Response to the Heart Foundation Position on Red Meat

The latest update to the Heart Foundation position statement on red meat suggests that Kiwis should actively try to reduce red meat intake and that it is a leading cause of cardiovascular disease and mortality.

What’s right in the position?

Before we get started into what (in my humble opinion) is ‘wrong’ with the position, let’s look at what’s right with it.

I fully concur with most of the advice in the statement. For example, to eat more vegetables, swap from refined grains to whole grains, eat healthy fats from nuts and seeds, avocado, and oily fish, and reduce processed foods.

That’s all sound dietary advice.

Where the Heart Foundation position gets it wrong

On the other hand, some of the guidelines are in contrast to the evidence. For example, the advice to choose reduced-fat dairy products is in stunning contrast to the evidence.

some of the guidelines are in contrast to the evidence

Full-fat dairy

Evidence suggests that full-fat dairy promotes better outcomes for mortality and morbidity than low-fat dairy. Full-fat dairy in combination with a diet high in fruit and vegetables exerts a protective effect against coronary artery disease (an effect not seen with low-fat dairy)¹ and colorectal cancer.² In an investigation of close to 13,000 children (and contrary to the hypothesis of the authors), it was discovered that lower-fat varieties of milk products (and not dairy fat) were associated with weight gain.³ A recent review of the literature by Kratz and colleagues concluded that the recommendation to consume low-fat dairy foods is in contrast to the observational evidence to reduce cardiometabolic risk.⁴

full-fat dairy promotes better outcomes for mortality and morbidity than low-fat dairy

Reducing saturated fat

The recommendation to replace animal, palm, and coconut oils with ‘healthy oils’ from plants is a veiled way to state the old party line of ‘eat less saturated fat!’.

But again, this position is in contrast to the available evidence.

Cardiovascular disease is still the leading cause of death globally. Diet is seen as being the leading contributor to this, along with other lifestyle factors such as exercise, and we are increasingly aware of the roles of stress and mental health, and negative changes to sleeping patterns. Critical to the debate around cardiovascular disease and diet is the topic of saturated fat and whether or not it has a major role to play in the incidence and severity of heart disease and to all-cause mortality.

Cardiovascular disease is still the leading cause of death globally

A Cochrane review (the ‘gold standard’ of reviews) on the effect of modified or reduced-fat interventions on total disease and cardiovascular disease (CVD) mortality showed no appreciable effect of the diets on either,⁵ and other reviews and meta-analyses also fail to find evidence linking reduced saturated fat intake with CVD mortality.^{6, 7}

As previously discussed in The Carb-Appropriate Research Review, the overall evidence does not suggest a strong link between saturated fat and either all-cause or cardiovascular disease mortality and yet, the reduction of saturated fat is still universally recommended. Much of this recommendation relies on substitution data, especially from the Hooper analysis⁸ which has recently been subjected to criticism due to a reanalysis of the data using different (and probably more appropriate) statistical methods which showed no effect of limiting saturated fat for the prevention of cardiovascular disease.⁹ Most importantly though, the Hooper meta-analysis is flawed to support a population-wide restriction of saturated fat because it showed no effect of reducing saturated fat on all-cause mortality!

the overall evidence does not suggest a strong link between saturated fat and either all-cause or cardiovascular disease mortality

Did the Hooper study show benefit from reducing saturated fat?

While there was a small, yet potentially important effect on cardiovascular events associated with reduced saturated fat diets (by approximately 17%) there was no effect on cardiovascular mortality or stroke incidence. The only effect seen was when saturated fat was replaced with polyunsaturated fats, and not when saturated fat was replaced with carbohydrate or monounsaturated fats.

no effect on cardiovascular mortality or stroke incidence

Was the effect observed in the replacement analysis larger because of the statistical methods they used?

In the paper by Thornley et al. mentioned above, the authors explain that the ‘random effects models’ used by Hooper and colleagues to pool their data, has the effect of biasing the results in favour of smaller trials where those disagree with larger. This seems counter-intuitive to the idea that larger numbers are more likely to have greater relevance to populations (‘the law of large numbers’).

