Fats Still Get A Bad Wrap
Everything You Need to Know About Eating Fat
Should fats be avoided? Should we be eating more dietary fat? Is there anything “good” about dietary fat?
My philosophy is that all fats have gotten lumped into one large category labeled as either good or bad, much like carbs. However, just like carbs, there are different types of fats, various sources of fat. Some are healthier than others and should be included in the diet, while others should be minimized. Thus, not all fats should be avoided.
The research is conflicting, such as some studies suggesting that saturated fats are unhealthy and avoid them while unsaturated fats are healthy. For instance, a very new study published on January 20, 2021, suggests that saturated fat-induced LDL in healthy individuals may represent a normal pathological response (Zincoker et al., 2021). Thus, in this case, with SFA raising LDL, is this bad? Is it still a predictor or risk factor for CVD? Yamagishi et al. (2010) concluded that SFA intake was inversely associated with stroke mortality. In their meta-analysis, Siri-Tarino et al. (2010) concluded there is no significant evidence that saturated fat is associated with increased risk for CHD or CVD. The Minnesota coronary Experiment found that those who reduced their cholesterol levels had a greater risk of death (Ramsden et al., 2016). Yet, we associate fat intake with raising our total cholesterol and our LDL, thus increasing CVD risk.
Still, Conflicted?
Should You Avoid Saturated Fats?
An easy way to remember which fats are saturated think of the terms saturated and solid together. These fats are solid at room temperature. This can include coconut oil, butter, lard, ghee for instance.
I may suggest avoiding SFA from refined and processed foods such as processed meats (i.e., cold cuts, hot dogs) and processed, refined desserts such as pastries and pies for a client. But I may suggest that butter and coconut oil within moderation is okay for the individual. Thus, I think quality and quantity matter. My suggestion would be to prepare more homemade meals furthering the control of types and amount of fats. When you go out to eat, you have no idea nor any control over the quality and quantity of fats used. Most restaurants, even the high-end places, will use cheaper, refined, oxidized oils and may use a heavy hand when adding them to the pan and to dishes. Thus, I suggest to my clients to reduce the amount of eating out and look at it more of a treat, not an everyday occurrence. By doing so, you reduce your risk of diet and lifestyle issues.
We should not eat a high-fat diet or a low-fat diet, but a balanced diet that includes all three macronutrients. I do not believe in extremes for most individuals, with some exceptions. Thus, a ketogenic diet or a low-fat diet is not a balanced diet.
I hope that most people have moved away from the concept that fat is bad. We require at least a minimum fat intake since it is essential. I once had a client tell me his doctor suggested a zero-fat intake diet. I am not sure how this is even possible! We need fats to store energy, to transport our fat-soluble nutrients for our cell membranes, to protect vital organs, and assist with temperature regulation (Haas & Levin, 2006, p. 64)
It may be better to break fats down into the SCFA, MCFA, and LCFA’s. But even within that, it can get complicated and confusing. For instance, within MCFA, lauric acid (12 carbons) seems to raise LDL more so than the MCFA caprylic acid (8 carbons) (Hass & Levin, p..65). Additionally, saturated fats will stabilize cell membranes, and unsaturated fatty acids provide flexibility to the cell membranes; therefore, both are required (Haas & Levin, 2006, p. 66).
Which ones are healthy to be used on salads?
Which ones are healthy when cooking?
Based on studies I have been reviewing, I lean to the fats included in the Med-diet. Thus, for oils, my go-to for raw and lightly cooked meals is EVOO. EVOO is monounsaturated fat. EVOO has been widely studied, and there is evidence supporting its use for the prevention of type 2 diabetes and CVD when used as part of the Med-diet (Forouhi et al., 2018).
Much like there is a great debate on fat in our food, the same exists for oils. For instance, I used to suggest avocado oil to clients over refined vegetable oils, only to find a new study that most avocado oils are fake (Green & Wang, 2020). The same issue applies to olive oil, and many are not pure olive oil. Thus, I provide a handout for clients on brands that I have found to be reputable, what to look for in quality oil and what temperatures to use certain oils. Therefore, not oils are the same. I use Olea Estates EVOO for my raw dishes. For my lightly cooked dishes, I use Braggs EVOO. For dishes, at higher temperatures, I will still use avocado oil but I try to reduce high-temperature frying.
