On March 6th, a blog was posted on the Nutrition Coalition web site. The post was about an announcement on the USDA web site that “The U.S. Departments of Agriculture (USDA) and Health and Human Services (HHS) currently are asking for public comments on topics and supporting scientific questions to inform our development of the 2020-2025 Dietary Guidelines for Americans.”

The Nutrition Coalition drew specific attention to two areas of the guidelines, which the USDA is seeking to review: low carb diets and saturated fat. For adults (aged 19-64), the USDA is seeking input on the topics “Dietary patterns to promote health and normal growth and meet nutrient needs” and “Saturated fats.”

i) The question being asked in the dietary patterns area is: “What is the relationship between specific dietary patterns (Dietary Guidelines-related, Mediterranean-style, Dietary Approaches to Stop Hypertension (DASH), vegetarian/vegan, and low-carbohydrate diets) consumed during adulthood and 1) body weight or obesity; 2) risk of cardiovascular disease; 3) risk of type 2 diabetes; and 4) risk of certain types of cancer?”

ii) The question being asked in the saturated fats area is: “What is the relationship between saturated fats consumption (types and amounts) during adulthood and risk of cardiovascular disease?”

Please support the Nutrition Coalition in the ways that they suggest on their post: tweet; Facebook; blog; and – most importantly – submit a comment as invited on the USDA web site. The rest of this note contains the submission that I sent to the USDA and HHS… (my comment can be seen here).

My submission

Dear USDA & HHS,

My PhD was entitled “An examination of the randomized controlled trial and epidemiological evidence for the introduction of dietary fat recommendations in 1977 and 1983: a systematic review and meta-analysis.”

I spent three and a half years researching all RCT and epidemiological evidence for the two dietary fat guidelines introduced in the US in 1977: 1) that total fat should be no more than 30% of daily calorie intake; and 2) that saturated fat should be no more than 10% of daily calorie intake (Ref 1). These guidelines, as you will know, have been reiterated in the Dietary Guidelines for Americans since the first edition in 1980 (Ref 2). The most recent edition has positioned the total fat guideline with the use of “Acceptable Macronutrient Distribution Ranges” (AMDRs). The range given for total fat is 20-35% and the AMDR for saturated fat is given as <10% – both as a percentage of daily calorie intake (Ref 3).

I would suggest that there are few people in the world who have studied these two guidelines for the length of time and at the academic level that I have. I have been entirely independent of any industry funding during all my research, which also sets me apart from many others in the field. I was a non-paid independent board member of the University Wales Institute Cardiff between 2006-2012 and I was a paid (a couple of days per month) independent board member of the National Health Service for Wales (2009-2012). The part time paid public health post aside, I have worked for myself since 2008. The declaration that may be relevant is that, when I started research in this field, I was a vegetarian and had been for almost 20 years. My confirmation bias would have been to find in favor of plant foods. Reluctantly my findings compelled me to admit that my dietary choices had been wrong. With this context, here is a summary of the evidence and a proposed way forward.

Introduction – facts about fat

I wish to start by saying that the notion that saturated fat could be harmful to human health makes no sense. There are three facts about fat that are not widely enough known:

1) Human beings must consume fat; we die without doing so. The word “essential” in nutrition means something that we must consume. There are two essential fats (omega-3 and omega-6) and four fat soluble vitamins (A, D, E and K), which must be consumed.

2) All food that contains fat contains all three natural fats: saturated; monounsaturated and polyunsaturated. It is impossible to consume unsaturated fat without saturated fat, or vice versa, in natural food. This second fact also establishes that saturated fat is no more synonymous with animal foods than unsaturated fat is synonymous with plant foods. All food that contains fat – plant or animal in origin – contains all three natural fats.

3) Dairy is the only food group that contains more saturated than unsaturated fat. The US “My Plate” inexplicably defines food groups as: fruit; veg; grains; protein; and dairy. Protein is a macronutrient. It is found in every food other than sucrose/pure fats. Protein is not a food group and the list of other food groups is incomplete. A better list of food groups would be: meat; fish; eggs; dairy; vegetables; fruit; nuts & seeds; legumes (beans, pulses, etc); and grains. The only one of these, for which the fat content is predominantly saturated, is dairy foods. Meat, fish, eggs, nuts, seeds, even lard, all have more unsaturated than saturated fat. Not that saturated is bad and unsaturated is good, but just to be clear about nutritional facts from the outset.