In their paper, Thornley and colleagues suggest that “inverse-variance heterogeneity’ analysis is more suitable because it widens confidence intervals, “yet retain[s] the favourable weights of the fixed effect method”. Using this method of statistical analysis, a pooled relative risk of 0.93, with a 95% confidence interval of 0.74 to 1.16 is produced. This means (because the 95% CI overlaps ‘1’) that there is no definitive effect of saturated fat on cardiovascular disease using this analysis.

no definitive effect of saturated fat on cardiovascular disease

What does this all mean?

The one analysis from the Hooper study which showed benefit from reduced saturated fat was for cardiovascular events, however, there are several considerations as to why this may not be a meaningful finding:

1. Greater weighting given to small studies

When smaller studies with a higher risk of publication bias are given a smaller weighting, the effects are no longer significant.

2. No effect when carbs substituted for saturated fat

When carbohydrate is consumed in greater amounts, with a lower intake of saturated fat, there is no reduction in CVD incidence or mortality. This suggests that it’s not the saturated fat that is the problem!

When carbohydrate is consumed in greater amounts, with a lower intake of saturated fat, there is no reduction in CVD incidence or mortality.

3. Positive benefits are only seen when polyunsaturated fats substituted for saturated fat

There was an effect shown when more polyunsaturated fats were consumed and less saturated fats. But because the same effect wasn’t seen with carbs, or with monounsaturated fats, it doesn’t make sense to label saturated fats as ‘bad’ but instead to look deeper into why polyunsaturated fats might be ‘good’ (i.e. greater intake of omega-3 fats, and/or greater intake of vegetables.)

it doesn’t make sense to label saturated fats as ‘bad’ but instead to look deeper into why polyunsaturated fats might be ‘good’

4. No effect on cardiovascular or all-cause mortality

The most important outcome is death. And the most important ‘death’ outcome is the overall rate, not necessarily grouped into different diseases. Put it this way, if we want to see what type of diet is ‘best’ overall, we need to see how many people get diseases, or die, from all causes, not from a particular illness. We don’t see a risk for all-cause or even CVD mortality from saturated fat in the diet.

We don’t see a risk for all-cause or even CVD mortality from saturated fat in the diet.

5. No substantive analysis of food ‘quality’

While ‘quality’ is vague, it is becoming clearer by the day, that more important than macro split in the diet, is how much of the diet is made up by refined and ultra-processed foods. In most observational data we can see a clear trend towards there being a greater impact of processed food and our modern food environment on mortality when compared to the amounts of macros, or sub-groups of macros that are eaten.

a clear trend towards there being a greater impact of processed food and our modern food environment

Adding to the weight of evidence against unnecessary vilification of saturated fat is a recent dose-response meta-analysis by Zhu and colleagues which appraised over 100,000 papers for inclusion and finally analysed 43 publications to determine the effect of saturated fat on cardiovascular mortality outcomes.

Some of the key findings included:

• No effect on cardiovascular risk from total fat intake (RR 0.97; 95% CI, 0.93–1.01)
• No effect of highest vs lowest intakes of saturated fat on cardiovascular risk (RR 0.97; 95% CI, 0.93–1.02)
• No influence of monounsaturated fat on cardiovascular disease risk (RR 0.97; 95% CI, 0.93–1.01)
• No effect of highest vs lowest intakes of polyunsaturated fats on cardiovascular disease risk (RR 0.97; 95% CI, 0.93–1.004)
• Highest vs lowest intakes of trans-fatty acids were associated with increased risk of cardiovascular disease (RR 1.14; 95% CI, 1.08–1.21)

Trends were observed for reduced risk with increased fat intake overall, increased saturated fat (to around 30% of calories), and monounsaturated fat, with reduced risk from baseline for increased % of calories from polyunsaturated fats, and worsened risk with increased intakes of trans-fats.¹⁰ When absolute intakes (grams per day) were analysed the results are even less clear as you can see in the graphs below.

reduced risk with increased fat intake overall, increased saturated fat

What does this tell us overall?

This study is consistent with the existing research. While some studies show an exceedingly small potential risk from saturated fats, others show no association or even benefit.

The overall effect, if there is any, is so small as to be ‘statistical noise’. In this particular study, the small effect sizes cross over the ‘risk line’ of 1.0 (meaning that we can’t be sure whether they benefit or harm) leaving us to conclude that they probably have no effect whatsoever.

The overall effect, if there is any, is so small as to be ‘statistical noise’.

