As you and millions of other people embark on new dietary journeys, you’re going to hear a ton about calories.
“Calorie counting is everything.”
“If you aren’t counting calories, you won’t lose weight.”
“Just eat less calories than you expend.” For one, it’s “fewer.” Two, that’s not the whole picture.
These statements aren’t wrong exactly, but they offer an overly simplistic picture of the relationship between weight loss and calories. They ignore context. And context is everything, especially when you’re talking about calories and weight loss.
Most people (even many scientists) believe that the body composition challenge is a relatively simple equation: to lose weight you must reduce calories (either eat less or burn more), to gain weight you must add calories (eat more or burn less), and to maintain weight you keep calories constant (eat and burn identical amounts). Calories in over calories out.
Right away, it sounds preposterous. Are people really maintaining perfect caloric balance by dutifully tracking and comparing their intake to their burn? Are they walking six fewer steps lest they lose an extra ounce off their midsection?
Are All Calories the Same?
The truth is, it’s more like a complex equation where you have to factor in many other very important variables:
- Am I getting calories from fat, protein, or carbs?
- Am I getting my calories through whole foods or refined processed foods?
- Are my glycogen stores full or empty?
- When’s the last time I exercised?
- Am I insulin-sensitive or insulin-resistant?
- Am I trying to lose “weight” or lose fat?
- How’s my stress level?
- Am I sleeping enough?
The answers to all those questions (and more) affect the fate of the calories we consume. They change the context of calories.
Ideally, all that complexity is handled under the hood. That’s how it works in wild animals. They don’t calorie count. They don’t think about what to eat or how to exercise. They just eat, move, sleep, and somehow it all works. I mean, they die, often violently, but you don’t see obese, metabolically-deranged wildlife—unless the obesity and metabolic derangement is physiological, as in bears preparing to hibernate. Somehow they figure it out. They’ve delegated the complex stuff to their subconscious.
This is generally true in “wild humans,” too. Hunter-gatherer groups by and large did not and do not show any evidence of metabolic derangement, obesity, or the other degenerative trappings of modern humans living in civilization. They are fully human in terms of physiology, so it’s not that they have special genetic adaptations that resist obesity. They’re living lifestyles and eating diets more in line with our evolutionary heritage. They’re moving around all the time, not going through drive throughs. They’re eating whole unprocessed foods that they have to procure, catch or kill.
What they don’t have is the ridiculous concept of calories and macronutrients floating around in their heads, informing their dietary choices. They don’t even think about food in terms of calories, or movement in terms of calories expended. Metabolically speaking, they consume their calories in the proper context.
But you? You might have to think about context. You might have to answer those questions and create the proper context.
Most people do not think about context. They home in on the number of calories the food database claims the food they’re eating contains, plot it against the numbers of calories the exercise database claims the exercise they’re doing expends, and then wonder why nothing’s working. That’s why “dieting doesn’t work”—because, as practiced in accordance with the expert advice from up high, it doesn’t. Almost invariably, the people who see great results from strict calorie counting, weighing and balancing, those types who frequent online weight lifting forums and have the freedom to spend hours perfecting their program, have the other relevant variables under control without realizing it.
They’re younger, with fewer responsibilities—and less stress and fewer disruptions to their sleep.
They’re lifting weights and training religiously, creating huge glycogen sinks and maintaining optimal insulin sensitivity.
They’re eating a lot of protein, the macronutrient that curbs hunger and increases energy expenditure the most.
They’re eating mostly whole foods.
They’ve had less time on this earth to accumulate metabolic damage.
Not everyone is so lucky.
Fat burning, glucose burning, ketone burning, glycogen storage, fat storage, gluconeogenesis, and protein turnover—what we do with the calories we consume—do not occur at constant rates. They ebb and flow, wax and wane in response to your micronutrient intake, macronutrient intake, energy intake, exercise and activity habits, sleep schedule, stress levels, and a dozen other factors. All of these energy-related processes are going on simultaneously in each of us at all times. But the rate at which each of these processes happens is different in each of us and they can increase or decrease depending on the context of our present circumstances and our long term goals. All of these processes utilize the same gene-based principles of energy metabolism—the biochemical machinery that we all share—but because they all involve different starting points and different inputs as well as different goals or possible outcomes, they often require different action plans. We can alter the rate at which each of these metabolic processes happens simply by changing what and when we eat and addressing the non-dietary variables. We can change the context.
But don’t controlled trials demonstrate that a “calorie is a calorie”?
People hear things like “in controlled isocaloric trials, low-carb diets have never been shown to confer a metabolic advantage or result in more weight loss than low-fat diets.” While often true, they miss the point.
People aren’t living in metabolic wards with white lab coats providing and precisely measuring all their food. They’re living in the real world, fixing their own food. Free living is entirely uncontrolled with dozens of variables bleeding in from all angles. In the lab situation, you eat what they give you, and that’s that. The situations are not analogous—real world vs. controlled lab environment.
In real world situations…
Why a Calorie Isn’t Just a Calorie
The macronutrient composition of the calories we eat alters their metabolic effects.
The metabolism of protein famously increases energy expenditure over and above the metabolism of fat or carbohydrate. For a given caloric load, protein will make you burn more energy than other macronutrients.
Protein is also more satiating than other macronutrients. Eat more protein, curb hunger, inadvertently eat less without even trying (or needing a lab coat to limit your intake).
Protein and fat together (AKA “meat”) appear to be even more satiating than either alone, almost as if we’re meant to consume fat and protein in the same meal.
The isocaloric studies tend to focus on “weight loss” and discount “fat loss.” We don’t want to lose weight. We want to lose fat and gain or retain lean muscle mass. A standard low calorie diet might cause the same amount of weight loss as a low-carb, high-fat diet (if you force the subjects to maintain isocaloric parity), but the low-carb approach has been shown to increase fat loss and enhance muscle gain. Most people who lose weight with a standard approach end up losing a significant amount of muscle along with it. Most who lose weight with a low-carb, higher-protein-and-fat approach lose mostly fat and gain or retain most of their muscle.
Take the 2004 study that placed overweight men and women on one of two diets: a very low-carb ketogenic diet or a low-fat diet. The low-carb group ate more calories but lost more weight and more body fat, especially dangerous abdominal fat.
Or the study from 1989 that placed healthy adult men on high-carb or high-fat diets. Even though the high-carb group lost slightly more body weight, the high-fat group lost slightly more body fat and retained more lean mass.
Both describe “weight lost,” but which is healthier?
Whether the calories come in the form of processed or whole food determines their effect.
We even have a study that directly examines this. For two weeks, participants either supplemented their diets with isocaloric amounts of candy (mostly sugar) or roasted peanuts (mostly fat and protein). This was added to their regular diet. After two weeks, researchers found that body weight, waist circumference, LDL, and ApoB (a rough measure of LDL particle number) were highest in the candy group, indicating increased fat mass and worsening metabolic health. In the peanut group, basal metabolic rate shot up and neither body weight nor waist size saw any significant increases.
