23 Mar Fats: We’ve Got It All Wrong
Somehow, the USDA still tells us not to consume more than 10% of our calories from saturated fat (1).
This is after they removed their recommendations to limit dietary cholesterol, and 4 years after TIME magazine declared that the war on fat had ended with a photo of butter on the cover and the mantra “Eat Butter” underneath.
In the TIME article they detailed how fat, specifically saturated fat, “has been the most vilified nutrient in the American diet” and that “our demonization of fat may have backfired in ways we are just beginning to understand.”
Yet, the battle against the evil, artery-clogging saturated fat rages on.
The article also explains the extremely flawed science that began the anti-saturated fat nonsense and details the lack of connection between saturated fat and heart disease. (Saturated fat has been blamed for heart disease because it raises LDL levels, although I explain the problems with this idea here.)
But while I agree with these points, if the TIME magazine article is any indication, we’re still completely lost when it comes to fats. The article shifts the blame to sugar, which I’ve already written several articles defending, and also touts the benefits of the polyunsaturated fats.
Herein lies an even bigger problem.
Not only are we still recommended to reduce our saturated fat consumption, we’re encouraged to replace these saturated fats with unsaturated fat, specifically the polyunsaturated fats.
What Are Polyunsaturated Fats?
While saturated fats are known as the heart-disease-causing fats, polyunsaturated fats are typically considered the “heart-healthy” fats.
Polyunsaturated fats, or PUFA, are the omega-3 and omega-6 fats that we’ve been encouraged to consume in place of the saturated fats. They’re found in fatty fish like salmon, nuts & seeds, and the vegetable oils that come from those nuts and seeds.
But, while the saturated fats have more or less been vindicated of their “artery-clogging” accusations, the general stance towards PUFA hasn’t changed. They’re still considered the angels of the fat world.
And they also contribute to virtually all other chronic conditions, including obesity & diabetes (6, 7), cancer (2, 8), fatty liver (9), and Alzheimer’s & Parkinson’s disease (10, 11, 12). This is not to mention that they’re also strongly immunosuppressive (13, 14, 15, 16).
So, how is it that these fats are so incredibly harmful?
Polyunsaturated fats have multiple double bonds in their carbon chains. This is what separates them from saturated fats, which don’t have any double bonds in their carbon chains.
The presence of double bonds in PUFA might sound like a minor detail, but it ends up causing problems at the most fundamental level of our health: energy balance.
Polyunsaturated fats inhibit energy production, drastically increase energy demands, and reduce the efficiency of energy usage.
These effects are so powerful that, beyond contributing to the chronic conditions I just mentioned, the PUFA content in our cells is also the primary determinant of lifespan and aging in all animals, including us humans! (17)
The reasons for these effects comes down to 3 properties of PUFA:
- They’re structurally weak
- They’re converted into harmful, inflammatory compounds
- They’re highly susceptible to damage
Let’s explore each of these properties a little more.
Polyunsaturated fats are structurally weak
We often only consider the fats we eat as sources of energy. But, fats serve functional and structural purposes as well.
As structural components of the cell, fats are extremely important for holding energy and allowing our cells to properly function.
This leads us to one of the major problems that results from consuming PUFA.
When we consume PUFA, they’re incorporated as structural components in our cells, including their mitochondria (18). But, the presence of double bonds in PUFA makes them weak, so they serve as extremely poor structural components.
As poor structural components, PUFA cause our cells, or more specifically our mitochondria, to leak energy! (19, 20, 21, 22, 23). And in addition to leaking energy, they also cause our cells to leak out ions like potassium (21).
When taken together, these two effects drastically increase our energy demands and reduce the efficiency of energy usage.
Polyunsaturated fats are converted into harmful, inflammatory compounds
When not used structurally, PUFA can be converted into various compounds, like the eicosanoids.
The eicosanoids are the major compounds responsible for inflammation in the body. These are the compounds that the various anti-inflammatory medications, like aspirin and ibuprofen, block.
Chronic inflammation is one of the primary markers of chronic disease, and this chronic inflammation requires PUFA. In other words, reducing PUFA consumption is a great way to reduce inflammation.
But, it doesn’t end there.
Again, these effects are disastrous for energy balance.
Polyunsaturated fats are highly susceptible to damage
The first 2 properties of PUFA have been predicated on the fats remaining intact. But, because of the double bonds in these fats, they’re extremely susceptible to damage through a process called lipid peroxidation (17).
And this damage wreaks havoc in our body.
Because of this extensive damage, lipid peroxidation is considered to be a crucial step in the development of many chronic conditions (31).
