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Health Benefits of Sunflower Oil

About the author: James Collier BSc (Hons), Registered Nutritionist. James has over 25 years of experience working in nutrition and dietetics, including 7 years as a Clinical Dietician in the NHS. Covering an array of clinical areas, he worked with people with a wide range of ailments and food intolerances.

Sunflower oil is a popular ingredient that’s rich in good fats but receives mixed reviews with some texts advocating a wealth of health benefits, whilst others suggest caution in respect of consuming too much. Consequently, there is a considerable amount of published misinformation, much of which is based on incomplete facts. This article will discuss sunflower oil’s qualities and will address the principal concerns people have, demonstrating why the sunflower oil used in Huel is both necessary and beneficial.

Sunflower oil is produced via the pressing of the seeds of the common sunflower plant (Helianthus annuus), and it is commonly used in both commercial food manufacture and home cooking as well as in cosmetics. The oil content of the seeds varies from 22% to 36% and is extracted from the seeds through expeller pressing[1]. The resulting oil is light amber in colour and has a pleasant, mild flavour. Sunflower oil has a relatively clean taste, making it relatively easy to incorporate into recipes.

Sunflower oil started to become a more popular choice of cooking oil in the late 1970s and 1980s[2], following the health claims surrounding the negative effects of saturated fats and the benefits of polyunsaturates on cardiac health[3-5]. Consumption also increased due to the rise in consumption of convenience junk foods, many of which contain sunflower oil rather than animal-derived fats due to the pressure on the food industry to lower the saturated fat content of these foods[5]). Because many fast foods contain sunflower oil, it has given rise to claims that sunflower oil is an unfavourable ingredient choice when, in reality, there’s more to consider.

Types of sunflower oil and their fat composition

There are four main types of sunflower oil produced through plant breeding and industrial processing, and these are categorised based on their principal fatty acid content. For information on the different groups of fatty acids, where each is found and what the benefits are, see our article Good Fats & Bad Fats.

Regular sunflower oils are 65-75% omega-6 polyunsaturates, principally the essential fatty acid (EFA) linoleic acid (LA), 20-40% monounsaturates (principally the omega-9 oleic acid (OA)), and the remainder is made up of saturates, principally palmitic and stearic acids. Due to the interest in the health benefits of monounsaturates, varieties of high-oleic acid sunflower oils (HOSO) have been developed and these are around 80% OA, less than 10% LA and lower in saturates. As well as these, there are degrees of sunflower oils in between with varying levels of monounsaturates and omega-6s with mid-oleic sunflower oils (MOSO) having around 50% OA. In addition to these, there are also high-stearic, high-oleic sunflower oil (HSHOSO) varieties with over 15% stearic acid and 70% OA, and these are used more so in cosmetics.

There are very low levels of omega-3 polyunsaturated in all types of sunflower oil and next to zero medium-chain triglycerides (MCTs) and trans fats. We have more detailed information on both omega-3 fats and MCTs in our articles Guide to EPA and DHA in Huel and Benefits of Medium-Chain Triglycerides respectively.

The following table shows the main categories of sunflower oil and the amounts of the four main fatty acids each contains (taken from various oil specifications):

Vitamins and minerals in sunflower oil

All types of sunflower oil are rich in vitamin E with about 40mg of alpha-tocopherol per 100g, as well as about 5mcg of vitamin K1. There are zero to negligible amounts of any other vitamins and minerals present.

Oxidation and sunflower oil

Oxidation – also known as rancidity – is the process where harmful free-radicals are produced, and these can have a number of negative health implications including being atherosclerotic and increasing the risk of cardiovascular disease (CVD)[6].

The smoke point of a fat or an oil refers to the temperature at which it begins to produce a bluish smoke[7] and is an indicator of how temperature affects the susceptibility of it to oxidation. Unrefined sunflower oil has a low smoke point of 107ºC/225ºF; refined sunflower oil has a high smoke point of 227-232ºC/440-450ºF. Fats and oils with a low smoke point are more susceptible to oxidation so should not be heated to high temperatures. Most sunflower oil that’s sold for home cooking is refined so is suitable for heating to a high temperature.

Temperature is not the only factor that affects the oxidation of a fat/oil; others include light, humidity, the presence of heavy metals and exposure to oxygen as well as the unsaturated fatty acid content. Oils with a high unsaturated fatty acid content are more prone to oxidation and fats/oils that are primarily comprised almost entirely of saturated fatty acids will not oxidise even in the presence of otherwise oxidation-promoting conditions.