Your current metabolic state determines the effect of calories.
In one study, a person’s metabolic reaction to high-carb or low-carb diets was determined by their degree of insulin resistance. The more insulin resistant a subject, the better they did and the more weight they lost on low-carb. The more insulin sensitive a subject, the better they did and the more weight they lost on low-fat. Calories were the same across the board.
In another study, insulin-sensitive obese patients (a rarity in the general population) were able to lose weight on either low-carb or low-fat, but insulin-resistant obese patients (very common) only lost weight on low-carb.
Whether you exercise determines the effect of calories.
If you’ve just finished a heavy lifting workout followed by a sprint session, your response to a given number of calories will differ from the person who hasn’t trained in a year.
Training: Your muscle glycogen stores will be empty, so the carbs you eat will go toward glycogen storage or directly burned, rather than inhibit fat burning. Your insulin sensitivity will be elevated, so you can move protein and carbs around without spiking insulin and inhibiting fat release. You’ll be in hypertrophy mode, so some of the protein you eat will go toward building muscle, not burned for energy.
Not Training: Your muscle glycogen stores will be full, so any carbs you eat will inhibit fat burning and be more likely to promote fat storage. Your insulin sensitivity will be low, so you’ll have to release more insulin to handle the carbs, thereby inhibiting fat burning the process. You won’t have sent any hypertrophy signals to your muscles, so the protein you eat will be wasted or burned for energy.
How you slept last night determines the effects of calories.
A single night of bad sleep is enough to:
- Give you the insulin resistance levels of a diabetic. Try eating carbs in an insulin-resistant state and tell me a “calorie is a calorie.”
- Make the reward system of your brain light up in response to junk food and dampen in response to healthy whole food. The more rewarding you find junk food, the more your brain will compel you to eat more of it.
- Reduce energy expenditure. Your “calories out” drops if you sleep poorly.
And those are just a few important variables that determine the context of calories. There are many more, but this post has gone on long enough…
The Take-Home Message
If calorie-counting works for you, great! You’re one of the lucky ones. Own that and keep doing what you’re doing. You’ve clearly got a good handle on the context of calories.
If calorie-counting and weighing and measuring failed you in the past, you’re not alone and there’s a way forward. Address the variables mentioned in this post that need addressing. Do you need better sleep? Do you need to manage stress better? Could you eat more protein or fat, eat more whole food and less processed food, or get more exercise, or lift more weights, or take more walks?
Handle those variables, fix those deficiencies, and I bet that your caloric context will start making more sense. The trick isn’t to increase the number of variables you plug into your calories in/calories out formula. It’s to make sure all your lifestyle and dietary ducks are in a row so that the caloric balance works itself out.
By understanding how these metabolic processes work, and knowing that we can control the rates at which each one happens through our diet (and exercise and other lifestyle factors) we needn’t agonize over the day-to-day calorie counting. As long as we are generally eating a PB-style plan and providing the right context, our bodies will ease into a healthy, fit, long-lived comfort zone rather effortlessly.
So, what’s your caloric context looking like? Thanks for reading today, everyone.
Pontzer H, Wood BM, Raichlen DA. Hunter-gatherers as models in public health. Obes Rev. 2018;19 Suppl 1:24-35.
Claesson AL, Holm G, Ernersson A, Lindström T, Nystrom FH. Two weeks of overfeeding with candy, but not peanuts, increases insulin levels and body weight. Scand J Clin Lab Invest. 2009;69(5):598-605.
Volek J, Sharman M, Gómez A, et al. Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body composition in overweight men and women. Nutr Metab (Lond). 2004;1(1):13.
Mccargar LJ, Clandinin MT, Belcastro AN, Walker K. Dietary carbohydrate-to-fat ratio: influence on whole-body nitrogen retention, substrate utilization, and hormone response in healthy male subjects. Am J Clin Nutr. 1989;49(6):1169-78.
Cornier MA, Donahoo WT, Pereira R, et al. Insulin sensitivity determines the effectiveness of dietary macronutrient composition on weight loss in obese women. Obes Res. 2005;13(4):703-9.
Ebbeling CB, Leidig MM, Feldman HA, Lovesky MM, Ludwig DS. Effects of a low-glycemic load vs low-fat diet in obese young adults: a randomized trial. JAMA. 2007;297(19):2092-102.
Benedict C, Hallschmid M, Lassen A, et al. Acute sleep deprivation reduces energy expenditure in healthy men. Am J Clin Nutr. 2011;93(6):1229-36.
***This article was substantially revised from the original version, which you can read here.
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Today’s guest post is generously offered up by Craig Emmerich, husband to—and co-author with—the queen of keto herself, Maria Emmerich. Enjoy!
When we consume macro nutrients, our bodies go through a priority for dealing with them. This priority can be very useful in understanding how our bodies work and how to leverage it for losing weight.
The body doesn’t like having an oversaturation of fuel in the blood at any time. It tightly manages the fuels to avoid dangerous situations like hyperglycemia or blood glucose that is too high. But it also manages and controls other fuels like ketones (beta hydroxybutyrate or BHB levels) and fats (free fatty acids or FFA and triglycerides) to keep them under control and not oversaturate the blood with fuel.
It is like the engine of a car. You don’t want to give the engine too much fuel and blow it up. So the body controls the amount of fuels in the blood to ensure you don’t “blow up.” To do this, the body will address the most important (or potentially most dangerous) fuels first. It does this in a very logical way—in reverse order of storage capacity.
Here is a chart showing the breakdown of oxidative priority for dietary fuels.
Modified Source: Keto. By Maria and Craig Emmerich
Original source: Oxidative Priority, Meal Frequency, and the Energy Economy of Food and Activity: Implications for Longevity, Obesity, and Cardiometabolic Disease, Sinclair, Bremer, et al, February 2017.
The #1 oxidative priority is alcohol because there is zero storage capacity for it. It makes sense that the body would address this first, since it can’t store it anywhere and too high blood alcohol means death.
The second oxidative priority is exogenous ketones. These are ketone salts that raise blood BHB levels. There isn’t a storage site for ketones either, so the body must deal with this before addressing other fuels. That is why exogenous ketones aren’t the best option when trying to lose weight. They displace fat oxidation, keeping fat stored while it uses the exogenous ketones as fuel instead.
The third oxidative priority is protein. Protein is a bit different, as there is a limited storage space for protein, but protein is not a good fuel source. It takes 5 ATP to turn protein into a fuel (glucose through gluconeogenesis) and another 2 ATP to burn in the mitochondria. Why would your body expend 7 ATP for something it can do for 2 ATP by just burning glucose or fat from your body? Protein is only really used as a fuel when other fuels (glucose and fat) are not present and it is forced to use protein. Protein gets preferentially used to stimulate muscle protein synthesis. It builds and repairs lean mass.
The next oxidative priority is carbohydrates. It has a moderate amount of storage capacity at 1,200 to 2,000 calories.
