For the last few decades, saturated fat was thought of as a villain in the development of heart disease. I have also seen many who have a fear to take saturated fats. However many experts disagree with the view. Here we will explore factors, data we have about saturated fats as a heart disease risk factor as well as Saturated fats & heart disease risk itself: Evidence. Before going to that, have a glimpse of types of fats that we generally take
- Saturated fats: no double bonds in the carbon chain
- Monounsaturated fats: one double bond in the carbon chain (ex.-Oleic acid)
- Polyunsaturated fats: two or more double bonds in the carbon chain (Example: Linoleic acid or omega-6, omega 9, omega 7, omega 3 groups (Alpha-Linolenic acid, Eicosapentaenoic acid or EPA, Docosapentaenoic acid or DHA)
With the increasing number of double bonds in the carbon chain, fat or oil becomes less stable and has a higher tendency for oxidation.
Saturated fats
Sources of saturated fats include animal fats, poultry, Ghee, butter, cheese, egg and some more. But remember saturated fat is not a single type of fat, rather it is a group of fats further classified by the length of carbon chains such as short-chain, medium-chain, long-chain and very long chain. Each class again has different types of fatty acids subclass.
Many studies linked between consumption of saturated fatty acids with increased blood cholesterol. Dr. Ancel Keys first proposed the diet-heart hypothesis in the 1950s which suggests that consumption of saturated fat raises blood cholesterol levels and thus increases the risk of heart disease. Despite the disagreement of some scientists the hypothesis persisted and resulted in the belief that a heart-healthy diet should limit saturated fat. (1)
Cholesterol, development of plaque in blood vessel and risk of heart disease
Cholesterol is a major component of all cell membranes and a vital component in the metabolic process. Your body needs cholesterol to make hormones such as estrogen, testosterone, and adrenal hormones, fat-soluble vitamins like vitamin D, and bile acids to help you digest your food. Pure lipid or cholesterol doesn’t mix or dissolve in the blood. Therefore to carry cholesterol through blood your body needs a type of protein carrier called a lipoprotein. (2)
According to the type of lipoprotein carrier, it further classified into two majors as LDL or low-density lipoprotein and HDL or high-density lipoprotein. Another major form of lipid that runs through your blood is triglycerides. While your body uses cholesterol to build cells, certain hormones, and vitamins, it uses triglycerides for energy. Extra calories from your foods that your body doesn’t use right away convert to triglycerides. It is stored in your fat cells. A high level of triglycerides in your blood can increase your risk of heart disease. (3)It also needs lipoprotein to circulate through the bloodstream.
Development of plaque in blood vessel
The problem occurs when circulating LDL particles deposit inside the wall of the blood vessels. In normal conditions this doesn’t happen but when an LDL is oxidized problems begin to occur. (4,5) Which is like LDL and cholesterol are traveling through your bloodstream and suddenly an unstable reactive molecule with an unpaired electron (in simple called as free radical) hit LDL-C. As a result, oxidation occurs to LDL-C
Probably you may know that your white blood cells give protection to your body from harmful pathogens. When LDL-cholesterol got oxidized your immune system identifies them as harmful substances. That creates an inflammatory signal and your immune system deploys certain white blood cells against oxidized LDL. White blood cells literally “eat” the oxidized LDL particles but that process turns white blood cells into foam cells that can’t function properly and accumulate in the wall of blood vessels. This is called plaque build-up and the process is called atherosclerosis. (6)
This process narrows artery interrupts blood flow and contribute to the development of heart disease. A heart attack happens when there is a sudden complete blockage of an artery that supplies blood to an area of your heart. With blockage to the supply of blood to a particular area of heart occurs, the cells start to die in starvation. When an area of build-up plaque raptures blood cells and other substances of the blood sticks to the ruptured area and form blood clots. When a blood clot completely blocks the flow of blood heart attack occurs. (7)
Diving deeper in to LDL-C, HDL-C and Lipoproteins
We have read about LDL, HDL, and triglycerides. You may also hear about LDL and triglycerides as bad cholesterol and HDL as good cholesterol. That is actually due to lipoproteins type, rather than cholesterol. When cholesterols are carried by a particular type of lipoprotein, then the risk becomes greater. Lipoproteins are often classified as either “small, dense LDL” or “Large LDL”. People who predominantly have small, dense LDL called as Pattern B and who mostly contains Large LDL called as Patter A. And in study scientists found an individual with pattern B has much higher i.e. up to the threefold increased risk of heart attack than pattern A. (8)
That may be due to factors like increased risk of oxidation and increased ability to penetrate the wall of the blood vessel and self-associate of such kind of lipoproteins. Moreover, researchers also reported that small dense LDL particles have less affinity for the LDL-C receptor that receives LDL-C for functions. That results in LDL-C spends more time in circulation with increased susceptibility to oxidation. (9,10,11) Interestingly scientists found losing weight with reduced consumption of refined foods had led to a change of Pattern B to Pattern A.
