Review Sows Confusion About Saturated Fats

By distorting evidence, a recent review in The Journal of the American College of Cardiology will result in more harm than benefit

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Key Takeaways

  1. Authors of this JACC State of the Art review state that the United States’ Dietary Guideline recommendations to reduce saturated fat are not justified due to the existence of evidence suggesting it may not increase the risk of CVD.
  • Consistent evidence from dozens of RCTs and meta analyses of prospective cohorts including millions of participants has confirmed the role of saturated fat in increasing CVD risk, and the benefit of replacing it with PUFAs and high quality carbohydrates.
  • This rhetoric inappropriately instills a fear of carbohydrates in the reader due to their perceived negative impact on health. Such claims are highly misleading given that many foods rich in carbohydrates, such as legumes, whole grains, fruits, and vegetables, offer a myriad of health benefits and reduce the risk of CVD, metabolic syndrome, diabetes, hypertension, and many other common diseases.
  • Current recommendations clearly emphasize replacing saturated fat with PUFAs, MUFAs, and/or unrefined carbohydrates, so this discussion is tangential and unproductive.
  • Most of the exceptions the authors present to strengthen their argument (CETP inhibitors, progestin and estrogen therapy, and Mediterranean diet interventions) are actually characterized by changes (or lack thereof) in CVD risk consistent with those seen in LDL, and others are explained by observed changes in other metrics known to influence risk.
  • While small, dense LDL can correlate strongly with increased CVD in univariate analysis, it typically fails to maintain predictive power after multivariate adjustment for triglycerides and HDL. This is likely because it is part of a broader pathophysiology (e.g. high triglycerides, low HDL cholesterol, increased LDL particle number, obesity, insulin resistance, diabetes, metabolic syndrome) that accelerates atherosclerosis, not due to it have a greater intrinsic ability to increase the risk of cardiovascular disease.
  • The evidence on what constitutes a healthy dietary pattern is fairly strong and consistent, with most heterogeneity in outcomes from intervention trials being explained by differences in macronutrient quality, adherence, age, baseline, disease, and other well-acknowledged factors.
  • Genetic differences in responses to saturated fat discussed by the authors here don’t provide any rationale for dismissing its role in disease risks, and if anything emphasize that some groups may benefit to an even greater extent than others.
  • The evidence given for full fat cheese and yogurt is riddled with problematic methodology, including adjustments for serum cholesterol, lack of consideration for comparators, and populations with low mean intakes that prevent meaningful observations of the resulting CVD risk from being made.
  • Isocaloric substitution of dairy fats with omega 6 fatty acids, alpha linoleic acid, marine omega 3 fatty acids, and carbohydrates from whole grains significantly reduce CVD and stroke risk.
  • In accordance with these findings, controlled trials on cheese indicate it may increase LDL slightly less than butter, but only in those with baseline high values. However, it significantly increases LDL when compared to tofu, reduced fat cheese, and egg whites. Trials specifically on yogurt are lacking, but those involving an increase in full fat yogurt, cheese, and milk consumption reveal an LDL cholesterol raising effect.
  • RCTs on red meat demonstrate a similar cholesterol raising effect when compared to lower saturated fat alternatives, and numerous meta analyses and large pooled cohorts repeatedly demonstrate it significantly elevates CVD, type 2 diabetes, colorectal cancer, and stroke risk.
  • Additionally, there are numerous other foods, such as legumes, whole grains, tubers, nuts/seeds, and fish, that would not only offer a broad variety of nutrients, but would also confer substantial protection against many of the most common chronic diseases rampant in current day societies.
  • The dietary guidelines aren’t directed towards subgroups such as the elderly and malnourished, again leaving one questioning why such remarks are being made. Regardless, the aforementioned foods could serve a similar role as cheap, nutrient dense staples, and evidence suggests such patterns are associated with beneficial impacts on the health of the elderly.
  • No nutrients found in full fat dairy, unprocessed red meat, or chocolate that can’t be sourced from lower fat alternatives or other health promoting foods are even discussed.
  • In addition to the reality that a high saturated fat intake is not a necessity for a lower carbohydrate diet, the authors only cite a single short term trial that suggests they possess any sort of a beneficial effect on metabolic disease endpoints, hardly enough to even spark interest, and nowhere near that required to justify incorporating into population wide guidelines.
  • Even though the review incessantly attacks the dietary guidelines for giving advice centered only on nutrients, the reality is that they primarily emphasize exactly what the authors are demanding; specific foods and food groups that constitute a healthy dietary pattern. Only in addition to these do they offer specific nutrient recommendations that are based on the totality of the high quality evidence, not an inherent bias.
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The Origin of Recommendations to Reduce Saturated Fat Intake

The review begins by briefly discussing the history behind the initiation of dietary goals and recommendations to lower saturated fat intake dating back to the 1970s. It details that since the 80s, there have been specific goals of reducing saturated fat intake to less than 10% of total calories to reduce CVD risk. The authors declare that their main intention is to answer the question posed by the United States Department of Agriculture and Health and Human Services’ in 2018; “What is the relationship between saturated fat consumption (types and amounts) and the risk of CVD in adults?” by reviewing the effects of saturated fats on health outcomes, risk factors, and mechanisms underlying CVD and metabolic outcomes. The question is whether the review provides a sufficient answer that is backed by a substantial body of evidence, which will become quickly apparent is far from the case.

Inconsistent Results: A Cause for Confusion?

Harcombe et al, de Souza et al, Siri-Tarino et al, and Zhu et al.

Reviews on prospective cohort studies and case-control assessing the relationship between saturated fat intake and CVD by Harcombe et al., de Souza et al., Siri-Tarino et al., and Zhu et al. fall victim to the same major methodological problem. This is the inclusion of an appreciable amount of cohorts which adjusted for serum cholesterol or baseline hypercholesterolemia (5/10, 1/3, and 5/11 cohorts in de Souza for total CHD incidence, CVD mortality, and CHD mortality, 7/16 and 4/8 in Siri-Tarino for CHD and stroke events, 3/6 in Harcombe et al., and 14/40 and 7/22 in Zhu et al. for CHD in the highest vs. lowest comparison and dose-response analysis, respectively). The action of adjusting for a moderator variable (in this case LDL-c, which is increased by saturated fat and increases the risk of CVD) that lies on the causal chain of the outcome of interest pulls the results of the analyses towards null, creating a biased and inaccurate observation of the real relationship. Because nearly half of the cohorts in each of these reviews make such adjustments, any effect would be significantly muted. Scarborough et al. discuss this very issue in their comment responding to Siri-Tarino et al.’s authors closely following its publication22. While there are additional issues that may also contribute to the lack of effect, such as little to no variance in saturated fat intake among cohort’s sample population, the inclusion of multiple cohorts with intakes all above or below the threshold where the majority of the observed increase in CVD risk is detected, failure to disclose review protocols, and inclusion of only CVD mortality metric; just this alone is enough to invalidate the results of these reviews. Lastly, despite these over-adjustments, trans fat was still associated with significant increases with CHD mortality and CVD in Zhu et al., and de Souza et al., which will prove to be an important consideration concerning some of the other reviews.