The last oxidative priority is fat. This makes sense, as there is a theoretically unlimited storage capacity for fat. There are people with upwards of 400 pounds of stored body fat, which represents 1.6 million calories.
Oxidative priority can help you understand what happens when you put certain fuels into your body. If you are drinking alcohol while eating carbs and fat, the carbs and fat will primarily go into storage while the body deals with the elevated alcohol.
To understand the power of oxidative priority take the case of an alcoholic. Alcoholics will have very low A1c levels (in the 4s) no matter what they eat! If they eat tons of carbohydrates they will still have an A1c in the 4s because the chronically elevated alcohol levels force the body to store all glucose while dealing with alcohol, creating a low A1c. I am not recommending anyone become an alcoholic to lower A1c level—but quite the opposite actually.
So, what does this mean, and how can you leverage your body’s biology to lose weight?
If you avoid alcohol and exogenous ketones, get a just enough protein to support maintenance of lean mass (about 0.8 times your lean mass in pounds for grams of protein a day), limit the carbs and then reduce dietary fat a bit to force the body to use more stored body fat for fuel you will lose body fat. When you restrict carbs for long enough (4-6 weeks for most people) the body gets used to using fat as its primary fuel (keto adapted). This means it can burn body fat or dietary fat equally well. Eliminating other fuels and keeping dietary fat moderate allows the body to focus on body fat for fuel resulting in fat loss.
That is our bodies system for processing fuels coming in through the diet. Leverage it for improved results and body recomposition.
Craig Emmerich graduated in Electrical Engineering and has always had a systems approach to his work. He followed his wife Maria into the nutrition field and has since dedicated his time researching and looking at nutrition and biology from a systems perspective. Over the last 8 years he has worked with hundreds of clients alongside Maria to help them heal their bodies and lose weight leveraging their biology to make it easy.
Thanks to Craig for today’s keto insights, and thanks to everybody here for stopping in.
Questions about dietary fuels and oxidative priority—or other points keto? Share them down below, and have a great end to the week. Take care, folks!
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Hey, folks! Today’s post is written by Dr. Lindsay Taylor. Lindsay is my co-author on The Keto Reset Instant Pot Cookbook and The Keto Reset Diet Cookbook. She also heads up our Keto Reset and Primal Endurance Facebook communities, and you might have heard her on the Primal Blueprint and Primal Endurance Podcasts. I’ve asked Lindsay if she would pop over to Mark’s Daily Apple from time to time to give us some insights from the front lines of the world of keto in addition to a few other topics. Enjoy!
Hi, everyone, thanks for having me here! Today I want to sort out one of the more common questions we get over in the Keto Reset Facebook community: “Is ____ keto?”
Fill in the blank with any type of food—beets, carrots, tomatoes, soy milk, cassava flour, you name it. It really doesn’t matter what food you insert into that blank because the answer I’m going to give is always the same:
There is no such thing as keto and non-keto food.
Now let me explain what I mean there….
Remember, ketosis is a metabolic state defined by having measurable levels of beta-hydroxybutyrate (BHB) in the blood (or acetone in the breath if that’s how you’re measuring). A ketogenic diet is any way of eating that allows you to be in ketosis. And guess what? There are no foods that automatically kick you out of ketosis—i.e., that are guaranteed to bring your level of measurable ketones to zero upon ingestion. Even pure white sugar won’t knock you out of ketosis if you eat a small enough amount, hence the saying, “Any food is keto if you slice it thinly enough.”
Of course I understand that when someone asks, “Is ____ keto?” they’re really asking, “If I eat a reasonably sized serving of this food, will I be knocked out of ketosis?” And my answer is: I don’t know.
Embracing the Keto Context
I’m not trying to be difficult here, but the answer depends entirely on the context. Among the many variables that factor in are the given individual’s carbohydrate tolerance and insulin sensitivity, how active they are and whether they have recently exercised, and how much of that particular food they intend to eat and their individual response to that food (which itself probably depends on genetics and a whole host of other variables).
In order to be able to classify foods as keto and non-keto, a given food would have to reliably affect most people the same way (i.e., no difference between individuals), and it would have to affect the same person the same way in different contexts (i.e., no difference between situations). That simply isn’t how it works.
Let me give you an example. I recently went to a birthday party at a friend’s house… a friend who just happens to make the best chocolate cake in the world. I don’t even really like cake, except hers is amazing. I reined in my desire to go face-first into the cake and ate a moderate slice. Though I patted myself on the back for my admirable self-control, I expected be out of ketosis the next morning. Guess what? At 10 a.m. the following day: 3.2 mmol/L on my blood ketone meter (anything above 0.5 mmol/L is considered “in ketosis,” and 3.2 is pretty high, especially for me).
So, does that mean that chocolate cake is a keto food? “Yes” because it didn’t knock me out of ketosis? Or still “no” because it’s chocolate cake and everyone knows chocolate cake isn’t keto no matter what my ketone meter said? But if “no,” how did I get one of the highest blood ketone readings I’ve ever registered without extended fasting? Is this the start of the new hottest diet, choco cake-o keto??
The high ketone reading was probably due to the fact that I had done a long training run the morning before and had been somewhat calorie restricted in the days prior. I would not expect the same outcome if I ate the same amount of chocolate cake on a rest day, or if I ate three times as much cake (like I wanted to) even on a heavy training day. Nor do I expect that anyone training for a marathon can eat chocolate cake after runs and remain in ketosis. I might have to do some follow-up cake testing to find out, though. Purely for science, of course….
I think that we can all agree that chocolate cake is not a food that someone should eat regularly, if at all, particularly if being in ketosis is very important to them (or likewise if they care to adhere to Primal principles). Nevertheless, this helps illustrate why “Does it kick me out of ketosis?” isn’t the right metric to use for deciding whether to include a food in your regular keto repertoire.
Ketosis can be a finnicky state. Trying to micromanage it by fretting about whether certain foods are keto seems like a waste of time, especially since most of the foods that people stress over aren’t things like chocolate cake (a “no duh” food) but are otherwise nutritious items like beets, tomatoes, carrots, leeks, and so on. And, anyway, unless you’re following a ketogenic diet to address a serious medical issue like epilepsy, staying in ketosis 100% of the time isn’t required. Mark has written before on the question of whether constant ketosis is even desirable, let alone necessary to meet our health, fitness, and longevity goals.
Fielding Expert Guidance: e.g. “But so-and-so said I’m not allowed to eat ______ because it’s not keto!”
I know if you’ve spent any time researching a ketogenic diet online, you’ve undoubtedly found list after list of “keto foods” and “non-keto foods”… and many times those lists contradict each other. What gives?
Keto being such a hot dietary strategy right now, there are approximately a bazillion keto coaches, keto Facebook groups, YouTube channels, Instagram pages, and blogs all devoted to telling you how to go keto the “correct” way. One “expert” will say absolutely that dairy is not keto, then the next Instagram model will proudly display a bowl of cream cheese with the hashtag #ketobreakfast. One Facebook group will insist that you eat nothing that grows below the ground, while the next lets you eat any vegetables except nightshades, and this one over here only allows members to eat spinach and cabbage. No wonder keto newbies get so overwhelmed!