Therefore total numbers of LDL particles(LDL-p) give a better picture than simple LDL cholesterol measurement. That means having more small particles you will have a higher number of particles, carrying the same amount of cholesterol. That can increase the risk. On the other hand, having more large LDL particles indicates a lesser number of lipoprotein for the same amount of cholesterol.
Large LDL-C may be beneficial
In fact, large LDL may be beneficial. Your body uses cholesterol as an important molecule in many vital functions. According to Dr. Stephen Sinatra a Cardiologist with more than 40 years of clinical practice, research, and study, who practices with an integrative approach “large, “fluffy” LDL cholesterol your body needs for immune health, brain function, and more. In fact, low levels of this helpful form of LDL cholesterol can be harmful to your health.” (12)
In a review paper, Japanese Scientist Harumi Okuyama and colleagues mentioned high blood cholesterol as a predictor of longevity, lower mortality from cancer, infectious diseases, and all-cause mortality. (13)A 2016 review on a total of 68 094 elderly people concluded there was either no link between LDL and mortality or that lower LDL was linked to higher mortality risk, especially in older adults. (14) Another population-based study followed 12,815,006 Korean peoples from 2001 to 2013. Researchers found an association of the lowest mortality with total cholesterol range 210–249 mg/dL in each sex-age subgroup, except for the youngest groups of men, aged 18–34 years (180–219 mg/dL), and women aged 18–34 years (160–199 mg/dL) and 35–44 years (180–219 mg/dL). (15)
Apolipoprotein B or ApoB as risk factor of heart disease
Another marker called ApoB or Apolipoprotein B exists to determine LDL particles. Since each LDL particle has one molecule of ApoB, the higher the ApoB number indicates higher the LDL particle number. By looking at LDL-p or ApoB instead of LDL-C, then the picture of diet and heart disease risk factors changes dramatically. (16)
High-density lipoproteins of HDL
HDL basically works the opposite of LDL. It removes cholesterol from arteries and plaques, protects the inner lining of the blood vessels from damage, and inhibits LDL oxidation. Like ApoB for LDL particles, ApoA1, carries HDL particles. Therefore the ratio of ApoB to ApoA1 has been also considered as a better indicator of the heart-disease risk factor. (6)
Saturated fats & heart disease risk itself: Evidence-We know
Saturated fats on blood cholesterol and heart disease risk factors
In 2016 WHO’s Meta-analysis of 84 Randomized Controlled Trials (RCTs) (17) studied thoroughly effects of saturated fats on blood lipids. The study evaluated the effects of replacing 1% of caloric intake from carbohydrates or unsaturated fats with 1% of caloric intake from saturated fat. The Meta-analysis covers the effects of saturated fat, polyunsaturated fats, monounsaturated fats and carbohydrates on LDL-C, HDL-C, total cholesterol, triglycerides. The study didn’t cover the LDL particle number but cover ApoB. Some significant consideration and findings of the study include
Saturated fats and LDL-C, LDL-C and ApoB
The study found saturated fat increased HDL-C but also increased LDL-C about 10 times than HDL-C. Therefore LDL-C to HDL-C ration increased significantly. On the other hand, although replacing unsaturated fat by saturated fat increased ApoA1 it also increased ApoB. And the increase of ApoA1 increase was 30–60% than in ApoB which was much different than the change in LDL to HDL.
