Is saturated fat dangerous?

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Is saturated fat dangerous?

Saturated Fat

Saturated fat is a type of fat that is solid at room temperature and is primarily found in animal products such as meat, dairy, and certain plant-based oils like coconut oil and palm oil. Saturated fat is an important part of the diet and can serve as a source of essential fat-soluble vitamins such as A, D, E, and K.

Saturated Fat and Cholesterol

In the 1950s, researcher Ancel Keys hypothesized that saturated fat was the main cause of diseases and elevated cholesterol levels. However, subsequent research has questioned the validity of this theory, pointing instead to other factors in the modern Western diet. Studies have shown that the overconsumption of vegetable mono- and polyunsaturated fatty acids, trans fats, refined carbohydrates, and deficiencies in key minerals, vitamins, and antioxidants may play a more significant role in disease development than saturated fat alone.

According to Mozaffarian, D., et al., a combination of various dietary factors can lead to the formation of plaque and, subsequently, disease. Analysis of fat in blood clots has revealed that only about 26% is saturated fat, while the majority consists of unsaturated fats, half of which are polyunsaturated. This highlights the importance of a more nuanced perspective on fat consumption and its relationship with disease.

Is Saturated Fat Really as Harmful as Claimed?

Chow, C. K., & Gray, J. I. discuss saturated fat. Unaltered saturated fat—meaning not excessively heated or chemically processed—is vital for the body for the following reasons:

  1. Saturated fat makes up at least 50% of cell membranes, providing necessary structure and protection.
  2. Saturated fat is crucial for bone health, aiding in calcium incorporation into bones.
  3. Saturated fat lowers lipoprotein(a), a substance that can increase health risks.
  4. Saturated fat has a positive effect on the immune system.
  5. Saturated fat is needed for the body to effectively utilize essential fatty acids. Prolonged omega-3 fatty acids are better retained in tissues when the diet is rich in saturated fat.
  6. Saturated fatty acids with 16 and 18 carbon atoms are preferred by the heart, which is why fat surrounding the heart is highly saturated. This fat reserve is used during stress situations.
  7. Short- and medium-chain saturated fatty acids have important antimicrobial properties.

Breast Milk

Breast milk contains a higher proportion of cholesterol than most other foods. Additionally, almost 50% of its calorie content comes from fat, much of which is saturated fat. Both cholesterol and saturated fat are essential for children's growth, particularly for brain development. Is it likely that millions of years of evolution would produce a substance so critical for children's development that is simultaneously as harmful as the Lipid Hypothesis suggests? It appears that Ancel Keys' Lipid Hypothesis is flawed, not only from a statistical perspective but also from an evolutionary one. Of course, some fats are less beneficial for us, and to understand which fats are good and which are bad, we need to examine the chemistry of fats more closely.

The Chemistry of Fats

Fats consist of fatty acids with long chains of carbon and hydrogen atoms bonded together, with a carboxyl group (COOH) at one end and an omega group (CH3) at the other. Fats are generally categorized as saturated, monounsaturated, or polyunsaturated. Saturated fatty acids are fully saturated with hydrogen atoms and have no double bonds along the carbon chain. Monounsaturated fats have one double bond, and polyunsaturated fats have two or more double bonds along the chain.

Fats are also classified by the length of their fatty acid chains. Short-chain fatty acids, with four to six carbon atoms, are always saturated and have antimicrobial properties, protecting against bacteria, viruses, and fungi in the digestive tract. These fats do not require bile salts for digestion and are absorbed directly, which can influence their metabolism and potential role in weight regulation. Medium-chain triglycerides (MCTs), with eight to twelve carbon atoms, are primarily found in butter and coconut oil and also have antimicrobial properties. Lauric acid and caprylic acid are two medium-chain fatty acids with many health benefits. Long-chain fatty acids, with 14 to 18 carbon atoms, can be saturated, monounsaturated, or polyunsaturated. Very long-chain fatty acids, with 20 to 24 carbon atoms, are usually highly unsaturated, such as the omega-3 fatty acids EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid).

