Contrary to what we’ve been told, cholesterol didn’t evolve to give us heart disease. It’s not here to kill us. The actual roles of cholesterol in the body include insulating neurons, building and maintaining cellular membranes, participating in the immune response, metabolizing fat soluble vitamins, synthesizing vitamin D, producing bile, and kick-starting the body’s synthesis of many hormones, including the sex hormones. Without cholesterol, it’s true that we wouldn’t have heart disease, but we also wouldn’t be alive.
Given all the work cholesterol has to do, the liver is careful to ensure the body always has enough, producing some 1000-1400 milligrams of it each day. Dietary cholesterol is a relative drop in the bucket. And besides, the liver has sensitive feedback mechanisms that regulate cholesterol production in response to how much you get from your diet. Eat more cholesterol, make less in the liver. Eat less, make more in liver.
Now, if cholesterol is so important, why do we worry about it at all? How has it garnered such a bad reputation for giving us heart attacks?
History of Cholesterol and Heart Disease
Heart disease took off in the early part of the twentieth century, and doctors frantically searched for the cause throughout the next several decades. Early studies in rabbits found that feeding them dietary cholesterol reliably increased blood cholesterol levels and induced atherosclerosis that very much resembled human atherosclerosis. Human tests in the fifties initially showed an association between early death by heart disease and fat deposits and lesions along artery walls. Because cholesterol was found to be present in those deposits and because researchers had previously associated familial hypercholesterolemia (hereditary high blood cholesterol) with heart disease, they concluded that cholesterol must be the culprit.
And while it’s true that cholesterol is involved in heart disease, the direct cause-and-effect relationship has not been established. The reality is far more complicated. To get closer to the reality, we must first understand what these cholesterol numbers actually mean.
Cholesterol versus Lipoproteins
Back in those early rabbit studies, researchers discovered a curious thing: even though feeding the rabbits cholesterol spiked their blood cholesterol and gave them heart disease, bypassing the first step and injecting it directly into the blood had no effect. It was completely harmless.
As it turns out, cholesterol doesn’t normally float around the blood by itself. It is contained within lipoproteins. You can think of lipoproteins as delivery vessels. They contain cholesterol, antioxidants, and fatty acids and along the surface have various proteins that direct the lipoprotein to different sites around the body. It’s not the cholesterol that is involved with atherosclerosis. It’s the lipoprotein.
Let’s play the freeway analogy game. Both LDL-cholesterol (LDL-C) and HDL-cholesterol (HDL-C), the standard, basic readings you get from the lab, do not reflect the number of LDL or HDL lipoproteins, or particles, in your serum. Instead, they reflect the total amount of cholesterol contained in your LDL and HDL particles. Hence, the “C” in LDL/HDL-C, which stands for “cholesterol.” Measuring the LDL/HDL-C and then making potentially life-changing health decisions based on the number is like counting the number of people riding in vehicles on a freeway to determine the severity of traffic. It’s data, and it might give you a rough approximation of the situation, but it’s not as useful as actually counting the number of vehicles. A reading of 100 could mean you’re dealing with a hundred compact cars, each carrying a single driver, or it could mean you’ve got four buses carrying 25 passengers each. Or it could be a couple buses and the rest cars. You simply don’t know how bad (or good) traffic is until you get a direct measurement of LDL and HDL particle number.
How does this relate to heart disease?
In my opinion, the most convincing heart disease hypothesis goes like this:
- LDL receptors normally “receive” LDL particles and remove them from circulation so that they can deliver nutrients and cholesterol to cells, and fulfill their normal roles in the body.
- If LDL receptor activity is downregulated, LDL particles clear more slowly from and spend more time in the blood. Particles accumulate.
- When LDL particles hang out in the blood for longer stretches of time, their fragile polyunsaturated fatty membranes are exposed to more oxidative forces, like inflammation, and their limited store of protective antioxidants can deplete.
- When this happens, the LDL particles oxidize.
- Once oxidized, LDL particles are taken up by the endothelium – a layer of cells that lines the inside of blood vessels – to form atherosclerotic plaque so they don’t damage the blood vessel. This sounds bad (and is), but it’s preferable to acutely damaging the blood vessels right away.
- So it’s the oxidized LDL that gets taken up into the endothelium and precipitates the formation of atherosclerotic plaque, rather than regular LDL. OxLDL, poor receptor activity, and inflammation are the problems.
If that’s the case, what exactly is the deal with traditional blood lipid numbers—the ones you get on a standard blood test?
This information is how I view cholesterol as it relates to my individual biology. If you have questions about your cholesterol numbers, discuss them with a qualified health professional.
Standard view: Get that TC below 200, or else you’ll have a heart attack or you’ll have to pay a higher health insurance premium, if the insurers take you on at all.
My take: Mostly meaningless. Even though the epidemiological evidence suggests a TC between 200 and 240 mg/dl is best for all-cause mortality,https://www.ncbi.nlm.nih.gov/pubmed/19903920‘>2
There is an advanced lipid test that’s worth getting: ApoB.
