Saturated with Science

The Truth About Saturated Fat


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Saturated fats and their role in health

Hello, dear peoples from all corners!

Urgent news!

Today’s lesson is on a very important substance. So dangerous, that it has been blamed in the deaths of millions. So toxic is this, that it is still warned against by the authorities as a disease-causing, epidemic-inducing poison. It has been implicated in the spread of cardiovascular disease, cancer, obesity, diabetes, high blood pressure, and even alien invasions. This substance is so deadly, our bodies need it!

Wait… What?

Okay I’m done being a snot. Now for a more serious tone, but not too serious because I don’t want to sound like the Clear Eyes dude. Ahem. Saturated fatty acids are implicated in heart disease and other diseases, and reports abound that lowering it reduced the cardiovascular disease [CVD] rise. This completely ignores the reduction in smoking with the rise in awareness that it caused all the cardiovascular diseases “In addition, age-adjusted death rates per 100,000 persons (standardized to the 1940 population) for heart disease (i.e., coronary heart disease) have decreased from 307.4 in 1950 to 134.6 in 1996 … . During 1964-1992, approximately 1.6 million deaths caused by smoking were prevented … .” (1). Way to go using this victory to blame saturated fat. Bravo. Further, CVD and other diseases are now at an all-time high, or at least was for a vast majority of people, where saturated fat was at an all-time low (2), which negates this entirely as causal. The association of saturated fat with CVD dates back to Ancel Keys and the Lipid Hypothesis (3), in which dietary cholesterol was first blamed, but because specimens had a neutral response where serum cholesterol was almost unchanged, he set his focus on saturated fats.

Saturated fats do not affect serum cholesterol, and courtesy of Dr. Malcolm Kendrick and biochemical sciences (4), this explains why:

The absorbed saturated fat is then packed into a very large lipoprotein (known as a chylomicron). Once a chylomicron is formed it travels up a special tube, called the thoracic duct, and is released directly into the blood stream. It does not, and this is important, pass through the liver.

Chylomicrons then travel around the body and are stripped of their fat, shrinking down until they become about the size of an LDL. At which point they are called chylomicron remnants. These are absorbed back into the liver – using LDL receptors – and are then broken down into their constituent parts
Therefore, a small amount of fat that you eat will end up in the liver. However, the vast, vast, majority will go straight from the guts to fat cells (adipose tissue). Whereupon they are stored away for later use.

In fact, this is the fate of all types of fat: saturated, polyunsaturated, or monounsaturated. There is nothing unique about saturated fat in the way that it is absorbed and transported around the body. Anyway, as you may have noticed, none of this has anything to do with LDL whatsoever. Nothing. Ergo the consumption of saturated fat, or any fat, can have no direct impact on LDL levels.

So there’s the most glaring flaw in this theory, and it was based on flawed data, described in a paper by Denise Minger, an author and opponent of the food guidelines. Her views are unbiased and very detailed in every paper thus far I have read, where she uses the most credible evidence on both sides. She even provides evidence that he did not, in fact, place blame on dietary cholesterol because his controlled trials showed it simply does not happen (5). Another serious flaw is the fact that alone, saturated fatty acids not only do not affect cholesterol, they don’t even have an effect on circulating fatty acids (6).

The evidence against saturated fat is lacking (7-8), and the push for unsaturated fats prompted review because of the swift increase in disease (9-11).

In fact, saturated fatty acids and natural trans fats are quite healthy! CLA is a trans fatty acid found in dairy fat. They protect from cardiovascular disease and events (12), aid in weight loss (13-15), reduce abdominal obesity and have medicinal properties (16-19), among many other benefits. The lungs require saturated fats in the diet, whereas unsaturated fats negatively affect function and even cellular composition (20-22).

SFA intake was inversely associated with mortality from total stroke, including intraparenchymal hemorrhage and ischemic stroke subtypes, in this Japanese cohort.

