total fats, MUFA, PUFA, and n-3 PUFA were inversely associated with T2D among Japanese men.

Fat intake in children: Is there a need for revised recommendations?

Trans–fatty acid levels in sperm are associated with sperm concentration among men from an infertility clinic

Dietary fat intake and risk of cardiovascular disease and all-cause mortality in a population at high risk of cardiovascular disease

To examine whether high intake of total fat, saturated fatty acids (saturated fat), trans fatty acids (trans fat), and cholesterol and low intake of monounsaturated fatty acids (MUFA), polyunsaturated fatty acids (PUFA), n-6 PUFA, and n-3 PUFA are associated with increased risk of dementia and its subtypes. Data from the Rotterdam Study, a prospective cohort study among elderly, were used. At baseline (1990 to 1993), 5,395 subjects had normal cognition, were noninstitutionalized, and underwent complete dietary assessment by a semiquantitative food-frequency questionnaire. The cohort was continuously monitored for incident dementia, and re-examinations were performed in 1993 to 1994 and 1997 to 1999. The association between fat intake and incident dementia was examined by Cox's proportional hazards models. After a mean follow-up of 6.0 years, 197 subjects developed dementia (146 AD, 29 vascular dementia). High intake of total, saturated, trans fat, and cholesterol and low intake of MUFA, PUFA, n-6 PUFA, and n-3 PUFA were not associated with increased risk of dementia or its subtypes. Rate ratios of dementia per standard deviation increase in intake were for total fat 0.93 (95% CI 0.81 to 1.07), for saturated fat 0.91 (95% CI 0.79 to 1.05), for trans fat 0.90 (95% CI 0.77 to 1.06), for cholesterol 0.93 (95% CI 0.80 to 1.08), for MUFA 0.96 (95% CI 0.84 to 1.10), for PUFA 1.05 (95% CI 0.80 to 1.38), for n-6 PUFA 1.03 (95% CI 0.77 to 1.36), and for n-3 PUFA 1.07 (95% CI 0.94 to 1.22). High intake of total, saturated, and trans fat and cholesterol and low intake of MUFA, PUFA, n-6 PUFA, and n-3 PUFA were not associated with increased risk of dementia or its subtypes.

BackgroundSeveral epidemiological studies have investigated the association between dietary fat intake and cardiovascular disease. However, dietary recommendations based on systematic review and meta-analysis might be more credible.Methods and resultsPubmed, Embase and Cochrane library were searched up to July 1st 2018 for cohort studies reporting associations of dietary fat intake and risk of CVDs. By comparing the highest vs. the lowest categories of fat or fatty acids intake, we found that higher dietary trans fatty acids (TFA) intake was associated with increased risk of CVDs [RR:1.14(1.08–1.21)]. However, no association was observed between total fat, monounsaturated fatty acids (MUFA), saturated fatty acids (SFA), and polyunsaturated fatty acids (PUFA), and risk of CVDs. Subgroup analysis found a cardio-protective effect of PUFA in the studies that has been followed up more than 10 years [0.95(0.91–0.99), I2 = 62.4%]. Dose-response analysis suggested that the risk of CVDs increased 16% [1.16 (1.07–1.25), Plinearity = 0.033] for an increment of 2% energy/day of TFA intake.ConclusionsThis current meta-analysis of cohort studies suggested that total fat, SFA, MUFA, and PUFA intake were not associated with the risk of cardiovascular disease. However, we found that higher TFA intake is associated with greater risk of CVDs in a dose-response fashion. Furthermore, the subgroup analysis found a cardio-protective effect of PUFA in studies followed up for more than 10 years.