Every single LDL particle has a single ApoB, making ApoB an effective measurement of LDL particle count. By all accounts I could find, ApoB is reliable and accurate. Every LDL particle has one ApoB, and along with TC:HD ratio, ApoB count is a strong predictor of heart disease risk (again, with the caveat that these studies are on populations leading a decidedly unPrimal and highly inflammatory lifestyle).https://www.sciencedirect.com/science/article/abs/pii/S0306987718304729‘>6
But if you’re eating a healthy diet, your performance is good, your body comp is good (or trending that way), your energy and sleep are rock-solid, you don’t have any familial hypercholesterolemia genes—is it really dangerous to have elevated cholesterol numbers?
I don’t know. But I’m skeptical.
For one, “elevated” cholesterol isn’t necessarily linked to heart disease. Sometimes it’s even linked to lower mortality. For instance, in people older than 60, high LDL is associated with lower all-cause and cardiovascular mortality.http://atvb.ahajournals.org/content/20/6/1536.full‘>8https://www.sciencedirect.com/science/article/abs/pii/0891584993900745‘>10
To name a few. Could “high” LDL particles be closer to benign if they’re more resistant to oxidation? I would imagine so. Does resistance mean immunity to oxidation? Absolutely not. Don’t get cocky.
Substantially “elevated” cholesterol, low HDL or high LDL can be a real problem, but they may also just be a symptom of the larger concern rather than the main issue itself. Cholesterol profile can be impacted by other conditions such as hypothyroidism, untreated diabetes or pre-diabetes, pregnancy (surprise!), lactation, stress, liver conditions, heart disease (symptom, not cause of). Even weight loss or fasting can spike cholesterol numbers (turns out burning all that animal fat off your body can have a momentary effect on blood lipids). Talk to your doctor about what your numbers mean in the grand scheme of your health. And see if you can get a read on other markers, like C-reactive protein (an inflammatory indicator), oxidized LDL, and ApoB (or some other marker of LDL particle number).
High cholesterol shouldn’t be ignored, but it’s not the only thing that matters. You have to look at the whole picture. You have to take a step back (or several steps back) and consider everything—not just numbers on a readout.
If you have any more questions about this topic, drop them down below. Thanks for reading, everyone. Take care.
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At this point, intermittent fasting isn’t a new concept, nor is it a difficult one. You take in all of your calories for the day within a limited window of time, and the rest of the day, you stick with water, maybe a cup of coffee, or tea in the morning if you feel so inclined. The idea is that giving your body a period of time “off” from digesting food allows your cells to heal and renew in other ways.
A Practice Born Because Calorie Restriction is Unpleasant
Intermittent fasting became popular because calorie restriction was found to contribute to healthy aging. A few mouse and worm studies seem to show that drastic reductions in food intake over a long period of time could prolong your life.
The research is compelling, but I’m not convinced actively restricting your calorie intake through sheer will is the true path to enjoyable longevity. I don’t want to be thin, frail, distractible, or preoccupied with food. I’d rather be vibrant and full of zest. I want to eat big strapping meals of steak and veggies smothered in butter without worrying about calories. I want to maintain muscle mass and have enough energy to go on long hikes and have the legs to still leap for high passes (over the young guys) at the end of Ultimate games. And as I appreciate the neuroprotective and autophagy-promoting qualities of calorie restriction, I’d rather not expend the mental energy and fortitude required to maintain such a regimen day-in and day-out.
Intermittent fasting is the workaround. Pushing off breakfast for a few hours gives me all of the benefits of calorie restriction, without all the misery.
Fasting is the way to have your cake and eat it too. Beyond the already proven benefits of a Primal Blueprint low-carb lifestyle, fasting once in a while seems to offer many of the same benefits of calorie restriction – you know, stuff like increased longevity, neuroprotection, increased insulin sensitivity, stronger resistance to stress, some cool effects on endogenous hormone production, increased mental clarity, plus more – but without the active, agonizing restriction.
You just eat Primally, focusing on meat and vegetables with plenty of animal fat, and skip meals on occasion. A sixteen-hour fast is on the low-but-still-effective end, or you could opt for longer, more intermittent fasts – say, a full twenty-four hours once or twice a week. Women may need to time fasts a little differently than men. More on that here.
When you’re done with the fast, eat as much as you want (which usually isn’t an issue, once you’re keto-adapted). It essentially turns into “eat when you’re hungry,” because let’s face it: eating the types of foods we evolved eating induces powerful satiety and makes eating the right amount of food a subconscious act. Fasting becomes a whole lot easier (and intuitive) when you’ve got your food quality dialed in. And I’ll come back to that little caveat at the end here.
“Fasting” was the top search term for MDA last week, and I hadn’t done a big post on it in a while, so I thought I’d do a comprehensive rundown of all the benefits (some conclusive, others prospective) you can expect to obtain from IF.
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Intermittent Fasting and Longevity
Everyone wants to live longer, but I find longevity pointless if you’re not enjoying yourself. Otherwise, life becomes dreary.
