It’s been a long time since I published the Definitive Guide to Fish Oils.
Oh sure, here and there I’ve cited some research supporting the beneficial effects of fish fat, but it almost goes without saying that omega-3s are important. Everyone knows it. Even the most curmudgeonly, conventional wisdom-spouting, statin script-writing, lifestyle modification-ignoring doc will tell you to take fish oil. And research in the last few years has not only continually confirmed the health advantages but illuminated new applications—and new physiological explanations—for their essential function in the body.
But what are those benefits, exactly? Why should we be eating fatty fish or, barring access to high quality edible marine life, taking fish oil supplements?
A major reason is that fish oil can help us reclaim our ancestral omega-3:omega-6 ratio and thus restore the inflammatory backdrop of the human body.
Polyunsaturated fats convert to eicosanoids in the body. Both omega-6 and omega-3-derived eicosanoids are important signaling molecules, but each has different effects, both figuring prominently in the body’s response to inflammation. Omega-6 eicosanoids are generally pro-inflammatory, while omega-3 eicosanoids are anti-inflammatory. Omega-3-derived eicosanoids (the type we get from taking fish oil or eating fatty fish) actually reduce inflammation; in an unbalanced diet heavy in vegetable oils, the omega-6 eicosanoids far outnumber the omega-3s and contribute to a lot more inflammation.
The best available evidence points to ancient humans having an omega-3:omega-6 ratio of around 1 to 1. A typical ratio these days is 1 to 16!
As most diseases and health conditions have an inflammatory component, such lopsided ratios can predispose us to any number of health problems. Conversely, correcting those ratios with smart supplementation of fish oil has the potential to correct or prevent those health problems.
Let’s look at some of them and what the most recent research tells us.
How Omega-3s Benefit Health
Arthritis is an inflammatory disease, whether we’re talking autoimmune arthritis or wear-and-tear arthritis.
The potential mechanisms are there. In vitro studies using isolated joint tissue show that both DHA and EPA increase joint lubrication. Studies in people show that fish oil reduces inflammatory markers and may even stop the progression of inflammation into inflammatory arthritis.
In a recent study out of Thailand, knee arthritis patients who took fish oil improved their walking speed. “Everyone felt good and happy with the fish oil.” In psoriatic arthritis, fish oil reduced inflammatory markers and lowered patients’ reliance on pain meds.
Fish oil also helps reduce the symptoms of autoimmune rheumatoid arthritis (RA). In one paper, fish oil supplements had additive effects on top of RA drugs. 3-6 grams appears to be an effective dose range. If that sounds high, it is—but you need that much to quell the exaggerated inflammatory responses of RA.
Depression is another one of those conditions that we don’t often think of as an inflammatory disease, but it is. The evidence is considerable. Vets with the most severe depression also have the highest levels of inflammatory markers. Among Type 2 diabetes, depression and inflammation go hand in hand, with the latter appearing to play a causative role in the former.
There’s considerable evidence that the causation goes both ways: depression can increase inflammation, and inflammation can increase depression. Thus, treating one may treat the other. Since omega-3s are potent and broad-reaching anti-inflammatories, could fish oil treat depression?
Fish oil has proven effective with EPA having a greater effect than DHA. It’s even effective in patients with and without an official diagnosis of major depressive disorder. It’s effective in type 2 diabetics with depression.
The stress response is an inflammatory one. A healthy omega-3:omega-6 ratio—the foundation of our inflammatory response system—should produce a healthy stress response. Does it?
In response to mental stress, fish oil promotes a healthy, less reactive neurovascular response. It lowers resting heart rate, a good indicator of general stress resilience. When taken post-trauma, it even reduces psychophysiological symptoms (like pounding heart) in car accident survivors. And in alcoholics, fish oil reduces both perceived (subjective) stress and basal cortisol (objective).
General Inflammatory and Immune Responses
Name a disease and “elevated inflammation” or “exaggerated immune response” is probably part of the pathology. What effect does fish oil have on some of these inflammatory pathologies?
- Reduced inflammatory markers (HS-CRP) in Type 2 diabetes patients.
- Improved inflammatory markers in colorectal cancer, including HS-CRP.