It’s important to understand that when someone says that certain foods aren’t keto, they really mean that those foods aren’t allowed (a word I strongly dislike) on their version of a keto diet. However, as I said above, any way of eating that results in a state of ketosis—either through carbohydrate restriction, fasting, or a combination of the two—falls under the keto umbrella. There are many, many versions of the keto diet, and just because some “expert” says that certain foods aren’t keto doesn’t mean you can’t achieve your goals while eating those foods. It simply means that this person has decided that their particular version of keto is best, perhaps because it worked well for them, or perhaps because they based it on ethical beliefs or their good-faith interpretation of the available science or, frankly, sometimes because they don’t understand keto very well. And that’s fine–their audience, their rules. That doesn’t make their rules right for everyone, though.
Asking Better Questions
Lest it seem like I’m maligning anyone who sets any kind of parameters on a keto diet, let me be very clear: there are foods that we would and would not encourage members of our Keto Reset community to consume. However, we encourage our community to decide whether or not to eat something not by asking, Is it keto? but by asking, Do I believe this food is healthy?
Of course, because we are a community rooted in Primal sensibilities, we assert that some foods are more likely to promote optimal health—i.e., those in the Primal Blueprint Food Pyramid. And yes, if you decide to go keto, which restricts carbohydrate intake to less than 50 grams per day for most people, it will be harder to accommodate foods like sweet potatoes and seasonal fruit into your daily repertoire even though they fit the Primal mold. However, this is a matter of math, not an indictment of certain foods as “not keto.”
In the Primal version of keto, food quality and nutrient density reign supreme.
We also recognize that there is a lot of individual variability in terms of what constitutes an optimal diet, keto or otherwise. Whether any particular food belongs in your diet depends on how you feel and perform when you eat it, and whether it does or does not move you closer to achieving your goals. That’s highly personal.
Let’s take the example of beets, because this one comes up a lot. Beets are a highly nutritious food that are considered “approved” by Primal standards. They’re also relatively higher in carbs (8 grams per ½ cup) than other veggies, and they grow below the ground, which can feel like a no-no on a ketogenic diet.
Rather than ask:
- Are beets keto?
- Can I eat these beets?
- Am I allowed to eat these beets? (Let me be clear: you are allowed to eat whatever you want, even on a ketogenic diet. Your body, your choice. That doesn’t mean you should.)
Ask this instead:
- Do I want to eat these beets?
- How will I feel physically and mentally if I eat these beets?
- Do I consider these beets to be a healthy choice? (Note that this is about your values, not somebody else’s.)
- If these beets were to knock me out of ketosis, would I be ok with that?
For example, your answer to #4 might be, “No. I have only been dedicated to the Keto Reset Diet for a few weeks, and I choose to be conservative in my carb consumption still in order to optimize the adaptation process. This serving of beets has more carbs than I want to add to this meal.” Cool, that’s totally valid—skip the beets. Or it might be, “Yes, I’ve been craving beets, beets are super healthy, and I don’t really care if I’m in ketosis later or not.” Cool, also valid—eat the beets. (For what it’s worth, I have no problem eating beets and staying in ketosis, but YMMV.)
Remember, too, If you really want to know if a certain food affects your level of ketosis, you can get a blood or breath meter and test it systematically. In my opinion, this isn’t necessary for the average ketogenic dieter, but some people prefer a data-driven approach. Robb Wolf also provides an excellent protocol for testing how certain foods affect your blood glucose response in his book Wired to Eat.
Perfection Isn’t the Goal—Health Is.
When it comes to deciding what to eat, we’ll never be able to know exactly what the perfect diet looks like—keto or not. While I certainly applaud people for thinking deeply about the quality of their diets, I also hate to see someone fret because the restaurant served shredded carrots on their salad when they heard that carrots aren’t allowed (there’s that word again) on a ketogenic diet. I have to believe that the stress of worrying about the carrot is more detrimental than the 2.6 grams of carbs in ¼ cup of shredded carrots would ever be.
If you are using the Primal Blueprint as your guiding template, it’s really hard to go wrong. Sure, you might find that your first stab at the keto diet needs tweaking to make it work for you. Maybe you feel better satiated with more fat, or maybe you need more protein. Maybe you prefer to eat breakfast instead of fasting in the morning. Maybe you do better with less saturated and more monounsaturated fat.
You can experiment and adjust these things. You don’t have to be perfect from day one. If you try something and decide you don’t like the outcome, you can move forward with new and better information. This isn’t making a mistake—it’s learning. It’s what we should all be doing to keep moving forward on our personal paths toward optimal health.
That’s it for today. Thanks for reading, everyone. Comment below, or find me in the Keto Reset Facebook group if you have any questions. And as always, #liveawesome!
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For today’s edition of Dear Mark, I’m answering two questions from readers. First, is it possible to become deficient in omega-6 fats as an adult? What would that even look like, and is there anything that might make omega-6 more important?
Second is a question related to last week’s feature on prostate health. Is saw palmetto an effective supplement for prostate issues? It depends on the issue.
I have a question for “Dear Mark”
Here it is:
I am completely and totally primal for 10 years now. Can I become O6 deficient ? Since 90% of my fat intake is saturated or O3.
It’s technically possible to become deficient in omega-6 fatty acids. The early rat studies that discovered the essentiality of Omega-6s found that their complete removal made the subjects consume more food (without gaining weight), drink more water (without peeing more than rats on a normal diet), develop scaly skin, lose fur, urinate blood, go infertile, grow weird tails, and die early. All this despite eating an otherwise nutrient-dense diet with all the fat-soluble vitamins (they even removed the fat from cod liver oil and gave the vitamins), B vitamins, and other nutrients a rat could ever want. The only thing missing was a source of omega-6 fats.
Once they discovered the issue—a lack of omega-6—how’d they fix it?
Coconut oil didn’t work, for obvious reasons. It’s almost pure saturated fat.
Butter worked, but you had to use a lot. The omega-6 fraction of butter is quite low.
Cod liver oil worked, but it didn’t fully cure the deficiency disease.
Lard worked well, as did corn oil, liver, flax oil, and olive oil. All of those fat sources fully resolved the issue and eliminated the symptoms. They were all good to decent sources of omega-6 fatty acids.
They also tried pure linoleic acid (the shorter-chained omega-6 PUFA found in nuts and seeds and the animals that eat them) and arachidonic acid (the long-chain omega-6 PUFA found in animal foods). Both worked, but AA worked best.
Throughout all these trials, exactly how much omega-6 fat did the rats require in their diets to cure deficiency symptoms?
When they used lard to cure it, the rats got 0.4% of calories from omega-6 PUFA. If the numbers hold true for humans, and you’re eating 2500 calories a day, that’s just 10 calories of omega-6, or about a gram and a half of pure arachidonic acid to avoid deficiency.