Saturated fats and triglyceride
The triglyceride to HDL-C ratio is another independent predictor of heart disease risk factor when LDL-C levels are below 160 mg/dL. And elevated levels of triglyceride (TG) and low levels of HDL-C contribute to inflammation and atherosclerosis. (18)
Triglyceride-to-HDL-C ratio higher than 3.8 is associated with having more small, dense LDL particles, which are especially susceptible to oxidation and plaque development. The study found while reducing saturated fat with polyunsaturated fat reduced the ratio, eating more carbohydrates increased it.
However, the changes are not significant and had little effects on the ratio. A 10% reduction in calories from saturated fat would increase the triglyceride-to-HDL-C ratio by a mere 0.16 if more carbohydrates were eaten, and decrease it by only 0.04 if more polyunsaturated fat were eaten.
Strength and limitation of the Meta-analysis
The study maintained stringent criteria, so as to best isolate the effects of dietary substitution. For example, all food was provided to the participants, calories and protein were matched between diets. The meta-analysis included only studies that had thorough daily control of food intake. Elimination of the effect could be achieved by feeding the different diets side-by-side (parallel design) or by giving the diets to the volunteers in random order. Dietary periods had to be at least 13 days.
Tight control of dietary intake the study isolates specific effects of the particular nutrients. While the inclusion of only studies with strictly controlled diet the study provides valuable information on specific nutrients the study excludes some other factors that have also contributions to real life. The meta-analysis could not differentiate between the various food sources of the nutrients. Moreover, the study excluded diets that focused on hydrogenated oil, omega 3 PUFA (fish oils), and saturated fats as medium-chain fatty acids (MCFA). (6)The same study also reported this approach, while valuable in assessing specific effects of modifying SFA intake through the exchange of specific nutrients, does not provide a clear picture of what might happen in real-world settings in which modification of SFA intake might be accompanied by other changes in diet.
Saturated fats and Inflammation
Well, we know plaque development begins with the oxidation of LDL in a blood vessel. As such oxidation stimulates inflammation, therefore reducing such oxidation and inflammatory response is an important strategy. Saturated fat increases the absorption of lipopolysaccharides(LPS) type of bacterial endotoxins in the intestine that stimulates immune action. But the role of saturated fat on inflammation may not be that straight forward. Findings of one small study do not support a detrimental role of dietary SFA in low-grade inflammation among adolescents. (19) But in other studies, the effects of dietary saturated fat on inflammatory parameters yielded mixed results. (20,21)
One RCT reported that, compared to a diet high in saturated fatty acids (SFAs), a diet high in Monounsaturated Fatty Acid (MUFAs) decreased tendency of oxidation of LDL-C, a diet high in omega-6 (n-6) PUFAs increased it, and a diet high in omega-3 (n-3) Poly Un-saturated fatty acids (PUFAs) did not affect it. (22)
Another clinical study also suggests that a MUFA-rich diet may have favorable effects on cardiovascular risk since it prevents the oxidation of LDL and reduces the development of plaque. (23)
Findings of a review of 37 human clinical studies on saturated fats and inflammation
In the present time, this area appears as far from the settlement. A review of 37 human clinical studies from 2010 to 2016 found no significant associations between saturated fat and inflammation. According to the researchers due to small effects, large inter-individual differences and insensitive methods, dietary health effects are difficult to measure. This might explain why they did not find any effects after intervention with single nutrients or foods in the review. However, nutrients in whole diets may have synergistic effects, and thereby be able to affect the inflammatory system with more beneficial effects. (24)
Read more 8 lesser-known foods that cause inflammation in your body.
