Defiant Health Radio with Dr. William Davis
Defiant Health Radio with Dr. William Davis
What's the REAL story with fish oil?
Nearly 30 years of misinformation, disinformation, and misleading marketing have left most people confused: Do omega-3 fatty acids from fish oil reduce cardiovascular risk, dementia, and other conditions? Or are there adverse effects to expect, or greater benefits from other products?
Let's cut through 30 years of imprecise thinking and get to the bottom of this question. Final conclusion: Omega-3 fatty acids are among the most important components of diet you can consume to reduce both cardiovascular risk--even facilitate regression--and dementia.
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Let's discuss many of the facts and fictions surrounding omega-3 fatty acids. Because there have been several decades of confusion, misinformation, misinterpretation, and it but it's become very clear now how and when we should supplement omega-3 fatty acids for actually very significant benefits, even though that was not clear in the earlier years. Let's also be clear on what we're talking about. We're talking about the EPA and DHA that come mostly from fish. We're not talking about the linolenic acid that comes mostly from plant sources. And I point that out because you'll see a lot of misleading marketing. That's a lot of the source of misinformation here, is the misleading marketing, people trying to grab a portion of a very significant market for omega-3 fatty acids. So for instance, you'll see products that say, or like grain products that say rich in omega-3 fatty acids. That means it's rich in linolenic acid, not EPA and DHA. Now there's nothing wrong with linolenic acid, it actually has its own collection of benefits, separate and distinct from the EPA and DHA. But it's the EPA and DHA that have, and we'll discuss this in a moment, greater cardiovascular and brain health benefits that linolenic acid does not have. So don't fall for the misleading marketing that many food companies will use, and sometimes supplement companies, that are hawking their linolitic acid sources. It's fine to get linolitic acid, but it has nothing to do with EPA and DHA. So the excitement over omega-3 fatty acids, EPA, and DHA got its start when epidemiologic studies suggested that fish-consuming cultures, like the Inuit, the Eskimos, the Japanese, and some other cultures had fewer cardiovascular events compared to Western cultures. So studies were performed, most famously the GISI Prevenzioni, Italian trial, 11,000 participants, and people who got what we would regard as a very modest dose of 1,000 milligrams of EPA and DHA per day experienced a marked reduction in cardiovascular events like heart attack, but especially sudden cardiac death, a 45% reduction in sudden cardiac death. So that launched a lot of enthusiasm for omega-3 fatty acid supplementation. Unfortunately, that study was followed by a series of relatively smaller studies that were came up with uneven results. Some showed benefit, some did not. One of the reasons for the great uncertainty that was introduced by some of these smaller trials from a few years ago was that there are numerous methodological problems that were not addressed. For instance, one glaring problem is that there was no weight adjustment. So here's an issue. Just like vitamin D, very dependent on weight. That is, let's say I had somebody with a very low starting level, blood level of 25 hydroxyvitamin D. Let's say 17 nanograms per milliliter, which is very low. We're aiming for 60 or higher. So that person, let's say, takes 8,000 units of an oil-based gel cap of vitamin D. And that person's slender. Maybe they're 170-pound guy, right? And his 25 hydroxy vitamin D blood level goes from 17 to 63. Okay, perfect, right? Just where we want it. What if that guy was 270 pounds and he started with a 25 hydroxy vitamin D blood level of 17? He takes the very same 8,000 unit dose and his blood level goes to 37, much reduced because fat sequesters vitamin D. Well, the very same phenomenon occurs with omega-3 fatty acids. So if you have a lot of overweight people, which is the case in most of these clinical trials, right? Because most Americans and other people, other countries, are overweight or obese. So when you give people a standard fixed dose of omega-3 fatty acids, many people will not have much of a rise in their blood levels of omega-3s. Now, one of the great things to know is a test called an RBC, red blood cell omega-3 index. This is a test invented by Dr. William Harris, who has published dozens and dozens of studies validating this measure. It's very, very helpful. We know that the average American has an RBC, omega-3 index of 2.3% or thereabouts, meaning only 2.3% of all the fatty acids in the membrane, the cell membrane of the red blood cell, is our EPA and DHA. If you consume fish on occasion, you might go to 3.5, 4.1%. We're aiming for 10% in my programs. We're aiming for an RBC omega-3 index of 10% or greater because that's where we're confident we achieve effects like a reduction in sudden cardiac death, reduction