When they used liver to cure it, the rats got 0.1% of calories from omega-6 PUFA. If the numbers hold true for humans, and you’re eating 2500 calories a day, that’s just 2.5 calories of omega-6, or about a third of a gram of arachidonic acid to avoid deficiency.
The truth is that omega-6 deficiency is extremely hard to produce, even when you’re trying your hardest. Way back in the 1930s, the early omega-6 researchers tried to induce deficiency in an adult by giving him a 2 grams fat/day diet for months. Nearly all fat was removed, particularly the omega-6 fats, and the rest of the diet was fat-free milk, fat-free cottage cheese, orange juice, potato starch, sugar, and a vitamin/mineral supplement. Maybe not the ideal Primal diet, but better than some.
He ended up improving his health, not hurting it. There was no sign of deficiency.
Omega-6 fats are everywhere in the food environment, even if you’re actively avoiding concentrated sources of them. No one is developing a deficiency these days. However, certain conditions might increase the tolerable or beneficial upper limits of omega-6 intake.
If you’re strength training with the intent to gain lean mass, a little extra arachidonic acid can improve your results. The dose used was 1.5 grams per day. Average intake through food runs about 250-500 mg, though Primal eaters heavy on the animal foods are probably eating more.
If you’re recovering from injury or healing a wound, a little extra arachidonic acid can speed it up. AA is an important co-factor in the inflammatory response necessary for tissue healing.
Well done, Mark. My doc just prescribed saw palmetto to reduce multiple nighttime visits to the bathroom, though the research I’m looking at says there’s no clinical evidence to support saw palmetto for prostate problems. Your take?
It depends on the problem.
Large observational trials have found no connection between saw palmetto supplementation and prostate cancer risk. It neither helps nor harms.
Saw palmetto does seem to help benign prostatic hyperplasia, a non-cancerous growth of the prostate. This won’t cause serious health issues directly, but it can impede the flow of urine and lead to multiple nighttime bathroom visits. Saw palmetto is quite effective at reducing nighttime urination. If that’s what your doc is trying to help, I’d say give it a shot.
You might ask about combining saw palmetto with astaxanthin. It’s been shown to reduce the conversion of testosterone into estradiol that can sometimes result from plain old saw palmetto supplementation.
That’s it for today, folks. Take care and be well. Chime in down below if you have any questions or comments.
Mitchell CJ, D’souza RF, Figueiredo VC, et al. Effect of dietary arachidonic acid supplementation on acute muscle adaptive responses to resistance exercise in trained men: a randomized controlled trial. J Appl Physiol. 2018;124(4):1080-1091.
Oh SY, Lee SJ, Jung YH, Lee HJ, Han HJ. Arachidonic acid promotes skin wound healing through induction of human MSC migration by MT3-MMP-mediated fibronectin degradation. Cell Death Dis. 2015;6:e1750.
Bonnar-pizzorno RM, Littman AJ, Kestin M, White E. Saw palmetto supplement use and prostate cancer risk. Nutr Cancer. 2006;55(1):21-7.
Saidi S, Stavridis S, Stankov O, Dohcev S, Panov S. Effects of Serenoa repens Alcohol Extract on Benign Prostate Hyperplasia. Pril (Makedon Akad Nauk Umet Odd Med Nauki). 2017;38(2):123-129.
Vela-navarrete R, Alcaraz A, Rodríguez-antolín A, et al. Efficacy and safety of a hexanic extract of Serenoa repens (Permixon ) for the treatment of lower urinary tract symptoms associated with benign prostatic hyperplasia (LUTS/BPH): systematic review and meta-analysis of randomised controlled trials and observational studies. BJU Int. 2018;
Angwafor F, Anderson ML. An open label, dose response study to determine the effect of a dietary supplement on dihydrotestosterone, testosterone and estradiol levels in healthy males. J Int Soc Sports Nutr. 2008;5:12.
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Consistency is key in everything we do.
Training in the gym: The most optimal workout imaginable won’t do a thing if you only get around to it once every two weeks.
Sleep: A solid 8 hours of shut eye every night beats 10 hours one night, 6 the next.
Learning a new skill: Practice for an hour each day and you’ll become a master. Spend twelve hours one time and never again, and you’re remain a beginner.
The same is true for nutrition. A consistent, reliable way of eating—especially with a diet like keto, where extended consistency actually builds new fat-burning mitochondria and establishes habits—tends to produce the best results.
But what if you wanted to be a little less consistent? What if you wanted to cycle between Primal and keto? Is such a thing even possible?
Yes. Just make sure you do it right—and for the right reasons.
When Deciding Whether You Should Even Cycle At All…
Stick With Keto For At least a Month Before Cycling
Four to six weeks is usually a sufficient period of time. Then, once your muscles have become better adapted to the burning and utilization of actual fatty acids—not just ketones—you’re in a good place to start cycling between Primal and keto, or drift in and out of ketosis as you like.
Premature cycling without a sufficient base of fat adaptation will produce lackluster results across the board. You’ll never quite reach fat-adaptation, so the carb cravings will persist, your aerobic efficiency will suffer, and your fat burning machinery won’t be complete. And if you try to “cycle” without actually being fully ketogenic, you’ll be back at square one. Metabolic limbo is no place to be.
Do It For a Legit Reason
Don’t “cycle” because you’re five days into keto and feel terrible.
Don’t “cycle” because you miss French fries.
Don’t “cycle” because you took the stairs instead of the elevator and totally burned, like, 30 grams of glycogen from each quad.
Cycle because you’ve earned and fine-tuned your fat-burning ability, and now wish to support higher-intensity, higher-volume physical pursuits. Or because you just feel better with a more relaxed approach to macronutrients. Or because you really, really love purple sweet potatoes (I don’t blame you).
Watch Out For the Signs Of Poor Metabolic Flexibility
If every time you eat a carb you get sleepy in an hour and show signs of high blood pressure, even if it’s after an intense training session that should have depleted enough glycogen to make those carbs tolerable, rapid cycling is not for you.
If every time you “cycle” back to keto you feel like a truck hit you and it takes a week to get over the keto flu, rapid cycling is not for you.
When Cycling Back Out Of Keto…
Reduce Fat Intake To Make Room For Any Added Carbs
Fat and carbs together is a fattening combination. Most of the worst processed junk food, the stuff responsible for the obesity epidemic—soybean oil soaked French fries, potato chips, donuts and the like—are bags of fat and carbs. They spike glucose, raise insulin, depress lipolysis, and increase fat deposition while being so nutrient-poor that you’re hungry again in half an hour. But it’s not just the junk food that makes this combo dangerous. If you’re dropping a half stick of butter into your baked potato, even if the butter’s from grass-fed cows who snacked on natto, did CowFit, and fell asleep to a Weston A. Price audiobook recording every night and the potato is an ancient heritage variety unearthed at Machu Picchu, you’re still overdoing it.