Saturated fats to the rescue
Even individually, these 3 properties of PUFA make them incredibly harmful. And given all of them together, I would stay as far away from these fats as possible.
But this is easier said than done.
These fats are probably the biggest contributor to the health problems we’re seeing today, and they are EVERYWHERE!
They’re found in many baked goods, processed foods, cooking oils, fake butters & margarines, salad dressings, and fried foods. Plus, they’re encouraged as health foods in the form of nuts & seeds, fatty fish, and fatty chicken and pork.
But luckily, all the harmful properties of PUFA are directly contrasted by the saturated fats.
Saturated fats are everything PUFA are not. They’re stable, so they don’t leak energy and are extremely resistant to damage, and they aren’t converted to dangerous compounds. And, they even protect against the effects of PUFA! (32)
So, replacing PUFA with saturated fats like butter and coconut oil will go a long way for improving energy balance.
While it might go without saying, reducing or avoiding PUFA might take a bit of work. But it’s well worth it if you care about your health.
- “2015-2020 Dietary Guidelines: Answers to Your Questions.” Choose MyPlate, USDA, 7 Jan. 2016, choosemyplate.gov/2015-2020-dietary-guidelines-answers-your-questions.
- Zaminpira, Somayeh, and Sorush Vegetable Oils Consumption As One Of The Leading Cause Of Cancer And Heart Disease. 2017.
- Okuyama, Harumi, et al. “Medicines and Vegetable Oils as Hidden Causes of Cardiovascular Disease and Diabetes.” Pharmacology, 98, 3-4, 2016, pp. 134–70. doi:10.1159/000446704.
- Diniz, Yeda Sant’Ana, et al. “Diets rich in saturated and polyunsaturated fatty acids: Metabolic shifting and cardiac health.” Nutrition (Burbank, Los Angeles County, Calif.), 20, no. 2, 2004, pp. 230–34. doi:10.1016/j.nut.2003.10.012.
- Felton, C. V., et al. “Dietary polyunsaturated fatty acids and composition of human aortic plaques.” Lancet (London, England), 344, no. 8931, 1994, pp. 1195–96.
- Deol, Poonamjot, et al. “Soybean Oil Is More Obesogenic and Diabetogenic than Coconut Oil and Fructose in Mouse: Potential Role for the Liver.” PloS one, 10, no. 7, 2015, e0132672. doi:10.1371/journal.pone.0132672.
- Alvheim, Anita Røyneberg, et al. “Dietary linoleic acid elevates the endocannabinoids 2-AG and anandamide and promotes weight gain in mice fed a low fat diet.” Lipids, 49, no. 1, 2014, pp. 59–69. doi:10.1007/s11745-013-3842-y.
- Rose, D. P. “Effects of dietary fatty acids on breast and prostate cancers: Evidence from in vitro experiments and animal studies.” The American journal of clinical nutrition, 66, 6 Suppl, 1997, 1513S-1522S.
- Varela-Lopez, Alfonso, et al. “Gene pathways associated with mitochondrial function, oxidative stress and telomere length are differentially expressed in the liver of rats fed lifelong on virgin olive, sunflower or fish oils.” The Journal of nutritional biochemistry, 52, 2018, pp. 36–44. doi:10.1016/j.jnutbio.2017.09.007.
- Snowden, Stuart G., et al. “Association between fatty acid metabolism in the brain and Alzheimer disease neuropathology and cognitive performance: A nontargeted metabolomic study.” PLoS medicine, 14, no. 3, 2017, e1002266. doi:10.1371/journal.pmed.1002266.
- Farooqui, Akhlaq A., et al. “Modulation of inflammation in brain: A matter of fat.” Journal of neurochemistry, 101, no. 3, 2007, pp. 577–99. doi:10.1111/j.1471-4159.2006.04371.x.
- Lauretti, Elisabetta, and Domenico Praticò. “Effect of canola oil consumption on memory, synapse and neuropathology in the triple transgenic mouse model of Alzheimer’s disease.” Scientific reports, 7, no. 1, 2017, p. 17134. doi:10.1038/s41598-017-17373-3.
- Haw, M. P., et al. “The effect of dietary polyunsaturated fatty acids (PUFA) on acute rejection and cardiac allograft blood flow in rats.” Transplantation, 60, no. 6, 1995, pp. 570–77.
- McHugh, M. I., et al. “Immunosuppression with polyunsaturated fatty acids in renal transplantation.” Transplantation, 24, no. 4, 1977, pp. 263–67.