Ramsden and Hamley

Apart from the four reviews just discussed, two additional reviews have suggested there may not be an association between saturated fat intake and CVD, one of which the authors of the JACC mentioned in their brief comments on the subject. Ramsden et al. and Steven Hamley carried out these reviews, both including randomized controlled trials focused on determining the potential benefit of replacing SFAs with mostly polyunsaturated fatty acids (PUFA). Ramsden et al’s review included discussion of recovered data from the Minnesota Coronary Experiment (MCE) and also carried out a meta-analysis of an additional 4 RCTs, the Sydney Diet Heart Study (SDHS), the Rose Corn Oil Trial (RCOT), the Los Angeles Veterans Trial (LA Vet), and the Medical Research Council Soy Oil Trial (MRC-Soy). They also performed a sensitivity analysis on the previous 5 in addition to 3 more, the Diet and Re-Infarction Trial (DART), the Oslo Diet-Heart Study (ODHS), and the St. Thomas Atherosclerosis Regression Study (STARS). Not only was the MCE flawed in numerous ways that prevented meaningful conclusions from being drawn, but there were also multiple issues with the other smaller trials included in their analysis (for which MCE ended up weighed the most). As for the MCE, the main problems were the insufficient power to detect effects on mortality due to the high dropout rate (>75%), utilization of likely trans-fat-containing margarine in the intervention group, the main difference in mortality being observed only in subjects over 65 years of age, and the lack of essential metrics such as smoking status, LDL cholesterol, detailed dietary intake data, weight loss, and coronary disease status. The smaller size (and weaker statistical power), exclusion of mortality as the primary endpoint, and inclusion of trans-fat-based margarine in the experimental group of another trial (SDHS) were further issues that rendered the findings of the analyses unuseful. As for Hamley’s review of RCTs, he chose to exclude individual trials based on “inadequate control,” and other factors that he posits would impact the results, including suspicions that the control group had a higher trans fat intake, were exposed to cardiotoxic medications and had lower vitamin E intake. His meta-analysis ended up incorporating the same trials as Ramsden et al. ‘s, with the one exception being LA VET, which he replaced with DART. Ironically, this means he included both MCE and SDHS, which exposed the intervention groups to higher trans fat intake, alongside other small studies underpowered to detect meaningful effects on the chosen endpoints.

2020 Cochrane Review

Directly contradicting both of these trials is the recent Cochrane Review on reducing saturated fat for cardiovascular disease. This publication was subject to far more rigorous pre-review protocols and analyzed the results of 15 RCTs (even including SDHS) to find that long-term reductions in saturated fat intake resulted in significant reductions in combined cardiovascular events17. Furthermore, they conducted a meta-regression that demonstrated more significant reductions in saturated fat (and consequently, more significant reductions in cholesterol) led to greater events reductions. Unfortunately, no such regression was carried out for CVD mortality. However, in the subgroup analysis stratifying by absolute saturated fat reduction, a clear trend towards significant decreases in mortality can be observed, with the trial in which the most notable reduction was achieved reaching significance (Veterans Admin).

Chemical Structure of Saturated Fatty Acids

Next, the review moves on to discuss the variation in chemical structures of SFAs found in a wide variety of foods, explaining that SFAs vary based on their carbon chain length, their melting point, and state at room temperature (solid vs. liquid), the presence or absence of methyl branches (branched vs. straight-chain fatty acids), and their origin (exogenous vs. endogenous). Furthermore, they exclaim that food sources of such SFAs contain different proportions of specific fatty acids and other nutrients that impact their physiological and biological effects. They continue, saying “Branched-chain SFAs are found primarily in dairy, beef, and other ruminant-derived foods (13), and have similar physicochemical properties as unsaturated fatty acids, in particular lower melting point (or more accurately, phase transition temperature). In experimental animal studies, branched-chain fatty acids alter the microbiota composition in the direction of microorganisms that use these fatty acids in cellular membranes (14), and because they are normal constituents of the healthy human infant gut (15), these fatty acids could play a role in normal colonization.” It seems odd for them to be focusing on mechanistic studies in animal models (given the variability in their relevance to humans) in order to insinuate some innate requirement for these fatty acids, especially given that they also bring up the ability of intestinal flora and the liver to synthesize them shortly after that. That being said, the comment is followed by a remark that fatty acids are synthesized de novo from “excess carbohydrate and protein” and reference to a study linking specific plasma phospholipid concentrations of fatty acids and adverse cardiovascular outcomes, seemingly hinting at the notion the process is inherently harmful. However, that may not be the case. They then re-emphasize the earlier point that different circulating saturated fatty acids exert differing effects on blood lipids, glucose-insulin homeostasis, insulin resistance, and diabetes. While this is certainly a valid point, it does not purely suggest such effects follow changes directly resulting from consumption of the respective fatty acids given the potential for de novo synthesis and various pathophysiological processes to exert effects on plasma concentrations. This section’s final paragraph raises concerns regarding the failure to distinguish between fat and fatty acids, saying that the former comprises fatty acids in differing proportions and other components such as glycerol. Another valid point, but not necessarily pertinent to any of the claims they have put forth so far.

The Effects of Saturated Fat on Health

Old Research, Shifting Dietary Patterns, and Lessons from Finland

The next section of the review directs its focus towards the evidence on saturated fat’s health effects. Like the earlier paragraph briefly discussing the matter, the authors make numerous claims that are extremely misleading and not backed by the majority of the scientific literature. They begin by offering up typical rhetoric about current guidelines being based upon observations from ecologic research (including the Seven Countries Study) throughout the 1950s on diet and coronary heart disease. Next, they exclaim, “In recent decades, however, diets have changed substantially in several regions of the world. For example, the very high intake of saturated fat in Finland has decreased considerably, with per capita butter consumption decreasing from ∼16 kg/year in 1955 to ∼3 kg/year in 2005, and the percent energy from saturated fat decreasing from ∼20% in 1982 to ∼12% in 2007 (28). Therefore, the dietary guidelines that were developed based on information from several decades ago may no longer be applicable.” First, the fact that diets have changed in recent decades is not at all reason to completely dismiss previously established guidelines, and even more astonishing, the specific country they mention (Finland) is a prime example of evidence cutting directly against their position. The same article they reference explains the implementation of a widespread preventative health intervention originating in North Karelia (and later expanding to other regions in Finland) that aimed to modulate citizen’s dietary habits, mainly focusing on reducing saturated fat intake and replacing it with unsaturated fat, as well as increasing vegetable intake, and reducing sodium intake. This program’s results, which have been demonstrated to be attributed almost entirely to dietary changes, were that the working-age population experienced a considerable reduction in blood cholesterol levels and a remarkable 80% reduction in annual CVD mortality rates23. However, the authors of the JACC review make no mention of this whatsoever.

