Are we right to be afraid of dietary saturated fats? Dr Emma Feeney, Food for Health Ireland, University College Dublin, considers this controversial question
With more energy per gram (9 kcal) than any other macronutrient, the consumption of dietary fats (and high-fat foods) is believed to promote weight gain via an energy imbalance. For this reason, reducing dietary fat intake can be a successful weight loss or weight maintenance strategy. However, fats provide more than just calories — they are also required for a number of vital structural and nutrient-absorption functions. Accordingly, dietary fat can influence health outcomes other than body weight (for example, saturated fat intakes have been implicated in heart health).
This functional variety results in part from the fact that dietary fat is not a single substance, rather a collective of individual fatty acid types. Chemically, fatty acids consist of a carboxyl group (-COOH) attached to a long hydrocarbon chain, which can either be saturated (that is, contains no double bonds) or unsaturated (one or more double bonds). Thus, fats tend to be grouped based on their chemical make-up into three types: saturated fatty acids (SFAs), monounsaturates (MUFAs) and polyunsaturates (PUFAs).
The level of saturation can affect the fat’s physical properties. Generally, the more unsaturated the fat, the lower the melting point, and these tend to come mostly from plant-based sources, whereas saturated fats are generally derived from animal sources, with coconut oil being a notable exception. SFAs range in their carbon chain (C) length, from C:4–C:20, with the majority being C:12–C:16.
Dietary guidelines typically exist at two levels; at a nutrient level and also translated into a food-based level. Traditionally, the (nutrient-based) guidelines for SFAs are to keep intakes low, generally no more than 10–11% of total calories, with the most recent European Food Safety Authority position advising to keep intakes “as low as possible.”1–3 At the food level, the general recommendation from the World Health Organization involves following a pattern “based on whole foods (fruit and vegetables, whole grains, nuts, seeds, legumes and long chain polynsaturated fatty acid-rich seafood),” and a “lower intake of energy dense processed and fried foods, and sugar-sweetened beverages; and to avoid the consumption of large portion sizes.” However the contribution of the “moderate consumption” of dairy, lean meats and poultry to a healthful diet is acknowledged.3
The story appears to be more grey than the simple black and white picture that has sometimes been portrayed in public health messages
The origins of such recommendations to restrict intakes of SFAs can be traced to studies such as the Framingham and the Seven Countries studies, published in 1961 and 1970, respectively. These demonstrated some of the first correlations between total cholesterol and the risk of coronary heart disease (CHD), and between SFA consumption and CHD.4,5 The central principle, that saturated fat raises cholesterol and in turn increases the risk of developing heart disease, has become engrained in the public psyche, through numerous public health messages in the following 40-plus years.
More recently, however, the story appears to be more grey than the simple black and white picture that has sometimes been portrayed in public health messages. Advances in cholesterol measurement techniques, together with improvements in food intake estimates, have actually resulted in more ambiguous results, rather than cementing the link between SFA and heart disease.
In SFA and heart health studies, the biochemical outcomes assessed usually include total cholesterol, high density lipoprotein (HDL-C or “good” cholesterol) and low density lipoprotein (LDL-C or “bad” cholesterol). However, within LDL-C, there are two further types; large, buoyant LDL-C (pattern A) and small, dense LDL-C (pattern B), with pattern B reported to be approximately three times more artery damaging than pattern A.6
Although it is known that SFA can not only increase total cholesterol and LDL-C, but also, in some cases, HDL-C levels as well, what remains less characterised is the influence of SFA on these subclasses of LDL-C.7 Furthermore, not all saturated fats appear to act in an equal manner. The consumption of SFAs found mainly in milk and dairy products (such as C:4–C:10) are actually associated with fewer of the small, dense LDL-C particles.
The food matrix in which the SFAs are consumed adds yet another dimension to consider. For example, a number of studies have shown that saturated fats in certain types of dairy products, such as yoghurt and cheese, may actually improve cholesterol profiles and other CHD risk markers.8,9 Unfortunately, neither the current fatty acid nomenclature, nor the dietary guidelines based on them, take this functional diversity into account, and all SFAs are tarred with the same “unhealthy” brush. This problem is acknowledged by expert panels, who have considered revising the current system. However, until such time as a more useful and meaningful system is developed, the present widely used groupings are likely to remain.