Overall, I may have a client incorporate a variety of oils into their diet, such as EVOO (monosaturated), sesame oil (polyunsaturated omega 6), flaxseed oil (polyunsaturated omega-three oil) (Haas & Levin, 2006). Additionally, I may suggest coconut oil (unrefined, use in cooking up to 350 degrees F), olive oil (up to 375 degrees F.), and rice bran oil (up to 490 degrees F.) (Masterclass, 2020). Supposedly refined avocado oil can withstand temperatures up to 520 degrees F., but I have read conflicting information on this.
Additionally, the method used for cooking matters. I encourage clients to incorporate raw cooking and cooking methods other than frying such as stir fry, boiling, instant pot, slow cooker, steamer, and braising as healthier cooking options to reduce the number of oils used for cooking.
What About Coconut Oil?
Do the benefits that apply to medium-chain triglycerides (MCTs) apply to coconut oil?
No, the benefits of MCT do not apply to coconut oil. This actually was new information for me. I had once thought that coconut oil was an MCT, but actually, it is an LCT.
MCT are oils that are predominantly made up of caprylic acid (50-80%) and capric acid (20-50%). Coconut oil has 9% caprylic and 7% capric, with the bulk as lauric acid at 47%. While lauric acid can be classified as a medium-chain or a long-chain fatty acid, it behaves more like a long-chain fatty acid since the bulk of it is absorbed as chylomicrons. Medium-chain fatty acids are absorbed directly into the portal vein.
They also differ in chain length, which is essential when we look at absorption rate. Medium-chain acids are absorbed at a faster rate than long-chain fatty acids. Triglycerides containing lauric acid, such as coconut oil, have a higher molecular weight at 638, whereas MCT has a molecular weight of 512. This lower molecular weight of MCT facilities pancreatic lipase action. Therefore, MCT is broken down and absorbed faster than coconut oil. The MCT has a carbon number of C24:0 to C30:0, whereas only 4% of the coconut oil triglycerides are this length. Therefore, we cannot say that coconut oil is an MCT (Eyres et al., 2016).
Since I mentioned that LCFA’s are absorbed as chylomicrons, it might help if I explain briefly what that means. Chylomicrons are made in the enterocytes from exogenous triglycerides; thus, they are directly proportional to the amount of fat consumed in the diet (Gropper & Smith, 2018, p. 147). Chylomicrons travel via the lymphatic system and enter the bloodstream via the thoracic lymph duct, bypassing the liver to deliver triglycerides to the muscle and adipose tissue (Gropper & Smith, 2018, p. 145).
How and Why Do saturated fat and trans-fat intake increase LDL levels?
While the increase in LDL is a multifactorial issue, saturated fats and trans-fats have been linked to its increase because they are long-chain fatty acids (LCFA). LCFA (14-18 carbon chains) would include lauric acid, myristic acid, and palmitic acid. However, stearic acid, an 18 carbon chain LCFA, is not associated with an increase in LDL (Gropper & Smith, 2018, p. 155). Stearic acid is found in various animal and plant fats such as cocoa butter and shea butter, and animal fat.
Trans fats, found in processed foods, mimic saturated fats in the body, thus raising LDL (Clifford & Kozil, 2017).
LDL is a carrier of cholesterol from the liver to the body’s organs and can be deposited as plaque on the arterial walls.
The liver has LDL receptors so that LDL can be taken in and broken down by the liver. Too much saturated fat in the diet can downregulate these receptors; thus, the cholesterol builds up in the blood as it carries cholesterol from the liver to the organs. Therefore, the excess as it travels can build up along the arterial wall as plaque (Clifford & Kozil, 2017).
Dana-Farber Cancer Institute (2005) has found that the damage caused by trans fats and saturated fats may be due to these fats activating liver cells called PGC-1beta. When these cells are activated, it sends signals leading to an increase in the liver’s production of VLDL, the precursor to LDL (Dana-Farber Cancer Institute, 2005).
The Diet-Heart hypothesis
The diet-heart hypothesis suggested that replacing saturated fats with vegetable oil rich in linoleic acid would reduce cardiovascular disease because it would lower serum cholesterol levels.