The popular c. elegans worm enjoys increased longevity with both twenty-four and forty-eight hour IFs via signaling through a gene that we all have.full PDF) from the 1940s found that varying amounts of twenty-four hour IFs (every other day, every fourth day, every eighth day, etc) prolonged the lifespan of rats without retarding or stunting the growth (as occurred with calorie restricting them). Female rats responded best to every eight day fasts, while males responded best to every other day fasts.
Reductions in brain insulin signaling have been shown to increase lifespan in animals, either by calorie restricting or actively knocking out brain insulin receptors.http://www.ncbi.nlm.nih.gov/pubmed/21244426‘>3
Going in and pharmaceutically manhandling your cholesterol synthesizing equipment is one thing; eating real food and exercising, resulting in possible alterations to your lipid profile, is another. We don’t set out to force your blood lipids into submission, but lifestyle changes that happen to change them for “the better” are usually a good thing. Fasting brings potent changes to blood lipids in an “organic” way – you’re just letting your machinery do its thing on its own – and this is probably a very good thing.
Intermittent fasting is as effective or even more effective than calorie restriction in improving metabolic syndrome markers in overweight women, and it’s a whole lot easier to stick with.http://www.ncbi.nlm.nih.gov/pubmed/20300080‘>5
I discussed this last week, but it can’t hurt to mention that short-term alternate day fasting wrought improvements in LDL particle size and distribution in obese adults.http://www.ncbi.nlm.nih.gov/pubmed/20815899‘>7
Heck, intermittent fasting even helped cocaine addicts stick to their treatment and rehab program.http://www.ncbi.nlm.nih.gov/pubmed/18184721‘>9 In fact, here’s a review of most of the animal anti-cancer evidence.http://www.ncbi.nlm.nih.gov/pubmed/19135806‘>11 This is refreshing news. A preliminary studyhttp://ajpregu.physiology.org/content/296/1/R29.full‘>13 I’ve found this to be the case for me. If the body “needs” food right after a workout, why would hunger be blunted? This is why I tend to hold off on the eating post-workout. Every little bit helps, especially as you age.
Fasting doesn’t cause your brain tissue to waste away, contrary to what some people will tell you. It’s actually good for brain health. Any dietary restriction tends to increase neuronal plasticity and promote neurogenesis, but it was IF that had the greatest effect (with the fewest downsides).http://onlinelibrary.wiley.com/doi/10.1046/j.1471-4159.2003.01586.x/full‘>15 That is, mice who ate larger meals more infrequently saw greater increases in brain and overall bodily health. Still another study found that IF was beneficial for peripheral nerve function in mice by promoting the maintenance of the neuronal pathways responsible for locomotor performance.http://www.ncbi.nlm.nih.gov/pubmed/21106691‘>17), which is the process by which cells recycle waste material, eliminate or downregulate wasteful processes, and repair themselves. Why is autophagy so important? It’s required to maintain muscle masshttp://www.ncbi.nlm.nih.gov/pubmed/20104028‘>19 It reduces the negative effects of aginghttp://www.ncbi.nlm.nih.gov/pubmed/17934054‘>21
Without the autophagy that fasting provides, you would get very few of the benefits. Fasting even increases neuronal autophagy,http://www.ncbi.nlm.nih.gov/pubmed/21051570‘>23 (which mean better performance down the line), improved muscle protein synthesis,http://www.ncbi.nlm.nih.gov/pubmed/20187284‘>25 (you’ll earn your meal and make more muscle out of it if you train on an empty stomach). Studies on Muslim athletes during Ramadan show no effect on performance while fasting,http://www.ncbi.nlm.nih.gov/pubmed/19787180‘>27 in those who exercise and fast rather than just fast. When you train in a fasted state, glycogen breakdown is blunted28 and more fat is burned, leaving you more glycolytic energy in the tank for when you really need it and less body fat. Those are just a sampling of the benefits to fasted training; there are dozens more.
Mental Well-being and Clarity
A lot of health influencers will tell you that failure to eat something every few hours will cause mental fog and sluggishness, so keep a banana or a granola bar on your person at all times. Of course, this is all based on an assumption that we need to supply exogenous carbs on a regular basis to properly fuel the brain. This notion that fasting is only the province of anorexics or “caveman” has kept many people from experiencing the vast array of benefits.
I maintain that one’s comfort in handling intermittent fasting effortlessly does increase dramatically when you’ve reprogrammed those cells (and genes) to predispose your body to derive most of your day-to-day energy from fat, as opposed to constantly dipping into glycogen stores (as happens when we rely so much on refeeding carbs every few hours).
Overall, fasting just seems right. It’s like a reset button for your entire body, presumably across a large spectrum of maladies and dysfunctions. It puts your body into repair mode – at the cellular level – and it can restore normal hormonal function in the obese or overweight. Now, you don’t have to fast, but it’s definitely something to consider.
Have you tried intermittent fasting yet? Let me know how intermittent fasting has worked – or hasn’t – with your lifestyle in the comment section!
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When describing someone that has successfully made the transition to a Primal or Keto way of eating I often refer to them as “fat-adapted” or as “fat-burning beasts”. But what exactly does it mean to be fat-adapted? How can you tell if you’re fat-adapted or still a sugar-burner?