- Reduced airway inflammation in asthma patients.
- Pre-op fish oil improved post-op inflammatory and immune markers in cancer surgery patients.
- Reduced inflammatory marker IL-10 in chronic Chagas cardiomyopathy, a serious heart condition.
- Reduced inflammatory gene expression in humans.
I could go on and on. And these are just studies done in the last year or two.
Fish Oil and Cardiovascular Disease
Not everything is so cut and dry. When it comes to certain conditions, like cardiovascular disease, the fish oil literature is confusing. Sometimes it helps, sometimes it doesn’t. What are we to make of it?
One thing that is unequivocal is that a high omega-3 index—the proportion of omega-3 fatty acids in the red blood cell membrane—is protective against cardiovascular disease (see the chart; as omega-6 content goes up, so does cardiovascular mortality). So the question isn’t if long chain fatty acids from fish oil are helpful. It’s: Are those fatty acids reaching your red blood cell membranes and being incorporated?
How To Improve Bioavailability
Several factors affect whether fish oil will increase omega-3 index and thus have the effects we’re looking for:
Omega-6 fats and omega-3 fats compete for space in the red blood cell membranes. If omega-6 intake is too high, fewer omega-3s will make it into the membranes, thereby inhibiting or even abolishing the positive effects of fish oil.
If omega-3 index is low, we’ll see effects. If it’s high enough, further fish oil has no additive effect. We see this in studies such as this one, where only older adults with a low omega-3 index experienced cognitive benefits from omega-3 supplementation. In another study of older adults and cognition that didn’t control for omega-3 index, they found no benefit.
Or in this study, where fish oil had benefits in congestive heart failure patients because they had low baseline levels of omega-3.
Or this study, where autistic patients—who tend to have lower omega-3 statuses than the general population—improved some behavioral measures after taking fish oil.
To take advantage of the full effects of fish oil, however, one must also limit the amount of omega-6 fats they eat. In one study, taking fish oil with saturated fat increased incorporation of omega-3s into red blood cell membranes, while taking it with omega-6 prevented omega-3 incorporation. The best way to do it is to eliminate seed oils—the most concentrated source of omega-6 fatty acids in the modern diet. If you don’t limit seed oils and other dense sources of omega-6s, you’ll have to consume extremely high doses of fish oil to make a dent in your inflammatory status.
Making It Easier To Get Your Omega-3s…
Thanks for reading today, folks. I take this information very personally in my life and business. To that end, this week I just released a new formula of Primal Omega-3s that enhances bioavailability and adheres to stricter environmental sustainability standards—all in a smaller capsule. The idea was to optimize benefits and maximize ease. And right now I’m also offering a deal to make this level of quality more affordable….
I’m kicking off the new formula with a BOGO deal. Buy one new Primal Omegas, get the second bottle free now through 8/10/18 at midnight PDT. Just add two Primal Omegas to your cart and use code NEWOMEGAS at checkout. Limit 1 per customer. One-time purchase only.
Thanks again, everybody. Have a great end to the week.
The post Omega-3 for Health: What the Latest Research Shows appeared first on Mark’s Daily Apple.
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For today’s edition of Dear Mark, I’m answering several questions drawn from the comment board of last week’s post on fasting vs carb restriction. First, how do I square my recommendations with the successful reports of potato dieters losing weight on a high-carb tuber diet? Second, is Leangains optimal for mass gain? Third, how do I use extra virgin olive oil, butter, and ghee? Fourth, could exogenous ketones help a man with dementia, MS, and seizures? Fifth, how should a woman with stalled weight loss integrate fasting?
Walter Sobchak asked:
If “carbs” are so bad, how do people eat only potatoes and lose large amounts of weight? Andrew Taylor (SpudFit.com) and Penn Jillette (Penn & Teller) are two high-profile people, but there are lots more. Of course, I wouldn’t recommend an unbalanced diet of only one food, but the point is that potatoes are a natural food and are not inherently detrimental.
I agree that potato-only diets are a quick weight loss hack.