And anti-inflammatory foods but lesser-known to protect your health.
The Big Picture –Heart disease itself than heart disease risk factor
In above we have discussed about risk factors of heart disease rather than heart disease itself. Many studies found that saturated fat intake may increase heart disease risk factors, but not heart disease itself.
Atherosclerosis or development of heart disease is an inflammatory disease, mostly developed from the oxidation of cholesterol and multi-factorial. In present researcher indicated an association of multiple factors with cardiovascular disease and suggests a holistic approach in the prevention of heart disease. (25) Some of the major controllable factors include high blood pressure-hardening of artery or stiffness of blood vessel, inflammatory high blood sugar (we discussed earlier this about enlarged fat cells, weight gain, chronic inflammation), high blood cholesterol levels (more accurately lipoprotein number), smoking, overweight or obesity; lack of physical activity; unhealthy diet, chronic stress, lack of sleep and more. (26)
Also read
Foods that reduce blood pressure.
The food matrix rather than single nutrient
Food research with a reductionist approach or nutrient focused approach that evaluated the effect of a single nutrient group linking one nutrient to one health effect ignoring the effects of other nutrients of food (food matrix) will not give a real-world picture. This may partly explain why discrepancies exist in nutritional research. (27)
For example cheese and butter both contain saturated fat (SFA) but both have different food matrices. A clinical study reported that butter but not cheese has a greater influence in increasing the capacity of HDL in clearing LDL from white blood immune cells. In conclusion, researchers support that the food matrix modifies the association between SFAs and cardiovascular disease risk. (28) Another example-Ghee a form of clarified butter high with saturated fats contains beneficial short-chain saturated fat butyrate, monounsaturated fat, vitamin A, E and K and also helps to absorb fat-soluble vitamins. (29)
Saturated fats & heart disease risk itself: Evidence
Studies on Saturated fat and heart disease itself
Reanalysis of unpublished data recovered and published in the British Medical Journal reported replacing saturated fat with linoleic acid-containing vegetable oils increased mortality risk despite significant reductions in LDL and total cholesterol. (30) Several more meta-analyses and systematic reviews further cast doubt over the effect of SFA on CVD outcomes. In fact, recent research and meta-analyses have demonstrated the benefits of full-fat dairy consumption, based on higher bioavailability of high-value nutrients and anti-inflammatory properties. (27)
Another 2014 Meta-analysis of 32 observational studies (530,525 participants) of fatty acids from dietary intake; 17 observational studies (25,721 participants) of fatty acid biomarkers; and 27 randomized, controlled trials (103,052 participants) found no significant association between saturated fat intake and heart disease. (31) Another systematic review and meta-analysis of observational studies showed no association between saturated fat consumption and (1) all-cause mortality, (2) coronary heart disease (CHD), (3) CHD mortality, (4) ischaemic stroke or (5) type 2 diabetes in healthy adults. (32)
One more systematic review and meta-analysis of 10 dietary trials including 62 421 participants found no significant difference in all-cause mortality or CHD mortality, resulting from the dietary fat interventions. (33)
Bottom Line
Presently the reputation on saturated fat is changing from it had earlier. Moreover, several large studies didn’t found significant evidence on the consumption of Saturated fats & heart disease risk itself. One thing I again wish to tell you that saturated fat is not a single type of fat, rather it is a group of different types of fatty acids. Another very important factor is the usage of heat in fat before consumption. Burnt and overheated fats are always unhealthy. Similarly, I don’t have faith in highly processed fats where the possibility of oxidation of fats as well as the loss of other nutrients becomes high during processing. When you heat fats or oils, they release toxic aldehydes the amount of which depends on the types of fats. I will come with the coming articles about that.
