Sunday, January 8, 2012

DGA 2011 - Total Fat and Saturated Fat: Part 2

You can read Part 1 here

Dietary Fat and Cardiovascular Disease

“This review confirmed that replacing SFA with unsaturated fatty acids may reduce the risk of coronary heart disease, and that replacing trans fats with unsaturated fats improves blood cholesterol levels. From a whole-of-diet perspective, this review found that reducing the risk of cardiovascular disease by replacing SFA with carbohydrate (as is the case in some low-fat diets) depends on effects on body weight [410].”

This study examined the difference in the total cholesterol:HDL cholesterol ratio (TC:HDL-C).  The lower this ratio the lower the risk of cardiovascular disease.  However this study did not measure cardiac events, just is a risk factor.

Relative to carbohydrates: unsaturated fats decrease the ratio by reducing LDL-C and increasing HDL-C, TFA increases the ratio by increasing LDL-C and reducing HDL-C, and SFA only slightly increases the ratio by increasing both LDL-C and HDL-C, but in a ratio that increases the TC:HDL-C.

Of the saturated fats only palmitic acid increases the TC:HDL-C ratio, the others decrease it.  Lauric acid improves the ratio more than the average MUFA and PUFA do.  The effects of stearic acid resemble the effect of MUFA, which makes sense as stearic acid can be converted to oleic acid by the delta-9-desaturase enzyme.  This is why it’s important to not generalise.

It’s important to see how foods affect this ratio, rather than just fatty acids, because all foods are a mix of various saturated, monounsaturated and polyunsaturated fatty acids.  This graph shows that every measured fat and oil outperformed carbohydrate on the TC:HDL-C ratio.  Even butter and shortening, rich in SFA and TFA respectively (the two fatty acid groups that increased the ratio), would result in an improvement in the TC:HDL-C ratio.

The authors attempt to explain why carbohydrates performed so poorly on the TC:HDL-C ratio.

“The unfavorable effect of carbohydrates on total:HDL cholesterol might be opposed by a favorable effect of carbohydrates on body weight, because low-fat diets may promote weight reduction. Isoenergetically replacing fat constituting 10% of energy with carbohydrates may reduce weight by 3 kg. The data of Leenen et al suggest that a weight loss of 3 kg may lead to a decrease of 0.24 in total:HDL cholesterol. If a high-carbohydrate diet reduces energy intake sufficiently to cause a 3-kg weight loss, then the effect on total:HDL cholesterol would be approximately equal that of isoenergetic replacement of SFAs constituting 10% of energy with cis unsaturated oils. This underlines the importance of weight management in the reduction of CAD risk. Unfortunately, the effects of low-fat diets on body weight over the long term are uncertain. The introduction of low-fat, high-carbohydrate foods in the United States does not appear to have reduced caloric intake; rather, carbohydrates seem to have been added to existing intakes. However, further studies on the long-term effect of high-carbohydrate diets on body weight are urgently needed.”

“Thus, it is not certain whether weight loss per se is a strong argument for replacing fat with carbohydrates. Without doubt, reducing the high prevalence of obesity should be a major public health target, but increased intakes of carbohydrates could be shown to be insufficient to counter the effects of low energy expenditure and high caloric intake that characterize modern societies.”

The authors are uncertain whether carbohydrates aid in weight loss.  This uncertainty is not expressed in the dietary guidelines.

“From a whole-of-diet perspective, this review found that reducing the risk of cardiovascular disease by replacing SFA with carbohydrate (as is the case in some low-fat diets) depends on effects on body weight [410].”

From the previous study both low carbohydrate, high fat and low fat, high carbohydrate diets aided weight loss.  The possibility that dietary fat or certain fatty acids would aid weight loss was not considered.  Lauric acid aids in weight loss by increasing fat metabolism and thermogenesis [9], yet lowers the TC:HDL-C ratio beyond any fatty acid.  As this study points out excess body weight is coinciding with an increased intake of carbohydrate and the obesity epidemic is getting worse, not better.  Minor reductions in body fat from our high carbohydrate diets, something  that is not occurring in the general public, is unlikely to be an accurate explanation.

Instead, the findings of this study would suggest that replacing carbohydrate with fats and oils reduces the risk of cardiovascular disease by improving the TC:HDL-C ratio.

“An additional justification for using total:HDL cholesterol might be that it includes the amount of cholesterol in the triacylglycerol-rich VLDL fraction, which also positively correlates with CAD risk.”