Queue the War on Carbohydrates

After this, they bring up what they claim to be a few large and well-designed prospective cohorts carried out recently that supposedly demonstrate replacing saturated fat with carbohydrate does not result in a lower risk of coronary heart disease, and may increase mortality risk8, 24,25. However, one of these is an editorial (Hu 2010) and echoes what the results from the other two (Jakobsen et al. 2009 and Liu et al. 2000) demonstrate, which is that replacing saturated fat with refined carbohydrate does not reduce, and may increase, the risk of CVD. Additionally, Jakobsen et al. showed that the replacement of SFAs with PUFAs elicited significant reductions in both CVD events and mortality. Hu’s editorial declared that increased intake of refined carbohydrates and SFA were independent risk factors for CVD. Moreover, although he believes that reducing refined carbohydrate intake may be most important, he states that low fat, high complex carbohydrate or moderately restricted carbohydrate diets rich in fat and protein from vegetable sources may confer protection against CVD. This is surprising given that the authors spent quite a bit of time discussing the importance of not looking at saturated fat as a single uniform nutrient, yet they are willing to do it for carbohydrates. Once again, this shows they are making misleading statements and providing studies that either do not relate to their position or invoke evidence contradicting it. They continue by saying, “Furthermore, a number of systematic reviews of cohort studies have shown no significant association between saturated fat intake and coronary artery disease or mortality, and some even suggested a lower risk of stroke with higher consumption of saturated fat (3,6,32,33).” The significant issues with three of these have been addressed previously (Zhu et al., de Souza et al., and Siri-Tarino et al.), and the fourth is on saturated fat intake and its potential protective effect against stroke26, which is a separate consideration entirely. The authors end this paragraph by commenting on a meta-analysis of prospective cohorts demonstrating that biomarkers of long-chain SFAs in plasma or serum were not associated with CHD27. It is entirely unclear as to why this was included, given that previous similar publications have noted these SFAs in plasma are unlikely to result from diet28. Not only that, only shortly after the authors claim that “it is important to distinguish between dietary saturated fat and serum SFAs”.

PURE and UK Biobank

Next, they refer to the PURE study, and although this study was an incredibly ambitious undertaking, it is unfortunately ridden with numerous critical flaws that dozens of researchers have discussed via comments responding to the original publication. As the JACC review’s authors discuss, 80% of the sample population was from low- and middle-income countries, which explains the origin of one of its most massive blunders; bias from malnutrition. In addition to focusing on lower-income countries, authors included energy intakes down to as low as 500 kcal/day. Higher carbohydrate consumption as a percentage of energy and the consequential lower percentage from fat was strongly correlated with low income, food availability, pollution, and healthcare access29,30. Therefore, comparing increasing quintiles of fat consumption to the lowest quintile is essentially comparing to a likely malnourished population. Even just minor decreases in the incidence of death and disease would deem fat intake protective when, in reality, an unfair comparison is just skewing the results. Further issues are failure to report the type of food frequency questionnaire used, lack of baseline health status and adjustment, failure to distinguish between types of carbohydrates, and large differences in the data from PURE and China Health and Nutrition Survey (CHNS) on China’s fat intake31–33. Finally, it seems the JACC review’s authors again selectively choose to showcase the observations they feel support their assertions and ignore those that do not, remarking that stroke incidence is reduced with increased saturated fat consumption. They fail to mention that rates of myocardial infarction are highest in the top quintile (the fact this does not factor in adjustments for confounders prior to calculation of an HR is unfortunate, and it would undoubtedly be of interest to see the resulting values). Further, mortality and incidence of all other observed outcomes were lowest in the third and fourth quintiles of saturated fat intake, which are unsurprisingly those where subject’s intakes were below 10% of their total caloric intake. In a demonstration of consistency, they then cite a recent prospective cohort of UK Biobank participants, exclaiming that it does not show an association between saturated fat and incident CVD, and that “Although there was also a positive relation of saturated fat intake with all-cause mortality, this became significant only with intakes well above average consumption.” While the former was shockingly correct, the latter was not, as the relation between saturated fat intake and all-cause mortality became significant at above around 12% of calories (Figure 1), with the average intake of the study’s sample being over 13% (seen in Table S2)34. To follow that up, in a sentence mentioning the macronutrient distributions associated with the lowest hazard ratio for all-cause mortality, they conveniently leave out a few lines following what they quote, which happened to be, “…5–10% from SFA (2.66 v 3.59 per 1000 person-years, 0.67 (0.62 to 0.73) compared with high (20% of energy) intake)…”, clearly emphasizing the benefit of reducing saturated fat intake to 5–10% of calories. Lastly, they declare that for dietary carbohydrate, higher consumption (from starch and sugar) is associated with higher CVD and mortality, and there is little need to restrict intakes of total or saturated fat for most populations in the context of contemporary diets, where reducing refined carbohydrates may be more relevant for decreasing the risk of mortality in individuals with insulin resistance and type 2 diabetes. While their final point is an important consideration, these conditions and refined carbohydrates’ contribution to adverse health outcomes are not being ignored. Oddly, they do not recommend reductions in refined carbohydrates and saturated fat, which is strange when considering the pattern with the lowest hazard ratio for all-cause mortality involves precisely that. Lastly, the dietary guidelines their entire review has set out to criticize do indeed suggest that refined carbohydrate and saturated fat intake should be reduced, and highlight healthy food patterns that will help achieve such reductions35, leaving one questioning what issues they have with them.