Potato-only diets work well because they’re so monotonous. When your only option is a plain potato, it’s extremely hard to overeat. It’s the combination of fat and carbohydrates that’s so easy to overeat, and that causes the most metabolic problems.
Potatoes are surprisingly nutrient-dense. They have complete protein, containing all the necessary amino acids. You won’t be bodybuilding on all-potatoes, but there’s enough protein in there to stave off muscle loss for a week or so.
I could recommend the potato-only diet, ditch the keto/low-carb/Primal talk, and people who listened to me would still lose weight. But they’d miss out on all the other benefits, not least of which is the delicious food. In short, the potato-only diet isn’t the worst thing out there, but I wouldn’t recommend it as a long-term strategy.
Mattias Carlsson asked:
I have a question for advice if someone know. According to most sources I find the so called anabolic window persist at least 24 hours after resistance training. How can then an intermittent fasting with 8 hour eating as in lean gains, from what I understand, be optimal on training days. It seems to me that a bit of overeating on carbs and protein during all this time would be most beneficial?
I don’t know that it’s optimal for sheer mass gain. But it does seem to strike a nice balance between “gains” and “staying lean.” You may not bulk up as quickly as you would cramming food in your gullet. You will gain lean mass without gaining so much of the squishy mass that normally accompanies what passes for “gains.”
Michael Levin wondered:
Question: EVOO, Ghee and grass-fed butter–which to use when and for what?
EVOO: salads, marinades, sautéing. It’s actually far more resistant to heat than most people think; the polyphenols protect against oxidative damage.
Butter: Cooking eggs and other breakfast items, melted with broccoli/shrimp, finishing steaks and reduction sauces.
Beth Olson asked:
What are your thoughts on exogenous ketones? My dad has MS and dementia and seizures way too often. Should we try adding these?
I can’t give your dad any medical advice. You can talk to his doctors, however, and show them this study where exogenous ketones reduced seizure activity in mice. You can show them that coconut oil and MCT oil—two other routes for generation of ketones—have shown efficacy against cognitive decline in patients with Alzheimer’s or dementia.
I suspect exogenous ketones can help. I also suspect they’d be far more helpful on top of a low-carb, high-fat diet with plenty of healthy lifestyle modifications.
That’s the thing with dementia: there isn’t a pill that fixes everything, or even a single intervention. In the one study that actually got major results, researchers had Alzheimer’s patients undertake a dramatic diet, exercise, and lifestyle shift. Here’s what each subject did:
- Eliminate all simple carbs and follow a low-glycemic, low-grain (especially refined grains) diet meant to reduce hyperinsulinemia.
- Observe a 12-hour eating window and 12-hour fast each day, including at least three hours before bed.
- Stress reduction (yoga, meditation, whatever works for the individual).
- Get 8 hours of sleep a night (with melatonin if required).
- Do 30-60 minutes of exercise 4-6 days per week.
- Get regular brain stimulation (exercises, games, crosswords).
- Supplement to optimize homocysteine, vitamin B12, CRP levels.
- Take vitamin D and vitamin K2.
- Improve gut health (prebiotics and probiotics).
- Eat antioxidant-rich foods and spices (blueberries, turmeric).
- Optimize hormone balance (thyroid panel, cortisol, pregnenolone, progesterone, estrogen, testosterone).
- Obtain adequate DHA to support synaptic health (fish oil, fish).
- Optimize mitochondrial function (CoQ10, zinc, selenium, other nutrients).
- Use medium chain triglycerides (coconut oil, MCT oil). You could possibly use exogenous ketones here too.
Bring that study to your dad’s doctors and see what they have to say. If they aren’t blown away by the possibilities and open to give it a try, I’d be shocked. Hopefully your dad is game. I’d love to hear how it works.
Lisa Chupity asked:
I went Primal/Paleo back in March of 2012. I lost the 15 pounds I wanted to lose. In 2015, 7 pounds crept on, and for the life of me, I can’t lose ‘em! April of this year, I went Keto. I track my macros, and do my best to keep my carbs to 20 grams per day, tho I don’t beat myself up if I have 24. I haven’t lost an ounce! I’m going to have to do the IF thing, I’m sure. As it is, my breakfast is bone broth (1 1/2 cups) and a mug of Coffee with Brain Octane in it. Lunch is yer basic “Big Ass Salad”. Dinner is good, too, and within Keto guidelines. I try to keep my caloric intake to ~1600 calories/day.