“High-fat diets lower fasting triacylglycerol concentrations, which may reduce cardiovascular disease risk”

Low carbohydrate, high fat diets improve the TC:HDL-C ratio, reduce VLDL-C, reduce triglycerides, reduce the proportion of the atherogenic pattern B LDL particles and increase the proportion of the non-atherogenic pattern A LDL particles [10].  It would appear low carbohydrate, high fat diets are superior to low fat, high carbohydrate diets on all these measurements and biomarkers used to predict the risk of cardiovascular disease.  In addition carbohydrate intake is positively associated with atherosclerosis whereas saturated and monounsaturated fatty acids are negatively associated with atherosclerosis [11].  It should hardly be surprising that people struggle and fail to improve their blood lipids while eating a low fat, high carbohydrate diet in accordance with their doctor’s advice.

“However, the effect of carbohydrates on total:HDL cholesterol justifies some caution in the application of high-carbohydrate diets to the prevention of heart disease.”

“The link between dietary saturated fat, cholesterol levels, atherosclerosis and other components of cardiovascular disease has been well established in previous guidelines, and was not reviewed here.”

The research reviewed in the previous dietary guidelines for all Australians (2003) found that saturated fatty acids tend to increase LDL cholesterol and that increased LDL cholesterol increases the risk of cardiovascular disease [12].  However, no research was cited that found a direct link between saturated fatty acids and cardiovascular disease.  If higher intakes of saturated fats did indeed appear to contribute to cardiovascular disease, the study would have been included in the previous dietary guidelines.  As such the evidence against saturated fat only amounts to intermediary variables.

There is some evidence suggesting the same as what the lack of evidence in the 2003 guidelines suggests, that dietary saturated fatty acids are not associated with cardiovascular disease [13] [14].

Mechanistically, it does not make much sense for saturated fats to contribute towards cardiovascular disease.  Cardiovascular disease begins with plaque formation (atherosclerosis) in the arteries.  The plaque is the end product of a foam cell neutralising the potential harm of oxidised lipids and lipoproteins.  Polyunsaturated fatty acids (PUFA) are uniquely susceptible to oxidation by having two or more double bonds [15] and a greater linoleic acid (18:2) leads to more linoleic acid in the LDL membrane and more oxidised LDL (relative to oleic acid (18:1)) [16] [17] .  Once the PUFA in the LDL membrane become oxidised they may damage the adjacent apolipoproteins, which then oxidises the LDL particle, the LDL particle penetrates the endothelium and encourages macrophages to form foam cells [11].  Saturated fatty acids on the other hand have no double bonds, and are therefore the most chemically stable of all fatty acids.

There is more evidence that high PUFA diets increase lipid peroxidation leading to oxidised LDL and atherosclerosis.  One measure of LDL oxidation was 16.1% higher in omega 6 PUFA rich diets compared with SFA rich diets and 17.5% higher than MUFA rich diets.  The same study found a different measure of LDL oxidation was 75% higher in omega 6 PUFA rich diets compared with SFA rich diets and 47.2% higher than MUFA rich diets.  This is despite the vitamin E in LDL was higher in the PUFA rich diet group followed by the MUFA rich diet group [18].  A different study found LDL oxidation is over 31% higher in n-6 PUFA rich diets compared with SFA and MUFA [19].  In these studies LDL oxidation of omega 3 rich diets was even higher than omega 6 rich diets.  (In both studies above one could expect more dramatic results against the PUFA groups if the studies lasted longer as more PUFA would displace the safer SFA and MUFA in the cell membranes and promote oxidative stress).  Low total fat, low saturated fat but high PUFA diets increases oxidised LDL relative to the participants’ normal diet, regardless of adding fruits and vegetables [20].  PUFA are positively associated with atherosclerosis, whereas SFA are negatively associated with atherosclerosis [11].

