The Exoneration of Seed Oils

A Review of Misinformation and the Evidence

Anyone aware of my work will be familiar with my rants about nutrition misinformation spread by pseudo-influencers on social media and podcasts. Shoddy dietary advice is nothing new, of course: magazines, newspapers, books and TV programmes have been propagating fad diets since nutrition science has been a thing. Yet never, I feel, has dangerous pseudoscience been as prolific as now. Spend a few short minutes scrolling social media and you’ll likely come across someone blurting out oodles of quackery on a subject matter on which they claim to be an authority. Eating is an activity in which we all partake, so it’s understandable that nutrition is a field where everyone has an opinion. Food appeals to our curiosity. Most of us want to live longer, happier and healthier lives, and a good diet is integral to these goals. And we enjoy eating, too. Few fields are as hyped as nutrition and dietetics, and the internet is rife with health and fitness influencers pushing out fake information to suit their own agenda, which, incidentally, needn’t be financially driven: popularity, gaining followers and ideological motivations are equally persuasive. With so much conflicting information leaching into our brains, it can be hard to discern between the useful and the bullshit.

Of particular concern is the hostility aimed at specific foods or food groups where claims are made that consuming a certain food is linked to an increased risk of contracting a specific disease. Often the influencer will use technical jargon and cite research which, they assert, supports their position. Nutrition science is incredibly nuanced, however, and rarely should a specific food be singled out as a cause of a particular illness. Of course there are exceptions, especially when it comes to food allergies, autoimmune diseases or inborn errors of metabolism. In these circumstances, however, only susceptible individuals are affected, and targeting particular foods shouldn’t be part of general advice. Worryingly, this is exactly what these influencers are doing.

One recent trend I’ve noticed is influencers claiming that the consumption of seed oils is harmful to human health. Alarmingly, they tell us that consuming seed oils is linked to cardiovascular disease (CVD), inflammation, cancer and other health issues. But is there any truth to these claims? To what extent are these self-proclaimed fitness gurus merely parroting the narrative of others without looking at the evidence themselves? And where did these claims originate?

What Are Seed Oils?

Before we dive into the research, we should clarify what’s meant by the term “seed oil” and outline the principal fatty acids they contain. When people talk about seed oils they typically mean sunflower, rapeseed (canola), safflower, corn and soybean oil. Most of these are high in omega-6 fatty acids, particularly linoleic acid (LA). LA is one of two essential fatty acids, the other being alpha-linolenic acid (ALA), an omega-3. Omega-3s and -6s are both types of polyunsaturated fatty acids (PUFAs). As humans, we must consume both ALA and LA regularly in our diets to prevent illness or death. In the absence of dietary LA, children will fail to grow and adults may experience fatty liver, skin lesions, reproductive failure and, eventually, death. Thankfully, due to LA’s prevalence in human diets, deficiency is rare. Bizarrely, however, many of the online fitness quacks denounce LA as the malevolent villain in their anti-seed-oil story, claiming it to be the key fatty acid behind an array of lifestyle-related maladies.

Other vegetable oils, such as rapeseed oil, are rich in monounsaturated fatty acids (MUFAs), particularly oleic acid, a high intake of which has been shown to improve blood cholesterol profiles [1]. What about flaxseed and chia seed oils? Although these are seed oils, it’s not always clear if the anti-seed-oil influencers are including them in their demonisation narrative. I feel that often – though I could be wrong – flax and chia oils get a pass because, rather than containing significant amounts of LA, both are rich sources of ALA. It is true that many modern Western diets contain too few omega-3s, and, although hotly debated, some academics feel the ratio of omega-3 to omega-6 is too low, an issue I previously discussed. So I’m going to give the influencers the benefit of the doubt and assume that flax and chia oils are not included in their seed-oil denouncements. Incidentally, another popular oil, olive oil – which, like rapeseed, is rich in oleic acid – seems to be favoured by these influencers, possibly because olives are a fruit rather than a seed.