To add to the mess, I have Multiple Sclerosis, so stuff like Cross Fit is outta the picture. I can manage some stationary cycling, and some Pilates, with lighter modifications. Any advice?
If you try IF, do the “early restricted feeding” rather than late. You’re already doing a kind of “fast” in the morning, just drinking broth and coffee with MCTs, and it doesn’t seem to be working.
Eat some fat and protein for breakfast with a few carbs. Eggs and bacon with a side of cantaloupe or berries. An omelet with spinach and onions and cheese. Steak and greens and half a banana. Emphase whole-food fat and protein. Have coffee and broth, too, if you like. This and lunch should be your biggest whack of calories.
Eat your Big Ass Salad for lunch. Drop dinner, or make it really light and no later than 5 or 6 PM.
Terry Wahls has a great Primal-friendly MS protocol. Check out her Ted talk and go from there if it interests you.
Good luck and keep us apprised of your results.
That’s it for today, folks. Take care, be well, thanks for reading and writing!
The post Dear Mark: Potato Diet, Lean Gains, EVOO/Butter/Ghee, Exogenous Ketones, and Early IFing appeared first on Mark’s Daily Apple.
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For today’s Dear Mark, I’m answering just one question from a reader. What are we to make of the new study purporting to show that saturated fat is the most harmful substance a liver can encounter? Should we remove all traces of it from our diets? Should we eat pure sugar? Quaff soybean oil? How relevant is an overfeeding study to a community of people dedicated to eating a sustainable, weight-reducing or -maintaining diet that includes saturated fat?
Let’s find out:
Did you see this study? http://care.diabetesjournals.org/content/early/2018/05/24/dc18-0071
What’s your take on it? Just got one of those classic emails from my vegetarian friend with only a link to the study and a smug emoji.
Oh yes, I knew this would come up after I linked to in on Weekend Link Love.
The title is “Saturated Fat is More Metabolically Harmful for the Human Liver Than Unsaturated Fat or Simple Sugars.”
I have a human liver. Do you? Probably. This is highly relevant to all of us, right?
Well, the first thing to understand is that this was an overfeeding study. Participants didn’t just eat a eucaloric diet with different energy sources. They each got a daily 1000 calorie snack on top of their normal diet for three weeks.
The SFA group ate 1000 extra calories in the form of butter, coconut oil, and blue cheese. The SFA:MUFA:PUFA ratio was 76%:21%:3%. Their liver fat increased by 55%.
The UFA group ate 1000 extra calories in the form of pecans, olive oil, pesto, and butter. Their SFA:MUFA:PUFA ratio was 21%:57%:22%. Their liver fat increased by 15%.
The Sugar group ate 1000 extra calories in the form of orange juice, soda, and candy. Their snack had no fat, all sugar. Their liver fat increased by 35%.
Saturated fat also increased lipolysis—the breakdown of fatty acids for energy—while unsaturated fat decreased it. Lipolysis normally increases during fasting or exercise. In that context, it’s a good thing and you end up losing body fat. If you have a steady stream of extra fat calories coming in, you won’t lose body fat. The researchers could have seized on this point and screamed “unsaturated fat inhibits lipolysis!” but they didn’t. Wonder why.
Also notable is the observation that overeating sugar increased de novo lipogenesis (creation of fat from sugar) in the liver by 98%. I was told that didn’t happen in humans, that de novo lipogenesis was a myth. Guess it can happen.
But, again, the most important thing to realize is that this was an overfeeding study. It wasn’t a weight loss study. It wasn’t designed to see which kind of diet spontaneously results in the most weight loss. It was designed to get people to eat 1000 extra calories from different nutrient sources to see how they affect liver fat. And they didn’t construct the entire diets around the hypothesis. From what I can tell, the participants ate their normal diets. Only the 1000 calorie overfeeding snacks were provided by the researchers.