“The American Heart Association (AHA) and individual scientists advise consumption of at least 5–10 % of energy as n-6 PUFA to reduce CHD risk. They note that randomised controlled trials (RCT) of CHD outcomes are considered to be the ‘gold-standard’ for guiding clinical practice decisions. Individual RCT, and two meta-analyses combining seven RCT, are cited as providing ‘the most convincing’ and ‘decisive’ evidence-base, with ‘immediate implications’ for ‘population and individual level recommendations’ to substitute n-6 PUFA-rich vegetable oils for SFA. However, the conclusions of these meta-analyses have been questioned due to their (1) omission of relevant trials with unfavourable outcomes; (2) inclusion of trials with weak design and dominant confounders; (3) failure to distinguish between trials that selectively increased n-6 PUFA, from trials that substantially increased n-3 PUFA; (4) failure to acknowledge that n-6 and n-3 PUFA replaced large quantities of trans-fatty acids (TFA), in addition to SFA, in several trials.” [21]

“RCT that substituted mixed n-3/n-6 PUFA in place of TFA and SFA reduced CHD risk. By contrast, n-6 specific PUFA interventions tended to increase CHD risk. These increased CHD risks from n-6 specific PUFA diets may be underestimated as they replaced TFA and SFA; reductions of these potentially atherogenic fats would be expected to reduce CHD risk. Consistent with this, we found that the substitution of n-6 PUFA for TFA and SFA produced an increased risk of death from all causes” [21]

“Advice to specifically increase n-6 PUFA intake, based on mixed n-3/n-6 RCT data, is unlikely to provide the intended benefits, and may actually increase the risks of CHD and death.” [21]

The current recommendations for reducing chronic disease risk are for linoleic acid (LA) (18:2 n-6) to make up 4-10% of total calories, alpha-linolenic acid (18:3 n-3) to make up 0.4-1.0% of total calories and 500 mg of long chain omega 3 PUFA (for men).  This puts the recommended omega 6:3 ratio at approximately 10:1 [22].  In contrast the omega 6:3 ratio of hunter-gatherers is about 1:1 and the ratio that improves health outcomes is between 2:1 and 5:1.  A ratio of 10:1, which is recommended is associated with worse health outcomes [23].  If a health promoting omega 6:3 ratio of 2:1 to 5:1 is used, the recommended LA intake would be between 2-5% of total calories, half the current recommendation.  Reducing of LA, rather than increasing omega 3 PUFA, is likely to be healthier as high PUFA diets will increase lipid peroxidation and high LA diets are also associated with insulin resistance and cancer [24].

Saturated Fatty Acids, Natural trans-Fatty Acids and Artificial trans-Fatty Acids

The dietary guidelines group SFA and TFA together as ‘bad’ fats because they tend to increase LDL cholesterol.  However, the two groups produce very different biological effects.

“Dietary SFA and dietary TFA have been associated with raised plasma LDL-cholesterol, and dietary TFA has been associated with a reduced plasma HDL-cholesterol [88].”

SFA increase LDL-C, but also increase HDL-C and are chemically stable.  More important than blood lipids is that SFA are negatively associated with atherosclerosis and (along with MUFA) result in less oxidised LDL than PUFA (see above).  TFA up regulates cholesterol ester transfer protein, which transfers cholesterol and triglycerides between LDL and HDL particles.  Up regulating CETP has the effect of increasing LDL-C while decreasing HDL-C [25].  A mechanism by which TFA cause atherosclerosis is by supressing transforming growth factor β (TGF-β), a protein that protects against atherosclerosis [26].  Saturated fat does not have this effect.

Serum lipoprotein A (LpA) is a strong risk factor for CVD as it is related to the quantity of LDL particles, which is likely to be more predictive than LDL-C (because lipoproteins oxidise before cholesterol).  High SFA diets produced the lowest LpA, high MUFA and PUFA diets produced non-significant differences between each other and a small significant increase in LpA, high TFA diets produced a large significant increase in LpA.  SFA decreases LpA and TFA increases LpA relative to cis unsaturated fats [27].

For linoleic acid and alpha-linolenic acid to be useful as eicosanoids they undergo a number of changes catalysed by enzymes.  The elongase enzyme adds two carbons to the hydrocarbon tail, desaturase enzymes remove two hydrogens and form a double bond and cyclooxygenase (COX) enzymes add oxygen to form the eicosanoid.  TFA block desaturase enzymes and COX1.  This can contribute to an essential fatty acid deficiency and cause imbalances in the eicosanoids, often promoting clotting [28].  SFA do not have this effect.

TFA increase C-reactive protein (CRP), a biomarker for inflammation which is associated with CVD [29].  SFA do not increase CRP, but in fact coconut oil (rich in lauric acid) seems as anti-inflammatory as fish oil [30] and stearic acid can be converted to oleic acid, which is anti-inflammatory.

