06 Apr Omega-3s Are NOT The “Healthy Fats”
Omega-3s are all the rage nowadays.
Everybody’s taking fish oil – it’s the new miracle cure, featured on the news, on every health site, and in the supermarkets.
Foods like salmon, flaxseeds, and walnuts are considered the ultimate health foods because of their “heart-healthy” omega-3 fats, which are supposed to benefit everything from heart disease to diabetes to cancer.
And this is coupled with ridiculous claims of boosting the immune system, improving memory, and anti-aging effects.
But, omega-3s don’t have all the benefits that they’re claimed to have. They’ve been found not to protect against heart disease and stroke (1, 2, 3, 4, 5), cancer (4, 5), macular degeneration (6), IBD (7), aging (8), or dementia, Alzheimer’s disease, and other neurological disorders (9, 10).
Not only do omega-3s not benefit many of the diseases they’re claimed to, they also contribute to many of them.
But, before we get too carried away on all the problems omega-3s cause, let’s first talk about what omega-3s are, and how they differ from their omega-6 siblings.
Omega-3s vs. Omega-6s
Omega-3s and omega-6s are polyunsaturated fats. As I talked about in this article, these fats are incredibly harmful.
The omega-6 fats are mostly found in vegetable oils, nuts, and seeds, and were promoted as the healthy replacement for the “artery-clogging” saturated fats. But, it’s become more well-recognized that the omega-6 fats, which were once touted for their “heart-healthy” qualities and other supposed benefits, are harmful to our health.
The omega-3 fats, on the other hand, are found in fish, flaxseeds, chia seeds, walnuts, and some other foods. These fats have come onto the health scene more recently than the omega-6 fats and are now replacing them as the “healthy fats.”
As I explained in the aforementioned article, the polyunsaturated fats, including both the omega-3s and omega-6s, are harmful for 3 reasons:
- They’re structurally weak
- They’re converted into harmful, inflammatory compounds
- They’re highly susceptible to damage
Well as it turns out, the omega-3s are even worse than the omega-6s when it comes to these 3 parameters.
You Thought Omega-6s Were Weak?
If you thought omega-6s were weak, just wait until you hear this.
The omega-3s have more double bonds than their omega-6 counterparts, making them even less stable. This leaves them structurally weaker and about twice as susceptible to damage than the omega-6s.
For example, DHA is one of the omega-3 fats that’s considered to be extremely beneficial. But, the amount of DHA used structurally in our cells is directly related to aging and lifespan (11). In other words, the more DHA in our cells, the faster we age and shorter we live.
This is because DHA is one of the weakest and least stable fats. When used as a structural component of the mitochondria, it increases the leakage of energy more than any other polyunsaturated fat (12). And, it’s 320 times more susceptible to damage than monounsaturated fats! (11)
As I mentioned in the last article on fats, when the polyunsaturated fats become damaged through lipid peroxidation they wreak havoc on the body. And, not only are omega-3s more susceptible to this damage, they’re also converted to compounds that are even more destructive.
When the omega-3s undergo lipid peroxidation they’re converted into hydroperoxides and endoperoxides. These compounds, as well as their reactive aldehyde breakdown products such as acrolein, HNE, and MDA, are extremely harmful.
These compounds damage proteins and DNA, including the cellular components that are needed for energy production (4, 13, 14, 15, 16). These compounds are also implicated in cancer, diabetes, heart disease, liver disease, Alzheimer’s disease, aging, and are known to be neurotoxic (16, 17, 18, 19, 20).
Now, the argument may be made that eating these polyunsaturated fats doesn’t mean that they’ll become damaged and cause this destruction. But, many studies have discredited this argument by showing that increased omega-3 consumption (and PUFA consumption in general) does increase lipid peroxidation and the presence of their harmful breakdown products (21, 22, 23, 24, 25, 26, 27, 28, 29).
Omega-3s Are NOT The “Healthy Fats”
Maybe it’s overkill by now, but just to hammer the point home…
Because of the damaging effects of omega-3s and their derivatives, omega-3s have been implicated in causing cancer (30, 31, 32, 33), fatty liver (34, 35, 36), and insulin resistance (37, 38). And, like the omega-6s, they’re also strongly immunosuppressive (39, 40, 41).
And, while the omega-3s are currently recommended during pregnancy and infancy, they’ve been shown to cause shorter lifespans, lower body weights, and neurological abnormalities in children whose mothers consumed large amounts of them (42).
So with all that being said, can we stop promoting the omega-3s as healthy already? Or are we going to have to wait another 30 years to figure it out?
And while we’re at it, maybe we should reconsider all the fish oil supplementation.