I’m not saying to “go low-fat.” I’m suggesting you reduce fat calories as you increase carb calories. What does that look like in practice? A gram of fat has roughly twice the number of calories as a gram of glucose (it’s actually 4 calories per gram of carbs and 9 calories per gram of fat, but close enough). For every two grams of carbs you add, reduce fat by one gram.
Remember That Primal Is Still Compatible With “High-Fat,” Meaning You’ll Probably Still Be Fat-Adapted
Primal has always been primarily about high-fat eating (while being agnostic enough about macronutrients to encompass moderate-carb approaches, too) and the resulting fat-adaptation. Keto isn’t the only path there.
It may take longer. You might never get to the point where you could get someone ketone-drunk by breathing into their mouth. But plain old low-carb Primal will turn you into a fat-burning beast. It’s important to realize that “ketosis” isn’t even the primary goal for most people doing it—the primary goal is building the fat-burning infrastructure that will give you food freedom for years to come.
Consider Time Restricted Feeding/Intermittent Fasting
Restricted eating windows and/or intermittent fasting are great ways to make your transition away from keto onto a higher-carb Primal approach go more smoothly. You’re not leaving ketosis entirely, since for the duration of the fasting period you’ll be consuming your own body fat and generating ketones. You get a nice guaranteed dose of ketosis every day (and night) while enjoying the benefits of relaxed macronutrient ratios—a wider variety of plant foods, in-season fruit, more carbs for athletic pursuits that warrant them.
This could very well be the dietary approach you stick with for the long haul, and that’s okay.
Go For a Hard Workout
Anything done with sufficient volume and intensity will turn your muscles into glycogen sinks—the perfect scenario for someone trying to ease their way back to a more relaxed macronutrient intake. If you have any residual physiological insulin resistance from being keto, a hard training session will re-sensitize you.
When Cycling Back Into Keto…
Remember To Get Extra Salt, Magnesium, and Potassium
Even if you have extensive experience being fat-adapted and your mitochondrial infrastructure is set up to utilize fats and ketones, you’ll still lose a lot of intracellular water, electrolytes, and plasma volume switching back to keto—low insulin has that effect, regardless of prior adaptation. That means eating more sodium, more magnesium, and more potassium. Salt to taste (maybe even a bit more than that), take a good magnesium supplement, and eat potassium-rich foods.
Side note: An unappreciated and keto-friendly source of potassium is zucchini. Seriously, you probably don’t realize it, but a large zucchini has very few digestible carbohydrates and about a gram of potassium. Have at ’em.
Maintain Your Training
Some people suggest taking it easy during the transition. They say to let your body “ease” into the change. Hogwash. Consistent exercise is a great way to upregulate fat burning in muscle tissue. In one study, obese people—a population known for impaired fat oxidation—increased their ability to burn fat by a factor of 2.7 through moderate exercise alone. Imagine the effect it’ll have on you.
The good news is that it gets easier the longer you do this. At this point, 15-ish years into my low-carb, high-fat lifestyle and 3 years into my keto lifestyle, switching between Primal and keto is effortless. It just happens. And if I eat some carbs, I’m no worse for wear.
Of course, you don’t have to cycle between Primal and keto. Stick with one or the other. Or neither. Whatever works, works. Just be honest with yourself.
Thanks for reading, everyone. Take care, leave your tips for the transition down below, and have a great rest of the week.
Berggren JR – Am J Physiol Endocrinol M (2008) Skeletal muscle lipid oxidation and obesity influence of weight loss and exercise
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For today’s edition of Dear Mark, I’m answering a single, significant question. It concerns the latest “anti-low-carb” study claiming that we’re all killing ourselves by not eating bread. A reader wonders if the study is legit and if we should be worried about eating fewer carbs than “normal” people.
I don’t think we should be concerned, and I’ll explain why in detail. Let’s take a look and break it down.
I’m sure you’ve seen this latest study to claim that low-carb diets will kill us all: https://www.thelancet.com/journals/lanpub/article/PIIS2468-2667(18)30135-X/fulltext
Is it legit?
Yes, I’ve seen it.
Where to start?
This study came from Walter Willet, he of the voluminous mustache and unbridled enthusiasm for seed oils.
The most glaring weakness is the way they gathered the data. Over the course of 25 years, participants were asked to accurately report their diet reaching back as far as six years. This is an inherent issue in most nutrition data gathering, so it’s not unique to this study, but come on. Can you remember what you ate 6 years ago? Did your diet change at all, or was it stable enough to encompass with a curt summary?
The characteristics of the participants differed greatly.
Low-carbers were far more likely:
- To be men—Males have a higher risk of mortality than women.
- To be diabetic—Diabetes lowers lifespan, especially in the 1980s (when the bulk of the data was collected).
- To be sedentary—Failure to exercise is a major risk factor for early death, and ill health in general.
- To smoke cigarettes—Again, this is an elementary variable. Nothing like being able to smoke indoors. Remember smoking sections on airplanes? I do.
- To eat fewer fruits and vegetables—Carnivory is popular these days, and may work for some, but plants are still good for you and actually complement a low-carb, high-meat diet quite nicely.
- To be overweight—All else being equal, the fatter you are, the unhealthier you are.
Even if they were able to “control for” all those variables, you can’t control for the overall health and wellness trajectory of a person hellbent on ignoring their personal health. What other unhealthy things are they doing that weren’t captured and accounted for by the researchers?
For instance, alcohol intake. They didn’t look at alcohol intake in this trial. Seriously, search for “alcohol” in the paper and you’ll come up blank. It’s very likely that the low-carbers were drinking more alcohol, as similarly-conducted epidemiological research has found that “carbohydrate intake [is] the first to decrease with increasing alcohol consumption.” (2) Alcohol can take a serious toll on health and lifespan if you aren’t careful with your intake.
Oh, and low-carbers were also more likely to be on a diet. This might be the most crucial variable of all. Who goes on a diet, typically? People who have a health or weight problem. Who doesn’t diet? People who are happy with their health and weight. There are exceptions to this, obviously, but on a population wide scale, these trends emerge. Did the low-carb diet actually reduce health and lifespan, or did the health conditions that prompted the diet in the first place reduce health and lifespan?
Ultimately, this was all based on observational studies and epidemiological data. It can’t establish cause-and-effect, it can only suggest hypotheses and avenues for future research.
Luckily, we have controlled trials that demonstrate the health benefits of low-carb dieting, all of which correspond to better longevity:
- Improved cardiovascular risk factors. (3)
- Improved metabolic and vascular health. (4)
- Reduced inflammation. (5)
- Improved insulin sensitivity. (5)
You could make the argument that the positive health effects are purely short-term and that in the long run, those benefits turn to negatives. It wouldn’t be a very good argument, though, because we don’t have any indication that it actually happens. If you go reduce carbs or go keto and you lose body fat, gain lean muscle, improve your fasting blood sugar, normalize your lipids, and reduce inflammatory markers, I see no plausible mechanism by which those improvements lead you to an early grave. Do you?