The Women’s Health Initiative, PREDIMED, and Faulty RCTs

Following the discussion of PURE and the UK Biobank data is another common talking point among skeptics of the diet-heart hypothesis; that the evidence for the dietary guidelines recommendations to reduce SFAs had important methodological flaws, one being that they were small in size. Authors then bring up the Women’s Health Initiative (WHI), one of the larger and more recent trials on reducing CVD via lifestyle intervention, and briefly remark that the low-fat diet providing 9.5% of calories from saturated fat did not reduce the risk of heart attack or stroke. Again, numerous relevant details are being left out. The major one is that based on the failure of subjects to reach the studies adherence assumptions (that the intervention group would reduce the percentage of energy from total fat 13% and 11% compared to the control group at 1 and 9 years, respectively, and the control group incidence rate would be one third greater), the projected power to detect differences in CHD was only 40%36. The researchers’ chance to detect a difference between the intervention and control group was already incredibly low based on this limited power. This was further compounded by the less than moderate beneficial changes in the intervention group (and even some potentially detrimental ones) in comparison to the control group. Such paltry changes included a difference of weight loss of about 1 kg after three years, a less than 3% and 1% reduction in calories from saturated and trans fat, respectively, and a one serving difference in fruit and vegetable intake. Harmful alterations were increased refined grain consumption and decreased intake of nuts. As such, the changes in biomarkers of interest in the intervention group, especially LDL-c, were similarly small, with the reduction being 3 mg/dl greater than the control. Given these factors, it is unsurprising that no significant reduction in risk was seen. However, despite the extremely limited power, when authors directed their attention towards subjects who achieved the lowest intake of saturated fat (<6% of energy), they remarkably still observed a marginally significant reduction in CHD risk. This once again demonstrates the value of reducing intake of saturated fat, even in a relatively healthy population with a lower baseline intake (~13% of energy) and a lower overall incidence of CHD (<1% of the subjects over about eight years of follow up). Moving onward, they bring up PREDIMED, saying, “Despite an increase in total fat intake by 4.5% of total energy (including slightly higher saturated fat consumption), major cardiovascular events and death were significantly reduced compared with the control group.” It is unclear how they even came to this conclusion, given that the supplementary data from the study itself shows that both the intervention groups reduced their intake of saturated fat as a percentage of calories from 10% to just about 9% (Table S9)37. It is also worth noting that they reduced red meat and dairy consumption, both of which are foods this review’s authors seem to emphasize there shouldn’t be limits on the consumption of. They then conclude this paragraph by claiming that the six most recent reviews and meta-analyses of RCTs demonstrated that replacing saturated fat with polyunsaturated fat does not significantly decrease coronary outcomes or total mortality, citing three publications (Ramsden et al. 2016, Hooper et al. 2015, and Hamley 2017.). Two of these have major problems that have been previously addressed, and the highest quality review (Hooper) demonstrated a significant benefit of reducing saturated fat intake on CVD events. Also, in their updated 2020 review mentioned earlier, their meta-regression indicated that the extent of saturated fat reduction and the corresponding decrease in serum cholesterol was responsible for said effect. After the previous comment, authors then state, “Even if these analyses were to be challenged, for example, based on the criteria for study selection or other lines of evidence (42), an important possibility to consider is that an apparently lower risk of CVD with substitution of SFAs by polyunsaturated fatty acids could be attributed to a possible beneficial effect of polyunsaturated fatty acids and not necessarily to an adverse effect of SFAs”, followed by, “…the evidence from both cohort studies and randomized trials does not support the assertion that further restriction of dietary saturated fat will reduce clinical events.” Firstly, the initial statement is quite a speculation given that reducing saturated fat or replacing it with PUFAs, certain MUFAs (such as olive oil and nuts in PREDIMED), and whole grains consistently reduces CVD events38. Second, even if this were true, why would one choose to consume a nutrient that does not lower the risk of the leading cause of death in the United States over almost all others (aside from refined carbohydrate)? After considering that almost everything the authors have cited up to this point has had notable flaws they failed to disclose, and that many of their sources cut against their position, the erroneous nature of the closing statement for this section is incredibly clear.

LDL, Insulin Resistance, Carbohydrate Condemnation, and Circulating Fatty Acids

Questioning the Utility of Serum LDL-c

In the next section, the authors attempt to instill doubt in the reader about the utility of LDL cholesterol as a biomarker for assessing the effect of saturated fat on cardiovascular risk. After declaring that it is quite clear LDL plays a causal role in the development of CVD, they stipulate that the reduction of LDL through diet cannot be inferred to result in CVD benefit without having the means to assess other biological effects that accompany this reduction. Whether or not there are means to assess other biological effects (which there are), as repeatedly displayed throughout this entire commentary, saturated fat reduction consistently and reliably reduces CVD incidence, so this point is entirely tangential. To follow up this stipulation, they note that postmenopausal estrogen plus progestin therapy and cholesteryl ester transport protein (CETP) inhibitors elicit no CVD benefit despite decreasing LDL cholesterol. They make mention of Mediterranean style interventions and pharmaceutical inhibition of sodium-glucose cotransporter type 2’s ability to reduce CVD risk while increasing LDL, suggesting that these supposedly unexplained deviations from the typical pattern somehow denigrate the relationship between dietary reductions of LDL and CVD risk. As for the increased risk associated with estrogen and progestin therapy, subgroup analysis showed that the risk was driven by those with the highest baseline LDL, for whom even the observed maximum reduction in LDL would not bring close to a normal value (Figures 1 and 4)39. The reference they cite for CETP inhibitors clearly describes the reasons for discrepancies in the results of four different trials. It highlights the success of anacetrapib (which did significantly reduce CVD events) being due to the trials’ longer duration and its sustained effect on LDL-c (or non-HDL-C/apoB). The other trials were of substantially shorter duration, or resulted in less notable reductions in LDL-c, explaining the variance in observed results40. Regarding the Mediterranean-style interventions reducing CVD risk, the two trials they cite are the Lyon Diet Heart Trial and a subgroup study of LDL oxidation biomarkers in PREDIMED participants. This is odd given that both demonstrated that significant reductions in LDL from reducing/replacing dietary saturated fat conferred protection against CVD, precisely the opposite of what they claimed these interventions show. Finally, given the positive benefit of SGCT2 on blood glucose and blood pressure, its ability to offer nephroprotection in CKD (which can compound the risk of CVD events in those with an established disease), and the “minimal changes in lipids” it causes, it is unsurprising they have also shown benefit concerning the risk of adverse cardiovascular outcomes41. None of these change the existence of the relationship between LDL-c and CVD; they just highlight the multifaceted nature of cardiovascular disease and the existence of other risk modifiers. Therefore, it is inappropriate to suggest they somehow indicate that diet-induced reductions in LDL cannot be inferred to result in CVD benefit.

Honing in on sdLDL

The following paragraph brings up a few more common points of discussion. One is that because saturated fat restriction does not lower the more atherogenic sdLDL particle, and lowers HDL (with a negligible effect on the total: HDL ratio), the decrease in saturated fat intake cannot be inferred to yield a proportional reduction in CVD risk. While it has been consistently shown that small dense LDL and the total cholesterol to HDL ratio do indeed correlate well with CVD risk, in no way does this indicate that sdLDL is inherently more atherogenic or that HDL and total cholesterol are the central dictators of cardiovascular disease risk. Accordingly, most studies show that while sdLDL possesses a significant univariate association with CHD risk, it is seldom an independent predictor after multivariate adjustment for triglycerides and HDL. Therefore, Rizzo et al. suggest that “the increased risk associated with smaller LDL size in univariate analyses is a consequence of the broader pathophysiology of which small, dense LDL is a part (e.g. high triglycerides, low HDL cholesterol, increased LDL particle number, obesity, insulin resistance, diabetes, metabolic syndrome).”42 Furthermore, a recent pre-print of a Mendelian randomization that observed the effects of various lipoprotein subfractions on CVD risk provides additional support that sdLDL is not inherently more atherogenic, with the authors concluding, “LDL and VLDL subfractions appear to have nearly uniform effects on CAD across particle size. Therefore, the results do not support the hypothesis that small, dense LDL particles are more atherogenic.”43 While the point being raised here is important (i.e., that LDL cholesterol reductions are not necessarily the only metric that should be considered with respect to CVD risk reductions via dietary interventions), the other metrics are not being ignored. Even in most of the trials the JACC review authors claim changes in LDL did not correspond with reductions in cardiovascular events (PREDIMED and WHI); they did, as they do across a wide variety of therapeutic interventions44.