As sunflower oil is primarily composed of monounsaturates and polyunsaturates, it is important that it is stored in a sealed container and in a cool, dark and dry place. And, whilst it’s fine to heat sunflower oil and other vegetable oils to high temperatures a single time for immediate consumption, they should not be reheated and exposed to oxygen or light continuously. This is a significant reason why many fast-foods and junk foods are atherosclerotic: the oil – e.g. sunflower – used for frying – is exposed to a significant oxidation-promoting environment before the food is consumed[6].

Why sunflower oil is beneficial

As sunflower oil is low in both saturated and trans fats, it is an attractive choice of oil for use in home cooking and food manufacture. Many convenience food recipes use regular sunflower oil as an ingredient – and consequently contain a high level of omega-6s – due to the pressure on manufacturers to lower the saturated fat content of foods[5]. This has led to a plethora of confusing articles and blog posts: some sources claim that there is overconsumption of omega-6s in the Western diet and we should be lowering our intake of them[5, 8-12]. As regular sunflower oil is high in omega-6s, some information may lead people to think that sunflower oil is an oil to be avoided or that HOSO is the preferred choice as it’s lower in omega-6s and higher in monounsaturates.

On the other hand, we have information encouraging a high intake of polyunsaturates – both omega-3s and -6s. Sunflower oil, with its relatively low saturated fat content, its low susceptibility to temperature-induced oxidation and the fact that it’s rich in one of the two most important fatty acids for health, is therefore recommended.

This is understandably confusing, and the reality is we absolutely should be including a good intake of omega-6s in our daily diets, although the quality of the omega-6s we ingest is important. Indeed, maybe it’s not the overconsumption of omega-6s that’s the key issue, rather the ratio of omega-3s to -6s in our diets[13]; i.e. we should be eating greater amounts of foods which contain the omega-3s alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA) and/or docosahexaenoic acid (DHA) derived from nuts, seeds (like flaxseed) and other plant sources, or from oily fish and marine algae (more information)[14]. As well as consuming adequate amounts of omega-3s, of equal importance are omega-6s[15] – especially LA – as long as they are in the right form and are not adulterated by oxidation.

In poor-nutritional-quality overly processed junk foods, vegetable oils that are susceptible to oxidation are damaged and lose their health benefits. Therefore, overconsumption of omega-6s from these foods could indeed contribute to CVD risk as observational studies may have indicated[12, 16], and this is apparently where the claims that overconsumption of omega-6-rich oils like sunflower oil are bad come from. However, this absolutely in no way means that consuming omega-6-rich oils is undesirable, and this misinterpretation of the literature is one of the reasons that’s leading to the incorrect information being disseminated.

LA is one of the two EFAs that humans require in our diet; it’s the only omega-6 that is essential and is the most abundant omega-6 in the human diet accounting for typically 90% of omega-6 PUFA intake[8, 17]. Indeed, consuming 5-10% of total energy from omega-6s is associated with a reduced risk of CVD relative to low intakes[9-11]. LA has also been shown to be the most potent fatty acid for lowering both blood total cholesterol and LDL cholesterol levels, more so than omega-3s[18, 19]. An increased intake of both omega-3 and omega-6 polyunsaturates has been shown to reduce CVD risk and is recommended for both primary and secondary prevention of CVD[10, 20, 21].

Are omega-6s inflammatory?

Inflammation is a necessary physiological response to injury or infection to help fight off foreign bodies and to aid the healing process. However, low-grade inflammation – defined as the chronic production of inflammatory factors at a low level as a result of an unresolved inflammatory response – may have an involvement in disease development and has been linked to obesity, CVD, depression, chronic pain and poor gut health[22-26].

Poor dietary habits may be associated with low-grade inflammation[26, 27], and there have been claims made that omega-6s – and hence, sunflower oil – are ‘pro-inflammatory’ through being linked to low-grade inflammation and subsequently overconsumption of them increases the risk of some diseases[28-30]. The reasoning behind this speculation is due to the omega-6 fatty acid arachidonic acid (AA) being involved in the production of various inflammation-promoting factors. 

AA is synthesised in the body from LA and is sometimes referred to as a semi-essential fatty acid in circumstances where there’s insufficient LA. Both AA and the omega-3 EPA are necessary for the production of eicosanoids, critical chemical messengers for the immune and inflammatory responses. The response from AA-derived eicosanoids is different to the response from EPA-derived eicosanoids, however, with the latter being less potent inducers of inflammation[8, 31]. Nevertheless, it’s an oversimplification to label all AA-derived eicosanoids as pro-inflammatory as they also inhibit pro-inflammatory factors like leukotrienes and cytokines and induce anti-inflammatory lipoxins[8, 28]. Therefore, an adequate amount of AA will actually help to maintain an optimal inflammatory response.

As a good intake of omega-3 fatty acids has a beneficial effect on inflammation[32] and, as the ratio of omega-3s to omega-6s is often suboptimal in a population[13-15], this may lead people to wrongly assume that omega-6s are pro-inflammatory when, in fact, the problem lies with the lack of omega-3s being the pro-inflammatory issue[33].