- Aung, Theingi, et al. “Associations of Omega-3 Fatty Acid Supplement Use With Cardiovascular Disease Risks: Meta-analysis of 10 Trials Involving 77 917 Individuals.” JAMA cardiology, 3, no. 3, 2018, pp. 225–34. doi:10.1001/jamacardio.2017.5205.
- Rizos, Evangelos C., et al. “Association between omega-3 fatty acid supplementation and risk of major cardiovascular disease events: A systematic review and meta-analysis.” JAMA, 308, no. 10, 2012, pp. 1024–33. doi:10.1001/2012.jama.11374.
- Fodor, J. George, et al. “”Fishing” for the origins of the “Eskimos and heart disease” story: Facts or wishful thinking?” The Canadian journal of cardiology, 30, no. 8, 2014, pp. 864–68. doi:10.1016/j.cjca.2014.04.007.
- Peskin, B. S. “Why fish oil fails: A comprehensive 21st century lipids-based physiologic analysis.” Journal of lipids, 2014, 2014, p. 495761. doi:10.1155/2014/495761.
- Hooper, L., et al. “Omega 3 fatty acids for prevention and treatment of cardiovascular disease.” The Cochrane database of systematic reviews, no. 4, 2004, CD003177. doi:10.1002/14651858.CD003177.pub2.
- Lawrenson, John G., and Jennifer R. Evans. “Omega 3 fatty acids for preventing or slowing the progression of age-related macular degeneration.” The Cochrane database of systematic reviews, no. 4, 2015, CD010015. doi:10.1002/14651858.CD010015.pub3.
- Cabré, Eduard, et al. “Omega-3 fatty acids and inflammatory bowel diseases – a systematic review.” The British journal of nutrition, 107 Suppl 2, 2012, S240-52. doi:10.1017/S0007114512001626.
- Magalhães, João Pedro de, et al. “Fish oil supplements, longevity and aging.” Aging, 8, no. 8, 2016, pp. 1578–82. doi:10.18632/aging.101021.
- Burckhardt, Marion, et al. “Omega-3 fatty acids for the treatment of dementia.” The Cochrane database of systematic reviews, 4, 2016, CD009002. doi:10.1002/14651858.CD009002.pub3.
- Assisi, Alessandro, et al. “Fish oil and mental health: The role of n-3 long-chain polyunsaturated fatty acids in cognitive development and neurological disorders.” International clinical psychopharmacology, 21, no. 6, 2006, pp. 319–36. doi:10.1097/01.yic.0000224790.98534.11.
- Hulbert, A. J. “On the importance of fatty acid composition of membranes for aging.” Journal of theoretical biology, 234, no. 2, 2005, pp. 277–88. doi:10.1016/j.jtbi.2004.11.024.
- Hulbert, A. J., et al. “How might you compare mitochondria from different tissues and different species?” Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology, 176, no. 2, 2006, pp. 93–105. doi:10.1007/s00360-005-0025-z.
- Marnett, L. “Endogenous DNA damage and mutation.” Trends in Genetics, 17, no. 4, 2001, pp. 214–21. doi:10.1016/S0168-9525(01)02239-9.
- Niedernhofer, Laura J., et al. “Malondialdehyde, a product of lipid peroxidation, is mutagenic in human cells.” The Journal of biological chemistry, 278, no. 33, 2003, pp. 31426–33. doi:10.1074/jbc.M212549200.
- 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.
- Del Rio, Daniele, et al. “A review of recent studies on malondialdehyde as toxic molecule and biological marker of oxidative stress.” Nutrition, metabolism, and cardiovascular diseases: NMCD, 15, no. 4, 2005, pp. 316–28. doi:10.1016/j.numecd.2005.05.003.
- Pocernich, Chava B., and D. Allan Butterfield. “Acrolein inhibits NADH-linked mitochondrial enzyme activity: Implications for Alzheimer’s disease.” Neurotoxicity research, 5, no. 7, 2003, pp. 515–20.
- Butterfield, D. Allan, et al. “Evidence that amyloid beta-peptide-induced lipid peroxidation and its sequelae in Alzheimer’s disease brain contribute to neuronal death.” Neurobiology of aging, 23, no. 5, 2002, pp. 655–64.
- Reed, Tanea, et al. “Redox proteomic identification of 4-hydroxy-2-nonenal-modified brain proteins in amnestic mild cognitive impairment: Insight into the role of lipid peroxidation in the progression and pathogenesis of Alzheimer’s disease.” Neurobiology of disease, 30, no. 1, 2008, pp. 107–20. doi:10.1016/j.nbd.2007.12.007.
- Roberts, L. J., et al. “Formation of isoprostane-like compounds (neuroprostanes) in vivo from docosahexaenoic acid.” The Journal of biological chemistry, 273, no. 22, 1998, pp. 13605–12.
- Allard, J. P., et al. “Lipid peroxidation during n-3 fatty acid and vitamin E supplementation in humans.” Lipids, 32, no. 5, 1997, pp. 535–41.