Swapping out the saturated fat and replacing it with vegetable oil did reduce serum cholesterol levels. This data is supported by research. However, while LDL and TC were reduced, it did not reduce CVD mortality levels. Those in the linoleic, vegetable oil group had a greater risk of death (Ramsden et al., 2016)
This study used a high amount of linoleic acid (PUFA, corn oil/omega 6), which Ramsden et al. (2016) states are almost twice as much as consumed in the average American diet. This study also looked at those who were institutionalized, which simplified controlling the diet. However, 25% of the study subjects were 65 years old or older. Having one-fourth of the study subjects in this population may skew the number of deaths. For instance, the study (Ramsden et al., 2016) states that the deaths associated with lower cholesterol levels were found in those over 65. In those younger than 65-year-old, there was no relationship between serum cholesterol and death.
Thus, my question at this point would be, are higher cholesterol levels protective in old age but not in those younger than 65? And actually, not going into this topic, but yes, it appears based on data that a higher cholesterol level is heart-protective as we age!
Therefore, based on this information I think we are testing all wrong. I would like to see health professionals test different lab markers. Instead, I would like to look at hs-CRP as a marker for inflammation since atherosclerosis is an inflammatory disease. Thus hs-CRP is a known biomarker for atherosclerotic CVD risk (Direct Labs, n.d.). Additionally, I would test APO A and ApoB. APO A is an HDL component, and a low level of this indicates an increased CVD risk (Direct Labs, n.d.).
ApoB is a component of VLDL and when this is elevated is an indicator of CVD (Direct Labs, n.d.).
Therefore while this study showed no association between reduced lipid markers and lower CVD risk we also must note the subset of the population that these results were in.
Should you consume Saturated fats, Unsaturated fat?
While reducing saturated fats in the diet, such as in coconut oil, can lower cholesterol markers, this does not necessarily mean it will prevent CVD, according to Ramsden et al. (2016). Eyres et al. (2016) state that coconut oil consumption does not raise HDL levels but raises LDL and TC levels. Additionally, some studies they reviewed found that coconut oil and safflower oil can reduce triglyceride levels.
Therefore, we must question whether saturated fats are harmful because they increase serum cholesterol levels. According to Ramsden et al. (2016) saturated fats may not pose an increased risk for CVD.
It might be wise to include saturated fats into the diet, to incorporate coconut instead in its whole food form, such as coconut flesh, since this would consist of polyunsaturated omega-three fats (Eyres et al., 2016). Additonally, there is a recent very small study on the benefits on coconut oil for this new virus. The study can be found at this link. It would be interesting to see the reustls on a much larger scale.
As practitioners guiding our clients, we need to consider one’s complete diet and lifestyle. For instance, I know people in the Philippines who consume coconut water, coconut flesh, and coconut milk on a regular, almost daily basis as part of their diet. However, their diet also consists of other traditional local foods, including an abundance of fruit varieties. This diet differs vastly from the westernized standard American diet that we see in the United States. Therefore, in this context, as a local food incorporated into a whole foods diet, it is not the same as coconut oil used for frying food at high temperatures as part of the westernized diet. Thus, I think coconut products can be part of a healthy diet when chosen and incorporated wisely.
If replacing saturated fat with polyunsaturated fats or carbohydrates are both unhealthy, what could be a health-promoting replacement for saturated fats?
If saturated fats are unhealthy for us, especially in excess, there are healthy swaps we can make. The answer is not to replace saturated fat with more carbs and other harmful fats. Instead, we should incorporate foods rich in omega-three essential fatty acids such as those found in the Mediterranean diet. Switching to the Med-diet would include nuts, seeds, nut and seed oils, fatty fish such as salmon, and pure extra virgin olive oil (EVOO). The Med-diet would be a healthier option instead of swapping saturated fats for carbs and a low-fat diet. The Lyon Heart study showed that a Mediterranean diet reduces all-cause mortality (DiNicolantonio, 2014). Therefore, it may be wise to incorporate the Mediterranean diet into our lifestyles.
Bottom Line
EAt a whole food diet, with fats in their natural state such as in a coconut, in nuts and seeds, in avocado and so forth. Start minimizing the processed food, the take-out food, the fast food, food in a bag or box, and so forth and you will automatically reduce unhealthy fats in the diet.
References
Direct labs, Direct Laboratory Services, LLC. (n.d.). Cardiovascular/heart health. Retrieved from https://www.directlabs.com/OrderTests/tabid/55/language/en-US/Default.aspx
Forouhi, N. G., Misra, A., Mohan, V., Taylor, R., & Yancy, W. (2018). Dietary and nutritional approaches for prevention and management of type 2 diabetes. BMJ, 361, k2234. http://doi.org/10.1136/bmj.k2234 (Links to an external site.)