According to the present Guidelines for Americans that are also considered in some others, saturated fat intake should be less than 10% of total calorie intake in a day. (34)
Disclaimer: Information provided here are generalized information for informational and entertainment purpose only, not intended to provide one to one health consultation or replace practice of a qualified practitioner.Different people may have different health condition and may have different reaction to the same food. Hence it has been advised to consult with health care provider before application of any of above information Source and references: 1.DuBroff R, de Lorgeril M Fat or fiction: the diet-heart hypothesis BMJ Evidence-Based Medicine Published Online First: 29 May 2019. doi: 10.1136/bmjebm-2019-111180 2.https://www.betterhealth.vic.gov.au/health/conditionsandtreatme nts/cholesterol 3.https://www.mayoclinic.org/diseases-conditions/high-blood- cholesterol/in-depth/triglycerides/art-20048186 4.Lau BH. Suppression of LDL oxidation by garlic. J Nutr. 2001;131(3s):985S–8S. doi:10.1093/jn/131.3.985S 5.Tuttolomondo A, Di Raimondo D, Pecoraro R, Arnao V, Pinto A, Licata G. Atherosclerosis as an inflammatory disease. Curr Pharm Des. 2012;18(28):4266–4288. doi:10.2174/138161212802481237 6."Is saturated fat bad for your health?," Examine.com, published on 12 August 2014, last updated on 24 February 2020, https://examine.com/nutrition/is-saturated-fat-bad-for-you/ 7.https://www.heartfoundation.org.au/your-heart/heart- conditions/heart-attack 8.Austin MA, Breslow JL, Hennekens CH, Buring JE, Willett WC, Krauss RM. Low-density lipoprotein subclass patterns and risk of myocardial infarction. JAMA. 1988;260(13):1917–1921. 9.Ivanova EA, Myasoedova VA, Melnichenko AA, Grechko AV, Orekhov AN. Small Dense Low-Density Lipoprotein as Biomarker for Atherosclerotic Diseases. Oxid Med Cell Longev. 2017;2017:1273042. doi:10.1155/2017/1273042 10.Krauss RM. Heterogeneity of plasma low-density lipoproteins and atherosclerosis risk. Curr Opin Lipidol. 1994;5(5):339–349. doi:10.1097/00041433-199410000-00005 11.Bowden RG, Wilson RL, Beaujean AA. LDL particle size and number compared with LDL cholesterol and risk categorization in end-stage renal disease patients. J Nephrol. 2011;24(6):771–777. doi:10.5301/JN.2011.6376 12.https://www.drsinatra.com/the-heart-health-benefits-of- coconut-oil 13.Okuyama H, Langsjoen PH, Ohara N, et al. Medicines and Vegetable Oils as Hidden Causes of Cardiovascular Disease and Diabetes. Pharmacology. 2016;98(3-4):134–170. doi:10.1159/000446704 14.Ravnskov U, Diamond DM, Hama R, et al, Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review BMJ Open 2016;6:e010401. doi: 10.1136/bmjopen-2015-010401 15.Yi SW, Yi JJ, Ohrr H. Total cholesterol and all-cause mortality by sex and age: a prospective cohort study among 12.8 million adults. Sci Rep. 2019;9(1):1596. Published 2019 Feb 7. doi:10.1038/s41598-018-38461-y 16.https://www.medicalnewstoday.com/articles/318712#what- increases-ldl-cholesterol? 17.https://www.who.int/nutrition/publications/nutrientrequirement s/sfa_systematic_review/en/ 18.Welty FK. How do elevated triglycerides and low HDL- cholesterol affect inflammation and atherothrombosis?. Curr Cardiol Rep. 2013;15(9):400. doi:10.1007/s11886-013-0400-4 19.Harris CP, von Berg A, Berdel D, et al. Dietary saturated fat and low-grade inflammation modified by accelerometer-measured physical activity in adolescence: results from the GINIplus and LISA birth cohorts. BMC Public Health. 