in heart attack, and even maximum protection of brain health from dementia. But more recently, larger studies using higher doses. Now recall that omega-3 fatty acid are a component of food, right? They're in fish and shellfish mostly. And whenever we're talking about food, we need to talk about larger quantities. In other words, if I said to you, uh beef is good for you, let's just say, right? And I said you can have 50 grams or 50,000 milligrams, that would be a teensy weensy little piece. So when we talk about food, we need to talk about larger quantities, especially gram or even kilogram quantities. So when we talk about omega-3 fatty acids, a natural fat component of foods, we need to talk about gram quantities, several grams. But that was not recognized until recently. And so more recently, larger studies have been performed that have indeed shown dramatic reduction in cardiovascular events, stroke and heart attack. That even better. That argument has gained terrific momentum, thank goodness, for several studies using CT carony angiography. And all that means, these are CAT scan CT devices using 3D reconstruction of the various components of arteries. I tried to do that study 18 years ago, but the software we had 18 years ago was insufficient, was not enough to measure what are called voxels or 3D pixels in space. But now that technology has advanced, and several studies, three studies, have used CT, quantitative CT coronary angiography, not just to look at the detail in the coronary arteries, that is the arteries of the heart, but also break down how much soft plaque, that is fatty plaque, fibrous plaque, and calcium you have. So it breaks the components of artery of uh of carneur artery atherosclerotic plaque into its various components. And in these three studies, such as the hearts or the evaporate trial, in which higher doses of omega-three fatty acid were used, and then baseline, and then a follow-up CT cardioranticram was performed, showed not only was there a reduction in cardiovascular events, but there was actual regression, shrinkage, reduction of the fatty elements. That's important because it's the fatty elements in the coronary arteries that rupture and cause heart attack. That's how heart attack is caused. People think heart attacks are caused by the progressive worsening of a blockage. 30%, 50%, 70%, 100%. No, most of the time it's the rupture of a small plaque, maybe only 35% reduction in the diameter of the artery, but it erupts suddenly, closes off the artery. That's how most heart attacks occur. Well, we now know with very good evidence provided to us by these CT carnearandrographic studies, that it's the fatty rupture-prone components that regress with omega-3 fatty acids. And interestingly, in all these three trials, because statin cholesterol drugs are felt to be the prevailing standard, they thought it was unethical to use a placebo group. So everybody's on statin, all three of these trials. And some had the addition of omega-3s, some did not. And only the people who got the omega-3 fatty acids experienced regression of plaque, mostly fatty plaque. The people on statin drug alone all experience progression, worsening. So the real pivotal finding here is that omega-3 fatty acids not only reduce heart attack and sudden cardiac death, also reduce the fatty components of carneur atherosclerosis and achieve regression of carneur atheroscleron plaque. So for that reason alone, we are using, I advocate, 3,600 milligrams or more of EPA and DHA total per day. There are some subsets of people like lipoprotein A people where we use higher doses. But for the most part, 3600 milligrams in those studies, 3,000 to 3,300 milligrams of EPA and DHA were used. I've been using higher doses for many, many years. That works very, very well. So we use 3,600 milligrams total EPA and DHA. Not 3,600 milligrams of fish oil, but 3,600 milligrams of the EPA and DHA combined. Now another area where the evidence is good that omega-3 fatty acids as EPA and DHA, not lenolinic acid, are beneficial is in preservation of cognitive health. So let me make this issue because it's very confusing and it's leading to a lot of misinformation. There are two groups of beneficial supplements or drugs for brain health. There are things that are nootropic, and there are things that are neurotrophic. And that's a big difference. Something that's nootropic is something that improves memory or creativity or your ability to learn and concentrate or recall data temporarily. Caffeine would be a good example. You have a cup of coffee and you're a little bit faster on your feet, your concentration is a little bit better, energy is a little higher for a few hours, and then you're back to normal. Is your brain actually any healthier? No. That's a nootropic effect. There's a long list of factors that are nootropic, such as uh these are things you might not have heard of, like uh dimethyl aminoethanol or hooperzine or vinposetine or paracetam, uh many ginkgo bloba, long list of things that improve your brain function temporarily by boosting various neurotransmitters like