You also have to consider choline. The more fat you eat, the more choline your liver needs to process that fat. In rats with fatty liver, supplementing with extra choline directly reduces liver fat. In Chinese women, a high choline intake protects against fatty liver. If the subjects didn’t increase choline as they increased fat overfeeding, they were bound to gain more liver fat. Remember: this was the whole point of the study.
Now with that out of the way, who is this study relevant for?
Those people who think keto gives them free license to consume as many calories as they can cram into their mouths. Don’t do that. Especially don’t do that with isolated sources of fat, including saturated fat. Overfeeding anything is bad news, unless you’re trying to gain lean mass, lifting hard and heavy on a regular basis, and the thing you’re overfeeding is whole food rather than isolated fat.
That’s it for today, folks. What are your thoughts? Does this study tell you anything new, or is it old news?
Let me know what you think down below. Take care, be well, and have a great day.
The post Dear Mark: Saturated Fat More Harmful to Liver Than Sugar? appeared first on Mark’s Daily Apple.
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One of the more exciting developments over the past few years has been the explosion in population genetics research. People are a diverse lot, and even though we’re all people who essentially want the same things out of life (and we’re working with the same basic machinery), there’s a lot of wiggle room. It’s not just information for curiosity’s sake. The information researchers are uncovering about human ancestry can have real ramifications for how said humans should eat.
A couple years ago, I wrote a post laying out a few guidelines for using your personal ancestry to inform your diet. Today, I’m going to talk about another one: polyunsaturated fat metabolism.
For years, it’s been “common knowledge” in alternative health circles that most people just aren’t very good at converting the omega-3s (ALA) in plant foods into the long-chained omega-3s found in seafood (DHA, EPA), and that everyone should just eat fish for their omega-3s. This remains solid advice, but the reasoning needs a little tweaking. It turns out that the genes that encode the proteins responsible for conversion of ALA into DHA/EPA (and linoleic acid into arachidonic acid)—known as FADS—have a couple variants. Some variants make conversion less effective and some make conversion more effective. Furthermore, the distribution of these variants vary across populations.
For instance, the variant that increases conversion of ALA into DHA and EPA is more common in South Asian (Indian, Pakistani, Bangladeshi, Sri Lankan) populations and African populations than any other group, while it’s moderately common in Europeans and East Asians and rarest in Native Americans and Arctic natives. Why?
In Africa, anatomically modern humans initially crowded along the coasts because that’s where the food was, especially the omega-3-rich seafood that provided the nutrients necessary for brain expansion. When humans began expanding into the omega-3-deficient interior of the continent, those with the FADS gene variant for improved long chain PUFA conversion were more successful. They could live in areas totally bereft of marine foods and still make enough EPA and DHA to survive and produce big-brained babies. Researchers estimate that the new variant became entrenched in African populations around 85,000 years ago due to positive selection. To this day, African populations almost exclusively carry the variant that increases conversion.
Then, as modern humans left Africa and moved into Europe and Asia carrying that same genetic variant, they encountered new environments that placed new demands on their genes.
In South Asia, the gene variant persisted. Plants were plentiful and long-chained omega-3s were not due to warm water reducing the omega-3 content of marine life, and the ability to efficiently convert fats offered a survival advantage. About 3/4 of the population carries it today.
In East Asia, about 1/2 of the population carries it.
In Europe, meat and fish were more widely available. Conversion was less necessary when you had a regular intake of pre-formed EPA, DHA, and arachidonic acid. Thanks to European admixture with existing archaic populations who still had the conversion-decreasing variant, its frequency increased until the arrival of farmers from the East, whose agricultural innovations selected for and genes contributed to the conversion-increasing variant.
In Native American populations, including Arctic, North American, and Latin American natives, the variant is almost completely absent. They were getting all their long-chain PUFAs directly from animal and marine foods, and it shows in the genes.
That’s a broad overview. The story’s more complicated than that, of course. East Asia is a big place with many different ethnic groups. Same goes for Europe, and Africa, and everywhere else. Except for the Africans and Native Americans, the frequency of the variants vary within these populations.