The claim also assumes that a higher dietary LA intake is directly related to the level of AA in the blood; i.e. an increased intake of LA leads to a higher conversion to AA and this, in turn, is converted to inflammatory eicosanoids. This is not the case as there is a negative feedback control in place; i.e. AA and eicosanoids are only produced on demand[28, 30].

Furthermore, serum levels of C-reactive protein (CRP) – a key blood marker for inflammation – have been shown to be lower with a higher serum LA level[29, 30, 34], indicating that a good intake of LA actually protects against low-grade inflammation. It has also been shown that even a very high intake of linoleic acid does not increase inflammatory responses, nor has a significant impact on AA levels[35-38].

Therefore, the claim that a high intake of omega-6 fatty acids, or indeed LA-rich sunflower oil, can promote low-grade inflammation by increasing the body's AA levels is overly simplified and, in fact, the reverse is true.

Sunflower oil in Huel

Huel Powder contains sunflower oil powder. This is produced by spray-drying regular sunflower oil onto a carrier. You can read about the process here and this maintains all of the oil’s nutrition and aroma properties whilst increasing its versatility and shelf life.

As Huel contains all the nutrients you need for optimum health, it’s paramount that it contains an adequate amount of LA to provide enough to at least cover all essential requirements and sufficient for conversion to AA.

The omega-6 content of Huel products are as follows:

Per 2,000kcal % total energy
Huel Powder

(based on EU v2.3 Vanilla)

15.7g 7%
Huel Bar

(based on EU v3 Cocoa)

23.2g 10%
Huel Ready-to-drink

(based on v1.0 Vanilla)

20.5g 9%
Huel Granola

(based on v1.1 Original)

19.5g 7%

As a proportion of total energy intake, these are all in line with a lower CVD risk[9-11] and reflect optimum nutrition targets.

What is sunflower lecithin?

Lecithins are natural fatty substances found in both plant and animal tissues which are amphiphilic; i.e. they attract both water and oils. They are often used in foods to create a smoothing texture and to reduce stickiness. Sunflower lecithin is in the form of phosphatidylcholine, and 0.1-0.2% of sunflower oil is lecithin. Huel Ready-to-drink and Huel Bar both contain sunflower lecithin to help with smoothness and texture whilst providing some nutrition.

Main points

  • There are different types of sunflower oil
  • Standard sunflower oil is rich in the essential omega-6 fatty acid linoleic acid
  • Sunflower oil is rich in vitamin E and contains some vitamin K1
  • Sunflower oil is susceptible to oxidation
  • Vegetable oils used in the production of convenience junk foods are likely to be unfavourable
  • It is a misconception that sunflower oil is pro-inflammatory
  • The sunflower oil in Huel is beneficial and a crucial source of linoleic acid