As I’ve mentioned before, fat-adaptation is the normal, preferred metabolic state of the human animal. It’s nothing special. It’s just how we’re meant to fuel ourselves. That’s actually why we have all this fat on our bodies – turns out it’s a pretty reliable source of energy.
Here’s what you need to know about the benefits of becoming fat adapted, or keto adapted, and why it works with your biology.
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Are Being in Ketosis and Being Fat Adapted the Same Thing?
Fat-adaption does not necessarily mean you’re in ketosis all the time. Ketosis ketosis describes the use of fat-derived ketone bodies by tissues (like parts of the brain) that normally use glucose. That happens after you’ve depleted your glucose stores, and your body starts producing ketones for energy. When you’re in ketosis, you can usually detect ketones in your bloodstream.
Fat-adaption describes the ability to burn both fat (through beta-oxidation) and glucose (through glycolysis).
The Disadvantages of Primarily Burning Sugar for Energy
To understand what it means to be fat adapted, it’s useful examine what it means to depend on sugar for energy.
It Is More Difficult to Access Stored Fat for Energy When You’re Dependent on Sugar
What that means is, when your body is primarily looking for sugar for fuel, your skeletal muscle doesn’t as readily oxidize fat for energy.
What happens when a sugar-burner goes two, three, four hours without food, or skips a whole entire meal? They get ravenously hungry. A sugar-burner’s adipose (fat) tissue even releases a bunch of fatty acids 4-6 hours after eating and during fasting, because as far as your biology is concerned, your muscles should be able to oxidize them. After all, we evolved to rely on beta oxidation of fat for the bulk of our energy needs. Once your blood sugar is all used up (which happens really quickly), hunger sets in, and your hand reaches into the chip bag yet again.
A Sugar Burner Doesn’t Readily Access Dietary Fat for Energy
As a result, more dietary fat is stored than burned. Unfortunately for them, they’re likely to end up gaining lots of body fat. As we know, a low ratio of fat to carbohydrate oxidation is a strong predictor of future weight gain.http://onlinelibrary.wiley.com/doi/10.1111/j.1748-1716.1970.tb04764.x/abstract?systemMessage=Due+to+scheduled+maintenance+access+to+the+Wiley+Online+Library+may+be+disrupted+as+follows%3A+Monday%2C+6+September+-+New+York+0400+EDT+to+0500+EDT%3B+London+0900+BST+to+1000+BST%3B+Singapore+1600+to+1700‘>2 If you’re unable to effectively beta oxidize fat (as sugar-burners often are), you’d better have some quick snack options on hand.
Sugar Burners Use Stored Glucose Quickly During Exercise
Depending on the nature of the physical activity, glycogen burning could be perfectly desirable and expected, but it’s precious, valuable stuff. If you’re able to power your efforts with fat for as long as possible, that gives you more glycogen – more rocket fuel for later, intenser efforts (like climbing a hill or grabbing that fourth quarter offensive rebound or running from a predator). Sugar-burners waste their glycogen on efforts that fat should be able to power.
The Benefits of Being Fat Adapted
There are some compelling advantages to being fat adapted or keto adapted, which may move you to make the switch if you haven’t already.
People Who are Fat Adapted Often See Improved Insulin Sensitivity
A ketogenic diet “tells” your body that no or very little glucose is available in the environment. The result? “Impaired” glucose tolerance http://www.ncbi.nlm.nih.gov/pubmed/19407076‘>4
Being Fat Adapted Means You Go Longer Between Meals
A fat-burning beast can effectively burn stored fat for energy throughout the day. If you are fat adapted, chances are, you can handle missing meals and are able to go hours without getting ravenous and cranky (or craving carbs).
You Can Better Utilize the Fat You Eat for Energy
A fat-burning beast is able to effectively oxidize dietary fat for energy. If you’re adapted, your post-prandial (after mealtime) fat oxidation will be increased, and less dietary fat will be stored in adipose tissue.
When You’re Keto Adapted, You Always Have a Fuel Source
A fat-burning beast has plenty of accessible energy available in the form of body fat, even if he or she is lean. If you’re adapted, the genes associated with lipid metabolism will be upregulated in your skeletal muscles.http://www.ncbi.nlm.nih.gov/pubmed/18801964‘>6 If you can handle exercising without having to carb-load, you’re probably fat-adapted. If you can workout effectively in a fasted state, you’re definitely fat-adapted.
You Can Still Burn Glucose When Fat Adapted
It’s not that the fat-burning beast can’t burn glucose – because glucose is toxic in the blood, we’ll always preferentially burn it, store it, or otherwise “handle” it – it’s that we do not depend on it. I’d even suggest that true fat-adaptation will allow someone to eat a higher carb meal or day without derailing the train. Once the fat-burning machinery has been established and programmed, you should be able to effortlessly switch between fuel sources as needed.
A fat-burning beast will be able to burn glucose when necessary or available, whereas the opposite cannot be said for a sugar-burner. Ultimately, fat-adaption means metabolic flexibility. It means that a fat-burning beast will be able to handle some carbs along with some fat. When you’re fat adapted, you will be able to empty glycogen stores through intense exercise, refill those stores, burn whatever dietary fat isn’t stored, and then easily access and oxidize the fat that is stored when it’s needed.