This is true not just for saturated fats, but for all fat types and fat intake overall. The only fat to show harm is trans-fat and even that has a fairly modest effect. Not that I suggest people eat trans-fats but the harm from inadvertently ingesting small amounts of trans-fats is likely to be minimal and some naturally occurring trans-fats are likely to be health-promoting (like vaccenic acid from meat and dairy).

The only fat to show harm is trans-fat and even that has a fairly modest effect.

As mentioned, some studies (including the Hooper meta-analysis) do show a positive effect on mortality or morbidity when saturated fat replaces polyunsaturated fats (PUFAs). However these also fail to find the same effects when monounsaturated fats or carbohydrates replace saturated fat,^11-16 so we can only determine from these studies that PUFAs (in particular the Omega 3 fats) are beneficial, not that saturated fats are harmful.

In a study published in the British Medical Journal,¹⁷ 18 well-known researchers have disputed the World Health Organisations dietary guideline to reduce saturated fat to less than 10% of daily calories, and have stated that this dietary guideline is not backed by evidence.

The authors summarised the key points of the paper as:

• 2018 WHO draft guidelines on dietary saturated fatty acids and trans-fatty acids recommend reducing the total intake of saturated fat and replacing it with polyunsaturated and monounsaturated fatty acids
• The recommendations fail to consider evidence that the health effects of saturated fat vary depending on the specific fatty acid and food source
• Maintaining general advice to reduce total saturated fatty acids will work against the intentions of the guidelines and weaken their effect on chronic disease incidence and mortality
• A food-based translation of the recommendations for saturated fat intake would avoid unnecessary reduction or exclusion of foods that are key sources of important nutrients

Overall, the take-home message is that your overall fat intake, or the type of fat that you consume, is not likely to be a significant modifier of your future health. The key priority should be, that the fats, and the foods overall that you consume, are mostly natural, whole, and unprocessed wherever possible.

your overall fat intake, or the type of fat that you consume, is not likely to be a significant modifier of your future health

Should we reduce red meat intake?

The primary reason provided for reducing red meat is because of its high saturated fat content (around 50% of the fat in meat is saturated). However, according to the evidence, this does not increase all-cause or CVD mortality risk.

So, we need to look directly at the evidence for meat and mortality outcomes. The primary evidence used to support the Heart Foundation position was a meta-analysis by Bechthold et al.,¹⁸ which showed a 16% increase in heart disease and stroke risk between the lowest and highest meat consumers. Additionally, a meta-analysis by Schwingshakl and colleagues demonstrated an ~10% increase in mortality risk[1] for those eating greater quantities of red meat.¹⁹

So, the evidence at least suggests some, albeit small relative risk from eating red meat…but is that the whole story?

It must be remembered that these risks are statistically exceedingly small, confounded, and prone to influence that cannot be adequately accounted for by statistical adjustment.

these risks are statistically exceedingly small, confounded, and prone to influence that cannot be adequately accounted for by statistical adjustment

For example, I discussed in a past Carb-Appropriate Review a very widely reported prospective cohort study Association of changes in red meat consumption with total and cause-specific mortality among US women and men: two prospective cohort studies by Yan Zheng and colleagues which concluded “Increases in red meat consumption, especially processed meat, were associated with higher overall mortality rates.²⁰ However, in this study, as in the meta-analyses above, the association shown between increased red meat intake of ½ serving per day and the risk of early death is quite low. A hazard ratio of 1.1 is equivalent to a 10% greater risk of death over the 8-year study period. This might seem compelling but is exceptionally low when we consider the 95% confidence intervals (1.04-1.17) and that small hazard ratios are inaccurate for showing causation because of the large array of other factors that could affect the outcome.

---

[1] RR: 1.10; 95% CI: 1.04, 1.18

In this study, attempts were made to adjust for baseline and change in factors such as smoking, alcohol use, diabetes, heart disease, cholesterol, total energy intake, consumption of food groups (sugar, fruit, vegetables, whole grains) and exercise. However, it is extremely difficult to effectively model for all of these and when the hazard ratio is low, the result is typically considered to be statistical noise.

This ‘noise’ is further exacerbated when lifestyle factors that could affect the outcome accumulate.

What factors affect mortality outcomes?