Inversely associated = prevented or reversed the risk/cured. The ingestion of saturated fatty acids was protective of this often deadly occurrence (12). This is completely contrary to what we’ve been told as a whole and contradictory to the current methods in place.

In fact, this specific kind of disease and others can be attributed to seed foods and their proteins called agglutinins (23-26). This works by a process known as agglutination, which is the binding together or clotting of proteins of a specific type (27). These foods also contain lectins, a type of inflammatory protein. Lectins, in and of themselves, cause problems for a large amount of people, and from specific sources such as grains and legumes [all seeds have them], and for some people eggs [the white], or dairy, (28-32).

Other diseases plunked onto saturated fat? Well, those can be explained too, like PUFA or polyunsaturated fatty acids (33-36); sugar in cancer (37-40)—also involved in a cover-up when the sugar industry found their product to cause cardiovascular disease and cancer (41)—and other diseases (42-45); excessive general carbohydrate (46-53); alcohol (54-55); and many other things which had been postulated as healthful.

The link between animal products [meat and saturated fat pretty much go hand-in-hand] and disease is nonexistent (56-58), with studies even retracting previous associations after correcting for variables (59).

Processed “meat” ingredients: hot dogs
Mechanically Separated Chicken, Water, Pork, Dextrose, Modified Corn Starch, Salt, Contains 2% or Less of the Following: Beef, Corn Syrup, Flavorings, Sodium Phosphates, Potassium Lactate, Potassium Acetate, Sodium Diacetate, Sodium Erythorbate, Oleoresin of Paprika, Sodium Nitrite, Smoke Flavoring.


So, some chicken, water, pork, sugar, sugar, salt, beef, sugar, petroleum by-products, random isolated chemical names that may or may not be natural, a weird mix of paprika instead of just using, you know…paprika, and some random concoction instead of actually smoking the meat.

All these random and scientific jargon ingredients and they said it was the meat?

Say now, fair spirit, that you jest poor little Puck?


You see, this is why all claims against saturated fat can be dismissed as junk science, pseudoscience, and even as propaganda or fearmongering. That and the fact that we evolved and thrived on it since the dawn of human beings, and only recently has the health crisis happened, and continued to worsen the more the misinformation is heeded as legitimate.

I have more studies but I scrolled up and realized this is already long…

Shout out:

Doctor Malcolm Kendrick

Denise Minger



Statistics abuse
1. CDC. Website. 5 Nov 1999. Achievements in Public Health, 1900-1999: Tobacco Use -- United States, 1900-1999. Accessed 1 Sept 2018 from

2. Credit Suisse. YouTube video. 18 Jan 2016. The Truth on Fat. Retrieved from

The Lipid Hypothesis
3. “lipid hypothesis.” McGraw-Hill Concise Dictionary of Modern Medicine. 2002. The McGraw-Hill Companies, Inc. Accessed 1 Sep. 2018 from

Valuable blogs
4. Malcolm Kendrick, MD. Why saturated fat cannot raise cholesterol levels (LDL levels). Accessed 3rd July 2018 from

5. Denise Minger. (22 Dec 2011) THE TRUTH ABOUT ANCEL KEYS: WE’VE ALL GOT IT WRONG. Retrieved on 2 Sept 2018 from

Saturated fat evidence
6. Volk BM, et al. (2014) Effects of Step-Wise Increases in Dietary Carbohydrate on Circulating Saturated Fatty Acids and Palmitoleic Acid in Adults with Metabolic Syndrome. PLoS ONE 9(11): e113605.

7. Patty W Siri-Tarino, et al. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. The American Journal of Clinical Nutrition, Volume 91, Issue 3, 1 March 2010, Pages 535–546,

8 . de Souza Russell J, Mente Andrew, Maroleanu Adriana, Cozma Adrian I, Ha Vanessa, Kishibe Teruko et al. Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies BMJ 2015; 351 :h3978

9. Hamley S. The effect of replacing saturated fat with mostly n-6 polyunsaturated fat on coronary heart disease: a meta-analysis of randomised controlled trials. Nutr J. 2017 May 19;16(1):30. doi: 10.1186/s12937-017-0254-5.