To analyze the intake of fat and fatty acids and their food sources of pregnant women in Chengdu. Participants were from a cohort study in 2017, which was conducted among 1652 healthy singleton pregnant women within 6-14 weeks of gestation in a maternity out-patient clinic of maternal-and-child health care institution in Chengdu, Sichuan Province. Data on maternal demographic characteristics was collected by questionnaire. In three trimesters, 3-day 24-hour dietary recall method was applied to collect dietary intakes data, with the information of docosahexaenoic acid(DHA) supplement intake being collected by questionnaire. The intakes and sources of daily fat and fatty acids in three trimesters were calculated using the National Nutrient Database of USDA and China Food Composition Tables(6th edition). The intake levels of fat and fatty acids were evaluated according to 2013 Chinese Dietary Reference Intakes. The study showed that the intakes of total fat and fatty acids increased during pregnancy. The mean intake of total daily fat was 64.8 g/d, 81.2 g/d, 88.5 g/d in three trimesters, respectively. The proportion of energy from total fat &gt;30%E during three trimesters were 67.7%, 77.6%, 82.9%, respectively. The proportions of energy from saturated fatty acids(SFA) were 7.9%E, 8.9%E, 9.7%E, and those higher than 10%E were 20.9%, 31.9%, 44.7% in three trimesters, respectively. The proportions of energy from monounsaturated fatty acids(MUFA) were 12.9%E, 13.5%E, 14.2%E, and the proportions of energy from polyunsaturated fatty acids(PUFA) were 8.5%E, 8.4%E, 8.8%E in three trimesters, respectively. The proportion of DHA intake meeting recommendation(200 mg/d) in three trimesters were 3.6%, 21.7%, 21.1%, respectively. The radio of SFA, MUFA and PUFA(S∶M∶P) was 1∶1.6∶1.1 in the early trimester, and S∶M∶P was 1∶1.5∶1 in the second trimester and third trimester. Total fat and MUFA mainly came from edible oil and meat, and PUFA mainly came from edible oil and nuts. SFA mainly came from meat and milk, and the contribution of milk to SFA increased during pregnancy. The excessive intakes of total fat and SFA and the inadequate intake of DHA among pregnant women in Chengdu deserve attention.