In this cohort, the group that reduced red meat intake the most over the 8-years (and had the lowest risk of mortality) also reduced alcohol, and increased activity the most, with the smallest increase in weight (Figure 1). This is an example of confounding influences and the effects of committed ‘health changers’ undertaking multiple healthy habits.

This is an example of confounding influences and the effects of committed ‘health changers’ undertaking multiple healthy habits.

The groups also had a linear association between energy intake (calories consumed per day) and red meat decrease/increase and, given that energy intake is one of the key factors for obesity, metabolic syndrome and future health risk (see Can You Be Healthy at Every Size) this is a major flaw in this study. (Figure 4.)

So, there are several factors to ‘unpick’ here which can be informative for the entire saturated fat debate. There are a large number of other lifestyle factors that affect cardiac and general health outcomes. And, perhaps more importantly, the lifestyle factors above suggest that those with baseline markers like high cholesterol were advised to reduce red meat…AND alcohol and to exercise, and reduce portions. This is an example of a bias in study outcome based on highlighting committed health changers. In other words, the people who wanted to be healthier engaged in a range of health behaviours and made health changes, one of which was reducing red meat…but this might not have had any impact at all on later outcomes.

those with baseline markers like high cholesterol were advised to reduce red meat…AND alcohol and to exercise, and reduce portions

This is consistent with the advice provided at the time (in the low-fat crazed 1980s from which this data was drawn). Those who did reduce meat intake also reduced those factors indicated above and this also suggests that they were more active in their health.

While the effects of a reduction in fat, saturated fat and animal have little effect on health outcomes, an increase in natural unprocessed foods, reduced red-meat containing convenience foods (such as hamburgers and pizza which are typically found with high prevalence in these types of cohorts), reduced alcohol, and better energy balance and reduced weight gain are all-powerful impactors of health and so, that is likely to be the effect we are observing. Again, those who take positive health steps are typically more motivated, more active in their health, and achieve better results. This is a clear and undeniable fact that we have seen replicated thousands of times in the literature.

those who take positive health steps are typically more motivated, more active in their health, and achieve better results

The small percent increase in mortality from increased red meat consumption is not robust enough to warrant concern, especially when we see the range of other factors that have a higher likelihood of being responsible (in concert) for improving outcomes. Most importantly, it is highly likely that those who took control of their health by eating ‘better’ overall, regulated their energy intake, drank less alcohol, and were more active, achieved better results. So, eat natural foods, move, drink little alcohol (a little is fine!) and make sure that your diet allows both freedoms to live, AND an appropriate energy balance for you.

So, eat natural foods, move, drink little alcohol (a little is fine!) and make sure that your diet allows both freedoms to live, AND an appropriate energy balance for you.

Isn’t red meat carcinogenic?

This is correct but also flawed. Processed meats have a much stronger association with cancer than red meat, which is why some caution should be exercised with them but they are often lumped in with red meat or total meat (including white meats) and this confuses the issue of whether red meat is a significant factor in cancer development.

Processed meats have a much stronger association with cancer than red meat

Several other important things need to be considered:

1. World Health Organisation classifications for grouping of carcinogens reflect the strength of evidence that something can cause cancer, not that eating it WILL cause cancer
2. The WHO classifications characterise risk, not the risk related to dose and exposure
3. Therefore, small amounts of known carcinogens may not provide for any meaningful increase in risk

small amounts of known carcinogens may not provide for any meaningful increase in risk

That notwithstanding, the risks from red meat are far lesser than that of processed meats and again, any risks are both dose-dependent and need to be considered in the context of the diet overall.

So, what does this all mean?

While there might be some marginal statistical increase in risk from eating meat, conversely, this is unlikely to affect the quality or length of life in any meaningful way. Other lifestyle factors of activity, choosing refined foods, getting enough sleep, reducing the impact of media and stress, eating more vegetables, ensuring optimal intakes of protein and omega 3 fats, and ensuring general nutrient repletion are far more important. Indeed, if red meat is eschewed, there is some population-level risk of increasing nutrient insufficiencies which are already a major impactor of human health.

In short, in the context of a healthy diet and lifestyle, there is no need to reduce red meat intake.

In short, in the context of a healthy diet and lifestyle, there is no need to reduce red meat intake.