- Filaire, Edith, et al. “Effect of 6 Weeks of n-3 fatty-acid supplementation on oxidative stress in Judo athletes.” International journal of sport nutrition and exercise metabolism, 20, no. 6, 2010, pp. 496–506.
- Song, J. H., and T. Miyazawa. “Enhanced level of n-3 fatty acid in membrane phospholipids induces lipid peroxidation in rats fed dietary docosahexaenoic acid oil.” Atherosclerosis, 155, no. 1, 2001, pp. 9–18.
- Al-Gubory, Kaïs H. “Mitochondria: Omega-3 in the route of mitochondrial reactive oxygen species.” The international journal of biochemistry & cell biology, 44, no. 9, 2012, pp. 1569–73. doi:10.1016/j.biocel.2012.06.003.
- Malis, C. D., et al. “Incorporation of marine lipids into mitochondrial membranes increases susceptibility to damage by calcium and reactive oxygen species: Evidence for enhanced activation of phospholipase A2 in mitochondria enriched with n-3 fatty acids.” Proceedings of the National Academy of Sciences of the United States of America, 87, no. 22, 1990, pp. 8845–49.
- Gonzalez, M. J., et al. “Lipid peroxidation products are elevated in fish oil diets even in the presence of added antioxidants.” The Journal of nutrition, 122, no. 11, 1992, pp. 2190–95. doi:10.1093/jn/122.11.2190.
- Kjaer, M. A., et al. “Dietary n-3 HUFA affects mitochondrial fatty acid beta-oxidation capacity and susceptibility to oxidative stress in Atlantic salmon.” Lipids, 43, no. 9, 2008, pp. 813–27. doi:10.1007/s11745-008-3208-z.
- 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.
- Fang, J. L., et al. “Determination of DNA adducts of malonaldehyde in humans: Effects of dietary fatty acid composition.” Carcinogenesis, 17, no. 5, 1996, pp. 1035–40.
- Griffini, P., et al. “Dietary omega-3 polyunsaturated fatty acids promote colon carcinoma metastasis in rat liver.” Cancer research, 58, no. 15, 1998, pp. 3312–19.
- Sasaki, T., et al. “Effects of dietary n-3-to-n-6 polyunsaturated fatty acid ratio on mammary carcinogenesis in rats.” Nutrition and cancer, 30, no. 2, 1998, pp. 137–43. doi:10.1080/01635589809514653.
- Brasky, Theodore M., et al. “Plasma phospholipid fatty acids and prostate cancer risk in the SELECT trial.” Journal of the National Cancer Institute, 105, no. 15, 2013, pp. 1132–41. doi:10.1093/jnci/djt174.
- Brasky, Theodore M., et al. “Serum phospholipid fatty acids and prostate cancer risk: Results from the prostate cancer prevention trial.” American journal of epidemiology, 173, no. 12, 2011, pp. 1429–39. doi:10.1093/aje/kwr027.
- 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.
- Nanji, A. A., et al. “Dietary saturated fatty acids: A novel treatment for alcoholic liver disease.” Gastroenterology, 109, no. 2, 1995, pp. 547–54.
- Nanji, A. A., et al. “Dietary saturated fatty acids down-regulate cyclooxygenase-2 and tumor necrosis factor alfa and reverse fibrosis in alcohol-induced liver disease in the rat.” Hepatology (Baltimore, Md.), 26, no. 6, 1997, pp. 1538–45. doi:10.1002/hep.510260622.
- Borkman, M., et al. “Effects of fish oil supplementation on glucose and lipid metabolism in NIDDM.” Diabetes, 38, no. 10, 1989, pp. 1314–19.
- Vessby, B., and M. Boberg. “Dietary supplementation with n-3 fatty acids may impair glucose homeostasis in patients with non-insulin-dependent diabetes mellitus.” Journal of internal medicine, 228, no. 2, 1990, pp. 165–71.
- 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.
- Virella, G., et al. “Immunosuppressive effects of fish oil in normal human volunteers: Correlation with the in vitro effects of eicosapentanoic acid on human lymphocytes.” Clinical immunology and immunopathology, 61, 2 Pt 1, 1991, pp. 161–76.
- Bechoua, Shaliha, et al. “Influence of very low dietary intake of marine oil on some functional aspects of immune cells in healthy elderly people.” The British journal of nutrition, 89, no. 4, 2003, pp. 523–31. doi:10.1079/BJN2002805.
- Church, M. W., et al. “Excess omega-3 fatty acid consumption by mothers during pregnancy and lactation caused shorter life span and abnormal ABRs in old adult offspring.” Neurotoxicology and teratology, vol. 32, no. 2, 2010, pp. 171–81. doi:10.1016/j.ntt.2009.09.006.