We’ve all heard the story. Maybe we’ve even been the protagonist.
Person goes full keto. They lose a bunch of weight, normalize their pre-diabetic glucose numbers, resolve their high blood pressure readings, have more energy, feel great, and have nothing but high praise for the new way of eating.
Except for one thing, everything seems perfect: their cholesterol is sky-high. It throws a wrench into the whole operation, installs a raincloud over the procession, spoils their confidence.
“Could I be killing myself?”
“Are my health improvements just a mirage?”
In other words, are the apparent benefits of keto merely superficial if your cholesterol skyrockets?
The evidence is pretty clear that for the majority of adults who go keto, their cholesterol numbers improve.
In obese adults with type 2 diabetes, a ketogenic diet improved blood lipids and boosted fat loss compared to a low-calorie diet.
In lean, healthy adults without any weight to lose (and who didn’t lose any weight during the course of the diet), total cholesterol went up from 159 to 208 mg/dL and triglycerides fell from 107 to 79 mg/dL. A lipophobic doc might freak out at the rise in TC, but given that the triglycerides dropped, I bet the change reflects a rise in HDL and an overall positive, at worst-neutral effect.
Another study of lean adults with normal cholesterol numbers found that going keto improved their lipids, reducing triglycerides, increasing HDL, and leaving LDL unchanged. Those with small pattern B LDL particles (the “bad kind”) saw their LDL particle size increase, on average. All told, keto was beneficial.
But you aren’t everyone. You aren’t the average of a population. And, given the number of readers I have and the number of people trying a ketogenic diet, there are bound to be some people whose lipid profiles go in the other direction.
I don’t give medical advice here, and I always encourage people to partner with the physicians for health solutions. That said, let me share some thoughts on the keto-cholesterol question….
I’m not just talking about high total cholesterol or high LDL-C. I’m talking about what appears to be the real, legit risk factor for a cardiac event: elevated LDL particle number. According to experts like Dr. Peter Attia and Dr. Chris Masterjohn, atherosclerosis occurs when LDL particles infiltrate the endothelial lining of our arteries. Thus, it’s not high LDL cholesterol that increases the risk of atherosclerosis—LDL-C is the cholesterol found inside the particles— it’s a high number of LDL particles in circulation. The more LDL-P, the greater the chance of them becoming oxidized and infiltrating the arterial wall. There are many factors to consider, like oxidative stress, inflammation, and fatty acid composition of the LDL particles, but all else being equal, a greater number of LDL particles seems to increase the risk of a heart attack.
What Could Be Causing LDL Elevations On Keto?
I asked Dr. Cate Shanahan for her input on this topic, and she provided a beautiful explanation:
But when you stop eating so many carbs insulin politely steps aside, and your insulin levels plummet. Now your body fat can more easily and more often release its stores of fatty acids into your bloodstream.When your body fat releases stored fatty acids, any unused fatty acids quickly get picked up by the liver and packed into VLDL lipoprotein. VLDL is a precursor to LDL. So in reducing your insulin levels and increasing your body’s use of fat, you will raise your VLDL, LDL and total cholesterol. You are simply trafficking in fat more often now. And now, because your body stabilizes fat carrying lipoproteins with cholesterol, there is a need for more cholesterol in your blood. These are not bad consequences. They are in fact happy signs your diet is doing what its supposed to be doing.
If you’re actively losing weight, you will probably experience a rise in cholesterol. This is the transient hypercholesterolemia of major weight loss, and it’s a well-known phenomenon. Once your weight stabilizes, cholesterol should normalize—although to a lesser extent than other diets, given Dr. Cate Shanahan’s explanation of increased “trafficking in fat.”
Low Thyroid Function
The thyroid is a barometer for your energy status. If you have plentiful energy to spare, thyroid function is normal. If your body perceives low energy availability, thyroid function may down-regulate. Since the thyroid plays a big role in regulation of LDL receptor activity, its downregulation can lower LDL receptor sites. Fewer LDL-receptors clear LDL particles from the blood. Folks with genetic predispositions to heart disease often have low LDL receptor activity, causing elevated LDL particles. Folks with genetic variants that increase the activity and expression of LDL receptors have lower heart disease rates. Although genes often have different effects that may affect disease risk via other pathways, that’s pretty strong evidence that LDL receptor activity regulates, at least in part, one’s LDL-P and heart disease risk.
Read this post for maintaining thyroid function on keto, and check out Elle Russ’ Paleo Thyroid Solution for an even deeper, more thorough dive into thyroid health.
Eating Too Damn Much
Some keto people pride themselves on gorging. Some are doing it for a good cause—a quest to find the fabled metabolic advantage. Some are doing it to show off and for keto cred—look how much salami I can eat! Some are using keto to deal with unresolved issues with food itself.
Everything I say about doing keto presupposes that you are eating like a normal person. You’re eating as much as you need to fuel your brain and daily activities, fitness and performance goals. You’re leaving the table satiated, not stuffed. For most people, this happens without even trying. It’s why keto is so effective for weight loss.