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How Do You Know if You’re Fat Adapted or Keto Adapted?
There’s really no “fat-adaptation home test kit.” I suppose you could test your respiratory quotient, which is the ratio of carbon dioxide you produce to oxygen you consume. An RQ of 1+ indicates full glucose-burning; an RQ of 0.7 indicates full fat-burning. Somewhere around 0.8 would probably mean you’re fairly well fat-adapted, while something closer to 1 probably means you’re closer to a sugar-burner. The obese have higher RQs. Diabetics have higher RQs.http://www.ncbi.nlm.nih.gov/pubmed/20864947‘>8 What do these groups all have in common? Lower satiety, insistent hunger, impaired beta-oxidation of fat, increased carb cravings and intake – all hallmarks of the sugar-burner.
It’d be great if you could monitor the efficiency of your mitochondria, including the waste products produced by their ATP manufacturing, perhaps with a really, really powerful microscope, but you’d have to know what you were looking for.
No, there’s no test to take, no simple thing to measure, no one number to track, no lab to order from your doctor. To find out if you’re fat-adapted, the most effective way is to ask yourself a few basic questions:
- Can you go three hours without eating? Is skipping a meal an exercise in futility and misery?
- Do you enjoy steady, even energy throughout the day? Are midday naps pleasurable indulgences, rather than necessary staples?
- Can you exercise without carb-loading?
- Have the headaches and brain fuzziness passed?
Yes? Then you’re probably fat-adapted. Welcome to the human metabolism you were wired for!
That’s it for today, folks. Send along any questions or comments that you have. I’d love to hear from you guys.
The post What Does It Mean to Be Fat Adapted or Keto Adapted? appeared first on Mark’s Daily Apple.
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Cholesterol usually gets the gold for most demonized nutrient, and fats undoubtedly take the silver. It’s time to confront the misunderstandings around fats.
When I switched from a high-carb, low-fat diet and started to eat healthy fat as a nutrient, my health rapidly transformed. As important as fat is to your body, the fact remains that not all fats are created equal.
A few fats, including but not limited to trans fats, deserve every bit of disparagement they get and then some. But many types of fats are beneficial, and we’d like to put in a good word for them. Here, we’ll go through good fats, harmful fats, and how to eat more of the best kinds of fats. At the end of this article, I’ve included a video explaining how to get more healthy fats and why you would want to in the first place.
What are fats?
You may count your fat grams as part of your macro tracking, or you see them high up on your nutrition label. But what are fats, really?
Fats are compounds of carbon, hydrogen and oxygen atoms that exist in chains of varying lengths, shapes and orders. They’re one of the vital nutrients required by the body for both energy and the construction/maintenance of “structural” elements, such as cell membranes.
Saturated and Unsaturated Fats
It’s a common misconception that fats are categorized as either saturated or unsaturated. That’s not exactly how it works. All fats to some extent contain both saturated and unsaturated fatty acids, they are generally categorized by levels of saturation.
Biochemically speaking, these fatty acids sport a single double bond in their fatty acid chain. The more double bonds a fatty acid has, the more “fluid” it is. They are generally liquid at room temperature.
Monounsaturated fats are found in numerous oils, including avocado oil, olive oil, flaxseed oil, sesame seed oil, sunflower oil, safflower oil, corn oil and peanut oil. Notice that we use the word “found” and not comprise. The fact is, these oils contain varying levels of monounsaturated fat. The rest is a mix of polyunsaturated and saturated. Olive oil, for example, contains about 75% monounsaturated fat, and canola 60%. By the way, these fats are also found in avocados and nuts. They’re granted approval (as much as any fat is in conventional wisdom) as a “healthy fat.”
Polyunsaturated fats have more than one double bond in their fatty acid chain. They tend to be liquid even when refrigerated. Their problem is they also tend to go rancid easily, particularly when heated. When we heat them (and we often do), they often become oxidized. We’ve let in the Trojan Horse at that point and opened ourselves up to all kinds of free radical damage – everywhere from cell membrane damage to wrinkles to arterial plaque build up.
Polyunsaturated fats are found in grain products, soybeans, peanuts and fish oil.
Essential Fatty Acids
First off, we call them essential because the body can’t produce them itself and must obtain them from food. We’re talking about omega-3 and omega-6.
Omega-6. I fully acknowledge it’s important, but most of us get enough of it that we don’t have to think about it. Omega-6 fatty acids, found in corn and other grains as well grain-fed livestock, play a crucial role in dermal integrity and renal function among other things. But if left unchecked, they trigger inflammation. Ratio matters, but we’ll get to that in a minute.
What keeps omege-6 in check? Omega-3s, of course. While omega-3s were ignored for decades, they’re finally garnering respect, but it’s still not enough in my opinion.
