Facing the Fats: Should You Be Scared of Saturated Fat?

by Emily Groopman and Jen Guidera

Butter. Bacon. Heavy cream. While considered wholesome staples in 19th and early 20th century America, these foods are now seen as “greasy killers” rather than good nourishment (1, 2). The fear and even shame surrounding consumption of such items reflects a powerful nutritional paradigm. Associated with a plethora of unpalatable conditions, including obesity, cardiovascular disease (CVD), and Type II diabetes, saturated fat is the ultimate dietary taboo. Yet, despite favoring lard, butter, and beef tallow, populations such as the French are both leaner and less prone to CVD (3). The simultaneous rise in saturated fat phobia and obesity rates casts further doubt on its supposed dangers. Faced with such contradictions, consumers may begin to question mainstream beliefs. Though seen as a virtually fatal substance, how bad is saturated fat truly?

Fat 101: Saturation, Hydrogenation, and More

While well informed of the potential dangers of saturated fat, the average consumer likely lacks similar knowledge of its chemical structure or biological functions. Dietary fats are largely triacylglycerols (TAGs), which consist of three fatty acids attached to a glycerol backbone (4). TAGs can be classified by three biochemical properties: saturation, conformation, and chain length. Saturation refers to the state in which carbons are bonded to the maximum number (i.e., “saturated” with) hydrogen atoms (5). Thus, saturated fats have no carbon-carbon double (C=C) bonds, while unsaturated fats have one (monounsaturated) or more (polyunsaturated). This results in differing molecular shape and as well as structure: the double bonds create “kinks” in the fatty acid chains, increasing their surface area and preventing them from packing tightly together (5). Thus, at room temperature, unsaturated fats, derived from nuts, seeds, and fish, are fluid, liquid “oils,” whereas saturated fats, derived from animal products and coconut, are dense, solid “fats” (6).

Conformation is similarly important for TAG structure. Within unsaturated fatty acids, hydrogen atoms about the C=C bond can be on either the same (cis) or opposite (trans) sides. The latter conformation decreases the “kink” of the C=C bond, causing trans isomers to be structurally – and behaviorally – similar to saturated fatty acids (5). Finally, TAGs vary in chain length, the number of carbon atoms in the fatty acid backbone. Dietary fat largely consists of long (>14 carbon) chain fatty acids (LCFAs); however, some saturated fats, such as milk fat and coconut oil, contain significant amounts of short (<8 carbon; SCFAs) and medium (<14 carbon; MCFAs) fatty acids (4, 7). Shorter chain length increases solubility in the blood, enabling SCFAs and MCFAs to flow directly to the liver, where they are oxidized to generate energy (8, 9). As a result, they, unlike LCFAs, bypass adipose tissue – and therefore are not stored as body fat. MCFAs have also been shown to actively oppose body fat synthesis, via down-regulating involved genes and stimulating fat oxidation (9). Thus, substances high in these shorter chain fatty acids likely promote weight loss and/or maintenance – regardless of their degree of saturation.

But Is It Fattening? Assessing the Relationship Between Saturated Fat and Obesity Risk

It seems very intuitive that fat ingested is stored as fat in the body. However, fat, including saturated fat, has many other roles in the body than just adding padding. Saturated fat regulates gene expression as a transcription factor, releases hormones coordinating immunity and metabolic function, and is a vital component of cell membranes (5). Still, we might wonder, even given these other functions of fat, does fat lead to weight gain more so than other macronutrients like carbohydrates? We have good reason to ask this question–in the nutritional movements happening in our day and age, fat seems to have a special role in weight gain. Foods we typically think of as “fatty”–french fries, potato chips, M&Ms–have all been implicated in campaigns against obesity (10). The USDA, for example, states in their most recent Dietary Guidelines Consumer Brochure, “Make major sources of saturated fat–such as cakes, cookies, ice cream, pizza, cheese, sausages, and hot dogs–occasional choices, not everyday foods” (10). One thing we should notice is that many of these foods, including French fries, potato chips, M&Ms, cakes, cookies, ice cream, and pizza, are also high in highly processed carbohydrates.

The fact that many foods we normally consider high in saturated fat are often high in refined carbohydrates poses a challenge to those looking to study the effect of saturated fat on weight gain. Further, foods high in saturated fat are also often “calorie dense” foods, packing more energy per unit weight and per unit volume. You would have to eat, for example, five times as much broccoli by weight to intake the same number of calories that you would get from cheddar cheese. With all of these factors coming together in the same group of foods, it is indeed challenging to separate the variables and make conclusions about which variables are actually linked to weight gain.