- Kelley, D. S., and P. A. Daudu. “Fat intake and immune response.” Progress in food & nutrition science, 17, no. 1, 1993, pp. 41–63.
- Mascioli, E. A., et al. “Medium chain triglycerides and structured lipids as unique nonglucose energy sources in hyperalimentation.” Lipids, 22, no. 6, 1987, pp. 421–23.
- Hulbert, A. J., et al. “Life and death: Metabolic rate, membrane composition, and life span of animals.” Physiological reviews, 87, no. 4, 2007, pp. 1175–213. doi:10.1152/physrev.00047.2006.
- Hulbert, A. J., et al. “Dietary fats and membrane function: Implications for metabolism and disease.” Biological Reviews, 80, no. 1, 1999, pp. 155–69. doi:10.1017/S1464793104006578.
- Porter, R. K., et al. “Allometry of mitochondrial proton leak: Influence of membrane surface area and fatty acid composition.” The American journal of physiology, 271, 6 Pt 2, 1996, R1550-60. doi:10.1152/ajpregu.1996.271.6.R1550.
- Brookes, Paul S., et al. “The Proton Permeability of the Inner Membrane of Liver Mitochondria from Ectothermic and Endothermic Vertebrates and from Obese Rats: Correlations with Standard Metabolic Rate and Phospholipid Fatty Acid Composition.” Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology, 119, no. 2, 1998, pp. 325–34. doi:10.1016/S0305-0491(97)00357-X.
- Hulbert, A. J., and P. L. Else. “Membranes as possible pacemakers of metabolism.” Journal of theoretical biology, 199, no. 3, 1999, pp. 257–74. doi:10.1006/jtbi.1999.0955.
- Brand, Martin D., et al. “Proton conductance and fatty acyl composition of liver mitochondria correlates with body mass in birds.” The Biochemical journal, 376, Pt 3, 2003, pp. 741–48. doi:10.1042/BJ20030984.
- Hulbert, A. J., and P. L. Else. “Membranes and the setting of energy demand.” The Journal of experimental biology, 208, Pt 9, 2005, pp. 1593–99. doi:10.1242/jeb.01482.
- Cocco, Tiziana, et al. “Arachidonic acid interaction with the mitochondrial electron transport chain promotes reactive oxygen species generation.” Free Radical Biology and Medicine, 27, 1-2, 1999, pp. 51–59. doi:10.1016/S0891-5849(99)00034-9.
- Di Paola, Marco, and Michele Lorusso. “Interaction of free fatty acids with mitochondria: Coupling, uncoupling and permeability transition.” Biochimica et biophysica acta, 1757, 9-10, 2006, pp. 1330–37. doi:10.1016/j.bbabio.2006.03.024.
- Hillered, L., and P. H. Chan. “Role of arachidonic acid and other free fatty acids in mitochondrial dysfunction in brain ischemia.” Journal of neuroscience research, 20, no. 4, 1988, pp. 451–56. doi:10.1002/jnr.490200407.
- Greene, Jessica F., and Bruce D. Hammock. “Toxicity of Linoleic Acid Metabolites.” Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation, and Radiation Injury, 4, edited by Kenneth V. Honn et al., Advances in Experimental Medicine and Biology, vol. 469, Springer, Boston, MA 1999, pp. 471–77.
- Bruder, Eric D., et al. “An oxidized metabolite of linoleic acid stimulates corticosterone production by rat adrenal cells.” American journal of physiology. Regulatory, integrative and comparative physiology, 284, no. 6, 2003, R1631-5. doi:10.1152/ajpregu.00753.2002.
- Goodfriend, T. L., et al. “Oxidized products of linoleic acid stimulate adrenal steroidogenesis.” Endocrine research, 28, no. 4, 2002, pp. 325–30.
- Musatov, Andrej. “Contribution of peroxidized cardiolipin to inactivation of bovine heart cytochrome c oxidase.” Free radical biology & medicine, 41, no. 2, 2006, pp. 238–46. doi:10.1016/j.freeradbiomed.2006.03.018.
- Mylonas, C., and D. Kouretas. “Lipid peroxidation and tissue damage.” In vivo (Athens, Greece), 13, no. 3, 1999, pp. 295–309.
- Purohit, Vishnudutt, et al. “Role of fatty liver, dietary fatty acid supplements, and obesity in the progression of alcoholic liver disease: Introduction and summary of the symposium.” Alcohol (Fayetteville, N.Y.), vol. 34, no. 1, 2004, pp. 3–8. doi:10.1016/j.alcohol.2004.06.008.