It seems the burden of proof lies in the Willet camp. If the only healthy range of carbohydrate intake is between 50-55%, he would have to show that:
- No healthy, long-lived cultures or individuals have a carbohydrate intake that strays from the 50-55% range. Anthropological and ethnographical evidence must confirm.
- The benefits of low-carb diets, established through randomized controlled trials, are illusory and/or transitory, eventually giving way to health decrements that lower lifespan.
That’s a tough one. Hats off if he can pull it off. I doubt he can.
Thanks for writing in. I hope I allayed any concerns you might have had.
Take care, all, and be sure to share down below with your own comments and questions.
1. Seidelmann, Sarah, MD, et al. Dietary Carbohydrate Intake and Mortality. Lancet. 2018. (Online First)
2. Liangpunsakul S. Relationship between alcohol intake and dietary pattern: findings from NHANES III. World J Gastroenterol. 2010;16(32):4055-60.
3. Thorning TK, Raziani F, Bendsen NT, Astrup A, Tholstrup T, Raben A. Diets with high-fat cheese, high-fat meat, or carbohydrate on cardiovascular risk markers in overweight postmenopausal women: a randomized crossover trial. Am J Clin Nutr. 2015;102(3):573-81.
4. Ballard KD, Quann EE, Kupchak BR, et al. Dietary carbohydrate restriction improves insulin sensitivity, blood pressure, microvascular function, and cellular adhesion markers in individuals taking statins. Nutr Res. 2013;33(11):905-12.
5. Rajaie S, Azadbakht L, Saneei P, Khazaei M, Esmaillzadeh A. Comparative effects of carbohydrate versus fat restriction on serum levels of adipocytokines, markers of inflammation, and endothelial function among women with the metabolic syndrome: a randomized cross-over clinical trial. Ann Nutr Metab. 2013;63(1-2):159-67.
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For today’s edition of Dear Mark, I’m responding to four reader comments. First up, if a person can’t eat eggs, doesn’t like liver, but really wants choline, can they just supplement? Second, are a couple handfuls of almonds too much omega-6 for the average person? What if they eat fish? Third, a new study claims to show that keto dieting tanks hepatic insulin sensitivity. What should we make of it? Are we giving ourselves type 2 diabetes by going keto? And fourth, I highlight a great approach to drinking alcohol (and living in general) from one of our readers.
If I can’t eat eggs, and don’t like liver, can I supplement with choline? What would be a good dose?
Yes, you can supplement with choline. Men need around 550 mg per day. Women, 425 mg. Those requirements go up if you’re pregnant or nursing, and they very likely go up if you’re drinking.
It’s very possible that those are good levels for the average person eating a low-moderate fat diet. If you’re eating a high-fat diet or engaging in cognitively-demanding work, you may benefit from higher doses.
What jumped out at me was high O6 from snacking on almonds…this was in the fish oil post too, and it’s got me looking twice at how much is too much. I have a handful or two almost every day, and not supplementing with O3 ( although just started an experiment with daily supplements or fish). Too much?
Thanks as always for the excellent post—I’ve been wondering about alcohol too!
Don’t get me wrong. Almonds are a nutrient-dense whole food. They’ve got tons of magnesium, prebiotic fiber, polyphenols. Their health effect profile is impressive:
- Almond consumption improves fatty acid profile of serum lipids.
- Almonds reduce lipid oxidation biomarkers in older adults.
- Almonds reduce 24-hour insulin secretion in non-diabetics.
- Almonds improve glycemic control in type 2 diabetics.
- Almonds improve satiety and postprandial glucose when consumed as snacks and do not increase overall energy intake.
- Almonds possess potent prebiotic fibers, particularly in the skins.
- Almond consumption improves the endocrine profile of women with PCOS.
But they are high in linoleic acid. Absent fish, two handfuls a day is probably excessive. Having some fish fat will balance it nicely.
Try this: Replace one of your handfuls of almonds with a can of sardines or smoked oysters.
Does keto cause liver insulin resistance? Just saw this study and don’t want type 2 diabetes…
First of all, it’s a mouse study.
Second of all, it was a three-day study designed to look at the short-term transitory effects of going keto. Anyone who’s gone keto knows that the early days are a bit rough. Your mitochondria aren’t good at burning fat or ketones yet. You haven’t built the metabolic machinery required to extract the energy you need from the new balance of macronutrients. This period of transition coincides with the “keto flu”—that period of fatigue, listlessness, and headaches.
If you stick with the diet and make it through to the point where you can crank out and utilize ketones, everything changes. You can suddenly start making ATP from all that body fat you’re burning off, giving you a virtually limitless supply of energy at all times. It’s great.
But in the meantime, for that early period it’s rough. You’re insulin resistant, yet unable to burn much fat. Your liver is perpetually overloaded with energy, making insulin resistance almost unavoidable (if transitory).
Third, the composition of this study’s “keto” diet was about as bad as you could get (PDF). The fat came from Crisco—the classic trans-fat laden version—rounded out with a bit of corn oil. Trans-fats and omega-6 linoleic acid. Does this look like the diet you’re eating? Does this look like the keto diet anyone is eating? If the researchers set out to get the worst possible results for the keto group, it wouldn’t have looked any different. almost looks like they were trying to get the worst possible results.
Alcohol in ketosis is just one aspect of alcohol use in a healthy lifestyle. For me personally I perceive alcohol to play not a vital but an extremely useful role.
I drink about 40 gm of ethanol just about every day in the form of a classic gin martini made with 3.5 oz of premium gin (healthy fats in that olive, brother). I consider gin to be a very special spirit because it is comprised of water, ethanol, and botanical substances like the l-terpenes from juniper berries which are known to have a tonic effect on the human organism – and none of the hundreds of dubious organic chemicals (referred to as “cogeners”) contained in whisky or tequila. I always consume this martini between 5:00 and 7:00pm, and I very rarely drink anything else at any time of day or night. I have this drink immediately before and with the evening meal which I personally prepare from scratch with fresh ingredients and consume with my wife of 51 years.
The martini seems to me to punctuate and enhance the transition from “doing” – being responsible, making things happen, solving problems, exerting myself – to “not doing” – resting, refreshing, nourishing, regenerating. Subjectively, I feel like this one drink, consumed with food, stimulates the parasympathetic nervous system. The alcohol research, so-called, tends to produce the opposite result, but in my opinion, virtually all of the alcohol effects research is dreadful – just about the junkiest junk science you can find anywhere.
I will be 80 on my next birthday, my resting heart rate, measured with a Polar FT7 heart rate monitor as an average over 3-5 minutes is 51-52. I ride a mountain bike on intermediate level trails – often in a fasted state – and recently recorded a maximum heart rate of 167. This is considerably higher than the HRmax predicted by any of the recently validated formulas. My GGT level is 16, so I have to conclude that my liver thrives on classic gin martinis. I take no prescription medications and no over-the-counter medications. I am not trying to brag here, I am just trying to document that by just about any measure my health and physical condition is exceptional for a person my age.