Given that we must consume fat to survive, let alone thrive, and given that we cannot avoid saturated fat, it would make no sense that nature has provided component parts of food, which are trying to help and harm human beings at the same time. As this extract from my first journal article put it: “Using a 100 g steak, as an example, with 5.4 g of fat, it is difficult to accept that the 39% of the fat which is saturated is damaging to the cardiovascular system while the 61% of the fat which is unsaturated is protective. Keeping in mind that the total fat content of the steak will provide all but 3 of the 13 vitamins and 16 minerals that are a pre-requisite for the maintenance of good health” (Ref 4).

The beef-steak facts may surprise some people. So might the fact that, gram for gram, olive oil (Ref 5) has 14 times the total fat of beef (Ref 6) and 7 times the saturated fat. A counter may be that human beings don’t eat large quantities of olive oil. Yes, but 1 tablespoon of olive oil has more saturated fat than a 100g pork chop (Ref 7). And the oily fish (Ref 8) , which we are advised to eat, has twice the total fat and one and a half times the saturated fat of that red meat we are told to avoid (Ref 6). People who know something about nutrition can make a mockery of dietary guidelines and we are doing just this – world wide.

The RCT evidence





Randomized Controlled Trials are superior to epidemiological studies in the hierarchy of evidence. A systematic review and meta-analysis of RCTs is better still (Refs 9 & 10). This was thus the logical place to start my investigation. The primary outcome measure was set as mortality – all-cause and from heart disease – as this is the most important outcome measure to examine. There is no point dying less from one condition to die more from another.

The first paper published from my PhD was a systematic review and meta-analysis of the RCTs available at the time the 1977 dietary committee was deliberating (Ref 11) (the five key papers from my PhD are included in this submission). This paper found that there were exactly the same number of deaths in the control and intervention groups and no significant differences in deaths from Coronary Heart Disease (CHD). The paper also concluded that fewer than 2,500 sick men had been studied (no women and no healthy men), with no findings in support of introducing dietary fat guidelines, and yet “Dietary recommendations were introduced for 220 million US and 56 million UK citizens by 1983, in the absence of supporting evidence from RCTs.” This article achieved global coverage and became the 64th most impactful paper in any discipline for 2015 (Altmetric).

During media discussions on the day of publication, I was surprised by the readiness of Public Health England (PHE – the UK dietary guideline setting body) to accept that the evidence was not there at the time the guidelines were introduced. The spokesperson for PHE claimed that the advice had been forthcoming since. This was timely, as I was in the process of submitting our follow-up paper (Ref 12). This paper reported that women and healthy men were now included in RCTs available for review. However, the pooled RCTs again found no significant differences in all-cause or CHD mortality. Additionally, the pooled RCTs revealed that only 1 of the 10 RCTs included healthy men and women and thus, even if results had been found, they would still not have been generalisable to the whole population (Ref 13).

The full papers detail the interventions. Some were to reduce fat; some were to modify fat (to replace saturated fat with unsaturated fat). None made a case for change individually – indeed a number cautioned that their vegetable oil interventions were potentially harmful/toxic – and there was no case for change collectively in meta-analysis.

An additional valuable finding from both papers was that “Mean serum cholesterol levels decreased in all intervention groups and all but one control group. The reductions in mean serum cholesterol levels were significantly greater in the intervention groups; this did not result in significant differences in CHD or all-cause mortality” (abstract) (Ref 12). These papers thus undermined the diet-heart-cholesterol hypothesis at the same time as finding no evidence for total or saturated fat reduction, or dietary modification to replace saturated with unsaturated fat.

An important point to make here is that I also researched how replacing saturated fat with unsaturated fat could lower cholesterol without improving heart disease. My research found that the contrary – increased risk of heart disease – was more likely and this editorial explained how (Ref 14).

The epidemiological evidence

Notwithstanding that epidemiological evidence is weaker than that of RCTs, for completeness, my PhD sought to examine the epidemiological evidence available at the time dietary guidelines were introduced in the US (and subsequently the UK) and the epidemiological evidence available today. The paper on the epidemiological evidence at the time found that there were six studies to systematically review. These studies could not be subjected to meta-analysis, as the data were not conducive. The conclusion of the paper was “None of the six studies found a significant relationship between CHD deaths and total dietary fat intake. One of the six studies found a correlation between CHD deaths and saturated dietary fat intake across countries; none found a relationship between CHD deaths and saturated dietary fat in the same population” (abstract) (Ref 15).