Polyunsaturated Fatty Acids – Not Always Healthy

It is politically correct to say that polyunsaturated fats are healthy while saturated fats are harmful to health. This has resulted in a shift in fat consumption. At the turn of the last century, dietary fats were predominantly butter, lard, tallow, coconut oil, and small amounts of olive oil. Today, fat intake largely consists of polyunsaturated vegetable oils from soy, corn, sunflower, and rapeseed oil. Up to 30% of the calories in the modern Western diet come from polyunsaturated vegetable fats, which have been linked to various health problems. Trans fatty acids from hydrogenated vegetable oils are particularly dangerous. According to Ramsden, Christopher E., et al., one reason polyunsaturated fats cause health problems is their tendency to oxidize or become rancid when exposed to heat, oxygen, and moisture. Rancid fats contain free radicals that attack cell membranes and red blood cells, causing DNA/RNA damage and triggering unhealthy mutations in tissues.

Too Much Omega-6 and Too Little Omega-3

Simopoulos, Artemis P., emphasizes the importance of the ratio between omega-6 and omega-3 fatty acids for maintaining health. The study also discusses the modern diet's imbalance between omega-6 and omega-3 and how this imbalance can negatively impact inflammatory processes and other health issues. The research highlights the effects of various sources of omega-3 and stresses the importance of maintaining a balanced diet with the correct ratio of omega-6 to omega-3.

Although the essential omega-6 fatty acid is necessary, the modern Western diet provides excessive amounts of omega-6 relative to the essential omega-3 fatty acid. The ideal ratio should be around 2:1, meaning two parts omega-6 to one part omega-3, with approximately 4–5% of total calorie intake coming from both combined. Today, the ratio is about 20:1, leading to an imbalance that affects prostaglandin production, increasing the tendency for inflammation. The lack of omega-3 has also been linked to other health issues. Polyunsaturated vegetable oils contain very little omega-3 compared to omega-6.

Unfortunately, commercial agricultural practices have also reduced omega-3 content in eggs, fish, and meat, which naturally contain higher omega-3 levels compared to omega-6. For example, organic eggs from hens fed their natural diet (insects and green vegetation) have an omega-6 to omega-3 ratio of approximately 1:1, while commercial eggs can contain up to 19 times more omega-6 than omega-3. Flaxseed oil is not a good source of omega-3 because only 1–5% of the precursor form ALA (alpha-linolenic acid) in flaxseed oil is converted into the easily absorbable omega-3 forms EPA and DHA. Additionally, much of the flaxseed oil available on grocery store shelves is rancid.

Why Does Saturated Fat Have Such a Bad Reputation?

Why does saturated fat have such a bad reputation? The answer lies in the Lipid Hypothesis. This hypothesis, which became known as the Lipid Hypothesis, gained enormous media attention. Ancel Keys continued studying the correlation between fats and cardiovascular problems. His most famous study, "The Seven Countries Study," began in 1958 and continued until 1970. The study involved more than 12,000 men aged 40–59 in 16 different regions across seven countries. Ancel Keys and his colleagues concluded that countries with high saturated fat consumption had higher rates of heart disease. But was this really the case?

Excluded Data

If Keys' theory had been correct, areas with high cholesterol levels should logically have high death rates and vice versa. However, when analyzing all the data, this was not the case. It turned out that Ancel Keys had excluded data that contradicted his theory. For example, the Corfu group had even slightly lower cholesterol levels than the Crete group, yet their mortality rate was seven times higher. It was found that areas with roughly the same cholesterol levels in Italy, Slovenia, and Finland had completely different mortality rates. "The Seven Countries Study" was based on several fundamental flaws in its observational selection. Statistician Russell H. Smith commented on the study:

“… the evaluation method of the observations was very inconsistent and questionable. A thorough examination of death rates and the relationship between diet and mortality reveals significant inconsistencies and contradictions… It is almost inconceivable that 'The Seven Countries Study' was conducted with such a lack of scientific method. It is also astonishing how NHLBI/AHA ignored such sloppiness in their many enthusiastic reviews of the study… In summary, the relationship between diet and [the diseases saturated fat has been accused of causing] for 'The Seven Countries Study' cannot be taken seriously by objective and critical researchers."

"The Seven Countries Study" has been heavily criticized and dismissed over the years, but unfortunately, the media has not let go of its flawed findings. Subsequent studies have been unable to show that saturated fat and cholesterol are harmful.

MONICA

The World Health Organization (WHO) chose to investigate the same connections as Ancel Keys in its MONICA study. However, this time they included 21 countries instead of seven. The MONICA study revealed what "The Seven Countries Study" should have shown if Keys had not manipulated the data—both high and low mortality rates occurred in areas with high cholesterol levels among the population. When considering all observations in both "The Seven Countries Study" and the MONICA study, the link between high cholesterol levels, i.e., saturated fat intake, and disease could be questioned. Tunstall-Pedoe, Hugh, et al., discuss this connection in detail.