Impact of Insulin Resistance on Atherosclerosis

The next paragraph begins with a description of insulin-resistant states, their increasing prevalence in the US, and a brief discussion of how they can increase atherogenesis. Authors then exclaim that individuals with insulin resistance experience impaired skeletal muscle glucose oxidation, increased hepatic de novo lipogenesis, and atherogenic dyslipidemia after a high carbohydrate meal. They also remark these individuals have a higher propensity to convert carbohydrate to fat, which further aggravates the insulin-resistant phenotype, including increases in circulating SFAs and lipogenic fatty acids such as palmitoleic acid. This is an incredible oversimplification that implies that once an individual is insulin resistant, any carbohydrates will exacerbate obesity, hypertension, hyperglycemia, hyperinsulinemia, and numerous other adverse effects associated with this phenotype. Additionally, the statement that subjects experienced significant detriments following a high carbohydrate meal is grossly misleading, as the diets fed in the study the authors linked were both high in fat (35% of kcal) and carbohydrate (55% kcal), contained an additional 25% of subjects daily energy requirements in the form of sucrose, and the quality of the foods and nutrients provided was unclear45. While refined carbohydrates are indeed the last thing that an insulin-resistant individual should center their diet around, diets including appreciable amounts of whole food complex carbohydrates such as legumes, whole grains, fruits, and vegetables have been repeatedly demonstrated to exert a host of beneficial effects on metabolic function. These include but are not limited to, improvements to insulin resistance, reductions in HbA1c, weight loss, decreased blood pressure, and improvements in lipids46–58. This lack of acknowledgment of essential differences in food/macronutrient quality and their impacts on health again seems quite hypocritical given that one of the authors’ main contentions with dietary guidelines recommending reductions in saturated fat is that it fails to do so.

Serum Fatty Acids and Carbohydrate Calumny

The next two paragraphs put much effort into distinguishing between dietary saturated fat and circulating SFAs, starting by saying while some studies suggest increased saturated fat intake does not increase chronic disease risk, people with higher circulating even-chain SFAs have an increased risk of numerous chronic diseases. While the latter may be true, the former is most certainly not, and unsurprisingly they cite two studies mentioned previously that do not support such an assertion (Siri-Tarino et al. and Jakobsen et al.). They then say that circulating SFAs in the blood tend to track closer with dietary carbohydrate intake (again, no specification of quality here), and that changes in saturated fat intake of 2–3 fold have no effects on serum SFAs in the context of diets lower in carbohydrate. Adding on to this, they explain that the primary fatty acid product of de novo lipogenesis (DNL), palmitoleic acid, is a good proxy of DNL due to its low presence in the diet and that larger proportional increase when carbohydrates are converted to fat. Following this preface, they then discuss how multiple studies show a close link between increased dietary carbohydrate intake and increased serum palmitoleic acid levels independent of body weight changes and saturated fat intake59–62. Thereafter, they exclaim how increased palmitoleic acid levels are associated with substantial increases in the risk of stroke, heart failure, and coronary artery disease. They do not mention that every single one of these studies involves diets high in refined carbohydrates, and only one trial62 reduced saturated fat intake below the limit recommended by the dietary guidelines and numerous other nutritional science organizations. Interestingly, this trial only looked at serum FA content and select inflammatory markers, and the low carbohydrate intervention involved a reduction in calories accompanied by an increase in MUFA, no significant change in SFA intake, and reduced refined carbohydrate. In contrast, the low-fat intervention also decreased calories, slightly reduced SFA intake, increased refined carbohydrate intake, and increased alcohol intake. Not only are results pertinent to actual metabolic function lacking, but the comparison seems unfair, and the potentially detrimental changes in the dietary patterns of the low-fat intervention are not representative of those recommended by any competent nutritional organization. Their attempt at portraying carbohydrates as inherently harmful to those with insulin resistance by referencing trials involving the consumption of highly processed sources, accompanied by other negligible diet changes, appears very disingenuous. Finally, they conclude that “Clearly, the impact of dietary SFAs on health must consider the important role of carbohydrate intake and the underlying degree of insulin resistance, both of which significantly affect how the body processes saturated fat. This intertwining aspect of macronutrient physiology and metabolism has been consistently overlooked in previous dietary recommendations.” As already acknowledged, it is certainly crucial to consider these factors. Nevertheless, it is unclear how the studies they brought up in this section, showing excess refined carbohydrate intake is harmful to health, change the well established harmful effects of excess saturated fat. Furthermore, the adverse effects attributed to carbohydrates are almost entirely insinuated to be in part via increases in DNL, reflected in increased serum palmitoleic acid. Such statements are very reductionist and ignore the complexity of changes in DNL commonly observed with metabolic syndrome63. As repeated almost ad nauseam up to this point, the fact they mention intertwining aspects of macronutrient physiology and metabolism again is astounding given the continued indiscriminate vilification of carbohydrates displayed just prior.

Imperfections in Nutritional Science, Ancestry, Nutrigenomics, and Process Contaminants

No “One True Diet”

The review’s subsequent section begins with comments on the failure of the scientific community to determine “the one diet” that achieves optimal metabolic health for all. They then bring up the heterogeneity of dietary intervention outcomes, which they postulate to be a result of the fact some individuals have better outcomes from specific diets than do others. According to them, the objective should be to match each individual to their best, culturally appropriate diet. While it is true that for some individuals modifications may need to be made dependent upon their life stage, the presence of health conditions, and food availability (among other factors), results of well-controlled dietary intervention studies for improving health status have been relatively consistent. Heterogeneity is typically well explained by differences in macronutrient quantity and quality, the degree of subject adherence to interventions, age, baseline disease presence, and other critical factors. Many of these are factors the authors have repeatedly highlighted the importance of considering, yet they seem to selectively ignore them when it is convenient. Individualizing nutrition is most definitely valuable, and it is odd to think someone within the field of nutritional science would dismiss this. That being said, they can’t possibly expect the creators of the guidelines to create such recommendations that will apply to each and every person, and it is not their main goal.