Genes aren’t destiny, but they do modify and regulate our response to a given environmental input.
Some people are dietary cholesterol hyper responders. Unlike the majority of the population, they absorb tons of dietary cholesterol and do not down-regulate their endogenous production to accommodate. The result is an increase in cholesterol synthesis and absorption, leading to a spike in blood cholesterol.
Some people are sensitive to saturated fat. In response to it, they produce elevated numbers of LDL particles. If your keto diet is high in saturated fat and you have a genetic sensitivity to it, your cholesterol will probably skyrocket.
Some people have genes that reduce the activity of their LDL receptors. This will necessarily boost LDL particle numbers.
This topic—genetic variance and how it affects keto—could be an entirely separate post, so I’ll leave it at that (and probably come back to it in the future).
Too Much Butter
Huh? Too much butter, Sisson? Is such a thing even possible?
Maybe. Subjecting cream to the butter-making process strips it of something called milk fat globule membrane (MFGM). And when you compare equal amounts of dairy fat through either cream (with MFGM intact) or butter oil (with MFGM absent), you get very different metabolic effects. Those who ate 40 grams of dairy fat through butter oil saw their lipids worsen, including ApoB, a surrogate for LDL particle number. Those who ate 40 grams of dairy fat through cream saw their lipids unchanged, and in the case of ApoB even improve. That’s 4 tablespoons of butter compared to 4 ounces, or a half cup, of heavy cream.
Caveats apply here. The subjects weren’t eating a low-carb or ketogenic diet; they just added the butter or cream on top of their normal diet. But in keto people who are genetically susceptible, huge amounts of butter may be responsible for rising LDL-P.
I still love butter. It doesn’t affect my lipids like that. But your mileage may vary, and it’s something to think about if you’re in that situation.
So, What Can You Do If You See An Increase in LDL?
Start Chugging Soybean Oil
Kidding… It’s true that swapping out some of your animal fats for polyunsaturated seed oils will almost certainly lower your cholesterol levels. It does this by increasing LDL receptor activity, but, being far more unstable than other fats, omega-6 PUFAs also increase the tendency of the LDL particles to oxidize. And since oxidized LDL are the ones that end up wedging in the arterial walls and causing issues, loading up on PUFAs might not be the right path.
You know what just occurred to me? This is an aside, but maybe linoleic acid (the primary fatty acid in seed oils) up-regulates LDL-R activity because the body recognizes the inherent instability of linoleic acid-enriched LDL particles and wants to clear them out before they can cause trouble. I hope some researchers take this idea further.
Stop Being a Keto Caricature.
Half a package of cream cheese for a snack.
Dipping an entire stick of pepperoni into homemade alfredo sauce and calling it dinner.
I’m not saying cream cheese is bad. It’s great. Nor am I suggesting you never eat pepperoni, dipped in alfredo sauce or not. But the amounts are unreasonable. And turning those into regular meals is a bad idea. There’s no reason you can’t go keto while eating a hamburger patty or ribeye over a Big Ass Salad. Far more nutrients, far more micronutrients, and it tastes way better.
Maybe if you’re a nomadic horselord sweeping across Europe in the early Bronze Age, you need to eat an entire lamb intestine stuffed with marrow and organs, and you should wash it down with a quart of creamy mare milk. Such a meal would provide the calories you need to see your enemies driven before you and go great with the lamentations of their women. But you’re not a Yamnaya nomad. You’re you.
You probably don’t need that much food, that many calories, and that much fat—since there’s plenty of it on your body already, waiting to be liberated and converted into energy. Therein lies the beauty of keto. That’s what this is all about: Getting better at burning your own body fat.
Balance Your Fats
The overzealous and protracted drive to demonize all sources of saturated fat as evil has led to a vociferous backlash from the other direction. But just because the supposed experts got the saturated fat issue wrong doesn’t mean the opposite is true: That all the fat we eat should be as saturated as possible.
For one thing, eating nothing but saturated fat is very hard to do using whole foods. Very few animals exist in the world, past or present, with only saturated fat. The only exception I can recall is the coconut, a curious sort of beast that spends most of its time hanging from a tree impersonating a large hairy drupe. Your average slab of beef fat runs about 50% saturated fat, 45% monounsaturated fat, and 5% PUFA. That differs from cut to cut and depending on the diet of the animal, but not by much. It’s similar for other ruminants like bison and lamb. And the most prominent saturated fatty acid in ruminant fat is stearic acid, a fat that converts to monounsaturated oleic acid in the body and has an effect on cholesterol indistinguishable from MUFA or PUFA.
Or take the fatty acid composition of game meat—the type humans encountered and consumed for our entire history.