Types of Research

As any debunking of pseudoscientific claims involves delving into the research, to enable a better understanding, I should briefly outline three types of studies. Observational studies draw inferences from a sample population where the variable is not under the control of the researcher. For example, an observational study might look at the consumption of vegetable oils in a population and see how it relates to incidence of CVD. Observational studies are useful for making general observations, but we should be cautious about drawing firm conclusions from them. A major problem with observational studies is that there are confounding factors, some of which may be unknown. From the above example, we should be reluctant to draw any hard link between vegetable oil use and CVD as populations will likely also consume foods containing other types of fats, like saturates, sugar and salt, and low amounts of fibre and antioxidants, or there may be some other unknown influence.

In randomised controlled trials (RCTs), subjects are randomly assigned to a treated group – of which there may be more than one – or a control group. Often RCTs are performed in a double-blind format, where neither the subject nor those performing the experiment are aware of which group the subject is assigned to. This helps to minimise the risk of bias, which would lessen the validity of the findings.

Meta-analysis is the gold standard in research. These studies systematically assess the results of previous research that have explored the same question. Meta-analysis can involve consolidating findings from either observational studies, RCTs or both, and, although each individual study will likely involve reporting measurements with a degree of error, the aim is to use statistical approaches to derive a pooled estimate closest to the unknown common truth based on how this error is perceived. Meta-analysis results are considered the most trustworthy source of evidence by the evidence-based literature in the life sciences.

Seed Oils and Heart Disease

We’re now ready to take a critical look at the evidence to assess whether seed oils are hazardous to human health, and if their regular use increases the risk of certain diseases. Indeed, what does the research reveal about seed oil consumption and health protection? Crucially, when reviewing the science, we should be mindful of what good research looks like.

As part of my investigations for this article, I had to painfully trudge through numerous videos where influencers used what they claimed to be a science-based assertion that seed oils were dangerous for health. One hugely popular carnivore said that the largest RCT ever done on saturated and polyunsaturated fats proved that seed oils are dangerous. This guy has a massive social media following and speaks with such conviction that he comes across as highly credible which makes his claims particularly dangerous. When opining that the consumption of seed oils leads to increased rates of death, he cited the Minnesota Coronary Experiment. In this study, the researchers set out to compare a diet high in saturated fats with one high in polyunsaturates. They enrolled 9,570 patients who’d been hospitalised for mental illness, and they intended to run the study for more than three-and-a-half years to allow sufficient time to adequately test the effects of the diets. The results showed a 22 percent increased risk of death for each 30mg/dl (0.7 mmol/l) reduction in total blood cholesterol. The authors concluded that replacing saturated fats with LA from vegetable oils does not translate to a lower risk of dying from coronary heart disease (CHD)*. They stated that “Available evidence from randomised controlled trials shows that replacement of saturated fat in the diet with linoleic acid effectively lowers serum cholesterol but does not support the hypothesis that this translates to a lower risk of death from coronary heart disease or all causes.” They further claimed that there is “growing evidence [of an] overestimation of the benefits of replacing saturated fat with vegetable oils rich in linoleic acid.” [2]

Does this mean that the influencer is correct and vegetable oils do offer no benefit? Well, aside from the fact that he claimed that seed oils increase the risk of disease, not just that they offer no benefit over saturated fat, there’s a lot wrong with drawing a hard claim from this study when we delve into the methodology. Firstly, the subjects were given their assigned diets as inpatients and, because hospitalisation for mental illness gradually became less common as society developed a better understanding of mental illness, many ended up being treated as outpatients. Consequently, 75 percent were discharged within the first year, and, of the remaining 25 percent, only around half stayed in the study for at least three years. Due to the number of follow-up years being severely diminished, the results are of limited statistical power. There is, however, a more fundamental flaw: the patients in the polyunsaturates group were fed hydrogenated fat margarines. These contain trans fats which have since been banned due to them being strongly linked to CHD risk. When reviewing studies, it’s crucial to understand what strong evidence looks like. This study is a long way from strong evidence.