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. 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:2Δcholesterol = 2.74 ΔSFAs − 1.3 ΔPUFAs (where Δ = 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. 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/day10 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 arachidonic13 (20:4, n-6), do lower plasma cholesterol, but this is of little practical importance because of their low levels in most foods. High-dosefish 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 SFA14 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 ruminant meat and milk fat. They are produced by microorganisms in the rumen. The main natural trans-fatty acid in red meat is trans 11, 18:1, called vaccenic acid. Trans-fatty acids are also produced during hydrogenation of vegetable and fish oils to make harder fats in food processing. Here the isomers are chiefly trans 9 and trans 10, 18:1. Around half of the trans-fatty acids in the British diet16 and Australian diet17 were estimated to come from animal foods, and half from margarines and other processed fats.16 With reduction of the industrially produced trans-fatty acids since then, the proportion from ruminant fat may be higher. Effects of different fatty acids on total-cholesterol levels are approximately mirrored by effects on LDL-cholesterol levels. As to HDL-cholesterol levels, SFAs 12:0, 14:0 and 16:0 raise it, and unsaturated fatty acids have little effect on it.18 Fasting plasma triglycerides are lowered by omega-3 PUFAs. Effects of fatty acids on different plasma LDL- and HDL-cholesterol are summarised in Table 1. There is now a vast body of literature on the role of fatty fish, fish oils and long-chain omega-3 PUFAs in the prevention and amelioration of heart disease, as well as in supporting the development of infants and having a positive impact on several chronic diseases and mental function. This summary concentrates on CHD and long-chain omega-3 PUFA provided in diet as fatty fish (and less on the more numerous human experiments with pharmacological doses of fish oil). Interest started with observations in Greenland Eskimos living traditional lifestyles, who had high intakes of animal fat but low incidence of CHD. Their animal fat was largely marine animals—fish, seal, etc. Dyerberg et al. in the 1970s found their plasma fatty acids contained unusually high amounts of eicosapentaenoic acid (EPA),19 and they suggested this reduced the tendency to thrombosis via an altered pattern of prostanoids.20 In the early 1980s, researchers reported that fatty fish, as well as fish oils (both rich in omega-3 PUFAs), produced a much greater reduction of plasma triglycerides and VLDL than oils or foods rich in n-6 linoleic acid.21 By the mid-1980s, there were two further major discoveries. Kromhout and colleagues (one of the Seven Country Study team) reported that in the Zutphen (Dutch) cohort, people who ate more fish (about 1/3 fatty) experienced significantly fewer CHD deaths.22 The mechanism was not via any of the known risk factors for CHD; possibly there was reduced platelet aggregation. They produced a recommendation for one or two fish dishes a week in dietary guidelines for the prevention of CHD.22 At about the same time, researchers in Australia were finding that rats fed dietary fat rich in PUFAs showed significantly fewer episodes of ventricular fibrillation when a coronary artery was occluded. The protective effect of tuna fish oil was stronger than sunflower seed oil, especially in the reperfusion phase.23 These animal experiments were confirmed by others in the United States, working with cultured neonatal rat cardiac myocytes, that can be seen to contract rhythmically under the microscope. It was then found that polyunsaturated fat in the medium counteracts the effects of pharmacological agents that usually initiate arrhythmias.24 Since then, at least 13 cohort studies have been completed, involving over 200 000 subjects. Most studies found protective effects of fish, and these were significant in countries with high rates of CHD and in studies of high scientific quality.25 Two meta-analyses (with a somewhat different selection of studies) both found significantly lower relative risk of CHD death in regular fish eaters,26,27 and He et al.27 showed a striking dose–response relationship, where eating fish two to four times per week reduced the mortality risk to 0.77. From the animal experiments it would be expected that the effect of fatty fish consumption would be on prevention of sudden deaths due to ventricular fibrillation. This was indeed found in two intervention studies: with fish in Wales (the DART study),28 and with fish oil capsules in the Italian GISSI study.29 Later trials in patients with implanted cardioverter/defibrillators have not provided such clear answers,30,31 but these are very complex cases to manage. In the largest randomised controlled trial of patients with implanted cardioverter/defibrillators (n = 402), the trend in favour of fish oil was impressive but not statistically significant, although technical difficulties with recordings and poor compliance in taking the large fish oil capsules were reported.30 Recently, five expert bodies have made recommendations regarding omega-3 PUFA intakes. In 2004, the US Food and Drug Administration concluded that supportive, but not conclusive, research shows that consumption of EPA and DHA omega-3 may reduce the risk of CHD. The Scientific Advisory Group of Food Standards Australia New Zealand likewise considered the evidence was probable that fatty fish containing omega-3 PUFAs reduces the risk of CHD. In 2003, the Joint WHO/FAO Expert Consultation32 concluded that the evidence was convincing that fish and fish oils (EPA and DHA) reduce the risk of cardiovascular disease. The (Australian) National Heart Foundation33 advises that, to lower the risk of CHD in the general