10. James J DiNicolantonio. The cardiometabolic consequences of replacing saturated fats with carbohydrates or Ω-6 polyunsaturated fats: Do the dietary guidelines have it wrong? Open Heart. 8 Feb 2014; 1(1): e000032; doi:  10.1136/openhrt-2013-000032

11. Uffe Ravnskov, MD, PhD; James J. DiNicolantonio, PharmD; Zoë Harcombe, MA; Fred A. Kummerow, PhD; Harumi Okuyama, MD, PhD; and Nicolai Worm, MD, PhD. The Questionable Benefits of Exchanging Saturated Fat With Polyunsaturated Fat. Mayo Clin Proc. April 2014;89(4):451-453;

Saturated fat benefits
12. Yamagishi K, et al. Dietary intake of saturated fatty acids and mortality from cardiovascular disease in Japanese: the Japan Collaborative Cohort Study for Evaluation of Cancer Risk (JACC) Study. Am J Clin Nutr. 2010 Oct;92(4):759-65. doi: 10.3945/ajcn.2009.29146. Epub 2010 Aug 4.

13. Miner JL. Conjugated linoleic acid (CLA), body fat, and apoptosis. Obes Res. 2001 Feb;9(2):129-34.

14. Arion Kennedy, et al. Antiobesity Mechanisms of Action of Conjugated Linoleic Acid. J Nutr Biochem. 2010 Mar; 21(3): 171–179. doi:  10.1016/j.jnutbio.2009.08.003

15. Leah D Whigham,  Abigail C Watras,  Dale A Schoeller. Efficacy of conjugated linoleic acid for reducing fat mass: a meta-analysis in humans. The American Journal of Clinical Nutrition, Volume 85, Issue 5, 1 May 2007, Pages 1203–1211,

16. K G Nevin, T Rajamohan . Effect of topical application of virgin coconut oil on skin components and antioxidant status during dermal wound healing in young rats. Skin Pharmacol Physiol. 2010 ;23(6):290-7.

17. S Intahphuak, P Khonsung, A Panthong. Anti-inflammatory, analgesic, and antipyretic activities of virgin coconut oil. Pharm Biol. 2010 Feb;48(2):151-7.

18. Assunção ML, et al. Effects of dietary coconut oil on the biochemical and anthropometric profiles of women presenting abdominal obesity. Lipids. 2009 Jul;44(7):593-601. doi: 10.1007/s11745-009-3306-6. Epub 2009 May 13.

19. Fabian M. Dayrit. The Properties of Lauric Acid and Their Significance in Coconut Oil. Journal of the American Oil Chemists' Society. January 2015, Volume 92, Issue 1, pp 1–15

20. Wolfe RR, et al. Dietary fat composition alters pulmonary function in pigs. Nutrition. 2002 Jul-Aug;18(7-8):647-53.

21. Marla Paul. (20 May 2014.) Vitamin E in Canola and Other Oils Hurts Lungs. Accessed 2 Sept 2018 from

22. Erman F, et al. Determination of saturated and unsaturated Fatty acids amount in leukocyte membranes from subjects fed with solid and fluid oils. J Biochem Mol Biol. 2006 Sep 30;39(5):516-21.

Lectins and agglutinins
23. Vector Laboratories. Fluorescein labeled Peanut Agglutinin (PNA). Retrieved on 3 Sept 2018 from

24. Hassan Y. Naim, et al. Effects of galactose-binding lectins on human blood platelets: Identity of the peanut agglutinin receptor with the von Willebrand factor receptor. Theodor Kocher Institute, University of Berne Freiestrasse 1, CH-3000 Bern 9 Switzerland. 15 June 1982; Volume 26, Issue 6, Pages 431–441. DOI:

25. Pusztai A, et al. Antinutritive effects of wheat-germ agglutinin and other N-acetylglucosamine-specific lectins. Br J Nutr. 1993 Jul;70(1):313-21.