The one study that found a relationship between CHD deaths and saturated fat intake across countries was the well known and invariably referenced Seven Countries Study (Ref 16). In this study, Keys asserted that smoking, activity levels/exercise and weight played no part in CHD. This study has been afforded huge regard in its contrary (among five peer papers) finding on saturated fat when it is known to be wrong on three other major risk factors. The most significant limitation of the study was that it was an inter-country comparison, rather than a CHD/CHD-free comparison. Men (and it was only men) who developed CHD in Japan were compared with men who developed CHD in the US, as opposed to men who developed CHD in Japan being compared with men who did not develop CHD in Japan. This introduced substantially more confounding factors, including, but not limited to: geography; lifestyle; Gross Domestic Product; climate; politics; other aspects of national diet; national health provision etc. When asked about the value of Keys’ work, a contemporary of the time, Professor Peter Elwood, described inter country studies as “the lowest form of evidence” (Ref 17).

Epidemiological evidence available in 2016 fared little better. The conclusion of the fourth part of my PhD found similarly to the other documents: “Epidemiological evidence to date found no significant difference in CHD mortality and total fat or saturated fat intake and thus does not support the present dietary fat guidelines. The evidence per se lacks generalisability for population-wide guidelines” (abstract) (Ref 18).

Other meta-analyses

To present the findings of my PhD team in context, we reviewed other systematic reviews and meta-analyses that had placed heart disease and mortality as the key outcome measures.

A number of meta-analyses of RCTs, examining dietary fat and mortality, have been undertaken by other authors (Refs 19-21). One meta-analysis of prospective cohort studies has been undertaken by other authors (Ref 22). Two additional meta-analyses reviewed both RCTs and prospective cohort studies (Refs 23 & 24). Skeaff and Miller sought to summarize the evidence from cohort studies and RCTs of the relation between dietary fat and risk of CHD. Their conclusion was “Intake of total fat was not significantly associated with CHD mortality. Intake of total fat was also unrelated to CHD events” (p.175) (Ref 23). Chowdhury et al set out to summarize evidence between fatty acids and coronary disease. Their review examined saturated, monounsaturated, polyunsaturated and trans fats, while also reviewing individual chain length fatty acids, palmitic (C16:0) and margaric (C17:0) as examples. The conclusion was “Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats” (p.398) (Ref 24).

Table 7.1 in the review paper from my PhD summarized the findings from other meta-analyses of RCTs and/or prospective cohort studies (Ref 25). There were 39 reports of risk ratios from meta-analysis with 95% confidence intervals; 35 of which were non-significant. Please pause for a moment for that to sink in. Reviews of evidence focus on findings. The fact that so much research has been undertaken, examining total fat, types of fat, mortality and heart disease, and that the vast majority has found nothing of any significance, is extremely important.

One of the four significant findings related to trans fats, not total or saturated fat. It found that trans fat intake was positively associated with coronary disease (Ref 24). Another of the significant findings came from the study of the impact of replacing saturated fat with polyunsaturated fat (Ref 21), which was criticized (Ref 26) for excluding two studies that would have moderated this conclusion (Refs 27 & 28) and including a favorable, but non-randomized, non-controlled, cross-over trial excluded by the other meta-analyses (Ref 29).

The Cochrane reviews (Refs 20 & 30), one an update of the other, provided the only ostensibly credible findings against saturated fat for cardiovascular (CVD) events, but not for total mortality, CVD mortality, fatal myocardial infarction (MIs), non-fatal MIs, strokes, coronary heart disease (CHD) mortality, CHD events or the diagnosis of diabetes. The Cochrane reviews included 4 small studies (646 people in total), not included in any other meta-analysis, which were primarily studies of: diabetes (Ref 31); skin cancer (Ref 32); hypercholesterolemia (Ref 33); and glucose intolerance (Ref 34), but for which unpublished, non-peer-reviewed CVD event information was obtained. No study of healthy people of both genders was included and thus even this one apparent finding, for events alone, lacked generalizability.

Hooper et al suggested that there may be a small reduction in cardiovascular risk with reduction of dietary saturated fat intake (Ref 30). However, the findings were inconsistent between studies (shown by the I2 test of 65%). A fellow researcher in the UK, Dr Trudi Deakin, observed that, when a sensitivity test included only the RCTs that had significantly reduced saturated fat (>52,000 participants), the CVD events finding reduced from 17% to 9% and was no longer statistically significant (Table 8, p121) (Ref 30).