Back in 2010 a systematic review and meta-analysis of six RCTs concluded that increased PUFA consumption in place of SFA significantly reduced rates of CHD [3]. Does this serve as a complete rebuttal to those anti-seed-oilists? After all, this is a meta-analysis of RCTs; surely robust evidence? Adhering to strong evidence and understanding the methodology must, of course, work both ways and, despite the review’s encouraging conclusion, the studies analysed did not include at least one of the core characteristics crucial to testing the hypothesis.

Instead, therefore, we will focus on four studies that make up the main body of evidence looking at both seed oils and SFA versus PUFA intake. When a meta-analysis is conducted on these core trials, we do indeed see a consistent and drastic reduction in CHD outcomes. The American Heart Association Core Trials Review in 2017 cited these four as the most robust evidence available on the topic on the basis of the quality of study design, execution and adherence [4]. These four trials all replaced SFA intake with PUFA and all used vegetable oils as part of the intervention. The key reasons why these trials provide strong evidence are as follows:

1. The dietary intake of both the intervention and control groups were controlled.

2. Subjects had at least two years of sustained intake of the relevant diets; crucial, because it takes time for PUFA to be aligned in tissues.

3. The trials all compared high SFA with high PUFA intake and did not include trans fats, which we know to be hazardous to health.

4. Researchers validated adherence by using biomarkers like serum cholesterol, blood or tissue levels of PUFAs, and they collected information on CHD events.

Collectively, these four trials indicated that a reduction in SFA and an increase in PUFA from seed oils led to a 29 percent reduced risk of CHD. These are the strongest RCTs comparing SFA and PUFA intake, in particular seed oils, and are as methodologically tight as you can get. Consistently, we see a drastic improvement in cardiovascular outcomes when decreasing SFA intake and increasing PUFA intake from seed oils. In short, the four core trials demonstrated better cardiovascular health.

What makes these four trials so robust? Let’s look at one of them to illustrate why. The 1969 LA Veteran Study was a controlled double-blind trial on 846 males living in an institution with an average age of 65 years old, 30 percent of whom had CHD. The intervention group were given corn, soybean, safflower and cottonseed oils (all high in LA) to replace the saturates in their diet. This study had a strict dietary control with participants eating their meals at an institution centre and the average duration for each participant was eight years. Dietary adherence was confirmed by objective testing of blood and tissue levels of LA, and the extent of atherosclerosis in the coronary arteries and aorta was analysed. The seed oil group reduced their serum cholesterol by 13 percent, myocardial infarction, sudden death or stroke went down by 34 percent, and there was a 31 percent reduction in total CHD events [5]. The strict dietary control and the eight-year-long intervention period ensured large differences in fatty acid intakes and allowed for a sufficient number of CHD events for statistical significance.

As well as these trials, there’s other strong evidence. For instance, a 2018 meta-analysis of 54 controlled studies showed all types of vegetable oil to be more effective at reducing LDLs when compared to butter [6].

An Inflamed Debate

Another claim online quacks make about omega-6s and vegetable oils is that they are “proinflammatory”. What could they mean by this? It’s likely that they’re linking seed oil use with low-grade inflammation and that their consumption increases the risk of diseases associated with inflammation [7]. Inflammation is a necessary physiological response to injury or infection and is part of the healing process. However, prolonged low-grade inflammation is involved in the development of diseases like CVD, some cancers, depression, chronic pain, poor gut health and obesity [8], and poor dietary habits are associated with low-grade inflammation [9].

The narrative stems from the speculation that arachidonic acid (AA), another omega-6 fatty acid, is involved in the production of various inflammation-promoting factors. AA is synthesised in the body from LA and is considered a semi-essential fatty acid, because it can reduce the requirement for LA. Along with the omega-3 EPA, AA is necessary for the production of eicosanoids, critical messengers necessary for the immune and inflammatory responses. However, the response from AA-derived eicosanoids is different to the response from EPA-derived eicosanoids, with the latter being less potent inducers of inflammation [10]. Nevertheless, it’s an oversimplification to label all AA-derived eicosanoids as “proinflammatory” as they also inhibit key proinflammatory factors [11]. Therefore, an adequate amount of AA may actually help to maintain an optimal inflammatory response. The claim also assumes that a higher dietary intake of LA leads to a higher conversion to AA and this, in turn, is converted to inflammatory eicosanoids. But this isn’t the case as negative feedback control is in place so AA and eicosanoids are only produced on demand [12].