Nevertheless, several studies have made an effort to separate these variables. For example, a study examining juvenile obesity found that caloric intake, not fat intake, correlated most closely with weight gain (11). Another study approached the fat-weight gain question from the weight loss angle, and also found that total caloric intake, not fat intake, correlated most closely with weight–subjects that were put on a low-fat diet lost the same amount of weight as subjects put on low carb diets (12). Based on these findings, it seems that total caloric intake is more closely tied to weight than is fat intake.

Interestingly, some studies have found that certain fat-rich foods are associated with weight loss. For example, a New England Journal of Medicine study looking at long-term changes in weight that found that peanuts were correlated with weight loss (13). Other studies show that fat reduces food consumption after a meal (14). But are certain fats more satiating than others? A recent study compared the satiety-effects of foods with different levels of saturated and unsaturated fats. The study found that chocolate, a food high in saturated fat, had similar satiety effects as peanuts, which contain primarily unsaturated fat (15). These findings suggest that saturated and unsaturated fat may have similar effects on satiety.

LDL and HDL: Assessing the Impact of Saturated Fat on CVD Risk

Though important, body mass index is not the sole measure of health: while obesity may strongly increase chronic disease risk, it is the diseases themselves that kill. Thus, the effects of saturated fat on CVD risk are as – if not more – important as its impact on body weight. For most Americans, exposed by the prevalent nutritional messages of the past 60 years, the association seems obvious: as a rich source of cholesterol, saturated fat raises levels of serum cholesterol, which “clogs” vessels, blocking blood flow to the heart and thereby resulting in CVD (16). However, evidence for this “Fat-Heart Disease” hypothesis was hardly conclusive. Supporting reports such as Ancel Keys’ famous “Seven Countries Study,” found a positive relationship between national saturated fat intake and per-capita CVD incidence, with countries with high intakes, like the United States, exhibiting higher rates than those with lower intakes, like Japan (17). Yet, such national-level analysis provided no insight on individual risk, as those consuming the most saturated fat may not have been the same persons developing CVD. Such broad analysis also fails to account for a plethora of potential confounds, including differences in intake of other nutrients, activity level, and relative genetic risk (18).

Assume, as did the US Department of Agriculture and American Heart Association in the 1980s, that these investigations provide sufficient evidence. Nevertheless, the “Fat-Heart Disease” remains unproven: for, despite the statements of such health authorities, total cholesterol is an unreliable marker of heart disease risk. Serum cholesterol is transported by two major carriers: low (LDL) and high (HDL) lipoprotein (18). While LDL accumulates in arterial walls, resulting in vessel narrowing and increasing CVD risk, HDL has the opposite effect, removing cholesterol from cells back to the liver, where it can be metabolized and eliminated (5). Thus, the LDL: HDL ratio, rather than absolute serum concentrations of the two, predicts CVD risk (19, 20). Recent randomized clinical trials (RCT) – the “gold standard” of dietary research – report that saturated fat has a neutral effect on LDL: HDL ratio, as it raises levels of both (21, 22). Further, saturated fat intake has even been negatively associated with CVD risk among certain groups: for instance, Mozaffarian, Rimm, & Herrington, found that postmenopausal women consuming higher saturated diets displayed less arterial narrowing and cholesterol blockage (23). Strikingly, intake of “good” polyunsaturated fat significantly increased CVD risk (23). Though requiring further validation by RCTs, such findings imply that saturated fat does not harm, and in some cases, may promote health.

 The Final Say on Saturated Fat

Contrary to what diet gurus and health magazines may claim, fat is more than fattening. Saturated fat has many key roles in the body, functioning as a transcription factor, regulator of hormone release, and building block of cell membranes. And, although calorie-dense, saturated fat does not necessarily lead to weight gain–total caloric intake seems to be the better predictor of weight gain. In fact, recent research suggests that some fat-rich foods may be satiating, promoting weight control.

Given the mixed and constantly fluctuating messages we receive from the nutritional mainstream, what should we do as consumers? While most dietary messages we receive revolve around weight, it is important to remember that health should be the focus. Further, we should keep in mind that health more than a number on the scale, and that likewise, food is more than the sum of its macronutrients. Ultimately, when making decisions, it is often wise to be wary of absolutes. Using moderation as a guide, we should make choices that both align with our current lifestyle and support a healthy and happy future.