Omega-3s are found primarily in fish, algae, flax and nuts. You also find good portions of them in eggs from chickens that are fed fish or flax meal. And you’ve heard us go on and on about the three forms: ALA (think flax) as well as EPA and DHA (think fish oil). Omega-3s have several key functions, including:
- Aiding circulation by naturally thinning the blood
- Fighting systemic inflammation
- Supporting brain function
- Easing symptoms of depression, anxiety and even ADHD
Now back to the ratio matter. Estimates vary, but experts generally characterize Western diets as anywhere between 10-30 parts omega-6 to 1 part omega-3 (10-30:1). What ratio should we be getting? What did our primal ancestors likely eat? Close to 1:1, although many will try to tell you that 4:1 is good enough. Supplements can bridge the gap if you want to rein in your ratios.
The sky high ratio of typical Western diets sets us up for inflammation, high blood pressure, blood clots, depressed immune function and sub-optimal brain development and neurological function.
So, what about the other oils, like olive oil? The ratio for olive oil is 3:1, which isn’t great in and of itself. But there’s yet another wrinkle. Olive oil is 75% monounsaturated and 14% saturated, which means that only 11% of it has the polyunsaturated ratio to begin with. In these relatively small amounts, ratio isn’t as much of a concern, particularly when the oil contains so many other good compounds like polyphenols that fight inflammation damage caused, in part, by the problematic ratio. Corn oil, on the other hand, contains only about 25% monounsaturated fat (and 13% saturated). The ratio matters big time here.
Saturated fats have been demonized for decades, largely due to the widely accepted lipid hypothesis that made a connection between lipid consumption and heart disease – and the advice that went along with it.
Saturated fats have all available carbon bonds paired with hydrogen atoms, which makes them highly stable. They don’t have the same tendency toward rancidity as polyunsaturated fats, even if heated. This is a good thing.
Saturated fats are an integral part of Primal living and are found in animal products and some oils, as part of a healthy diet, and I’ll say it again. Saturated fats serve critical roles in the human body. They make up 1/2 of cell membrane structure. They enhance calcium absorption and immune function. They aid in body’s synthesis of the essential fatty acids and provide a rich source of fat soluble vitamins.
Last but not least, they provide cholesterol. The human body makes its own, but it all balances out. Can I help that I’ve been won over by its many charms? Naturally occurring substances, natural body processes appeal to me – unlike our next categories.
We’ve all heard the story by now. The unnatural chemical modification process that created trans fats made products more shelf stable but wreak havoc for those who ingest them. (Quick fact: the hydrogenation process changes the position of hydrogen atoms in the fatty acid chain.)
The body doesn’t recognize the transformed fats. The trans fats are absorbed through cell membranes, where they initiate general disorder in cell metabolism. Trans fats have been associated with inflammation, associated atherosclerosis, diabetes, obesity and immune system dysfunction.
“What are these?” you ask. Good question. Insteresterified fats are a new-ish breed of chemically modified fats created to avoid the trans fat label. Like trans fats, these fats go through a kind of hydrogenation process along with the associated rearrangement of fat molecules and an enrichment with stearic acid. The point is the same as it was with the trans fat poison, er process: it makes the product more shelf stable.
So, this sounds all too familiar, no? Sound like splitting hairs? You got it. (Insert your own expletive.)
My suggestion: if hydrogenated is mentioned anywhere on the label, put it down and walk away.
How to Get More Healthy Fats
There are lots of ways to be smart about eating fat. The key is knowing what to look for. A few of my favorite fat sources include:
- Avocado oil
- Salad dressing made with avocado oil
- Olive oil
- High-quality lard and tallow from pastured animals
- Grass-fed meats
- Coconut oil
- Coconut butter
Here’s a video explaining how to add more healthy fats to your day, plus why you would want to.
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As a health-minded individual, you’ve no doubt gotten the memo that omega-3 fatty acids are important. You may dutifully eat your weekly servings of small, oily fish. Perhaps a fish oil pill is even part of your daily supplement routine. But do you know why?
Looking back, I used to write about omega-3s a lot in the early days of Mark’s Daily Apple (more than a decade ago, geez!) Since then, I’ve covered the topic here and there, but I thought it was time for a refresher. Today I’m going to focus on giving you a broad overview of their function and an update on the state of the research literature.
It would be impossible to cover all the reasons that omega-3s are important for health in a single post, nor all the areas of ongoing research. I’ll try to hit the big ones here. Let me know in the comments what else you’d like me to cover in future posts.
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What Are Omega-3 Fatty Acids?
Omega-3s are essential polyunsaturated fatty acids (PUFAs)—“essential” means the body can’t synthesize them. We have to get them from food or supplements.
As Primal folks, you might have an adverse reaction to the word “polyunsaturated.” It’s true that in the ancestral health world, we tend to be wary of PUFAs—or really, oils containing high proportions of PUFAs such as safflower and canola—due to their propensity to become rancid and be pro-inflammatory. However, this is a don’t-throw-the-baby-out-with-the bathwater situation. First, when it comes to overconsumption and inflammation, we are primarily concerned with omega-6 fatty acids, not omega-3s. Second, PUFAs, both omega-3s and even the oft-maligned omega-6s, serve many functions in the human body.
I’ll return to the issue of omega-6s vis-à-vis omega-3s later in this post. For now, I just want you to understand that omega-3s are polyunsaturated, essential, and important.