Green, H.S. & Wang, S.C. (2020). First report on quality and purity evaluations of avocado oil sold in the US. Food Control, 116, 107328. 10.1016/j.foodcont.2020.107328
Gropper, S., & Smith, J. (2018). Chapter 5: Lipids. In Advanced nutrition and human metabolism (7th ed.). Boston, MA: Cengage Learning.
Haas, E. & Levin, B. (2006). Staying healthy with nutrition. The complete guide to diet and nutritional medicine. Berkeley, CA: Celestial Arts.
Masterclass. (2020, Nov. 8). Cooking oils and smoke points: What to know and how to choose the right cooking oil. Retrieved from https://www.masterclass.com/articles/cooking-oils-and-smoke-points-what-to-know-and-how-to-choose#what-is-an-oil-smoke-point (Links to an external site.)
Ramsden, C. E., Zamora, D., Majchrzak-Hong, S., Faurot, K. R., Broste, S. K., Frantz, R. P., … Hibbeln, J. R. (2016). Re-evaluation of the traditional diet-heart hypothesis: Analysis of recovered data from Minnesota Coronary Experiment (1968-73). The BMJ, 353, i1246. https://doi.org/10.1136/bmj.i1246 .
Siri-Tarino, P. W., Sun, Q., Hu, F. B., & Krauss, R. M. (2010). Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. The American journal of clinical nutrition, 91(3), 535–546. https://doi.org/10.3945/ajcn.2009.27725 (Links to an external site.)
Yamagishi, K., Iso, H., Yatsuya, H., Tanabe, N., Date, C., Kikuchi, S., Yamamoto, A., Inaba, Y., Tamakoshi, A., & JACC Study Group (2010). 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. The American journal of clinical nutrition, 92(4), 759–765. https://doi.org/10.3945/ajcn.2009.29146 (Links to an external site.)
Zinöcker, M. K., Svendsen, K., & Dankel, S. N. (2021). The HOMEOVISCOUS adaptation to dietary Lipids (HADL) model EXPLAINS controversies over saturated fat, cholesterol, and cardiovascular disease risk. The American Journal of Clinical Nutrition, 113(2), 277-289. doi:10.1093/ajcn/nqaa322
Clifford, J & Kozil, A. (2017). Dietary fat and cholesterol. Retrieved from https://extension.colostate.edu/topic-areas/nutrition-food-safety-health/dietary-fat-and-cholesterol-9-319/
Dana-Farber Cancer Institute. (2005, Jan. 30). Scientists id molecular ‘switch’ in liver that triggers harmful effects of saturated and trans fats. Retrieved from https://www.sciencedaily.com/releases/2005/01/050128224527.htm
Davis, D. (n.d.). The end of the friedewald equation? The American society for clinical laboratory science. Retrieved from https://www.ascls.org/communication/ascls-today/325-ascls-today-volume-32-number-6/466-the-end-of-the-friedewald-equation
DiNicolantonio, J. J. (2014). The cardiometabolic consequences of replacing saturated fats with carbohydrates or Ω-6 polyunsaturated fats: Do the dietary guidelines have it wrong? Open Heart, 1(1), e000032. https://doi.org/10.1136/openhrt-2013-000032
Eyres, L., Eyres, M. F., Chisholm, A. & Brown, R. C. (2016). Coconut oil consumption and cardiovascular risk factors in humans. Nutrition Reviews, 74(4), 267–280. https://doi.org/10.1093/nutrit/nuw002.
Gropper, S., & Smith, J. (2018). Chapter 5: Lipids. In Advanced nutrition and human metabolism (7th ed.). Boston, MA: Cengage Learning.
Litchford, M. (2017). Laboratory assessment of nutritional status: Bridging theory and practice. Greensboro, NC: Case Software.
Ramsden, C. E., Zamora, D., Majchrzak-Hong, S., Faurot, K. R., Broste, S. K., Frantz, R. P., … Hibbeln, J. R. (2016). Re-evaluation of the traditional diet-heart hypothesis: Analysis of recovered data from Minnesota Coronary Experiment (1968-73). The BMJ, 353, i1246. https://doi.org/10.1136/bmj.i1246 .