A more important issue, perhaps, regarding the reduction of saturated fat intake, is the question of what to replace it with. Consider that the macronutrient content of the diet is a ratio; thus, reducing one nutrient will naturally alter the overall macronutrient ratios. Current evidence suggests that replacing SFA with carbohydrate, particularly fast-absorbed (high glycaemic) carbohydrates, such as sugar, may not be advisable, as it may increase the amount of LDL-C produced, specifically Pattern B — the type that is more associated with CVD.10 Replacing some SFAs with PUFAs, by contrast, has been associated with a more heart-healthy fatty acid profile.11
Dairy products have typically been considered to be a significant source of saturated fat, particularly cheese, and there is strong public belief that these foods ought to be limited in the diet, especially by those individuals who have high levels of blood cholesterol. This view has manifested in such newspaper headlines as “My love of cheese nearly cost me my leg,” referring to a man suffering from peripheral arterial disease who suffered a blood clot in his leg.12 A former smoker, he was also overweight, reported regularly eating takeaways and was fond of cheese. Although being overweight and smoking are two independent risk factors for CHD, the cheese consumption was the aspect that made the headline.
At least four independent studies conducted in the last 10 years have found that the saturated fat from cheese consumed for 4–6 weeks does not raise either HDL or LDL cholesterol levels when compared with the same amount and type of saturated fat given in butter form
From a scientific standpoint, however, at least four independent studies conducted in the last 10 years have found that the saturated fat from cheese consumed for 4–6 weeks does not raise either HDL or LDL cholesterol levels when compared with the same amount and type of saturated fat given in butter form (which does raise total LDL cholesterol).13,14 These results suggest that other compounds are present in cheese that may have beneficial effects on blood cholesterol. Researchers believe this may partly result from the high calcium content of cheese preventing absorption of dietary cholesterol, as well as its high protein content. Hence, a moderate daily intake of cheese may be enjoyed as part of a healthy diet.
Although food-based guidelines generally recommend a matchbox-sized portion of cheese (equal to approximately 25g), these studies suggest that as much as 45g daily has no negative impact on cholesterol levels, and in fact one study fed as much as 205g of hard cheese per 10MJ energy intake daily for three weeks without raising LDL-C levels (equivalent to 172g in an average 2000kcal diet).
Of course, cholesterol levels (and cholesterol subclasses) are just one biomarker of heart health; others also exist, such as blood pressure, inflammation and insulin sensitivity. However, in general, there is no clear relationship between SFA intake and any of these outcomes. Furthermore, the link between saturated fat intake and cholesterol levels appears to be dependent on genetic make-up. In other words, some individuals may be at greater risk of heart disease than others, regardless of diet.
Although we need at least some saturated fat in our diet, a great degree of uncertainty persists regarding exact intakes for disease prevention and for optimal health. Even though current guidelines suggest restricting SFA intake, it is important to remember that this is a very generalised guideline, based mainly on historical data. Many different types of SFAs exist under the umbrella term of ‘saturated fat.’ Research is still very much ongoing in this field, but dairy SFAs in particular appear to be associated with beneficial health effects. Future dietary guidelines may need to reflect the wide range of structures and functions of SFAs being identified.
1. Dietary Reference Values for Food Energy and Nutrients for the United Kingdom: www.sacn.gov.uk/pdfs/sacn_dietary_reference_values_ for_energy.pdf.
2. EFSA Panel on Dietetic Products, Nutrition and Allergies (NDA); Scientific Opinion on Dietary Reference Values for energy: www.efsa.europa.eu/efsajournal.
3. Joint FAO/WHO Expert Consultation on Fats and Fatty Acids in Human Nutrition: www.who.int/nutrition/topics/FFA_human_nutrition/en (2008).
4. W.B. Kannel, et al., Ann. Intern. Med. 55, 33–50 (1961).
5. A. Keys, Circulation 41(Suppl. 1), 1–211 (1970).
6. M.A. Austin, et al., JAMA, 260(13), 1917–1921 (1988).
7.>/b> R.P. Mensink, et al., Am. J. Clin. Nutr. 77, 1146–1155 (2003).
8. J.M. Steijns, Int. Dairy Journal 18(5) 425–435 (2008).
9. P. Sjogren, et al., J. Nutr. 134(1), 1729–1735 (2004).
10. J.S. Volek, et al., Progress in Lipid Research 47(5), 307–318 (2008).
11. A. Astrup, et al., AJCN, 93(4) 684–688 (2011).
12. The Daily Mail, “My Love of Cheese Nearly Cost Me My Leg,” 25 October 2011.
13. T. Tholstrup, et al., J. Am. Coll. Nutr. 23(2), 169–176 (2004).
14. P.J. Nestel, et al., EJCN. 59, 1059–1063 (2005).for more information Dr Emma Feeney Food for Health Ireland University College Dublin Tel. +353 1 716 2430 email@example.com www.fhi.ie