As well as debunking the claims made about the involvement of seed oil fatty acids in the physiological process of inflammation, we should also look at the epidemiology. Delving into published data forces us to see if we missed anything and if, indeed, an association of seed oil consumption and inflammation is revealed. Interestingly, this is an area where there has been considerable research. In one study, for example, 13 overweight men fasted overnight and then consumed a muffin either containing 50g of butter or 50g of sunflower oil. All subjects completed both interventions. After they ate the butter muffin, the inflammatory biomarker interleukin-6 (IL-6) increased, whereas after consuming the sunflower muffin, several inflammatory markers decreased. This indicated that sunflower oil reduced inflammation and butter increased it [13].

In another study, overweight subjects were split into three groups. One group consumed 20ml of rapeseed oil per day, another had 20ml of sunflower oil, and a control group consumed their habitual diet. The subjects consumed their oils every day for 12 weeks and were tested for various inflammatory biomarkers. After 12 weeks, all markers showed little change. In fact, at baseline the most consumed fats were butter and olive oil, indicating that when olive oil and butter are replaced with PUFAs, there’s no worsening of inflammatory markers [14]. Another team took 67 overweight people and, for 10 weeks, fed them either a diet high in omega-6-rich vegetable oil or one high in saturated fat from butter. The vegetable oil group lost liver fat and improved metabolic status without losing weight, whereas the butter group had higher liver fat, insulin, cholesterol, LDLs and triglycerides. These results tell us that vegetable oils don’t cause signs of inflammation [15]. Another trial on 486 middle-aged women showed that the consumption of sunflower, corn, rapeseed, soybean and olive oils was linked to lower levels of several inflammatory biomarkers including C-reactive protein (CRP) and IL-6 [16]. Moreover, CRP has been shown to be lower when serum LA is higher [17], indicating that LA might be protective against low-grade inflammation. It’s also been shown that not only does a high intake of LA not increase inflammatory responses, it also has little impact on AA levels [18].

Finally, a review of 37 RCTs looking at dietary fats and inflammatory markers found that, out of 10 controlled trials involving vegetable oils, none demonstrated convincing evidence of increased inflammatory markers. In fact, three of these studies found some beneficial effects on inflammation [19]. The claim that a high intake of omega-6 fatty acids or LA-rich seed oils can promote inflammation is unsubstantiated, and it's more likely the reverse is true: their consumption offers some protection. In one review, the authors concluded “that virtually no evidence is available from randomised controlled intervention studies among healthy [people] to show that addition of LA to the diet increases the concentration of inflammatory markers.” [20]

Why Pick On Seed Oils?

Over the past few decades, Western seed oil consumption has gone up. At the same time, incidences of diseases linked to lifestyle, such as CVD and cancer, have also risen. While it's easy to suggest a connection between these two variables, most of us are fully aware that correlation doesn’t mean causation. Nevertheless, this link has been exacerbated by those who claim that cutting seed oils from their diet made them “feel better”. Indeed, there could be a plausible link that involves oxidation. Oxidation is a process that results in the production of harmful free radicals with potentially negative health implications including an increased risk of CVD and cancers [21]. Oils are more likely to oxidise in the presence of heat, light, humidity, heavy metals and air. Unlike saturated fatty acids, unsaturates are prone to oxidation, so this includes all the omega-3s, omega-6s and MUFAs that we’re told are good for us. As vegetable oils primarily contain mono- and polyunsaturates, it’s crucial that they’re stored in suitable environments, and, while refined vegetable oils can be heated to higher temperatures and then consumed, they should not be reheated or exposed to oxygen or light continuously. This helps to explain the link between the consumption of fried convenience foods and disease: the unsaturated-rich vegetable oils used in the frying process have been exposed to a significant oxidation-promoting environment before the food is served [22]. Crucially, therefore, it’s the mistreatment of vegetable oils when making convenience foods that makes them unhealthy. Diets high in foods fried in vegetable oils – the junk food, fast foods and snacks we all know we should be eating less of – are linked to CVD and cancer risk. Regularly consuming foods high in saturates, sugar and salt, and low in fibre, micronutrients and phytonutrients, isn’t good for our health, and it just so happens that many of these foods often also contain seed oils. So, although there’s a link between diets high in vegetable oils and poor health outcomes, could it be the nutritional content – or lack thereof – of such diets that’s the real issue?