The Framingham Study

The Framingham Heart Study is sometimes cited as evidence supporting the Lipid Hypothesis. However, the study results point to entirely different conclusions. The Framingham Study began in 1948 and involved 6,000 people from the town of Framingham, Massachusetts. Two groups were compared at five-year intervals: those who consumed little cholesterol and saturated fat and those who consumed a lot. After 40 years, it was found that individuals who ate the most cholesterol and saturated fat consumed the most calories but weighed the least, had lower blood cholesterol levels (yes, you read that correctly), and had slightly lower risks of future health problems compared to those who ate little cholesterol and saturated fat. Castelli, William P., highlights this in his study.

A Study in the UK

In a large British study involving thousands of participants, half were asked to reduce their intake of saturated fat and cholesterol, quit smoking, and increase their intake of unsaturated fats such as vegetable oils and margarines. After one year, this group had doubled its mortality rate compared to the group that continued consuming saturated fats and cholesterol (despite continuing to smoke). However, a strong lobbying group advocating for polyunsaturated fats led the research leader to write, "The implication for Britain's health policy is that this preventive program might be effective," which was not true. The criticism has emerged later. Rose, Geoffrey, discusses this relationship in his study.

Should Have Improved Over the Years

When internist Paul Dudley White tried to introduce the German electrocardiograph (ECG) in the 1920s in the USA, his colleagues at Harvard University advised him to focus on a more profitable area of medicine because heart problems were so rare at the time. This was despite the diet not consisting of cholesterol-lowering fats.

From 1910 to 1970, the percentage of saturated fat from animal sources in the American diet decreased from over 80% to just over 60%, and the consumption of pure butter dropped from over 8 kg to less than 2 kg. Cholesterol intake from food increased by only 1%. Meanwhile, the intake of vegetable fats in the form of margarine, shortening, and other refined oils increased by about 400% during the same period. The decreased intake of saturated fats in favor of polyunsaturated vegetable fats should have led to a decline in certain diseases over time. Instead, the risk of these diseases increased and became the leading cause of death in the USA by the mid-20th century. Today, approximately 40% of all deaths are attributed to these diseases. These facts strongly contradict the hypothesis that saturated fats cause these diseases.

Conclusion

The Lipid Hypothesis or "The Seven Countries Study" changed the entire Western perspective on fats, leading to a 400% increase in the intake of unsaturated vegetable oils between 1910 and 1970. The price has been a significant increase in various diseases. Today, 40% of all deaths are related to these diseases. The idea that saturated fat is harmful is one of the greatest misconceptions in modern nutrition and health.

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Scientific references and sources

Show reference

Mozaffarian, D. et al. New England Journal of Medicine, vol. 354, no. 15, 2006, pp. 1601-13.

Siri-Tarino, P.W. et al. The American Journal of Clinical Nutrition, vol. 91, no. 3, 2010, pp. 535-46.

Chow, C. K., & Gray, J. I. (2019). Fatty Acids in Foods and their H. Implications. CRC Press.

Uffe Ravnskov (2008) Scandinavian Card. Journal, 42:4, 236-239, DOI: 10.1080/14017430801983082

Ramsden, Christopher E., et al. The BMJ 346 (2013): e8707.

Simopoulos, Artemis P. Biomedicine & pharmacotherapy 56.8 (2002): 365-379.

Keys, A., et al. Preventive medic. 13.2 (1984): 141-154.

Hubert H, et al, Circulation, 1983, 67:968; Smith, R and E R Pinckney. Vol 2, 1991, Vector Enterprises, Sherman Oaks, CA

Tunstall-Pedoe, Hugh, et al. The Lancet 355.9205 (2000): 688-700.

Castelli, William P. The American journal of medicine 76.2 (1984): 4-12.

Rose, Geoffrey. International Journal of Epidemio. 14.1 (1985): 32-38.

Castelli, W. P. (1992). The Canadian Journal of Cardi., 8(Suppl A), 5A-10A.

Portillo, M. P., Pellegrini, M., Casanueva, F. F., & Sanchez, J. (1998). International journal of obesity and related metabolic disorders: journal of the International Association for the Study of Obesity, 22(10), 947-9.

Dulloo, A. G., Jacquet, J., & Girardier, L. (1995). The American journal of clinical nutrition, 62(2), 301-9.

Kabara, J. J. (1978). The American Oil Chemists' Society, 1-14.