population, adults should consume two to three serves of fish (preferably oily fish) per week, thus obtaining 500 mg/day of marine omega-3 PUFA. The National Health and Medical Research Council's Dietary Guidelines for Australian Adults (2003, pp. 117–122),10 as the third point in its 20 pieces of practical advice on fats, say ‘Try to include in your diet fish high in omega-3 polyunsaturated fats—for example, sardines, tuna, salmon and herring’. When considering any possible effects of long-chain omega-3 PUFAs, note that trials with fish oils use much higher intakes than are obtainable from ordinary diets. In trials with food relatively high in omega-3 PUFAs, the OPTILIP Study34,35 found reduced fasting plasma triglycerides but no change in haemostatic factors or insulin. The Adelaide and Perth study (which did not get an acronym)36 found no differences in blood pressure, insulin or lipids, although red cell PUFA increased 50%. All this advice is about EPA (20:5) and DHA (22:6), the predominant omega-3 PUFAs in fish oil and oily fish. The third long-chain omega-3 PUFA is docosapentaenoic (DPA, or 20:5). Its concentration is about one-sixth of that of EPA and DHA in fish, and little seems to be known about its biological activity. The averages of these three fatty acids in herring, mackerel, pilchards, salmon, sardines and tuna are: 20:5 = 8.25%, 22:5 = 1.43% and 22:6 = 6.55% total fatty acids.37 When eaten, cholesterol, the sterol in the cell membrane of land animals, tends to raise plasma cholesterol, but less than might be expected. About half of the plasma cholesterol is synthesised endogenously from acetate in the liver, and there is a feedback mechanism so that this is downregulated if more is absorbed. Effects of dietary cholesterol on plasma cholesterol are inconsistent,38 evidently affected by the fatty acid composition of the diet and varying between individuals.39 In shellfish, the sterols are not of the cholesterol form;40 chromatography shows that they are mostly phytosterols from seaweed. Earlier bans on oysters, for example, in cholesterol-lowering diets were based on a chemical method that did not differentiate other sterols from cholesterol. Phytosterols (β-sitosterol, campesterol, stigmasterol, brassicasterol) are the corresponding sterols of plant cell membranes. They have a very similar chemical structure to cholesterol, only differing in one or two extra carbons at the side-chain end of the molecule. They reduce absorption of cholesterol by competitive inhibition. This affects both dietary cholesterol and cholesterol excreted in the bile, which is normally partly re-absorbed. In purified form (and higher intake), they can lower plasma cholesterol by a larger percentage than dietary cholesterol raises it.41 Dietary fibre,42,43 even coffee,44 can affect plasma lipids, but the most important dietary factor, other than type of dietary fat, is excess energy, leading to overweight. Overweight people tend to have raised plasma triglycerides and higher total LDL-cholesterol and lower HDL-cholesterol.45 Weight reduction by diet and/or exercise will usually reduce their cholesterol and triglyceride levels. In 1981 Sullivan46 suggested that the lower incidence of CHD in premenopausal women, compared with men and postmenopausal women, could be due to higher iron stores in the latter two groups. A number of studies have since investigated this possibility. As red meat is a major source of bioavailable iron, this question is of potential concern for the safety of high intakes. The Institute of Medicine in its dietary reference intake (DRI) report on 14 nutrients,47 including iron, reviewed the literature on high iron status and CHD to determine the tolerable upper intake level. They found: Serum ferritin and CHD: three positive, five negative studies Transferrin saturation and CHD: all five studies negative Serum iron and CHD: all four studies negative Total iron binding capacity and CHD: all four studies negative Sempos explained why the US Food and Nutrition Board had concluded that there was not enough evidence to support the hypothesis.48 At least one of the positive studies was seriously flawed. Also, there is no consistent convincing evidence that having haemochromatosis, especially the heterozygous form, is associated with an increased risk of CHD. This was against the background that iron deficiency remains the most common nutritional deficiency in the USA.48 In the large West of Scotland pravastatin trial, genotypes for the haemochromatosis gene were assayed in 482 people who developed a CHD event and 1100 who did not.49 There were no significant differences. A recent trial of phlebotomy in 1277 US veterans with symptomatic peripheral arterial disease and 4.5-year follow up found no difference in outcome between phlebotomy and controls or with reduction of iron stores.50 Perhaps this topic can best be summed up by noting that the ANZ NRV report11 did not address the iron stores/CHD question. A recent paper by the Harvard epidemiologists Qi et al. suggests that dietary haem iron is a risk factor for CHD in women with type 2 diabetes.51 The three tables in the paper do not appear to show how much haem iron or meat (including pig meat) was recorded for the different quintiles. The authors themselves admit that residual confounding by saturated fat was unavoidable even after careful adjustment. The Australian Dietary Guidelines (ADG) Report10 presents the SFA and MUFA contents of lean red meat as quite low, especially in lean beef (total fat 1.8 g/100 g), and about equal, with smaller amounts of PUFA. Recent data on individual fatty acids in red meat52 expressed as percentages of total fatty acids suggest, for example that lean beef rump contains less cholesterol-raising SFAs and more PUFAs (Table 3). As per cent of total fatty acids, the values for: SFA (14:0 + 16:0) are 2.6 + 21.8 = 24.4% cis-MUFA (16:1 + 18:1) are 3.0 + 