NAFLD may be a better risk factor for CVD compared to the metabolic syndrome, smoking, blood pressure and LDL-C [31].  TFA increase the risk of non-alcoholic fatty liver disease (NAFLD) by increasing oxidative stress (lipid peroxidation of PUFA can result in harmful TFA and oxidative stress) [32].  SFA protects against NAFLD, while high carbohydrate, high PUFA diets induce NAFLD [33].

“The protective effect of dietary saturated fatty acids against the development of alcoholic liver disease has long been known” [34]

TFA also impairs endothelial function [35], increases triglycerides [36] [37], insulin resistance [37] [38] and weight gain as fat (without caloric excess) [37] [38].  SFA do not impair endothelial function, they reduce triglycerides relative to carbohydrates and it’s inconclusive whether dietary SFA promotes insulin resistance and fat gain.

In the dietary guidelines there is no distinction between naturally occurring TFA (from ruminants) and those formed from artificial hydrogenation.  Plant oils (except olive oil, coconut oil and some higher quality oils) undergo a deodourisation process that weakly hydrogenates the oil, but actually produces more harmful artificial TFA  [37].  The natural TFA include trans-vaccenic acid and conjugated linoleic acids (CLA).  Trans-vaccenic acid is often converted to CLA.

The artificial TFA exert their toxic effects when they are incorporated in phospholipid membranes.  Cellular communication breaks down because TFA have a skewed hydrocarbon tail and no electric charge.  Natural TFA do not exert any toxic effects probably because they are not incorporated in phospholipid membranes [39].

Artificial TFA compromised immune function, whereas natural TFA improves immune function [40].  Artificial TFA decreases HDL-C and increases LDL-C and triglycerides, although natural TFA does not reduce HDL-C [41], but reduces LDL-C and triglycerides [42].  Artificial TFA promote fat accumulation [27] [28], but natural TFA may improve body composition (less fat, more muscle) [43].  Artificial TFA may promote cancer [44], but natural TFA blocks tumour cell growth [45] [46].


“The Guidelines recommend caution in choosing foods high in fat because of the implications for weight gain and cardiovascular disease risk”

The evidence provided reveals a few things:-

  • Low carbohydrate, high fat diets are equal, if not more effective than low fat, high carbohydrate diets for weight loss
  • All whole food fats are superior to carbohydrates in improving blood lipids as risk factors for cardiovascular disease
  • SFA are associated with less oxidised LDL, less atherosclerosis and are not associated with CVD
  • PUFA are associated with more oxidised LDL, more atherosclerosis and replacing SFA and TFA with omega 6 PUFA increases CVD
  • SFA, natural TFA and artificial TFA produce very different biological effects.  SFA and natural TFA tend to promote health, artificial TFA promote disease

The caution to avoid high fat foods is not grounded in the research behind the guidelines.  Rather, the research suggests low carbohydrate, high fat diets are equal, if not more effective than low fat, high carbohydrate diets for weight loss, and also that all whole food fats are superior to carbohydrates in improving blood lipids as risk factors for cardiovascular disease.

The section heading refers only to limiting saturated and trans fat, yet the guidelines recommend reducing all fat, which contradicts the evidence.  The guidelines group all SFA and all TFA together, as if increasing LDL-C is the only thing that’s important.  Despite increasing LDL-C, SFA are associated with less oxidised LDL, less atherosclerosis and not associated with CVD.  However, high PUFA diets increase oxidised LDL and atherosclerosis.

The guidelines do not distinguish between the health promoting natural TFA and the toxic, disease promoting artificial TFA.  Australians should entirely avoid artificial TFA and these fats should never be considered fit for consumption.  This also means deodorised oils (without a smell) should not be consumed.  These tend to be industrial oils such as canola, soybean, sunflower, safflower and palm.  The public message that ‘TFA decrease HDL-C and increase LDL-C’ does not convey the extent of the problems caused by artificial TFA, other effects include weight gain, NAFLD and cancer.  The messaging should be phrased as tangible health outcomes and effects, rather than somewhat abstract biomarkers and risk factors.

Based on the research cited the dietary guidelines should be sending a message that food quality may be more important than macronutrient ratios and replacing carbohydrate with fat actually improves blood lipids.

Instead of recommending: limit intake of foods and drinks containing saturated and trans fat.  What should be recommended instead is: to limit intake of foods and drinks high in polyunsaturated fat (except fish) and those that contain artificial trans fats (labelled partially hydrogenated and also any oils without a smell).

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