References

1.         Holmberg S, Thelin A, Stiernström E-L. Food Choices and Coronary Heart Disease: A Population Based Cohort Study of Rural Swedish Men with 12 Years of Follow-up. Int J Environ Res Public Health. 2009;6(10):2626-38.

2.         Larsson SC, Bergkvist L, Rutegård J, Giovannucci E, Wolk A. Calcium and dairy food intakes are inversely associated with colorectal cancer risk in the Cohort of Swedish Men. The American Journal of Clinical Nutrition. 2006;83(3):667-73.

3.         Berkey CS, Rockett HH, Willett WC, Colditz GA. Milk, dairy fat, dietary calcium, and weight gain: A longitudinal study of adolescents. Archives of Pediatrics & Adolescent Medicine. 2005;159(6):543-50.

4.         Kratz M, Baars T, Guyenet S. The relationship between high-fat dairy consumption and obesity, cardiovascular, and metabolic disease. Eur J Nutr. 2013;52(1):1-24.

5.         Hooper L, Summerbell CD, Thompson R, Sills D, Roberts FG, Moore H, et al. Reduced or modified dietary fat for preventing cardiovascular disease. Cochrane Database Syst Rev. 2011(7):CD002137.

6.         Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. The American journal of clinical nutrition. 2010;91(3):535-46.

7.         Mente A, de Koning L, Shannon HS, Anand SS. A systematic review of the evidence supporting a causal link between dietary factors and coronary heart disease. Arch Intern Med. 2009;169(7):659-69.

8.         Hooper L, Martin N, Abdelhamid A, Davey Smith G. Reduction in saturated fat intake for cardiovascular disease. The Cochrane database of systematic reviews. 2015(6):Cd011737.

9.         Thornley S, Schofield G, Zinn C, Henderson G. How reliable is the statistical evidence for limiting saturated fat intake? A fresh look at the influential Hooper meta-analysis. Internal Medicine Journal. 2019;0(ja).

10.       Zhu Y, Bo Y, Liu Y. Dietary total fat, fatty acids intake, and risk of cardiovascular disease: a dose-response meta-analysis of cohort studies. Lipids in Health and Disease. 2019;18(1):91.

11.       Mozaffarian D, Micha R, Wallace S. Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Med. 2010;7(3):e1000252.

12.       Jakobsen MU, O’Reilly EJ, Heitmann BL, Pereira MA, Balter K, Fraser GE, et al. Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Am J Clin Nutr. 2009;89(5):1425-32.

13.       Skeaff CM, Miller J. Dietary fat and coronary heart disease: summary of evidence from prospective cohort and randomised controlled trials. Ann Nutr Metab. 2009;55(1-3):173-201.

14.       Turpeinen O, Pekkarinen M, Miettinen M, Elosuo R, Paavilainen E. Dietary prevention of coronary heart disease: the Finnish Mental Hospital Study. International Journal of Epidemiology. 1979;8(2):99-118.

15.       Ramsden CE, Zamora D, Leelarthaepin B, Majchrzak-Hong SF, Faurot KR, Suchindran CM, et al. Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis. BMJ. 2013;346.

16.       Madsen L, Kristiansen K. Of mice and men. 2012.

17.       Astrup A, Bertram HCS, Bonjour J-P, de Groot LCP, de Oliveira Otto MC, Feeney EL, et al. WHO draft guidelines on dietary saturated and trans fatty acids: time for a new approach? BMJ. 2019;366:l4137.

18.       Bechthold A, Boeing H, Schwedhelm C, Hoffmann G, Knüppel S, Iqbal K, et al. Food groups and risk of coronary heart disease, stroke and heart failure: A systematic review and dose-response meta-analysis of prospective studies. Crit Rev Food Sci Nutr. 2019;59(7):1071-90.

19.       Schwingshackl L, Schwedhelm C, Hoffmann G, Lampousi AM, Knüppel S, Iqbal K, et al. Food groups and risk of all-cause mortality: a systematic review and meta-analysis of prospective studies. Am J Clin Nutr. 2017;105(6):1462-73.

20.       Zheng Y, Li Y, Satija A, Pan A, Sotos-Prieto M, Rimm E, et al. Association of changes in red meat consumption with total and cause specific mortality among US women and men: two prospective cohort studies. BMJ. 2019;365:l2110.