But this science-based justification fails to provide an explanation as to why so many influencers have jumped on board the seed-oil-demonising bandwagon. Truthfully, one can only guess at the reasons why seed oil bashing has become fashionable among zealots, though I’ve a hunch the narrative originated from online carnivore diet advocates. Currently in vogue, this way of eating involves consuming a diet that almost exclusively consists of animal products. Naturally, such a regimen mandates that pretty much any non-fauna-derived food will be subject to scorn. Indeed, other casualties include wholegrains, potatoes and even fruit. Could it be that the anti-seed-oil yarn originated from carnivores and has subsequently bled into other dietary ideologies?

While it’s not wholly clear why the meme has taken hold, I do have a hypothesis, albeit a rather cynical one: most people don’t understand the science behind the claims they make, nor do they care to. I’ll go further: in most cases they aren’t even concerned if the science exists! Few communicators are motivated to seek research to back up their assertions, let alone delve into it or assess the quality. A more likely explanation is that they’re committed to a claim because they’ve previously heard someone who they deem credible make a similar contention. At best, an influencer might perform a quick google to see if a published study exists that lends support to their position. In other words, they seek confirmation bias. But this isn’t science. One who adheres to the scientific method doesn't seek validation. However, many online communicators don’t even realise that they lack the necessary skills to critically review research and to comprehend the methodology behind it. Nor, even, do they acknowledge the existence of such skills. Fundamentally, the burden of proof should be on the individual to prove that seed oils are bad for health, not on others to prove otherwise. Sadly, this is not the world we live in, and academics and credible influencers – who, I should point out, do exist and, thankfully, seem to be growing in number, albeit too slowly – are compelled to spend valuable time debunking these myths. This could be time better spent researching, educating, pushing positive health messages and tackling the numerous food-related issues.

My hypothesis doesn’t just pertain to the animosity rallied against seed oils: it extends to any food where a non-scientific perspective has spread online. Nor does my cynicism end here. I can’t help but feel that it’s become cool in certain online camps to disagree with any mainstream view. There seems to be an anti-conventional-science rhetoric floating around. This is especially rife when it comes to health information and has worsened since the pandemic. Could it be that seed oils are merely another victim of anti-establishment conspiratorial ideologies?

When untrained individuals cite research, they are liable to interpret the findings incorrectly. Worse still is when a study's findings are deliberately misrepresented in order to push a particular narrative. Of course, you don’t need to be an academic to have the necessary skills to be able to interpret a scientific paper, but a worryingly large number of people who adopt the persona of a nutrition expert lack the competence to accurately communicate research findings. Influencers, sometimes with hundreds of thousands of followers, disingenuously drive their unqualified claims for their own dogmatic interest. This misinformation ranges from echoing something they’ve heard from another pseudo “expert” to outright lies and deliberate deception. I don’t doubt that, in some cases, influencers come with good intentions and truly believe their ideas are of genuine benefit to the health of their followers. However, lacking substantiation, any assertion is likely ideological and indicates an alignment with a particular dietary camp. For some, their very identity is attached to their nutrition beliefs. An honest actor who truly wishes to disseminate only reliable information should seek to be mindful of their own failure to understand the facts behind the claims they make, else they should refrain from commenting at all. A nutrition message that lacks the required level of rigour behind it will likely be hazardous to people’s health.

* More accurately, the term is coronary artery disease (CAD) due to the coronary arteries being the affected tissue. However, the commonly used term in many research papers is coronary heart disease (CHD), so I’ll use it here.