36.5 = 39.5% cis-PUFAs are 5.6 + 0.8 + 0.7 + 2.8 + 1.9 + 2.9 = 14.7% trans-fatty acids (18:1, 18:2 and 18:3) are 2.5 + 0.5 + 0.3 = 3.3% Most of the balance is stearic acid (13.2%) plus small amounts of 15:0, 17:0 and 14:1 fatty acids. The P/S ratio here is 0.60, whereas if the table in the Dietary Guidelines report is used, it would be only 0.22. Even if conjugated linoleic acid, 20:3, 20:5 and 22:6, are left out, the effective P/S for plasma cholesterol level is at least 10.3/24.4 = 0.42. The effect of red meat on plasma cholesterol in practice corresponds to what would be predicted from these recent Australian analyses of individual fatty acids in red meat cuts. Several controlled human studies find that lean red meat has a roughly neutral effect among foods on plasma cholesterol, suggesting it can be included in a cholesterol-lowering diet. A number of studies have shown the benefits of including lean red meat in prudent diets for cholesterol lowering. A group at St Thomas's Hospital London were able to reduce total- and LDL-cholesterol considerably in 15 free-living men with hyperlipidaemia on a diet, including increased P/S ratio and extra fruit and vegetables, that contained 180 g/day of lean red meat (8.5% fat). They concluded that providing care is taken to reduce total dietary fat, a moderate amount of meat and meat products may be included in a cholesterol-lowering diet.53 In Australia, Kestin et al. compared two fat-modified diets in 26 healthy men. One diet was vegetarian (LOV); the other contained 250 g/day lean meats (LOM). Total cholesterol fell 5% on diet LOM (10% on LOV). They concluded that a more widely accepted lean meat-containing prudent diet was almost as effective at lowering cholesterol levels as a plant-based prudent diet.54 Another Australian study involved 10 healthy subjects (men and women) given a very low-fat diet containing lean beef (500 g/day). Serum total cholesterol fell 20% and rose when beef dripping was added. The authors concluded that it was the beef fat, not lean beef itself, that was associated with elevations in cholesterol concentrations. The suggestion was that lean beef could be included in cholesterol-lowering diets (low saturated fat) provided that the meat was free of all visible fat.55 A further study in Texas, USA, gave 38 free-living men with hypercholesterolaemia a reduced-saturated-fat diet that included about 170 g either lean beef (8% fat) or chicken (7% fat) for five weeks. LDL-cholesterol fell 9% and 11% respectively, but the difference was not statistically significant. The authors concluded that lean beef and chicken were interchangeable in the NCEP Step 1 diet.56 In a long-term trial conducted in Chicago, Minneapolis and Johns Hopkins Lipid Clinic, 191 men with moderate hypercholesterolaemia were given 170 g/day of either lean red meat or lean white meat in their NCEP Step 1 diets. At the end of 36 weeks, LDL-cholesterol declined 1.7% and HDL-cholesterol increased 2.3% on the red meat; changes in the white meat group were not significantly different. (Lean red meat here, as is usual in the USA, was beef, veal or pork; lean white meat was poultry or fish.)57 Two other points are important about meat and plasma cholesterol. First, there is as much cholesterol in lean meat as in meat fat, chicken contains rather more cholesterol than beef, and kidney and liver contain four or five times more than muscle meat (see Table 2). These organs are richer in several good nutrients as well.37 Second, the fat of red meat has a more unfavourable fatty acid pattern than lean muscle meat. It contains more 14:0 and 16:0 SFA and less PUFA (see Table 3). By the method suggested above (omitting stearic acid), the P/S ratio in this lean meat is 0.42, while in the fat, it is 0.07. Of course, it contains about 20 times more total fatty acids than the lean muscle meat. This difference was first noted by Crawford,58 who compared the fatty acid patterns between very lean wild herbivores like and The to foods low in meat is a Australian analyses g in lean and British food tables similar for lean beef cuts the other lean red meat is rich in Australian for beef and mg/100 g for that about 9 The ratio is et blood of two of people with a moderate of One group ate 250 g/day of red meat for in of foods that the group was blood were significantly lower in the meat The authors suggest that the extra and in the meat may have added to the effect of less in reducing blood pressure. The against weight and the background papers the role of diet in the prevention and of and The report on the of a high body but does not a of which diets can be In the since the report was there has been research and much to find weight-reducing diets that are acceptable and The Total may much of its to the high protein of total energy and based this diet on their with diets reported in at least papers in the literature during the In one they report that over weeks, the diet in better changes in total- and in triglycerides and in blood compared with a diet, with no effects on or weight and in the men were not significantly different between the two possibly because of the of the et showed greater weight reduction with a protein intake of energy, compared with over a dietary Other have had similar with a dietary protein has been shown in human experiments to satiety and The for these changes have not been Low-fat, predominantly lean meat cuts have been shown to be acceptable in cholesterol-lowering diets. Meat is a good source of bioavailable iron, which does not appear to be a risk factor for heart disease. Meat is low in and high in and meat consumption does not appear to raise blood pressure. Overweight increases the risk of increased plasma cholesterol, increased blood pressure and diabetes. Meat is high in protein and contributes to weight reduction by increasing satiety and helping reduce energy intake in ad-lib weight-reducing diets.