A Quick Primer on Polyunsaturated Fatty Acids
Omega-3s and omega-6s are both types of polyunsaturated fatty acids. What does this mean? Fatty acids comprise chains of carbon atoms of differing lengths. Picture each carbon atom having four arms. They “hold hands” to form the chain. With the remaining hand(s), they hold on to one or more hydrogen atoms.
If each carbon atom uses one hand to hold the carbon on its left and one to hold the carbon on its right, that leaves two hands free for hydrogen. When each carbon is attached to two hydrogen atoms, these fatty acids are called saturated.
Sometimes carbons form double bonds, meaning they use two hands two grab a neighboring carbon. This leaves only one hand free for hydrogen. These are unsaturated fatty acids. When fatty acids only have one double bond along the carbon chain, they are called monounsaturated. When they have multiple double bonds, they are polyunsaturated.
The number in the name of the fatty acid tells you where you can find the first double bond. In omega-3s, the first double bond is on the third carbon atom from the omega (methyl) end. In omega-6s, it’s on the sixth carbon atom.
Double bonds form “kinks” in the fatty acid chains, affecting the shape, and ultimately the function, of the fatty acid. It is not inherently bad for a fatty acid to be polyunsaturated, but it does mean that they are especially vulnerable to oxidation. Omega-3 and omega-6 fatty acids (along with their less appreciated cousins, the omega-9 fatty acids) are each important in their own way.
The Three Main Types of Omega-3s
There are many forms of omega-3 fatty acids, of which three are particularly noteworthy for humans:
- Alpha-linolenic acid (ALA)
- Eicosapentaenoic acid (EPA)
- Docosahexaenoic acid (DHA)
ALA is the most abundant in the diet. In humans, its main biological function is as a precursor for EPA and DHA. ALA that is not converted to EPA or DHA is used mainly for energy.
Even though ALA is converted into EPA and DHA, the latter two are still considered essential (or “conditionally essential”) because conversion rates are too low to provide all the EPA and DHA needed for optimal functioning. Females are better able to convert ALA thanks to higher estrogen, but both sexes need to get EPA and DHA in their diet and/or from supplements.https://pubmed.ncbi.nlm.nih.gov/23668691/‘>2 https://www.ncbi.nlm.nih.gov/pubmed/29773586‘>4
On the other hand, a Cochrane Review published earlier this year takes a different stance.https://www.ncbi.nlm.nih.gov/pubmed/30415628‘>14 Multiple studies show a benefit, but at doses higher that you’re likely to take over the counter. To reduce triglycerides, the American Heart Association recommends taking 2 to 4 grams of EPA+DHA under a doctor’s supervision.https://www.ncbi.nlm.nih.gov/pubmed/26359502‘>16, and individuals diagnosed with depression may have chronically low levels of omega-3s in their cells.https://www.ncbi.nlm.nih.gov/pubmed/9513745‘>18
Some of the best sources of EPA and DHA are salmon, mackerel, anchovies, sardines, herring, and oysters. Cod livers are delightfully mild and pack a wallop of vitamins A and D to boot. Primal-friendly sources of ALA include flax seeds, chia seeds, and walnuts. You also get some omega-3s in meat and eggs (chickens are often fed omega-enriched feed). Grass-finished beef and pastured eggshttps://pubmed.ncbi.nlm.nih.gov/26795198/‘>32
The primary omega-6 fatty acid is linoleic acid (LA). LA and the primary omega-3 ALA use the same enzymatic pathways to convert into longer-chain fatty acids: arachidonic acid (AA, in the case of LA) and EPA and DHA (in the case of ALA). High LA levels can crowd out the ALA and make it so that it can’t make the all-important EPA and DHA.
You can directly impact the amount of omega-3s and omega-6s in your tissues by changing your diet.https://pubmed.ncbi.nlm.nih.gov/16387724/‘>34
Although some research suggests that the high ratio of omega-6 to omega-3 in modern diets puts people at risk for developing certain diseases such as heart disease and cancers,https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5093368/‘>36 Depending on whom you ask, modern diets may have a ratio of 1:10, 1:16, 1:20, or more!
I used to bang the drum about hitting the right omega-3:omega-6 ratio in your daily diet. In recent years I’ve backed off that stance somewhat. I still think modern diets like SAD are way too high in omega-6s, but the answer isn’t to pile on heaping servings of omega-3s to balance it and “correct” the ratio. The solution is to reduce consumption of omega-6s (mostly from refined seed and vegetable oils, and products containing those oils) while getting adequate omega-3s.
Should I Supplement With Fish Oil?
It is certainly possible to be deficient in omega-3s. Clinical deficiencies usually manifest as scaly rashes. Severe omega-3 deficiencies are rare in most parts of the world, though. Subclinical low omega-3 levels may manifest as brittle nails and hair, poor sleep, or mood disturbances.
Despite a mountain of evidence that omega-3s are essential for health, there is still no clear guidance about who exactly should supplement and how much. It seems to me that the best practice, and one I follow myself is: aim to get omega-3s from food, and supplement wisely as needed. In practice, this means I select grass-fed meat when I can, and I eat pastured eggs most days, and I eat a couple servings of small-oily fish every week. I take an omega-3 supplement most days, but I’ll skip that on the days when I eat fatty fish. Plus, I eat a lot of ALA-containing vegetables.