References:
1. (a) Allman-Farinelli, M. A. et al. (2005) ‘A Diet Rich in High-Oleic-Acid Sunflower Oil Favorably Alters Low-Density Lipoprotein Cholesterol, Triglycerides, and Factor VII Coagulant Activity’, Journal of the American Dietetic Association, 105(7), 1071-9; (b) Natali, F. et al. (2007) ‘Oleic Acid Is a Potent Inhibitor of Fatty Acid and Cholesterol Synthesis in C6 Glioma Cells’, Journal of Lipid Research, 48(9), 1966-75; (c) EFSA Panel on Dietetic Products, Nutrition and Allergies (2011) ‘Scientific Opinion on the Substantiation of Health Claims Related to Oleic Acid Intended to Replace Saturated Fatty Acids (SFAs) in Foods or Diets and Maintenance of Normal Blood LDL-Cholesterol Concentrations (ID 673, 728, 729, 1302, 4334) and Maintenance of Normal (Fasting) Blood Concentrations of Triglycerides (ID 673, 4334) Pursuant to Article 13(1) of Regulation (EC) No 1924/2006’, EFSA Journal, 9(4), 2043.
2. Ramsden, C. E. et al. (2016) ‘Re-evaluation of the Traditional Diet-Heart Hypothesis: Analysis of Recovered Data from Minnesota Coronary Experiment (1968-73)’, BMJ, 353, i1246.
3. Mozaffarian, D. et al. (2010) ‘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, 7(3), e1000252.
4. Sacks, F. M. et al. (2017) ‘Dietary Fats and Cardiovascular Disease: A Presidential Advisory from the American Heart Association’, Circulation, 136(3), e1-e23.
5. Dayton, S. et al. (1969) ‘A Controlled Clinical Trial of a Diet High in Unsaturated Fat in Preventing Complications of Atherosclerosis’, Circulation, 40(1s2), II-1–II-63.
6. Schwingshackl, L. et al. (2018) ‘Effects of Oils and Solid Fats on Blood Lipids: A Systematic Review and Network Meta-Analysis’, Journal of Lipid Research, 59(9), 1771-82.
7. (a) Calder, P. C. (2009) ‘Polyunsaturated Fatty Acids and Inflammatory Processes: New Twists in an Old Tale’, Biochimie, 91(6), 791-5; (b) Virtanen, J. K. et al. (2018) ‘The Associations of Serum n-6 Polyunsaturated Fatty Acids with Serum C-Reactive Protein in Men: The Kuopio Ischaemic Heart Disease Risk Factor Study’, European Journal of Clinical Nutrition, 72(3), 342-8; (c) University of Eastern Finland (2017) ‘Omega-6 Fatty Acids Do Not Promote Low-Grade Inflammation’, Science Daily, 13 November. Available at: https://www.sciencedaily.com/releases/2017/11/171113095430.htm (Accessed: 11 July 2023).
8. (a) Wellen, K. E. et al. (2003) ‘Obesity-Induced Inflammatory Changes in Adipose Tissue’, Journal of Clinical Investigation, 112(12), 1785-8; (b) Dantzer, R. (2012) ‘Depression and Inflammation: An Intricate Relationship’, Biological Psychiatry, 71(1), 4-5; (c) Dantzer, R. et al. (2008) ‘From Inflammation to Sickness and Depression: When the Immune System Subjugates the Brain’, Nature Reviews. Neuroscience, 9(1), 46-56; (d) Parkitny, L. et al. (2013) ‘Inflammation in Complex Regional Pain Syndrome: A Systematic Review and Meta-Analysis’, Neurology, 80(1), 106-17; (e) Minihane, A. M. et al. (2015) ‘Low-Grade Inflammation, Diet Composition and Health: Current Research Evidence and Its Translation’, British Journal of Nutrition, 114(7), 999-1012.
9. (a) ibid (7e); (b) Hotamisligil, G. S. (2006) ‘Inflammation and Metabolic Disorders’, Nature, 444(7121), 860-7.