The Relationship between Nutrition and Genetic and Relevance to Recommendations for Saturated Fat

Moving onward, the authors begin to discuss nutrigenomics, which is a fascinating up and coming field of study; however, their discussion is very narrow and seems focused almost entirely on exonerating saturated fat. They preface this discussion by saying that “the once apparently tight link between dietary SFAs and CVD appears to be loosening as a result of mounting evidence that casts doubt on previously established belief,” which is once again, blatantly incorrect. Then they say that some of the debate centers on the role of variation in food sources of SFAs (more on this to come) and some on interindividual variation in biological and clinical effects of saturated fatty acids. Such variation is suggested in part to be a result of genetic variants that result in a modulation of the relationship between dietary SFA and CVD-related biomarkers. One of the variants discussed is the APOE4 allele of the apo E gene, which predisposes individuals to an increased risk of CVD, hypothesized to result due to more significant fasting plasma and postprandial responses to saturated fat. Further, another study that observed saturated fat interacts with a weighted genetic risk score for obesity to modulate body mass index is mentioned, along with an apo A2 promoter gene for which saturated fat is associated with higher average body mass in those homozygous for the T allele. Appropriately, they do not put too much weight on the latter associations, but they do state that current information suggests that genetic predisposition modulates the association between saturated fat intake. They then state this segment of the population, which they deem “SFA-sensitive,” may experience a benefit in reductions of saturated fat intake, so it could therefore be recommended for them specifically. There does not seem to be any other way to classify this position than utterly baseless. It is ridiculous to suggest that only a subgroup of people with genetic predispositions to an even higher CVD risk resulting from a higher intake of saturated fat should consider reducing their intake. This subgroup’s existence in no way suggests an absence of risk in those outside of it, as evidenced by the reduced risk of CVD elicited from reducing/replacing saturated fat in millions of people both in epidemiological studies and RCTs. That being said, this section is concluded with a few similarly problematic statements. The authors emphasize that type 2 diabetes and obesity are significant contributors to CVD risk and declare that the “optimal diet” (what happened to there not being such a thing as “the one diet” based on current research?) should be based on an individual’s “carbohydrate tolerance,” apparently determined by insulin resistance and insulin secretion capacity. Next, they claim that a diet higher in fat and fiber seems to be optimal for type 2 diabetics, only based on a single trial64, and that a diet lower in total and saturated fat may solely be optimal for carbohydrate tolerant or insulin-sensitive individuals. While the dietary pattern they described as optimal can be beneficial to those with diabetes, it does not necessitate a higher intake of saturated fat, and individuals would serve to benefit from keeping it lower. Also, given the aforementioned success of high complex carbohydrate, low-fat diets in improving glycemia, lipids, blood pressure, and other disease risk factors in both healthy individuals and those with type 2 diabeties55–58, the suggestion that only carbohydrate tolerant individuals would serve to benefit from a diet low in saturated and total fat is unwarranted. The end of this section echoes the author’s earlier points about the increasing prevalence of type 2 diabetes and the need for a more personalized and food-based approach to recommend levels of total and saturated fat in the diet. As stated earlier, this is undoubtedly something considered by health professionals that have expertise in providing nutritional advice, and it does not indicate a need for any significant alterations in general dietary recommendations currently in place.

Dairy Saturated Fat: Uniquely Non-Atherogenic?

In the following section, authors begin by highlighting that the health effects of fats and oils may depend on their content of saturated and unsaturated fats, but are not only a sum of their lipid components. They state that they may also depend on the interacting effects of naturally occurring components and harmful components introduced by processing. They then reference the “trans-fat” story, which is a reasonably appropriate example, but just seems to be an aside that does not lead anywhere. Following a discussion of the history of suggestions to replace dairy fat with vegetable oils and the origin of the legislation that drove the saturated vs. unsaturated debate, they mention that the major component of vegetable oils (polyunsaturated linoleic acid) was recognized to decrease plasma cholesterol concentrations by the 1950s. In contrast, saturated fat could raise it; therefore, the former was estimated to have a more favorable effect on atherosclerosis. Incredibly, they then jump to state that despite being high in saturated fat, dairy does not promote atherogenesis, with a single reference. The reference they cite happens to analyze the relationship between dairy fat and incident CVD from 3 pooled cohorts with over 5 million person-years of follow up. It showed that when compared to carbohydrates (excluding fruits and vegetables — so likely the refined grains the authors spent so much time using to paint carbohydrates in a bad light) that dairy fat was not associated with a significant increase in the risk of CVD for a 5% increase in energy by a minimal margin, as the RR was 1.02 with a 95% confidence interval of 0.98 to 1.0565. However, in their analysis on the effect of isocaloric replacement of dairy fat with other nutrients/foods, almost every single replacement elicited a significant reduction in the risk of CVD, including vegetable fat, omega 6, ALA, marine omega 3, and carbohydrates from whole grains, ranging from RRs of 0.9 (0.87 to 0.93) to 0.72 (0.69 to 0.75) for vegetable fat and whole grains respectively. The only exceptions were carbohydrates from refined grains/starches and other animal fat. Henceforth, the authors conclude, “The results suggest that, compared with dairy fat, vegetable sources of fat and PUFA are a better choice for reducing risks of CHD, stroke, and total CVD, although other animal fat (e.g., from meats) may be a less healthy choice than dairy fat. In addition, we showed that types of carbohydrates made a difference; the replacement of dairy fat with high-quality carbohydrates such as whole grains was associated with lower risk of CVD, but the replacement with refined starch and added sugar did not appear beneficial.” How this supports their assertion that dairy fat is not atherogenic or the larger overall point that saturated fat reduction is not warranted is unknown, as it strongly suggests the opposite.

Appeals to Ancestry

After this, they begin to bring up an even stranger point, that due to the fact the ability of humans to digest lactose in milk has evolved separately numerous times, it is unequivocal that humans “required continuous dairy consumption for survival to reproductive age.” It seems as if they’re attempting to suggest this “requirement” for dairy milk, which was based on the fact that it may have offered a survival advantage in previous years (unsurprising given it is a concentrated source of calories), extends to present day, which is just outright false. This is especially problematic because the prevalence of lactose intolerance worldwide is suggested to exceed 65% of the population66. Expanding upon this, the authors also mention how bovine, goat, and sheep domestication coincided with the emergence of lactase persistence and that the meat from these species was likely a significant contributor of saturated fat to human diets, supplemented with some low polyunsaturated fruit oils (olive, avocado, and palm) where available. Continuing, they state that seed oil consumption would have been negligible back then and that these historical facts demonstrate that saturated fats were abundant, critical parts of the ancient human diet. Along with the lack of any research to support these final few assertions, there are numerous issues with this rhetoric, the main one being that any argument extending from this reasoning would be entirely founded on the logical fallacy “appeal to tradition.” Additionally, as they explicitly stated for milk consumption, these choices were likely made on the basis that they supported survival until reproductive age more than anything else. Therefore they would not necessarily have any relevance to constructing dietary patterns supporting a long (at least mostly) disease-free life, which is the goal of countrywide dietary guidelines. Interestingly, reviewing the best estimates we have on nutrient intakes of paleolithic populations, intakes of saturated fat were substantially lower than current-day populations, with estimates ranging from 7.5 to 12% of energy, indicating that a large fraction of the populations likely had intakes within the range recommended by dietary guidelines. Funnily enough, the JACC review authors specifically mention that domestication originated around 10,000 years ago with the advent of modern-day agriculture. The same publication mentions that some have hypothesized to be the origin of notable discordance between “older” and “newer” populations’ health67. That being said, this is the farthest thing from what we should be using to formulate current day guidelines on, especially when we have decades of recent high-quality data available.