acetylcholine, epinephrine, or dopamine, but then your bet your brain physiology reverts back to normal. Your brain's not healthier, you're not protected from dementia. You're just transiently a little bit smarter, a little bit better able to learn, be creative, recall lists of information, etc. To be distinguished, something that is neurotrophic, that is, factors that have been shown to actually benefit brain health and physiology in a long-term way. And these effects can be measured. For instance, if you did an MRI, for instance, of the brain, you can show that the hippocampus, the part of the brain that transac near-term memory into long-term memory, hippocampus shrinks with cognitive impairment and dementia. So if something is neurotrophic, it will protect the hippocampus and preserve its volume. Something that has neurotrophic effects will preserve the volume of the temporal or parietal lobes of the brain and prevent atrophy of the brain. Something with a neurotrophic effect will have beneficial effects on what are called trophic hormones, things that encourage brain growth, BDNF, brain-derived neurotrophic factor, IgF-1 alpha, and other growth factors. In other words, there are clear-cut benefits that we can list as neurotrophic that actually benefit the brain long term. In that short list of things that do that, omega-3 fatty acids are neurotrophic. So don't fall for all the claims for things that people say are good for brain health, like creatin, for instance, is nootropic. It does not actually improve brain health, does not protect you. At least no one's shown that from dementia. But omega-3 fatty acids at higher doses appear to protect. And just like the protect the doses used to protect from cardiovascular death and heart attack, that is north of 3,300 milligrams EPA and DHA per day, same thing with brain health, preservation of brain health. Higher doses because it's a component of food, right? So we want doses of at least 3,300 milligrams EPA and DHA per day. Let's talk for a moment about the form of omega-3 fatty acids that are important. So if you were to eat a piece of fish, let's say a piece of salmon, you're going to get the triglyceride form. And all that means is that there are three fatty acids on a backbone of glycerol. Triglyceride form, triglyceride, three tri fatty acids on a glyceride or glycerol backbone. That's how it occurs in fish, normally and naturally. When fish oil is produced, it's subjected to alcohol extraction, and those fatty acids are separated from the glyceride, the glycerol backbone, and you have so-called ethyl ester forms. And that's a perfectly fine form. It's just a little less well absorbed than the triglyceride form. So you can either get the triglyceride form, typically in liquid form, or the ethyl ester form, more common capsule form. Both work perfectly fine. And if you're tracking, say your RBC omega-3 index, you can always adjust your dose. If let's say you're getting 3,600 milligrams of EPADHA in the ethyl ester form, but your RBC omega 3 index is only 8.9%, boost the dose a little bit, right? So the the form in this case is not that important if you're tracking the blood levels of omega-3s. Now, many marketing claims are made for the phospholipid form. That's the form in krill oil. Well, the problem with that is while the phospholipid form is a very nicely absorbed form, it's better absorbed than the triglyceride form, better absorbed than the ethylester form. Problem is, most products like acrill oil, the quantity of EPA and DHA is so small as to be kind of useless. You'd literally have to take the entire bottle or more every day to even approach the intake, the RBC omega-3 index target of regular fish oil. So take krill oil if you want the astraxanthin carotenoid. Don't take krill oil if you want to achieve a truly beneficial level of RBC omega-3 index that protects you from cardiovascular events and from dementia. So put aside all that you've heard over the years, driven by poor science, sloppy science, methodological flaws, and know that the science has advanced, and we now know with confidence that supplementation of omega-3 fatty acids at a dose of at least 3,300 milligrams EP and DHA per day is the dose that provides maximum benefit. Now, of course, you can adjust your dose if you happen to eat some fish every uh every so often. But of course, eating fish is limited by the fact that we've tainted our oceans with mercury, shellfish with cadmium. And if you eat a lot of fish, you're going to get mercury toxicity, which has its own sets of concerns. So we use the well, I it's best to get it from the original source, like fish and seafood. We can't do that ad lib because of this mercury issue. And so we resort to supplements that have negligible amounts of mercury. Now, if you learned something from this video, I invite you to see my other videos on this YouTube channel, my Define Health Podcasts, my thousands of blog posts, on my William DavisMD.com. And if you'd like support in doing these kinds of things, join my conversations that we have most weeks on my inner circle.dr Davisinfinite Health dot com.