My personal belief is that alcohol in the right form and used properly is a health food. This conclusion is based on my personal experience, but I dearly wish that some enterprising biochemists, neurologists, and social psychologists would get together and design a quality research program to examine alcohol’s health effects under various real-world conditions. People like to drink, but a lot of what they drink is full of cogeners and sugar and genuinely toxic crap. Almost nobody has a clue what is in what they are drinking and what its health effects – positive or negative – might be. Millennials are currently destroying their livers in droves and even killing themselves with booze at distressingly early ages. Beliefs about alcohol and drinking in our culture are pathetically primitive.
I think I’ve got it figured out for me, but I think it would wonderful for the rest of the world to know the score.
I’m highlighting Daniel’s words even though he wasn’t asking a question. This man gets it. This is how to approach, appreciate, and consume alcohol. He’s drinking with complete lucidity, total awareness, and mindfulness. Alcohol isn’t “just” something you use to get loaded. It’s a sacred chemical that marks the transition from “doing” to “being.”
Many people blur the lines, drinking for the hell of it. Make it more of a special occasion, consume it mindfully and purposefully. Having a couple glasses of wine at night because I’m bored will ruin my sleep and throw off my tomorrow. Having those same two glasses of wine and some conversation with my wife or dear friends over cheese and olives has an entirely different physiological—not just psychological—effect. My liver actually processes the wine consumed with mindfulness differently.
That’s it for this week, everyone. Thanks for reading and be sure to chime in down below with your own comments, answers, or concerns.
The post Dear Mark: Choline Supplementing, Too Many Almonds, Keto and Insulin Resistance, and How to Drink appeared first on Mark’s Daily Apple.
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It’s a short one, maybe one of the shortest reader questions ever, and it represents one of the few cut-and-dry stances in ancestral health. Humans are omnivores, seed oils are bad for you, no curls in the squat rack, and farmed salmon is toxic poison.
Right? Maybe not.
What’s with the pic of the farm raised salmon?
First of all, I’m not certain that salmon was actually farm-raised. Second, while I’m on the topic, allow me to make the case for farmed salmon. That may surprise you. For years, I’ve been a huge proponent of wild-caught salmon. It’s the only one I ever buy or consciously seek out at restaurants. I’ll eat farmed salmon if it’s the best option available, or if I’m a guest and that’s what’s for dinner—and do so happily, by the way—but I’ve always been a wild salmon guy.
However, not everyone has the means to buy fresh or frozen wild-caught salmon on a regular basis, and not everyone wants to eat canned salmon. Sometimes you just want a big slab of tender salmon with a swathe of crispy, salty skin. Sometimes all five members of your family want their own big slab of tender salmon with the crispy skin. Is farmed salmon a good, safe, effective option?
Let’s look at the evidence. First, what are the benefits of salmon, and how does farmed salmon compare?
The main reason people eat salmon is to get the long chained omega-3 fatty acids—the ones we use to quell inflammation, balance our omega-6 intake, and shift the membrane composition of our cells and structures.
Farmed salmon is a great source. A 6-ounce portion of farmed Atlantic salmon has 4.4 grams of omega-3 fatty acids, which is actually more than wild. A 6-ounce portion of wild sockeye salmon has 2 grams of omega-3s.
But what about the omega-6 fats? Isn’t farmed salmon “loaded” with them? Well, that same portion of farmed salmon has 3.3 grams of omega-6 fats to the wild salmon’s 0.3 grams. The ratio is “worse” than the wild salmon’s. But even then, it’s great. While the wild salmon’s omega-3:omega-6 ratio of 1:0.15 is about as perfect as you can get, the farmed salmon’s ratio of 1:0.75 is fantastic. Besides, it’s also the absolute amount of omega-6s that matter. Admittedly, 3.3 grams is nothing compared to what most people are getting from seed oils, junk food, or even random handfuls of almonds and pecans throughout the day.
There’s more to fish fats than the omega-3s. For instance, many fish fats have subfractional layers with specific health effects. Fats derived from organic Irish farmed salmon possess anti-thrombotic qualities—they reduce the formation of blood clots.
Astaxanthin is a carotenoid that gives salmon its pink hue and may provide neuroprotective effects, especially combined with omega-3s. Wild salmon obtain astaxanthin from the krill and other pink sea creatures they consume. Farmed salmon obtain it from the feed they eat, which has it added. Both farmed and wild salmon provide astaxanthin to those who eat it, but a recent study found that the astaxanthin in wild salmon has higher bioavailability.
What about the drawbacks of farmed salmon, like contaminants?
Even this issue isn’t so clear cut. For example, a 2017 study found higher levels of persistent organic pollutants, metals, and DHA in wild Atlantic salmon compared to farmed Atlantic salmon. Farmed salmon had more overall fat, mostly from saturated, monounsaturated, and omega-6 fats, but farmed was still loaded with omega-3s.
A recent study actually tracked the changes in blood markers of contaminants in response to a high intake of farmed salmon. Eating almost a pound of farmed salmon each week had no effect on blood levels of persistent organic pollutants or mercury.
Surprisingly, European farmed salmon seems to have the biggest contamination issue. Good news, though: a 13-year study of contaminant levels in Norwegian farmed salmon found that toxins are dropping as the years go on.
What about when the rubber hits the road, when actual living and breathing humans eat farmed salmon? Does it help or harm? Let’s see what’s out there:
In one 2016 study, overweight men and women who ate farmed salmon twice a week for 4 weeks had higher HDL, larger LDL particles, lower triglycerides, and an overall improved cardiovascular risk profile. Their large LDL particle number also increased, but I’m not sure what happened to their overall LDL particle number. Another study found farmed salmon reduced triglycerides and increased HDL compared to lean chicken.
Eating farmed salmon twice a week modified the plasma phospholipid composition in a favorable way, increasing DHA and EPA and decreasing omega-6 fats.
Chinese men with a high risk for heart disease improved cardiovascular biomarkers after adding farmed salmon to their diets.
This was an interesting one. A group of otherwise healthy overweight adults were told to eat add a large dose of either fatty fish or lean fish to their normal diets for 8 weeks. The fatty fish was farmed salmon. The lean fish was wild cod. What happened?
- Cod increased DHA in white blood cell membranes. Farmed salmon increased overall omega-3s and reduced omega-6s in white blood cell membranes.
- Farmed salmon improved postprandial blood glucose control. Cod did not.
- Farmed salmon resulted in a smaller increase in postprandial insulin than cod.
I’m not suggesting farmed salmon is better than wild, or even equivalent, but I want to impress upon everyone who reads this blog that you don’t have to drop $15 a pound for wild caught salmon if your budget doesn’t allow it. Those $6 a pound Atlantic salmon fillets might not be as vibrantly red, might have a couple more grams of omega-6, and might have more or less pollutants depending on where they were farmed, but they’ll still have way more omega-3 than omega-6, they’ll still have astaxanthin, and they can still be part of an overall healthy diet.
Thanks for reading, everyone. I’d love to get your thoughts on this down below.
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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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