10. (a) Jump, D. B. (2002) ‘The Biochemistry of n-3 Polyunsaturated Fatty Acids’, Journal of Biological Chemistry, 277(11), 8755-8; (b) Flock, M. R. et al. (2013) ‘Long-Chain Omega-3 Fatty Acids: Time to Establish a Dietary Reference Intake’, Nutrition Reviews, 71(10), 692-707.
11. (a) ibid (10a); (b) ibid (7a).
12. (a) ibid (7a); (b) ibid (7c).
13. Masson, C. J. and Mensink, R. P. (2011) ‘Exchanging Saturated Fatty Acids for (n-6) Polyunsaturated Fatty Acids in a Mixed Meal May Decrease Postprandial Lipemia and Markers of Inflammation and Endothelial Activity in Overweight Men’, Journal of Nutrition, 141(5), 816-21.
14. Nicol, K. et al. (2022) ‘No Evidence of Differential Impact of Sunflower and Rapeseed Oil on Biomarkers of Coronary Artery Disease or Chronic Kidney Disease in Healthy Adults with Overweight and Obesity: Result from a Randomised Control Trial’, European Journal of Nutrition, 61(6), 3119-33.
15. Bjermo, H. et al. (2012) ‘Effects of n-6 PUFAs Compared with SFAs on Liver Fat, Lipoproteins, and Inflammation in Abdominal Obesity: A Randomized Controlled Trial’, American Journal of Clinical Nutrition, 95(5), 1003-12.
16. Esmaillzadeh, A. and Azadbakht, L. (2008) ‘Home Use of Vegetable Oils, Markers of Systemic Inflammation, and Endothelial Dysfunction Among Women’, American Journal of Clinical Nutrition, 88(4), 913-21.
17. (a) ibid (7b); (b) ibid (7c); (c) Kubota, Y. et al. (2015) ‘Serum Polyunsaturated Fatty Acid Composition and Serum High-Sensitivity C-Reactive Protein Levels in Healthy Japanese Residents: The KOBE Study’, Journal of Nutrition, Health and Aging, 19(7), 719-28.
18. (a) Kelley, D. S. et al. (1998) ‘Arachidonic Acid Supplementation Enhances Synthesis of Eicosanoids Without Suppressing Immune Functions in Young Healthy Men’, Lipids, 33(2), 125-30; (b) Thies, F. et al. (2001) ‘Influence of Dietary Supplementation with Long-Chain n-3 or n-6 Polyunsaturated Fatty Acids on Blood Inflammatory Cell Populations and Functions and on Plasma Soluble Adhesion Molecules in Healthy Adults’, Lipids, 36(11), 1183-93; (c) Rett, B. S. et al. (2011) ‘Increasing Dietary Linoleic Acid Does Not Increase Tissue Arachidonic Acid Content in Adults Consuming Western-Type Diets: A Systematic Review’, Nutrition & Metabolism, 8, 36.
19. Telle-Hansen, V. H. et al. (2017) ‘Does Dietary Fat Affect Inflammatory Markers in Overweight and Obese Individuals?—A Review of Randomized Controlled Trials from 2010 to 2016’, Genes & Nutrition, 12, 26.
20. Johnson, G. H. and Fritsche, K. (2012) ‘Effect of Dietary Linoleic Acid on Markers of Inflammation in Healthy Persons: A Systematic Review of Randomized Controlled Trials’, Journal of the Academy of Nutrition and Dietetics, 112(7), 1029-41.
21. (a) Leopold, J. A. and Loscalzo, J. (2009) ‘Oxidative Risk for Atherothrombotic Cardiovascular Disease’, Free Radical Biology and Medicine, 47(12), 1673-706; (b) Kummerow, F. A. (2013) ‘Interaction Between Sphingomyelin and Oxysterols Contributes to Atherosclerosis and Sudden Death’, American Journal of Cardiovascular Disease, 3(1), 17-26; (c) Saha, S. K. et al. (2017) ‘Correlation Between Oxidative Stress, Nutrition, and Cancer Initiation’, International Journal of Molecular Sciences, 18(7), 1544; (d) Liguori, I. et al. (2018) ‘Oxidative Stress, Aging, and Diseases’, Clinical Interventions in Aging, 13, 757-72.
22. ibid (21b).