Photo: Belchonock/Getty Images

A Brief Digression on Coconut Oil

Next, the authors discuss the 1970s animal experiments that used coconut oil of “unspecified origin,” which caused dramatic increases in hepatic and blood cholesterol and were therefore deemed atherogenic. They mention these oils were usually highly processed and fully hydrogenated (without a source), and that “virgin” coconut oils produced in recent years using gentler preparation methods do not possess the same LDL cholesterol-raising properties, citing a study demonstrating this lack of effect in humans68. While there was indeed no significant change in LDL following four weeks of consuming coconut oil daily, there are quite a few concerning factors that make this trial at least a bit suspect. First, baseline saturated fat intake was already relatively high (~15% kcal) in the coconut oil group. There was no information on post-trial intake, making it impossible to gauge the overall change in saturated fat intake, which is of critical importance. Given that the change in calories and total fat from baseline were only 71 kcal and 29 g when the coconut oil should have theoretically added about 430 kcal and 50 g of fat, it is very likely that significant alterations in dietary patterns were made, and that absolute saturated fat intake may have hardly changed. Regardless, another trial on virgin coconut oil69 showed that it did indeed significantly increase LDL cholesterol over 30 days, and a recent meta analysis70 including these two trials along with 14 others demonstrated a significant increase with coconut oil consumption in trials over two weeks, so this matter is far from settled.

Process Contaminant Paranoia

After mentioning these trials, the authors discuss the recent realization that high-temperature treatment of oils in the presence of trace metals generates process contaminants. Moreover, they describe an in vitro trial demonstrating that direct administration of different coconut oil samples subject to various leveling of processing elicited different effects on cholesterol metabolism, with greater processing associated with greater increases in cellular cholesterol. It is strange that after criticizing others for not basing their decisions on high-quality evidence that the authors defer to mechanistic studies, one of the weakest forms of evidence to support speculation about the effect of potential oil contaminants. Subsequently, they bring up a study using (mostly non-enzymatic) oxidation-resistant linoleic acid and claim that it supports the hypothesis that oxidation products and not specific fatty acids cause plaque formation in mouse models71. Such a statement is very misleading. The di-deuterated linoleic acid in this study only partially reduced atherogenesis of mice fed a high saturated fat and cholesterol diet, and alongside a reduction in oxidation products elicited significant decreases in LDL cholesterol. Pinning the entire process on oxidation products, especially when substituting common sources of PUFAs significantly reduces CVD incidence in humans, is unbecoming. Furthermore, placing so much weight on speculations stemming from rodent models such as this is a significant issue given the remarkable inconsistency in the predictive ability of said models for humans72. There is a reason they reside near the bottom of the evidence hierarchy.

Ostensible Problems with the AHA’s Presidential Advisory

In the following paragraph, authors state that human studies assuming all foods high in saturated fat are similarly atherogenic in many cases stem from an era before the recognition of process contaminants, which seems as if they are suggesting this is the only atherogenic characteristic of saturated fat-rich foods, and if so is an incredibly disturbing conjecture. Next, they claim that the recent Presidential Recommendation to avoid saturated fats from the American Heart Association is based on studies in the 60s and 70s, 3 in Europe, and 1 in America. This is an extraordinarily uncharitable and blatantly incorrect characterization of the AHA’s Presidential Recommendation. In reality, it analyzed these four trials, six smaller, lower quality “non-core trials,” the Lyon Heart study, PREDIMED, additional observational studies on populations following similar Mediterranean diets, RCTs reducing saturated fat intake and decreasing LDL-c (and vice versa), multiple meta-analyses of observational studies on SFA intake and CVD incidence, large scale cohorts observing the effects of replacing SFA on CVD incidence, and additional supplementary genetic and mechanistic evidence73. These considerations aside, the JACC review’s authors discuss that the 3 European trials are confounded because they used customary diets as comparisons, and supposedly partially hydrogenated fish oils were major constituents of European margarine during the 1960s and 70s, for which they cite a book titled “The Story of Margarine”. Unfortunately this book was inaccessible. Alas, they declare that The Oslo study explicitly estimated the partially hydrogenated fish oil intake at 40 to 50 g/day. Whether this pertains to the control or experimental group is unclear. However, the only information given in the publication is for the experimental diets’ composition, which was the following: “In an analysis of the experimental diet as consumed by 17 selected dieters, the mean daily intake was: protein, 92 gm.; fat, 104 gm.; carbohydrates, 269 gm.; and cholesterol, 264 mg. Daily intake of calories was 2,387. Calories derived from fat constituted 39 percent of the total. The sources of fat were: soybean oil (72 percent), fish fat (11.6 percent), animal fat (8.8 percent), cereal fat (5.0 percent), and fat from other sources (2.6 percent).”74 Given these numbers, and assuming “fish fat” is entirely partially hydrogenated fish oil, 11.6 percent of 104 g fat is still only 12 grams, way off from what they claim, so this bit is pretty confusing. Continuing in this vein, they assert that since the three European trials used customary diets as comparisons, it can be inferred that they were tests of polyunsaturated fats against trans-plus-saturated fats, and the effects cannot be ascribed to saturated fat alone. Henceforth, excluding these trials, as they see fit, only the (smaller and underpowered) US trial75 remains, which did not show a significant difference between the control and intervention group for its primary endpoint. However, for all endpoints combined and fatal atherosclerotic events, results were significant despite the relatively low total event rate and consequential low statistical power. A few things merit discussion here. First, the entire reason they suggest the European trials should be excluded is an inference they are confounded that is not conclusively proven. Second, even if this were the case, the large body of evidence from other RCTs and observational studies discussed in the AHA’s Presidential Report is sufficient to underscore the importance and benefit of reducing/replacing dietary saturated fat.

Food Matrix, Saturated Fat, and their Connection to Health

Finally, they conclude this section by saying, “…these observations strongly support the conclusion that the healthfulness of fats is not a simple function of their SFA content, but rather is a result of the various components in the food, often referred to as the “food matrix.”. Ample evidence is available from research on specific foods that other food components and the food matrix likely dominate over saturated fat content, as discussed in the following section. Recommendations should, therefore, emphasize food-based strategies that translate for the public into understandable, consistent, and robust recommendations for healthy dietary patterns.” Once again, the evidence they have brought forth does not seem to strongly suggest that the saturated fat content of foods is negligible with regard to a food’s healthfulness and impact on CVD risk. As for the food components and matrix, their actual relevance and implications for a foods’ impact on health will be addressed accordingly. Finally, as mentioned a few times previously, the current (and hopefully future) dietary recommendations are arguably already understandable, consistent, and robust, although there is always room for improvement.

Safe Sources of Saturated Fat?