Cohen, L. A., Thompson, D. O., & Maeura, Y. (1986). The Journal of the National C. Institute, 77(1), 43.

Rose, G., Hamilton, P. J., Colwell, L., & Shipley, M. J. (1983). Journal of epidemiology and community health, 37(3), 162-70.

"The Lipid Research Clinics Cor. Primary Prevention Trial Results. I. Reduction in Incidence of Coronary H. Dis." JAMA, 1984, 251(3), 351-364.

Kronmal, R. (1985). JAMA, 253(14), 2091-2095.

Nutrition Week. (1991). Nutrition week, 21(12), 2-3.

Lasserre, M., Polonovski, J., & Sauvant, P. (1985). Lipids, 20(4), 227-32.

Pinckney, E. R., & Pinckney, C. (1973). Los Angeles: Sherbourne Press, 127-131.

Harmon, D., Gardell, C., Malm, O., & Nilsson, S. (1976). The Journal of the American Geriatrics Society, 24(1), 292-8.

Meerson, Z., & Genin, E. (1983). Bulletin of Experimental Biology and Medicine, 96(9), 70-1.

Valero, E. L., Montero, E. G., & Cerdan, C. M. (1990). Annals of nutrition & metabolism, 34(6), 323-327.

Felton, C. V., Crook, D., & Davies, M. J. (1994). The Lancet, 344(8931), 1195.

Machlin, I. J., & Bendich, A. (1987). The FASEB Journal, 1(6), 441-5.

Kinsella, J. E. (1988). Food Technology, 42(10), 134-40.

Horrobin, D. F. (1983). Reviews in Pure and Applied Pharmacological Sciences, 4, 339-383.

Devlin, T. M. (1982). Textbook of Biochemistry. New York: Wiley Medical, 429-430.

Fallon, S., & Enig, M. G. (1996). Price-Pottenger Nutrition Foundation Health Journal, 20(3), 5-8.

Okuyama, H., Higashi, R., & Mizugaki, M. (1997). Progress in Lipid Research, 35(4), 409-457.

Simopoulos, A. P., & Salem Jr, N. (1992). The American journal of clinical nutrition, 55(3), 411-4.

Watkins, B. A., Lippman, H. E., & Le, B. (1996). Purdue University, Lafayette, IN, AOCS Proceedings.

Dahlen, G. H., Boman, H. G., & Birgegård, G. (1998). The Journal of Internal Medicine, 244(5), 417-24.

Khosla, P., & Hayes, K. C. (1996).  The Journal of the American College of Nutrition, 15(4), 325-339.

Clevidence, B. A., et al. (1997). Arteriosc., Thromb., and Vascular Biology, 17(9), 1657-1661.

Garg, M. L., Sebokova, E., & Thomson, A. B. (1988). The FASEB Journal, 2(4), A852.

Oliart Ros, R. M., & Hernández Martínez, C. (1998). AOCS Proceedings, 7.

Lawson, L. D., & Kummerow, F. A. (1979). Lipids, 14(6), 501-3.

Garg, M. L., Blake, R. J., & Wills, R. B. (1989). Lipids, 24(4), 334-9.

Felton, C. V., Crook, D., & Davies, M. J. (1994). The Lancet, 344(8931), 1195.

Prentice, R. L., & Caan, B. (2006). Randomized Controlled Dietary Modification Trial. JAMA, 295(6), 629-42.

Beresford, S. A., Johnson, K. C., & Ritenbaugh, C. (2006). JAMA, 295(6), 643-54.

Howard, B. V., Van Horn, L., & Hsia, J. (2006). JAMA, 295(6), 655-66.

Howard, B. V., Manson, J. E., & Stefanick, M. L. (2006). JAMA, 295(6), 39-49.

Michels, K. B., & Willett, W. C. (1996). Recent Results in C Research, 140, 295-305.

Prentice, R. L., & Sheppard, L. (1990). C. Causes and Control, 1(2), 81-97; discussion 99-109.

Prentice, R. L., & Sheppard, L. (1991). C. Causes and Control, 2(1), 53-8.

Willett, W., & Stampfer, M. J. (1990). C. Causes and Control, 1(2), 103-109.

Multiple Risk Factor Intervention Trial Research Group. (1982). JAMA, 248(12), 1465-77.

Willett, W. (1998). Nutritional epidemiology. New York: Oxford University Press.

Fallon, S., & Enig, M. G. (1996). Consumers' Research, 15-19.