26. Zhao Q, et al. Peanut agglutinin appearance in the blood circulation after peanut ingestion mimics the action of endogenous galectin-3 to promote metastasis by interaction with cancer-associated MUC1. Carcinogenesis. 2014 Dec;35(12):2815-21. doi: 10.1093/carcin/bgu216.

27. “agglutinin.” Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. 2003. Saunders, an imprint of Elsevier, Inc 3 Sep. 2018

28. Carolyn Pierini, CLS (ASCP), CNC. Lectins: Their Damaging Role in Intestinal Health, Rheumatoid Arthritis and Weight Loss. Vitamin Research Products. Accessed 3 Sept 2018 from

29. Rabia Hamid and Akbar Masood, 2009. Dietary Lectins as Disease Causing Toxicants. Pakistan Journal of Nutrition, 8: 293-303. DOI: 10.3923/pjn.2009.293.303

30. Medical News Today. (4 August 2007). How Lectin In Undercooked Red Beans And Rice Causes Food Poisoning. Accessed 3 Sept 2018 from

31. Miyake K, Tanaka T, McNeil PL (2007) Lectin-Based Food Poisoning: A New Mechanism of Protein Toxicity. PLoS ONE 2(8): e687.

32. Cordain L, Toohey L, Smith MJ, Hickey MS. Modulation of immune function by dietary lectins in rheumatoid arthritis. Br J Nutr. 2000 Mar;83(3):207-17.

33. Marian L. Neuhouser, et al. (n-6) PUFA Increase and Dairy Foods Decrease Prostate Cancer Risk in Heavy Smokers. The Journal of Nutrition, Volume 137, Issue 7, 1 July 2007, Pages 1821–1827,

34. Helmut Bartsch, et al. Dietary polyunsaturated fatty acids and cancers of the breast and colorectum: emerging evidence for their role as risk modifiers. Carcinogenesis, Volume 20, Issue 12, 1 December 1999, Pages 2209–2218,

35. Sonestedt E, et al. Do both heterocyclic amines and omega-6 polyunsaturated fatty acids contribute to the incidence of breast cancer in postmenopausal women of the Malmö diet and cancer cohort? Int J Cancer. 2008 Oct 1;123(7):1637-43. doi: 10.1002/ijc.23394.

36. C.V.FeltonPhD, et al. Dietary polyunsaturated fatty acids and composition of human aortic plaques. The Lancet; Volume 344, Issue 8931, 29 October 1994, Pages 1195-1196.

37. Simon J. Lawless, et al. Glucose represses dendritic cell-induced T cell responses. Nature Communications, 2017; 8: 15620 DOI: 10.1038/NCOMMS15620

38. X Wang, et al. Insulin resistance in vascular endothelial cells promotes intestinal tumour formation. Oncogene, 2017; DOI: 10.1038/onc.2017.107

39. VIB. 13 Oct 2017. Scientists reveal the relationship between sugar and cancer. Project started by Johan Thevelein, Wim Versées, and Veerle Janssens. Accessed 3 Sept 2018 from

40. Seely S, Horrobin DF. Diet and breast cancer: the possible connection with sugar consumption. Med Hypotheses. 1983 Jul;11(3):319-27.

41. Kearns CE, Apollonio D, Glantz SA (2017) Sugar industry sponsorship of germ-free rodent studies linking sucrose to hyperlipidemia and cancer: An historical analysis of internal documents. PLoS Biol 15(11): e2003460.