2019;19(1):818. Published 2019 Jun 25. doi:10.1186/s12889-019-7113-6 20.Santos S, Oliveira A, Lopes C. Systematic review of saturated fatty acids on inflammation and circulating levels of adipokines. Nutr Res. 2013;33(9):687–695. doi:10.1016/j.nutres.2013.07.002 21.Nettleton JA, Lovegrove JA, Mensink RP, Schwab U. Dietary Fatty Acids: Is it Time to Change the Recommendations?. Ann Nutr Metab. 2016;68(4):249–257. doi:10.1159/000446865 22.Kratz M, Cullen P, Kannenberg F, et al. Effects of dietary fatty acids on the composition and oxidizability of low-density lipoprotein. Eur J Clin Nutr. 2002;56(1):72–81. doi:10.1038/sj.ejcn.1601288 23.Moreno JA, López-Miranda J, Pérez-Martínez P, et al. A monounsaturated fatty acid-rich diet reduces macrophage uptake of plasma oxidised low-density lipoprotein in healthy young men. Br J Nutr. 2008;100(3):569–575. doi:10.1017/S0007114508911508 24.Telle-Hansen VH, Christensen JJ, Ulven SM, Holven KB. Does dietary fat affect inflammatory markers in overweight and obese individuals?-a review of randomized controlled trials from 2010 to 2016. Genes Nutr. 2017;12:26. Published 2017 Oct 4. doi:10.1186/s12263-017-0580-4 25.Poulter N. Coronary heart disease is a multifactorial disease. Am J Hypertens. 1999;12(10 Pt 2):92S–95S. doi:10.1016/s0895- 7061(99)00163-6 26.Hajar R. Risk Factors for Coronary Artery Disease: Historical Perspectives. Heart Views. 2017;18(3):109–114. doi:10.4103/HEARTVIEWS.HEARTVIEWS_106_17 27.Lordan R, Tsoupras A, Mitra B, Zabetakis I. Dairy Fats and Cardiovascular Disease: Do We Really Need to be Concerned?. Foods. 2018;7(3):29. Published 2018 Mar 1. doi:10.3390/foods7030029 28.Didier Brassard, Benoît J Arsenault, Marjorie Boyer, Daniela Bernic, Maude Tessier-Grenier, Denis Talbot, Angelo Tremblay, Emile Levy, Bela Asztalos, Peter JH Jones, Patrick Couture, Benoît Lamarche, Saturated Fats from Butter but Not from Cheese Increase HDL-Mediated Cholesterol Efflux Capacity from J774 Macrophages in Men and Women with Abdominal Obesity, The Journal of Nutrition, Volume 148, Issue 4, April 2018, Pages 573–580, https://doi.org/10.1093/jn/nxy014 29.https://www.medicalnewstoday.com/articles/321707 30.Ramsden Christopher E, Zamora Daisy, Majchrzak-Hong Sharon, Faurot Keturah R, Broste Steven K, Frantz Robert P et al. Re- evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73) BMJ 2016; 353 :i1246 31.Chowdhury R, Warnakula S, Kunutsor S, et al. Association of dietary, circulating, and supplement fatty acids with coronary risk: a systematic review and meta-analysis [published correction appears in Ann Intern Med. 2014 May 6;160(9):658]. Ann Intern Med. 2014;160(6):398–406. doi:10.7326/M13-1788 32.Malhotra A, Redberg RF, Meier P, Saturated fat does not clog the arteries: coronary heart disease is a chronic inflammatory condition, the risk of which can be effectively reduced from healthy lifestyle interventions, British Journal of Sports Medicine 2017;51:1111-1112. 33.Harcombe Z, Baker JS, DiNicolantonio JJ, et al Evidence from randomised controlled trials does not support current dietary fat guidelines: a systematic review and meta- analysis Open Heart 2016;3:e000409. doi: 10.1136/openhrt-2016- 000409 34.https://health.gov/sites/default/files/2019-10/DGA_Cut-Down- On-Saturated-Fats.pdf