Full Fat Dairy

In some of the review’s final paragraphs, the authors specify their reasons as to why they feel a few specific foods with high saturated fat content are unfairly discouraged. These foods include yogurt and cheese, dark chocolate, and red meat, discussed in that order. For yogurt and cheese, authors begin by describing that dairy is the primary source of SFAs in most diets and that major dietary guidelines recommend low or fat-free versions to limit SFA. However, that food-based meta-analyses consistently find the two are inversely associated with CVD risk, citing a cohort76, a literature review77, another cohort on type 2 diabetes78, and one actual meta analysis79. This seems as if it was just a citation error, but regardless the meta-analysis they cite actually provides weak, if any, evidence suggesting an inverse association of cheese and yogurt with CVD. The inverse association was only found for cheese and was attenuated when a single large study was removed in a sensitivity analysis. Furthermore, the subgroup analyses demonstrated the strongest inverse association with subjects below 50 years of age, a group in which CVD incidence would be lower and therefore possess far less of an ability to effectively gauge the effect on CVD risk. Even more concerning, numerous trials adjusted for hyperlipidemia, serum cholesterol, or saturated fat, which would also strongly impair their ability to pick up on an increased risk of CVD. One final consideration is that they chose to exclude one of the largest, and perhaps best quality studies (Hu et al. 1999), from their analysis, which demonstrated a significantly increased risk of CVD within the highest quintile of full-fat dairy consumption, and with a higher ratio of full to low-fat dairy consumption.

Dark Chocolate

After cheese and yogurt, the authors direct their attention to dark chocolate, stating that it contains stearic acid, which has a neutral effect on CVD risk, as well as that it contains other nutrients that may be more important for CVD/type 2 diabetes. They note that it possesses potential preventative effects on the two, supported by experimental and observational studies. While they provide no source for the stearic acid claim, the three meta-analyses they link97–99 do offer consistent evidence confirming a small protective effect of chocolate with respect to CVD and type 2 diabetes, in agreement with a meta-analysis100 on dark chocolate and cocoa powder’s effects on serum lipids and an RCT101 of its impact on insulin sensitivity.

Unprocessed Red Meat

The final food the author’s remark has insufficient evidence to suggest reducing intake based on saturated fat content is (unprocessed) red meat. They give four references to back up this claim: a meta-analysis of cohort studies102, two meta-analyses of RCTs(one on surrogate biomarkers103 and one on actual outcomes104), and a small cohort105. Aside from the fact that these publications do not even represent a modicum of the evidence on red meat intake and CVD, type 2 diabetes, and cancer, the three they gave to justify their claims are weak at best. The first meta-analysis they cite only includes 4 and 5 cohorts observing the effect of red and processed meat intake on CHD and type 2 diabetes incidence. Furthermore, three of the four observing the effect of red meat intake on CHD made adjustments for serum cholesterol, which, as discussed previously, is incredibly problematic given its role as a causal intermediate. Finally, although the association with diabetes was non-significant, it was by an incredibly small margin. Due to the limited number of studies considered and the range in intakes observed, it would be ill-advised to conclude this from this publication alone.

Comments on Gaps in Research and Potentially Distracting Dietary Guidelines

Before wrapping up their review, the authors comment on what they feel to be gaps in current research and essential considerations for future investigations. They initiate this paragraph by claiming that recommendations to reduce SFA intake without considering specific fatty acids and food sources are not aligned with current evidence. As a result, they suggest that these recommendations: “may distract from more effective food-based recommendations, and may also cause a reduction in the intake of nutrient-dense foods (e.g., dairy, unprocessed meat) that may help decrease not only the risk of CVD, type 2 diabetes, and other non-communicable diseases, but also malnutrition, deficiency diseases, and frailty, particularly among “at-risk” groups.” This is both false and incredibly hyperbolic. As demonstrated throughout this entire commentary, with the exception of dark chocolate, they continually failed to substantiate any of these claims. Regarding nutrient intake, full-fat dairy products hardly offer any advantage, if at all, over low-fat. Elimination of red meat does not necessitate decreased nutrient intake, especially given healthy substitutions such as fish, other lean meats, whole grains, legumes, and nuts/seeds are made. The full body of evidence shows that the effects of full-fat dairy are inconsistent at best, and low-fat dairy products appear to be favorable. Red meat is continually shown to have adverse effects on the risk of the diseases they mentioned, so the intention of including it in their sweeping claims is unknown. Next, they suggest that a focus on SFAs has had an unintended consequence of misleadingly guiding government, consumers, and industry towards foods low in SFA but rich in refined starch and sugar, and that guidelines should consider the types of SFAs, and more importantly, the foods containing them and their diverse effects on health outcomes. In addition to the fact that these choices were almost definitely motivated by factors other than the actual dietary guidelines, the consideration of different SFAs and foods containing them only seems to hold water to a very limited extent. Moderate amounts of dark chocolate and potentially whole coconut (which the authors interestingly chose not to discuss) are likely the only exceptions to the strong relationship between saturated fat intake and adverse health outcomes.

Closing Remarks

Processed Foods and Saturated Fat Bias

Finishing up this section and transitioning into their final paragraph, they strongly recommend a more food-based translation of guidelines to achieve a healthy diet, reconsidering the recommendations to reduce intake of total SFAs, and caution regarding the incorporation of processed foods “until much more is known about the health effects of specific process contaminants so that their levels can be minimized.” Carrying on, they claim the long-standing bias against foods rich in saturated fat should be replaced with a recommendation for diets consisting of healthy foods. Immediately following, they state, “We suggest the following measures: 1) enhance the public’s understanding that many foods (e.g., whole-fat dairy) that play an important role in meeting dietary and nutritional recommendations may also be rich in saturated fats; 2) make the public aware that low-carbohydrate diets high in saturated fat, which are popular for managing body weight, may also improve metabolic disease endpoints in some individuals, but emphasize that health effects of dietary carbohydrate — just like those of saturated fat — depend on the amount, type and quality of carbohydrate, food sources, degree of processing, etc.; 3) shift focus from the current paradigm that emphasizes the saturated fat content of foods as key for health to one that centers on specific traditional foods, so that nutritionists, dietitians, and the public can easily identify healthful sources of saturated fats; and 4) encourage committees in charge of making macronutrient-based recommendations to translate those recommendations into appropriate, culturally sensitive dietary patterns tailored to different populations.”

Missing the Mark

There are some excellent points here; however, their relevance is questionable. Regarding their recommendations encouraging a food-based translation of a healthy diet/a focus on diets consisting of healthy foods, it is almost sure that anyone interested in constructing policies for designing and implementing dietary guidelines would agree whole-heartedly. The panel in charge of creating the guidelines in 2015 was in such agreement that is exactly what they did. On the United States Department of Agriculture/Health and Human Service’s website it is explicitly stated, “A healthy eating pattern includes: A variety of vegetables from all of the subgroups — dark green, red and orange, legumes (beans and peas), starchy, and other, fruits, especially whole fruits, grains, at least half of which are whole grains, fat-free or low-fat dairy, including milk, yogurt, cheese, and/or fortified soy beverages, a variety of protein foods, including seafood, lean meats and poultry, eggs, legumes (beans and peas), and nuts, seeds, and soy products, and oils”35, which leaves one questioning precisely what the JACC review’s authors are even contesting.


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BSc in Nutritional Science. Fascinated in researching and sharing information on the links between food, exercise, and health.