42. Richard J Johnson, et al. Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. The American Journal of Clinical Nutrition, Volume 86, Issue 4, 1 October 2007, Pages 899–906,

43. DiNicolantonio JJ, Lucan SC. The wrong white crystals: not salt but sugar as aetiological in hypertension and cardiometabolic disease. Open Heart 2014;1:e000167. doi: 10.1136/openhrt-2014-000167

44. Pavel Grasgruber, et al. Food consumption and the actual statistics of cardiovascular diseases: an epidemiological comparison of 42 European countries. Food Nutr Res. 2016; 60: 10.3402/fnr.v60.31694. doi:  10.3402/fnr.v60.31694

45. Dr Mahshid Dehghan, PhD, et al. Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. The Lancet. Volume 390, Issue 10107, P2050-2062; 29 August 2017. DOI:

46. Dariush Mozaffarian, Eric B Rimm, David M Herrington. Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women. The American Journal of Clinical Nutrition, Volume 80, Issue 5, 1 November 2004, Pages 1175–1184,

47. Metin Basaranoglu, et al. Carbohydrate intake and nonalcoholic fatty liver disease: fructose as a weapon of mass destruction. Hepatobiliary Surg Nutr. 2015 Apr; 4(2): 109–116. doi:  10.3978/j.issn.2304-3881.2014.11.05

48. Meenakshi Ravichandran, Gerald Grandl, Michael Ristow. (Oct 03, 2017). Dietary Carbohydrates Impair Healthspan and Promote Mortality. Volume 26, Issue 4, P585-587. DOI:

49. Ian Spreadbury. Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity. Diabetes Metab Syndr Obes. 6 Jul 2012; 5: 175–189. doi:  10.2147/DMSO.S33473

50. den Biggelaar LJCJ, et al. Prospective associations of dietary carbohydrate, fat, and protein intake with β-cell function in the CODAM study. Eur J Nutr. 2018 Mar 10. doi: 10.1007/s00394-018-1644-y.

51. Elizabeth J. Parks. Effect of Dietary Carbohydrate on Triglyceride Metabolism in Humans. The Journal of Nutrition, Volume 131, Issue 10, 1 October 2001, Pages 2772S–2774S,

52. Siri PW, Krauss RM. Influence of dietary carbohydrate and fat on LDL and HDL particle distributions. Curr Atheroscler Rep. 2005 Nov;7(6):455-9.

53. Yunsheng Ma, MD, PhD, et al. Association between Carbohydrate Intake and Serum Lipids. J Am Coll Nutr. 2006 Apr; 25(2): 155–163.

54. S. J. Lowry, K. Kapphahn, R. Chlebowski, C. I. Li. Alcohol Use and Breast Cancer Survival among Participants in the Women's Health Initiative. Cancer Epidemiology Biomarkers & Prevention, 2016; 25 (8): 1268 DOI: 10.1158/1055-9965.EPI-16-0151

55. National Cancer Institute. Website. 24 June 2013. Alcohol and Cancer Risk. Accessed 3 Sept 2018 from

Meat and disease
56. MarijeOostindjer, et al. The role of red and processed meat in colorectal cancer development: a perspective. ScienceDirect. Meat Science; Volume 97, Issue 4, August 2014, Pages 583-596

57. Eunyoung Cho and Stephanie A. Smith-Warner. Meat and fat intake and colorectal cancer risk: A pooled analysis of 14 prospective studies. American Association for Cancer Research. April 2004. Volume 64, Issue 7 Supplement, pp. 113

58. D. D. Alexander,  C. A. Cushing. Red meat and colorectal cancer: a critical summary of prospective epidemiologic studies. obesity reviews; Volume12, Issue5; 27 April 2011; Pages e472-e493

59. Rohrmann S, et al. Meat consumption and mortality--results from the European Prospective Investigation into Cancer and Nutrition. BMC Med. 2013 Mar 7;11:63. doi: 10.1186/1741-7015-11-63. [After correction for measurement error, higher all-cause mortality remained significant only for processed meat.]

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