Seemingly having ignored that the only ‘finding’ was in fact non-significant and thus there were no findings, the paper continued to suggest that replacing energy from saturated fat with polyunsaturated fat “appears to be a useful strategy, and replacement with carbohydrate appears less useful” (p.2) (Ref 30) and replacement with mono-unsaturated fat unclear. Of the 11 interventions contributing to this conclusion, only 1 documented both saturated fat reduction and reported that this was mainly replaced with polyunsaturated fat (Ref 35).

Even if there were any findings in favor of polyunsaturated fat, it would be important to differentiate between polyunsaturated fats. The Diet and Reinfarction Trial (DART) provided early evidence for the benefit of omega-3 polyunsaturated fat, naturally abundant in fish (Ref 36). The only significant finding from this RCT was that all-cause mortality was lower for those following the fish advice, which was to increase fatty fish intake to at least two portions (200-400g) weekly. This significant finding was explored further by the research team, but not found to be replicated (Ref 37). Omega-6 polyunsaturated fats have pro-inflammatory properties, which can be mitigated by omega-3 intake (Ref 38), but any dietary advice on polyunsaturated fats needs to be specific and evidence based.

The American Heart Association (AHA) advisory report (Ref 39), which was published after my research, repeated the bias of Mozaffarian et al (Ref 21) by also excluding the same two studies that did not support replacing saturated fat with unsaturated fat (Refs 27 & 28) and by excluding another study that didn’t support the pro-unsaturated fat message (Ref 13) and by including the same favorable, but non-randomized, non-controlled, cross-over trial – the Finnish Mental Hospital study (Ref 29). The AHA report tried to rationalize exclusions, but the bias is clear to see to any independent researcher and the polyunsaturated fat/industry conflicts with the paper were not fully declared (Ref 40).

Dietary fat guidelines were introduced with the ambition of reducing deaths from CHD. In conclusion of the pool of evidence provided by many researchers in this field, no meta-analysis of RCTs and/or prospective cohort studies has found any significant difference for dietary fat interventions and all-cause mortality or deaths from CHD, or associations with dietary fat and CHD mortality (Refs 11, 19-24, 30).

A Way Forward

The Dietary Guidelines for Americans documented the sources of saturated fat in the American diet (fig. 3-4, p.26) (Ref 41). Pizza, desserts, candy, potato chips, pasta, tortillas, burritos and tacos accounted for 32.6% of saturated fat consumed in the diets of US citizens aged 2 years and older. 9.3% of dietary saturated fat came from sausages, frankfurters, bacon, ribs and burgers. 12.8% came from chicken and mixed chicken dishes, beef and mixed beef dishes, and eggs and mixed egg dishes. A further 24.5% was unaccounted for and collated as “All other food categories”; likely including, if not predominantly being, processed foods. The natural foods listed were cheese, milk, butter, nuts and seeds which collectively accounted for 20.8% of saturated fat intake. It would have been ideal for unprocessed chicken, beef and eggs to have been separated from processed meals containing these ingredients. The diagram presented in the Dietary Guidelines is clear nonetheless. Processed foods account for the majority of saturated fat intake in the diets of Americans.

There is opportunity for strong agreement among health professionals. If the public health message were revised to advise citizens to eat natural food and not processed food, saturated fat intake would fall accordingly although the health benefit would likely be the concomitant reduction in sucrose, trans fats and other processed ingredients deleterious to human health (Ref 42). Human beings evolved to eat foods available from the natural environment (Ref 43). It does not seem logical to advise populations away from carcass meat, dairy produce, eggs, nuts and seeds, in the name of saturated fat, when the modern processed foods, cookies, cakes, pizza, desserts and ready meals, are more sensibly related to modern illness (Ref 4).

Close

I have tried to summarize three and a half years of formal study of the dietary fat guidelines in this submission. I sincerely hope that this helps the USDA and HHS to review all evidence available on the subjects of both total fat (not indicated as ‘up for review’) and saturated fat, which has been identified as open to review.

The question being asked of contributors is “What is the relationship between saturated fats consumption (types and amounts) during adulthood and risk of cardiovascular disease?”

The answer is “none” and facts about fat inform us that it would make no sense for there to be any.

References

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