- African kudu (antelope family): 35% SFA, 24% MUFA, 39% PUFA
- African impala (antelope family): 51% SFA, 15% MUFA, 33% PUFA
- Elk: roughly 40% SFA, 30% MUFA, 30% PUFA
- Moose: roughly 33% SFA, 33% MUFA, 33% PUFA
I could go on, but you get the idea: Humans have been consuming a wide range of fatty acids for millennia. It probably makes sense to emulate that intake.
Once again, the folks whose cholesterol goes nuts on keto are outnumbered by those whose cholesterol improves. But if you’re one of the unlucky ones in the former category, try broadening your fatty acid intake (to, ahem, possibly include more nuts):
- Focus on monounsaturated fats and fat from meat, rather than isolated sources of saturated fat like butter and coconut oil. You probably don’t have to eliminate those fats. Just don’t make them the centerpiece of your diet.
- Eat more avocados, avocado oil, olives, olive oil, and mac nuts for monounsaturated fat. Salads are a great nutrient-dense way to incorporate high-MUFA foods.
- Eat more fish. A couple portions of farmed Atlantic salmon were enough to improve LDL-P in overweight men and women. And compared to plain keto, keto + omega-3s from fish has a superior effect on inflammation and metabolic health.
- Eat more kudu and impala (if you can get it). Sort of kidding. But really, eat them if you can.
They even have a version of keto called the Spanish ketogenic diet, which features a lot of extra virgin olive oil, olives, fish, and red wine. It works great and might be a good alternative for people whose cholesterol goes wild on saturated fat-heavy keto.
Are Traditional Lipid Markers Even Relevant for Keto Dieters?
Maybe, maybe not.
But be honest about it. You can’t oscillate between championing positive changes to blood lipids on a keto diet and pooh-poohing negative changes to blood lipids on a keto diet.
You can’t use positive changes to prove the efficacy and safety of the ketogenic diet, then turn around and claim that negative changes don’t count because keto dieters are understudied. What if those “positive” changes are actually negative in the context of a ketogenic metabolism? After all, keto dieters are largely understudied in both directions. If what’s unhealthy in a normal dieter might be healthy in a keto dieter, what’s healthy in a normal dieter may be unhealthy in a keto dieter.
I write these things as a strong proponent of spending a significant time in ketosis. As someone who frequently hangs out in a ketogenic state. As someone who wrote a book about keto and is writing another. But also as someone who insists on maintaining strict intellectual honesty and integrity.
We simply don’t know what very high cholesterol numbers mean in the subset of ketogenic dieters who experience them. I strongly suggest not being too flippant about them.
True: There aren’t any perfect studies examining the utility of conventional cardiovascular risk factors in people eating the type of keto diets you see in the ancestral health space. Maybe your elevated LDL particle number doesn’t mean what it means in the average overweight adult eating the Standard American Diet. Maybe your inflammation is low enough that the risk of atherosclerosis and oxidative modification of LDL is low. But I wouldn’t take that risk, not until we have more data.
What do you think, folks? How did keto affect your blood lipids? Did you make any changes, and if so, did they work? Thanks for stopping in today.
Note: This information isn’t intended as and shouldn’t be considered medical advice. Always consult your doctor in the management or treatment of any health issue.
Hussain TA, Mathew TC, Dashti AA, Asfar S, Al-zaid N, Dashti HM. Effect of low-calorie versus low-carbohydrate ketogenic diet in type 2 diabetes. Nutrition. 2012;28(10):1016-21.
Phinney SD, Tang AB, Waggoner CR, Tezanos-pinto RG, Davis PA. The transient hypercholesterolemia of major weight loss. Am J Clin Nutr. 1991;53(6):1404-10.
Phinney SD, Bistrian BR, Wolfe RR, Blackburn GL. The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation. Metab Clin Exp. 1983;32(8):757-68.
Kleinveld HA, Naber AH, Stalenhoef AF, Demacker PN. Oxidation resistance, oxidation rate, and extent of oxidation of human low-density lipoprotein depend on the ratio of oleic acid content to linoleic acid content: studies in vitamin E deficient subjects. Free Radic Biol Med. 1993;15(3):273-80.
Rosqvist F, Smedman A, Lindmark-månsson H, et al. Potential role of milk fat globule membrane in modulating plasma lipoproteins, gene expression, and cholesterol metabolism in humans: a randomized study. Am J Clin Nutr. 2015;102(1):20-30.
Raatz SK, Johnson LK, Rosenberger TA, Picklo MJ. Twice weekly intake of farmed Atlantic salmon (Salmo salar) positively influences lipoprotein concentration and particle size in overweight men and women. Nutr Res. 2016;36(9):899-906.
De luis D, Domingo JC, Izaola O, Casanueva FF, Bellido D, Sajoux I. Effect of DHA supplementation in a very low-calorie ketogenic diet in the treatment of obesity: a randomized clinical trial. Endocrine. 2016;54(1):111-122.
Pérez-guisado J, Muñoz-serrano A. A pilot study of the Spanish Ketogenic Mediterranean Diet: an effective therapy for the metabolic syndrome. J Med Food. 2011;14(7-8):681-7.
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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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