The association between prepregnancy dietary fatty acids and risk of gestational diabetes mellitus: A prospective cohort study

Total fat and fatty acid intakes and food sources in Mediterranean older adults requires education to improve health

A higher risk of colorectal cancer (CRC) has been associated with high animal fat intake, but not vegetable fat. To date, limited data provides the quantification of the effect exerted by fatty acids (FAs) on CRC overall and by anatomical sub-sites. This study aims to look at associations between some FAs intakes [cholesterol, total fat, total saturated fatty acids (SFAs), total monounsaturated fatty acids (MUFAs), total polyunsaturated fatty acids (PUFAs), total trans fatty acids (TFAs), oleic acid, myristic acid, total ruminant (rTFAs) and industrial fatty acids (iTFAs), eliadic acid (EA), conjugated linoleic acid (CLA), and CRC risk in a large case-control study (IROPICAN) in Iran . We analyzed 865 CRC cases (434 in colon, 404 in rectum, and 27 with unknown subsite) and 3,206 controls from seven provinces of Iran. Detailed information was collected by trained interviewers using validated lifestyle and food frequency questionnaires (FFQ). The different types of total and individual FAs intake were categorized into quartiles of intake. The odds ratios (OR) and 95% confidence intervals (CI) for the association between CRC them were calculated using multivariate logistic regression models by adjusting for the potential confounders. Furthermore, analyses were stratified by age (under and over 50) and also, we repeated the analyses for CRC subsites. There was a statistically significant positive association between CRC and high intake (quartile 4) compared to the low intake (quartile) of dietary total fat (OR=1.77, 95% CI=1.32-2.38), cholesterol (OR=1.58, 95% CI=1.22-2.05), total TFAs (OR=1.31, 95% CI=1.02-1.68), TFAs (OR=1.73, 95% CI=1.12-2.68), EA(OR=2.69, 95% CI=1.46-4.93), and SM (OR=1.45, 95% CI=1.00-2.09), as well as an inverse association with high intake of dietary rTFAs (OR=0.60, 95% CI=0.39-0.93), CLAs (OR=0.34, 95% CI=0.19- 0.60). Stratified analyses by age indicated that there was a statistically significant association between CRC and total fat intake [OR =1.30, 95% CI =1.16-1.46, p=0.006 for the interaction], cholesterol intake [OR =1.22, 95% CI=1.11-1.35, p=0.019 for the interaction], and iTFA intake [OR =1.31, 95% CI=1.06-1.62, p=0.02 for the interaction] after 50 years old. The results of our study indicate that decreasing fat consumption, particularly from industrial and animal sources, may reduce the risk of CRC. Citation Format: Monireh Sadat Seyyedsalehi, Paolo Boffetta, Kazem Zendehdel. Fatty acid intake as potential risk factor of colorectal cancer: A multicenter case control study in Iran [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 6450.

Nutritional status and dietary fatty acid intake among children from low-income households in Sabah: A cross-sectional study

BackgroundThe associations between changes in fatty acid intake over time and subsequent mortality are unclear. ObjectivesThe objective of this study was to prospectively examine associations between changes in fatty acid intake (as percentage of total energy) and mortality. MethodsAmong 65,179 adults from the Nurses’ Health Study and Health Professionals Follow-up Study, free from cardiovascular disease, cancer, and diabetes at baseline in 1994, we documented 20,571 deaths through 2020 (1,334,603 person-years). Diets were assessed every 4 years using validated questionnaires. Hazard ratios (HRs) and 95% confidence intervals (CIs) for mortality risk were estimated from Cox proportional hazards models. ResultsA 5% energy increment in total fat intake was associated with 5% lower all-cause mortality (HR: 0.95; 95% CI: 0.93, 0.96; isocaloric comparison was total carbohydrate). The HRs of all-cause mortality (95% CI) were 0.83 (0.78, 0.89) and 0.91 (0.87, 0.94) for a 5% increment in energy intake from polyunsaturated fatty acid (PUFA) and monounsaturated fatty acid (MUFA), respectively, and was 1.10 (1.04, 1.17) for a 1% increase in energy intake from trans fatty acid (TFA; all Ptrend ≤ 0.001). Changes in saturated fatty acid (SFA) were not associated with all-cause mortality. Increases in intakes of linoleic acid, marine n–3 PUFA, and MUFA from plant sources were each significantly associated with lower all-cause mortality. In substitution analyses, replacing 5% energy from SFA with PUFA was associated with 19% lower all-cause mortality (HR: 0.81; 95% CI: 0.75, 0.87), whereas replacing 0.3% of energy from SFA with marine n–3 PUFA was associated with 11% lower all-cause mortality (HR: 0.89; 95% CI: 0.84, 0.93). Isocaloric substitution of SFA by PUFA, particularly marine n–3 PUFA, was associated with lower mortality due to cardiovascular, neurodegenerative, and respiratory diseases. ConclusionsThese findings support replacing SFA with unsaturated fatty acids (especially from plant sources) and eliminating dietary TFA to reduce premature death.