References

  1. Cox J. Organic Gardening: Rodale Press; 1979.
  2. Sandbakken J & Kleingartner L. Sunflower Production  [Available from: https://www.ag.ndsu.edu/pubs/plantsci/rowcrops/a1331-03.pdf].
  3. Dietary goals for the United States: statement of The American Medical Association to the Select Committee on Nutrition and Human Needs, United States Senate. R I Med J. 1977; 60(12):576-81.
  4. NACNE (National Advisory Committee on Nutrition Education). A Discussion Paper on Proposal for Nutritional Guidelines for Health Education in Britain. 1983.
  5. Harcombe Z, et al. Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis. Open Heart. 2015; 2(1):e000196.
  6. Kummerow FA. Interaction between sphingomyelin and oxysterols contributes to atherosclerosis and sudden death. Am J Cardiovasc Dis. 2013; 3(1):17-26.
  7. American Oil Chemists’ Society. AOCS Official Method Cc 9a-48, Smoke, Flash and Fire Points Cleveland Open Cup Method.  Official methods and recommended practices of the AOCS. Champaign, Ill.: American Oil Chemists' Society; 2011.
  8. Linus Pauling Institute; Oregon State University. Essential Fatty Acids  [Available from: https://lpi.oregonstate.edu/mic/other-nutrients/essential-fatty-acids].
  9. Harris WS, et al. Omega-6 fatty acids and risk for cardiovascular disease: a science advisory from the American Heart Association Nutrition Subcommittee of the Council on Nutrition, Physical Activity, and Metabolism; Council on Cardiovascular Nursing; and Council on Epidemiology and Prevention. Circulation. 2009; 119(6):902-7.
  10. Kris-Etherton P, et al. The debate about n-6 polyunsaturated fatty acid recommendations for cardiovascular health. J Am Diet Assoc. 2010; 110(2):201-4.
  11. Harris WS, et al. n-6 Fatty acids and risk for CHD: consider all the evidence. Br J Nutr. 2011; 106(6):951-2; author reply 3-7.
  12. Massiera F, et al. A Western-like fat diet is sufficient to induce a gradual enhancement in fat mass over generations. J Lipid Res. 2010; 51(8):2352-61.
  13. Simopoulos AP. Evolutionary aspects of diet: the omega-6/omega-3 ratio and the brain. Mol Neurobiol. 2011; 44(2):203-15.
  14. Molendi-Coste O, et al. Why and How Meet n-3 PUFA Dietary Recommendations? Gastroenterol Res Pract. 2011; 2011:364040.
  15. Das UN. Essential fatty acids: biochemistry, physiology and pathology. Biotechnol J. 2006; 1(4):420-39.
  16. Patterson E, et al. Health implications of high dietary omega-6 polyunsaturated Fatty acids. J Nutr Metab. 2012; 2012:539426.
  17. US Department of Agriculture; Agricultural Research Service. Nutrient Intakes from Food: Mean Amounts Consumed per Individual, by Gender and Age  [Available from: https://www.ars.usda.gov/northeast-area/beltsville-md-bhnrc/beltsville-human-nutrition-research-center/food-surveys-research-group/].
  18. Mensink RP, et al. Effect of dietary fatty acids on serum lipids and lipoproteins. A meta-analysis of 27 trials. Arterioscler Thromb. 1992; 12(8):911-9.
  19. Fernandez ML, et al. Mechanisms by which dietary fatty acids modulate plasma lipids. J Nutr. 2005; 135(9):2075-8.
  20. Ramsden CE, et al. Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis. BMJ. 2013; 346:e8707.
  21. Mozaffarian D, et al. Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Med. 2010; 7(3):e1000252.
  22. Wellen KE, et al. Obesity-induced inflammatory changes in adipose tissue. J Clin Invest. 2003; 112(12):1785-8.
  23. Dantzer R. Depression and inflammation: an intricate relationship. Biol Psychiatry. 2012; 71(1):4-5.
  24. Dantzer R, et al. From inflammation to sickness and depression: when the immune system subjugates the brain. Nat Rev Neurosci. 2008; 9(1):46-56.
  25. Parkitny L, et al. Inflammation in complex regional pain syndrome: a systematic review and meta-analysis. Neurology. 2013; 80(1):106-17.
  26. Minihane AM, et al. Low-grade inflammation, diet composition and health: current research evidence and its translation. Br J Nutr. 2015; 114(7):999-1012.
  27. Hotamisligil GS. Inflammation and metabolic disorders. Nature. 2006; 444(7121):860-7.
  28. Calder PC. Polyunsaturated fatty acids and inflammatory processes: New twists in an old tale. Biochimie. 2009; 91(6):791-5.
  29. Virtanen JK, et al. The associations of serum n-6 polyunsaturated fatty acids with serum C-reactive protein in men: the Kuopio Ischaemic Heart Disease Risk Factor Study. Eur J Clin Nutr. 2018; 72(3):342-8.
  30. Science Daily. Omega-6 fatty acids do not promote low-grade inflammation 2017 [Available from: https://www.sciencedaily.com/releases/2017/11/171113095430.htm].
  31. Flock MR, et al. Long-chain omega-3 fatty acids: time to establish a dietary reference intake. Nutr Rev. 2013; 71(10):692-707.
  32. Reinders I, et al. Association of serum n-3 polyunsaturated fatty acids with C-reactive protein in men. Eur J Clin Nutr. 2012; 66(6):736-41.
  33. Sergeant S, et al. Gamma-linolenic acid, Dihommo-gamma linolenic, Eicosanoids and Inflammatory Processes. Eur J Pharmacol. 2016; 785:77-86.
  34. Kubota Y, et al. Serum Polyunsaturated Fatty Acid Composition and Serum High-Sensitivity C-Reactive Protein Levels in Healthy Japanese Residents: The KOBE Study. J Nutr Health Aging. 2015; 19(7):719-28.
  35. Thies F, et al. 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. 2001; 36(11):1183-93.
  36. Kelley DS, et al. Arachidonic acid supplementation enhances synthesis of eicosanoids without suppressing immune functions in young healthy men. Lipids. 1998; 33(2):125-30.
  37. Rett BS, et al. Increasing dietary linoleic acid does not increase tissue arachidonic acid content in adults consuming Western-type diets: a systematic review. Nutr Metab (Lond). 2011; 8:36.
  38. Kaikkonen JE, et al. High serum n6 fatty acid proportion is associated with lowered LDL oxidation and inflammation: the Cardiovascular Risk in Young Finns Study. Free Radic Res. 2014; 48(4):420-6.

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