The other thing I do, of course, is limit my omega-6 consumption by avoiding refined seed and vegetable oils. I’m not overly concerned with omega-6s found in nuts, which I don’t eat in huge quantities anyway, or other whole foods.
For folks who are already eating a lot of omega-3-rich foods, further supplementation may not offer a ton of benefit.If you’re on a high-fat ketogenic diet and running on a fat-based metabolism, you need access to fat. Some of it comes from your own body, but not all. A good portion of your body’s fuel will come from dietary fat, or the fat you eat. Especially if you are eating more fat than you’re accustomed to, you need to be able to absorb and then digest the fat you eat and turn it into useable energy. If you aren’t digesting fats, you may be in for some discomfort.
What are the signs and symptoms of poor fat digestion?
Signs You Aren’t Digesting Fats: What Does Fat Malabsorption Look Like?
Running a fat-based metabolism just doesn’t work if you can’t digest fats. Here’s what it looks and feels like:
Abdominal Pain and Discomfort After Fat-rich Meals
What happens to fat—or anything, really—that goes down the “wrong pipe”? When you consume fat but aren’t able to effectively digest it, that fat has to go somewhere. That fat goes where it isn’t supposed to be, and sometimes that causes pain and pressure.
Some misbegotten fat loss plans involve the active inhibition of fat digestion, either by consuming artificial fat-like substances that feel and taste like fat without providing any calories or taking lipase inhibitors which deactivate the intestinal enzymes that digest and absorb dietary fat. In both cases, the fat or “fat” is excreted when you go to the bathroom. Yeah. That’s not a good look, but it is a sure sign that you aren’t digesting fats.
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Fat is buoyant. If your poop is festooned with the fat you ate but didn’t digest, it will float more readily.
Passive leakage into your underwear is another common sign you aren’t digesting your fat. One of the most infamous processed “food” disasters was a line of “WOW” branded snacks that contained an indigestible fat substitute, which caused people to leak stool without warning. Same mechanism.
Apologies for the visual, but there’s no easy way to say it. People with poor fat digestion will often produce tangible, lasting results when they fart.
Unexpected Weight Loss
Not absorbing or digesting dietary fat will reduce your calorie absorption, and it may very well cause weight loss. But if you don’t have weight to lose, or if the weight loss comes with unwanted side effects (one study found that Orlistat users indeed lost weight, but they also lost more lean mass), you may want to pay attention.
Low Energy Levels
Trying to run on fat without actually being able to access dietary fat is a miserable exercise in futility. The boundless energy, the steady even keel, the ability to go for hours without eating or crashing—all the promises of fat-adaptation will elude you if you can’t digest the fat you eat.
Orlistat users are at an increased risk of oxalate-induced kidney damage.https://www.ncbi.nlm.nih.gov/pubmed/10757623‘>2
But it’s a real issue. You absorb fat-soluble vitamins alongside the dietary fat you eat. If you’re not absorbing the fat, you’re missing out on the nutrients. All those studies which find that eating fat-soluble vitamins like vitamin E and vitamin K2 alongside dietary fat improves nutrient bioavailability assumes that you’re able to digest the fat. If you can’t digest the fat very well, you’re missing out on the rest of the stuff you eat.
Not all of these are individual markers of poor fat digestion. It’s normal to have some floaty stool now and again. You aren’t always going to digest every bit of fat you consume. Everyone can name a time they felt bloated and had a stomach ache after eating. There are many other reasons why you could be losing weight without trying. But if they are co-incident, you might be dealing with poor fat digestion.
And you should probably do something about it.
How to Improve Your Fat Digestion
Okay, so any, some, or all of those symptoms are signs of poor fat absorption and digestion. It’s always a good idea to rule out larger health problems with your doctor. Until then, what can you do about it?
Chew your Food Thoroughly
Most fat digestion occurs in the GI tract, but it starts in the mouth with something called lingual lipase, the oral form of the major fat-digesting enzyme. To produce lingual lipase, however, you have to chew. The simple presence of fat in the mouth isn’t enough—you have to get those teeth and that tongue going. In one study, eating almonds and coconut triggered the release of lingual lipase, while eating almond butter (the same amount of fat) did not.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4446506/’>4 It doesn’t have to be some arcane bitter herb mix; even an espresso after a meal—that classic Italian custom—can improve fat digestion by increasing gastric acid production.https://www.ncbi.nlm.nih.gov/pubmed/31468384‘>6 Luckily, it’s an easy fix. Take a taurine supplement or eat more meat, especially hearts. Chicken, beef, lamb, turkey hearts are all great sources of taurine.
There you have it, folks. 9 signs and symptoms of poor fat digestion and 9 potential solutions to address the issue.
Do you have any problems digesting fat? Have you tried any of these recommendations? Do you have any recommendations of your own that weren’t listed here?
The post 9 Signs You Aren’t Digesting Fats and What To Do About It appeared first on Mark’s Daily Apple.
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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.
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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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