In European populations, for example, the conversion-increasing variant has the strongest selection in southern European populations (Tuscans), slightly less strong selection in Iberian populations (Spain/Portugal), moderate selection in Britain and northern Europe, and the weakest selection in far northern Europeans (Finns).
The ancient European groups that fed into modern populations followed a similar north-south pattern of variance. West and Scandinavian hunter-gatherers in the north show the least selection for the variant, since the cold waters of northern Europe offered plenty of cold water fatty fish and elongation of plant omega-3s just wasn’t very helpful or necessary. Pastoralists and farmers to the south show the most selection.
What’s it all mean?
People with African ancestry are almost certainly homozygous (2 copies) carriers of the increased-conversion variant. South Asians, including Indians, Pakistanis, Bangladeshis, and Sri Lankans, are also strong candidates to be homozygous carriers. Southern Europeans are most likely heterozygous (1 copy) carriers, Western and Northern Europeans less so.
Indigenous ancestry (unless African) probably means you’re a carrier of the decreased-conversion variant. Alaskan or Greenland Inuit, American Indian, Mexican mestizo—they tend to have lower FADS activity due to the relatively recent inclusion of agricultural foods in their ancestral diets. The farther north your people hail from, the more likely you are to carry at least one copy of the decreased-conversion variant.
If you carry the FADS variant that increases conversion:
- Watch your linoleic acid intake. A major reason linoleic—>arachidonic conversion was selected for was the rarity of both long-chain PUFAs and linoleic acid in the ancestral environment. Being able to convert all your linoleic acid to AA is great, assuming you’re not cooking with soybean oil, eating fries fried in corn oil, and snacking on potato chips in between meals. Seed oil high in concentrated linoleic acid is a historical aberration for everyone regardless of ancestry.
- Don’t think you can skip the fish and start glugging flax oil just because your mom was Sri Lankan and your dad was Tuscan. Studies show that the benefits of long-chained omega-3s like DHA are not modified by FADS gene status. Everyone can benefit from fish. Some people just need it more.
If you carry the FADS variant that reduces conversion:
- You need pre-formed DHA/EPA and arachidonic acid. You don’t make it very well. That means eating fish, shellfish, eggs, and other animal foods. Hard sell, I know.
- And if you eat a ton of vegetable oil—as most people do these days—you’re in trouble. Research shows that people with the conversion-decreasing variant who eat a lot of linoleic acid have lower HDL, higher triglycerides, and a bigger waist than those who eat very little.
- Your absorption and incorporation of DHA from food may be enhanced. One study in infants with the conversion-reducing variant found that taking fish oil increased DHA way more than in other babies. This could be a feature of infants with the variant—mom eats fish, passes DHA through breastmilk to baby, who absorbs every last drop—and not of adults.
Don’t know your FADS gene status? No problem. It’s actually more fun this way.
I would take the time to get your ancestry tested, unless you’re absolutely certain of your family tree—and it stretches far enough back to actually say something about your deep ancestry. That way you can look at the various populations from which you hail and make some educated guesses. And you can even plug the raw genetic data into a service that spits out your nutrition-and-health-related variants.
Even then, you may not get any hard and fast answers. FADS gene variant frequency data isn’t widely available for every possible ethnic group on Earth, so a lot of this is more art and intuition than hard science.
If the traditional diet of your immediate ancestry is plant-based—not vegan, just not buying steak from the non-existent grocery store—you probably carry at least one and perhaps two copies of the conversion-enhancing variant.
If your people lived near the sea or ate a decent amount of animal foods, you’re probably carrying one of the conversion-reducing variants.
Whatever you do, take it easy. Have fun with it. Very few people represent the tail end of an unbroken line of ethnic purity. Most people will vary a bit here or there, or a ton here and a ton there. I have a lot of Scandinavian ancestry, which explains my need for a lot of pre-formed DHA and EPA from wild seafood (I’ve confirmed with genetic tests).
As this topic is a moving target, with new data coming out constantly, I’ll probably revisit it from time to time. Until then, what do you all think about the field of ancestral influence and health? What’s your ethnic background, and what do you think it means for your ability to metabolize PUFA? And what other questions do you have regarding ancestry and diet?
Thanks for reading, everyone. Take care!
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