1.      G. Taubes, “What if It’s All Been a Big Fat Lie?,” New York Times, July 7, 2002 2002.

2.      H. Levenstein, Revolution at the Table: The Transformation of the American Diet.  (University of California Press, California, USA, 2003).

3.      M. de Lorgeril et al., Mediterranean diet and the French paradox: two distinct biogeographic concepts for one consolidated scientific theory on the role of nutrition in coronary heart disease. Cardiovascular research 54, 503 (Jun, 2002).

4.      H. Mu, C. E. Hoy, The digestion of dietary triacylglycerols. Prog Lipid Res 43, 105 (Mar, 2004).

5.      B. A. Griffin, S. C. Cunnane, in Introduction to Human Nutrition, M. J. Gibney, S. A. Lanham-New, A. Cassidy, H. H. Vorster, Eds. (Wiley-Blackwell, United Kingdom, 2009),  pp. 86-117.

6.      K. Sato, Crystallization behaviour of fats and lipids – a review. Chem Eng Sci 56, 2255 (Apr, 2001).

7.      S. Gallier et al., In vivo digestion of bovine milk fat globules: effect of processing and interfacial structural changes. I. Gastric digestion. Food Chem 141, 3273 (Dec 1, 2013).

8.      M. P. St-Onge, Dietary fats, teas, dairy, and nuts: potential functional foods for weight control? The American journal of clinical nutrition 81, 7 (Jan, 2005).

9.      B. Marten, M. Pfeuffer, J. Schrezenmeir, Medium-chain triglycerides. Int Dairy J 16, 1374 (Nov, 2006).

10.     U. S. D. o. Agriculture, U. S. D. o. Agriculture, Ed. (2011).

11.     L. J. Gillis, L. C. Kennedy, A. M. Gillis, O. Bar-Or, Relationship between juvenile obesity, dietary energy and fat intake and physical activity. International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity 26, 458 (Apr, 2002).

12.     I. Shai et al., Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. The New England journal of medicine 359, 229 (Jul 17, 2008).

13.     D. Mozaffarian, T. Hao, E. B. Rimm, W. C. Willett, F. B. Hu, Changes in diet and lifestyle and long-term weight gain in women and men. The New England journal of medicine 364, 2392 (Jun 23, 2011).

14.     V. Van Wymelbeke, A. Himaya, J. Louis-Sylvestre, M. Fantino, Influence of medium-chain and long-chain triacylglycerols on the control of food intake in men. The American journal of clinical nutrition 68, 226 (Aug, 1998).

15.     S. V. Kirkmeyer, R. D. Mattes, Effects of food attributes on hunger and food intake. International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity 24, 1167 (Sep, 2000).

16.     R. M. Krauss et al., Dietary guidelines for healthy American adults – A statement for health professionals from the Nutrition Committee, American Heart Association. Circulation 94, 1795 (Oct 1, 1996).

17.     A. Keys, Coronary heart disease in seven countries. Circulation 41, 186 (1970).

18.     W. C. Willett, M. J. Stampfer, Rebuilding the food pyramid. Scientific American 288, 64 (Jan, 2003).

19.     W. C. Willett, The dietary pyramid: does the foundation need repair? The American journal of clinical nutrition 68, 218 (Aug, 1998).

20.     L. Berglund et al., Comparison of monounsaturated fat with carbohydrates as a replacement for saturated fat in subjects with a high metabolic risk profile: studies in the fasting and postprandial states. The American journal of clinical nutrition 86, 1611 (Dec, 2007).

21.     R. P. Mensink, M. B. Katan, Effect of dietary fatty acids on serum lipids and lipoproteins. A meta-analysis of 27 trials. Arteriosclerosis and thrombosis : a journal of vascular biology / American Heart Association 12, 911 (Aug, 1992).

22.     A. A. Rivellese et al., Effects of dietary saturated, monounsaturated and n-3 fatty acids on fasting lipoproteins, LDL size and post-prandial lipid metabolism in healthy subjects. Atherosclerosis 167, 149 (Mar, 2003).

23.     D. Mozaffarian, E. B. Rimm, D. M. Herrington, Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women. The American journal of clinical nutrition 80, 1175 (Nov, 2004).

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

Connecting to %s

%d bloggers like this: