I’m continuing my crusade of keto mythbusting. Recently, there was keto crotch, then keto bloat, and today I’m returning to one of the O.G. myths—keto body odor. Yes, it seems detractors of the keto diet are hell-bent on making you think your body will become a stinky, bloated mess if you dare to drop your carbs below 50 grams per day…but is it true?

Here’s the spoiler: Yes, people in online keto diet forums occasionally complain about an unpleasant change in body odor when they first go keto. There is no scientific evidence that it actually happens, nor a clear, compelling explanation for why it would. Moreover, the anecdotal (and it’s all anecdotal) evidence suggests that if it does occur, it is rare and temporary. In other words, the whole idea of keto body odor seems to be exaggerated—shocking, I know.  

That said, significant dietary changes can result in other physiological changes that may manifest in a variety of ways. Since nobody wants to be the stinky kid, let’s take this opportunity to look at what might be plausible about keto body odor and what to do if you think you’ve been afflicted.  

What Causes Body Odor?

First, let’s clarify what’s meant by “body odor.” In the medical literature, the term is used in reference to aromas associated with breath, urine, feces, vaginal secretions, sweat (usually from the axilla, or armpits), and general bodily essence as it were. Because it’s such a broad term, the causes are also extremely varied. For the purposes of this post, I’m going to use the term “body odor” to mean aromas from sweat and general bodily funk, since that’s what’s usually meant by keto body odor.

Body odor arises when odorless compounds leave the body through glands in the skin and interact with microbes living on the skin’s surface. The microbes then release chemical compounds—what we actually detect as body odor. Typically, commercial deodorants target both pieces of the equation by using antiperspirants to minimize the excretion of the odor precursors and by creating an unfavorable environment for the microbes living on the skin. There is also a genetic component to how much individuals secrete compounds that cause body odor.

Although a huge industry is built around trying to help people mask their natural odors—and suggesting that body odor is always the result of poor hygiene—bodily scents are actually quite important. Just as other animals do, humans use olfactory cues for recognizing kin, making judgments about others’ personality traits and attractiveness, and even for detecting fertility. Although we rarely recognize it, the data suggests that smell probably factors into all our face-to-face social interactions.

Body odor can also result from illness. Before the use of sophisticated modern disease detection techniques, doctors were taught to use their sniffers as a diagnostic tool. Even today, smell can be an important clue that an individual is unwell. Often these odors emanate from the breath or urine, but certain infectious and metabolic diseases can be associated with distinctive body odors. In addition to perceptible body odor, the human olfactory system can detect infection and sense illness in others, presumably an important means of preventing the spread of communicable disease.

Diet and Body Odor

The whole notion that a keto diet can cause body odor rests on the assumption that how we smell is affected by what we eat. It turns out that there is scant evidence that that is actually the case.

When I’ve taken up the question of keto diet and body odor previously, I noted that there are really only two human studies that speak to this. One small study found that women judged men’s body odor more negatively when they ate a diet that contained red meat compared to when they abstained from red meat. However, the diets differed in other ways as well. In contrast, a different study found that women rated men’s body odor more positively when the men reported eating more fat, meat, and eggs, and more negatively when they ate more carbs. Hmm.  

Besides those two small studies, evidence that diet impacts body odor seems to come primarily from studies on guinea pig urine and meadow voles—not exactly the most compelling in my opinion.

Nevertheless, the common belief persists that certain foods will make you stinky: garlic, onions, cruciferous vegetables, and spicy foods especially. However, there is no evidence that this is actually the case beyond the obvious bad breath and, ahem, flatus that these foods can cause. In fact, the one study I found on the subject reported that garlic counterintuitively improved body odor.

So, Can Keto Make You Stinky?

As you can see, there’s minimal evidence at best linking body odor to diet, and none of it has to do with the keto diet itself. Nevertheless, the belief that keto causes body odor persists…thanks to the few complaints from some in the keto community (and, just maybe, those who have nothing to do with keto but want to cause a stir). While I don’t want to dismiss anecdotal evidence out of hand, I have noticed that once people go keto, their diet is immediately to blame for every weird smell, twitch, or symptom. It’s remarkable really.

In the interest of fairness, let’s look at the explanations that are typically offered for why keto might cause body odor:

Is It the Protein?

The first hypothesis is that keto dieters smell funky because they’re eating a lot more meat. As I already mentioned, there are only two small studies that speak to this, and the findings conflict. The idea at work: protein metabolism yields ammonia as a byproduct (true), which builds up because of eating “too much protein,” resulting in body odor.  

To which I object… First of all, it’s not necessarily true that going keto means eating more meat. My version of a keto diet certainly isn’t a steak-and-bacon fest—I still eat tons of veggies. If anything, my observation is that keto folks by and large remain fearful of eating “too much” protein lest it kick them out of ketosis. (The issue is not nearly so simple as that, as I’ve explained.) In any case, even if you’re eating a good deal of meat, a healthy liver should be able to convert the amount of ammonia generated into urea and send it off to the kidneys to be excreted as urine.

Maybe It’s the “Detoxing”?

Toxins such as environmental pollutants accumulate in adipose tissue, a.k.a. fat cells, and these toxins are then released into the bloodstream when people burn fat. Because the keto diet often results in increased burning of body fat, the theory goes that the body is “detoxing” all these pollutants, and that’s what causes body odor. Detoxing is a controversial subject, and while it is true that some of these toxins can be excreted through the skin, the actual amounts are fairly small (the majority get excreted via urine and feces). Plus, it’s not evident that the toxins that are excreted through the skin cause any particular odor. And wouldn’t any diet that actually does what it’s supposed to—i.e. burn fat—be subject to the same “stinky” detox effect? I think we can safely chuck this claim.

Are Ketones a Cause?

Maybe ketones themselves make you smelly? This one has the most potential validity, as it’s well documented that acetone—one of the three ketone bodies—gets excreted when you’re in ketosis. However, it’s the cause of the familiar keto breath, not body odor per se. I’ve seen no evidence linking acetone to actual body odor.

What To Do About It

Ok, I hear you saying, “Mark, I see that you’re skeptical, but I’m telling you… I stink!” What can you do about it?

Well, since there isn’t a clearcut cause, I can’t give a clearcut answer, but I’ll tell you what the general wisdom says:

First, you can support your body’s own detoxification pathways as I describe here. Your body should be able to do a fine job taking out the garbage—it’s designed to do so and is efficient at it—but hey, why not drink some coffee and throw some broccoli sprouts on your salad. This is a “can’t hurt, might help” situation.

Same thing goes for taking some nice epsom salt baths, another common recommendation. Whether there is any truth to their detoxifying nature, you’ll get a nice dose of transdermal magnesium with a hefty side of relaxation. Throw in some essential oils and olive oil and soak your cares away… hopefully taking some of the b.o. with it.

You can also experiment with eating less protein and more carbs, but I do see potential downsides to both. You definitely don’t want to eat too little protein, since it serves such a vital role in healthy functioning, and you don’t want to add back too many carbs if being in ketosis is your goal. That said, especially with regard to the protein you probably have room to play around, so feel free to experiment if you want. I’m not overly optimistic that this is the answer, but I’m always a fan of finding what works for you.  

Or, take a wait and see approach. Most keto side effects come and go as people become keto-adapted. If your problem is keto breath, not body odor per se, you can try chewing on some fresh herbs or taking chlorophyll supplements, but these will just mask the issue.

Lastly, if it is very noticeable and very bothersome, you can—and probably should—consult your doctor. If you are excreting significant ammonia, which usually happens via the breath, this is a sign of liver or kidney problems that need to be diagnosed asap.

The Bottom Line…

Because switching to a keto diet can initiate a profound metabolic shift, some people might experience side effects. And, sure, it’s conceivable that transient changes to body odor might be one of them. The lack of evidence that body odor is strongly affected by diet (as well as my own experience interacting with the thousands of people in my community who have tried keto) leads me to believe that this is a minor problem at most—and one that most people won’t experience at all. If it’s affecting you, feel free to try to solutions I described above. They might not resolve the problem immediately, but at least they’ll likely have other positive benefits.

Ok, what say you? Are your friends giving you a wide berth now that you’re in ketosis, or are you chalking this up to yet another thing the haters are blowing out of proportion?

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References:

Groyecka A, Pisanski K, Sorokowska A, et al. Attractiveness Is Multimodal: Beauty Is Also in the Nose and Ear of the Beholder. Front Psychol. 2017;8:778.

James AG, Austin CJ, Cox DS, Taylor D, Calvert R. Microbiological and biochemical origins of human axillary odour. FEMS Microbiol Ecol. 2013 Mar;83(3):527-40.

Natsch, A. What Makes Us Smell: The Biochemistry of Body Odour and the Design of New Deodorant Ingredients. CHIMIA Intl J Chem. 2015 Aug;69(7-8):414-420.

The post The Real Deal On Keto Body Odor appeared first on Mark’s Daily Apple.

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Move over, keto crotch. There’s a new fear-mongering anti-keto media blitz forming: keto bloat.

According to the “good scientists” of the Kellogg company food lab, an unprecedented number of young people are walking around with bloated guts and colons packed to the brim with impacted fecal matter, and it’s all because they’ve embraced ketogenic diets and “forsaken” fiber.

If this sounds like nonsense, that’s because it is.

Are millions of keto dieters suffering from bloating and constipation? I can find no evidence of this.

Is fiber necessary to prevent bloating and constipation? It’s complicated. I’ll explain later. But probably not.

Does the ketogenic diet necessarily exclude fiber? Not at all.

Are ketogenic diets as commonly practiced low in fiber? No.

What Is “Bloat” Anyway?

There are two things that people refer to as bloat: constipation and abdominal distension.

Constipation has different components. It’s being unable to make a satisfying bowel movement. It’s also feeling like you have to poop but are unable to. It’s being able to poop only a little bit. It’s struggling on the toilet bowl. Mostly, it’s being unhappy with your performance on the toilet.

Abdominal distension also can be different things. It might be trapped gas. It might be feeling “heavy” or “full.” It might mean your pants don’t fit after eating.

So, “bloating” can be any or all of these. You can pass hard small stools and feel like you’re bloated. You can poop just fine but have a lot of gas and feel like you’re bloated. You can spend hours on the toilet with not much to show for your effort and be bloated. So “Keto bloat” is difficult to pin down. That makes it easy to make claims and hard to disprove.

Let’s see how frequent bloating and constipation occurs in the ketogenic diet literature.

What Does Research Say About Constipation?

In a study of children with epilepsy placed on an olive oil-based ketogenic diet, about 25% of the subjects experienced constipation. So, was ketosis slowing them down? Not exactly. Those who experienced constipation were actually less likely to be in ketosis. Constipation went up as ketone readings went down, and epilepsy symptoms returned. Constipation improved as ketone readings went up and epilepsy symptoms subsided.

In adults with epilepsy on a ketogenic diet, constipation occurred in just 9% of patients. The authors note that this rate is lower than some other ketogenic studies and attribute the difference to “the heavy focus on importance of fiber from nutrient dense (fiber rich) vegetables, nuts, and seeds.” Note that they weren’t getting fiber from pills and powders. They were eating nutrient-dense foods that just so happened to contain fiber.

Another ten-year study compared the classical ketogenic diet, MCT oil-based ketogenic diet, and modified Atkins keto diet. They were all equally effective at reducing epilepsy symptoms in children, but the occurrence of constipation varied greatly. It was most common in the classic keto diet and medium chain triglyceride-based diet, both of which restrict protein. In the modified Atkins diet, which does not restrict protein, constipation was much rarer. Another study on the modified Atkins diet had similar results, with just 2 of 26 subjects reporting constipation.

Constipation does seem to be a common occurrence. However, the majority of keto diet studies are in epileptic populations following very strict clinical Keto diets. The extreme nature of these therapeutic ketogenic diets—extreme protein (7% of calories) and carbohydrate restriction—makes them an imperfect representation of how most people are eating Keto. And in studies of less-extreme, more realistic versions of the diet, such as modified Atkins (which allows more protein) or the version with “heavy focus” on vegetables, nuts, and seeds, constipation occurs at a much lower rate.

What Does Research Say About Bloating?

The only instance of something approximating bloating in the ketogenic diet literature occurred in studies using medium chain triglyceride-based diets. These are ones that use huge amounts of MCT oil to increase production of ketone bodies. It works great for curbing epilepsy symptoms, but it can also cause cramping, diarrhea, and abdominal pain. That’s not bloating per se. It’s literally the closest I could find.

Causes Of Bloating While Keto?

Okay, say you are dealing with constipation or bloating on a keto diet. What could be going on?

Not Enough Food

Constipation is often a consequence of low energy status. Everything that happens in the body requires energy, and if energy levels are low or energy availability is poor, basic functions will suffer. Bowel movements are no exception. The muscles and other tissues responsible for moving things along your digestive tract use energy. If you aren’t providing adequate amounts of energy, you’re depriving your tissues of the ATP they need to work best and sending your body a signal of scarcity which will only depress energy expenditure even more.

Low carb diets in general and keto diets in particular are very good at causing inadvertent calorie reduction. Great for fat loss, but some people take it overboard and go too far. I’m talking 800-1000 calories a day on top of CrossFit. That’s a recipe for disaster.

Water and Mineral Loss

When you go Keto for the first time, you shed tons of water. For every gram of glycogen you lose, you drop 3-4 grams of water. You also lose sodium and potassium with the water, and you need extra magnesium to regulate your sodium and potassium levels.

The water content of stool is what gives it that smooth texture we all desire. If you’re dehydrated, even mildly, you’ll have less water available for your bowel movements and be more likely to suffer from constipation.

Drink a big glass of salty water with lemon juice in the morning and sip on salty broth throughout the day. Zucchini is a great source of potassium, as is avocado.

Also, if you’re going to eat more fiber, you need to increase water intake for it to work.

Too Much or Too Little Fiber

The relationship between fiber and constipation is mixed. Some interventions do seem to help. Psyllium husk and flaxseed have both been shown to improve constipation. Galactooligosaccharides, a class of prebiotic fiber, improve idiopathic constipation. And inulin, another prebiotic fiber, improves bowel function and stool consistency in patients with constipation.

But there’s also evidence that more fiber can make the problem worse. In one 2012 study, patients with idiopathic constipation—constipation without apparent physiological or physical causes—had to remove fiber entirely to get pooping again. Those who kept eating a bit or a lot of it continued to have trouble evacuating. The more fiber they ate, the worse their constipation (and bloating) remained. Another review found mixed evidence; some people get less bloating and constipation with more fiber, others get less bloating and constipation with less fiber.

Personally, my toilet performance is stellar with or without a constant intake of voluminous levels of plant matter. Most days I eat a good amount—Big Ass Salads, broccoli, sautéed greens, berries—but on the days I don’t, I don’t notice any difference. I’m suspicious of the widespread calls for bowel-rending levels of fiber as the universal panacea for all things toilet, and I’m also suspicious of the people who claim fiber is unnecessary or even harmful.

Fiber helps some people and hampers others. There’s no one-size-fits-all with fiber, especially since there are many different types of fiber.

Too Many Sugar Substitutes

I get it. There are some interesting candies out there that cater to the Keto set and use various sugar alcohols—non-alcoholic, low-or-no calorie versions of sugar—artificial sweeteners, and fibers to recreate popular treats. It’s fun to eat an entire chocolate bar that tastes pretty close to the real thing and get just a few net carbs. But that’s a lot of fermentable substrate your gut bugs are more than happy to turn to gas.

If you want the opposite problem, you can always turn to Haribo sugar-free gummy bears.

FODMAP Intolerance

FODMAPs stands for fermentable oligosaccharides, disaccharides, monosaccharides, and polyols—the carbohydrates in plants that our gut bacteria usually mop up. Most people have gut biomes that can handle FODMAPs; indeed, most people derive beneficial short chain fatty acids from their fermentation. But some people’s gut biomes produce too much fermentation when they encounter FODMAPs. Fermentation begets hydrogen gas, which gathers in the gut and causes great distress. Common complaints of the FODMAP intolerant are bloating, stomach pain, and visits to the toilet that are either unproductive or way too productive—all of which fall into the bloating category.

The myth is that Keto people are eating salami and cream cheese for every meal. The reality is that many people go Primal or Keto and find they’re eating way more vegetables than they ever have before. These are great developments, usually, but if you’re intolerant of FODMAP fibers, you may worsen the bloating.

What Can You Do?

Eat enough protein. Most people can get away with eating 15-25% of their calories from protein and still stay in ketosis. Most people can eat even more protein and still get most of the benefits of fat-adaptation. The keto studies which had the lowest rates of constipation were far more tolerant of higher protein intakes.

Eat FODMAPs unless you’re intolerant. Most people can eat FODMAPs. In most people, FODMAPs improve gut health and reduce constipation and bloating. But if your gut blows up after a few bites of broccoli or asparagus, consult the FODMAPs list and try a quick FODMAP elimination diet.

Make sure you’re truly constipated. Your stool volume and frequency of toilet visits will decline on a normal ketogenic diet because there’s less “waste.” Make sure you’re not misinterpreting that as constipation or bloating. If there’s less poop, there’s less poop. If there’s more poop but it’s just not coming, and you have to go but can’t, that’s when you have an issue.

Experiment with fiber. Fiber clearly has a relationship to bloating and constipation. You just have to figure out what that looks like in your diet.

  • If you’re bloated and constipated on a high-plant Keto Diet, eat fewer plants.
  • If you’re bloated and constipated on a low-plant Keto Diet, try eating more plants. If that doesn’t help, go zero-plant.
  • If you’re bloated and constipated on a zero-plant Keto Diet, try eating more plants. .

We all have to find our sweet spot.

So, to sum up, “keto bloat” is mostly a myth. There’s a glimmer of truth there, but it’s highly exaggerated. Constipation is common on the most restrictive clinical keto diets, while eating fiber from whole plant foods, being less restrictive with protein, and making sure you’re drinking enough water and eating enough calories and electrolytes seems to avoid the worst of it.

What’s been your experience with bloating and constipation? How have you handled it?

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References:

Ho KS, Tan CY, Mohd daud MA, Seow-choen F. Stopping or reducing dietary fiber intake reduces constipation and its associated symptoms. World J Gastroenterol. 2012;18(33):4593-6.

Müller-lissner SA, Kamm MA, Scarpignato C, Wald A. Myths and misconceptions about chronic constipation. Am J Gastroenterol. 2005;100(1):232-42.

Guzel O, Uysal U, Arslan N. Efficacy and tolerability of olive oil-based ketogenic diet in children with drug-resistant epilepsy: A single center experience from Turkey. Eur J Paediatr Neurol. 2019;23(1):143-151.

Roehl K, Falco-walter J, Ouyang B, Balabanov A. Modified ketogenic diets in adults with refractory epilepsy: Efficacious improvements in seizure frequency, seizure severity, and quality of life. Epilepsy Behav. 2019;

Liu YM. Medium-chain triglyceride (MCT) ketogenic therapy. Epilepsia. 2008;49 Suppl 8:33-6.

Arnaud MJ. Mild dehydration: a risk factor of constipation?. Eur J Clin Nutr. 2003;57 Suppl 2:S88-95.

Noureddin S, Mohsen J, Payman A. Effects of psyllium vs. placebo on constipation, weight, glycemia, and lipids: A randomized trial in patients with type 2 diabetes and chronic constipation. Complement Ther Med. 2018;40:1-7.

The post Keto Bloat: Separating Fact from Fiction appeared first on Mark’s Daily Apple.

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Because people don’t have enough diets to choose from already, there’s a new one on the scene: the Pegan diet. Actually it’s not that new—Dr. Mark Hyman started writing about it back in 2014, but it’s gained traction since he published his latest book last year, Food: What the Heck Should I Eat?

According to Hyman, Pegan is a somewhat tongue-in-cheek play on the fact that it’s not quite Paleo and it’s not really vegan, hence Pegan. It claims to combine the best of both diets, namely a focus on eating lots of vegetables, as well as an emphasis on sustainable agriculture and ethical and ecologically sound animal farming.

Setting aside the obvious issue that it’s 100% possible to be a vegan who eats few to no vegetables, or to be a paleo dieter who cares naught about the environment, Pegan is touted as being easier to stick to than either vegan or paleo (presumably because Pegan allows for consumption of foods not allowed on either). Frankly, trying to frame it as a bridge between the two hasn’t proved to be a seamless, happy compromise based on social media conversation, but that’s probably of little surprise to anyone here.

I’ve had some readers ask me about the merits of Pegan and whether it offers any particular advantages over paleo/Primal, and I’m taking up that question today. (Note that I’m only focusing on the Pegan diet proposed by Dr. Hyman, not the “Pegan 365” diet offered by Dr. Oz. The latter isn’t paleo at all, allowing whole grain bread and pasta, corn, tofu, and a weekly “cheat day.” You can imagine my response to this version.)

Defining the Pegan Diet

These are the basic tenets of the Pegan diet in a nutshell:

Focus on sourcing high-quality food – Prioritize organically grown and pesticide-free produce as well as meat, eggs, and fats from pasture-raised and grass-fed animals and finally sustainably harvested seafood. Choose seafood with the lowest possible mercury content. Buy local when you can. Avoid CAFO meats and foods containing chemical additives.

Eliminate processed modern food-like substances and franken-fats – Processed carbohydrates have a high glycemic load and lead to excessive insulin production. Refined vegetable and seed oils such as canola and sunflower are pro-inflammatory. Avoid all such products.

Go gluten-free – Even if you don’t have celiac disease or an obvious gluten sensitivity, modern wheat is still a frankenfood, and gluten can damage the gut. Occasional consumption of heirloom wheat (e.g., einkorn) is ok if you tolerate it.

Go dairy-free – Dairy is problematic for most people and is best avoided. If you do decide to include some dairy, consider choosing goat and sheep milk products instead of cow. Grass-fed butter and ghee are acceptable.

Make vegetables the centerpiece of your diet – Vegetables (mostly non-starchy) should comprise 75% of your diet.

Enjoy healthy fats – Focus on omega-3s, as from small, oily fish. Eat plenty of healthy fats from grass-fed and pastured meats and whole eggs, nuts and seeds, avocados, and coconut products. Use olive oil, avocado oil, and coconut oil for cooking.

Eat meat sparingly – Dr. Hyman uses the term “condi-meat” to emphasize that meat should be a side dish, not the focus of the meal. He recommends no more than 4 – 6 ounces of meat per meal.

Include gluten-free grains and legumes in small quantities – You may eat ½ cup of gluten-free grains like amaranth or quinoa, plus ½ – 1 cup of legumes (preferably lentils) per day. If you are insulin resistant, you should limit these or refrain altogether.

Limit sugar – Avoid refined sugar and conventional “treats.” The bulk of your vegetable intake should be from non-starchy varieties, and opt for low-glycemic fruit. Natural sweeteners like honey should be used only sparingly for the occasional treat.

How Does Pegan Compare to Primal?

If you’re reading this and thinking, “Gee, Mark, this sounds an awful lot like the Primal diet,” I agree. While there are some differences between Pegan and Primal, they aren’t particularly dramatic:

Primal allows full-fat dairy consumption. Pegan discourages but doesn’t outright ban dairy.

I don’t actively encourage people to consume gluten-free grains and legumes, but I’m not as strongly opposed to them as others are in the ancestral community. I’ve said before that I consider quinoa, amaranth, wild rice, and legumes to be moderation foods (when well-tolerated, which is more an individual thing). They deliver pretty substantial carb hits relative to their nutritional value, but they certainly aren’t the worst options out there. I don’t think they should be dietary staples by any stretch—and daily consumption is too much in my opinion—but if Primal folks want to eat them occasionally, I’ve seen it work for people.

The biggest difference is in regard to protein. The Pegan diet explicitly limits protein consumption, while the Primal Blueprint recommends moderate protein consumption tailored to your activity levels, goals, age, and medical needs. On the surface, this might seem like a substantial difference, it’s probably not very disparate in practice. If a Pegan eats 3 eggs for breakfast, a large salad with 4 ounces of sardines at lunch, and 4 ounces of skin-on chicken thigh at dinner, that gets him or her to about 70 grams of protein, not counting the (admittedly incomplete) plant protein from the salad and any additional veggies included with breakfast and dinner, plus nuts and seeds. That’s within the realm of Primal guidelines, albeit less than I’d recommend for some populations.

That said, if Pegans are taking the whole “treat meat as a condiment” mantra to heart, they are probably at greater risk of underconsuming protein compared to the average Primal eater. This could present a problem for athletes and older folks looking to preserve lean mass. Likewise it is surely harder to get enough protein while also practicing time-restricted eating—and perhaps only eat one or two meals per day—and trying to follow Pegan guidelines. That isn’t a knock against Pegan per se, just a cautionary note.

Finally, while we’re on the subject of protein, I must object to Dr. Hyman’s appeal to environmentalism as a reason to limit meat consumption. I’m not at all convinced that raising livestock taxes the environment more than monocropping acres and acres of corn and soybeans.

In my opinion, Pegan could simply be called “vegetable-centric Paleo with permission to eat small amounts of quinoa and lentils if it suits you.” That isn’t catchy, though, so Pegan it is.

That said, I appreciate how Dr. Hyman for his version of the Pegan Diet emphasizes that there is no single diet that is exactly right for each individual and, like me, he advocates for self-experimentation. Dr. Hyman also speaks out against diet dogmatism and encourages his followers to focus on big-picture health. These are obviously messages I can get behind.

The Bottom Line

I’m a fan of anything that gets people thinking about food quality instead of just robotically tracking macronutrient intake and/or plugging calories into a magic weight-loss formula. Supporting sustainable agricultural practices, eating locally and seasonally, and avoiding environmental pollutants have always been part of the Primal Blueprint recommendations. In short, there is a lot I like about the Pegan diet.

However, I don’t agree that the Pegan diet is necessarily easier to implement than vegan or Paleo, which is supposed to be one of its big draws. If you’re a vegan who gets by on bagels, pasta, and Oreos, or a Paleo person who dutifully eschew grains but relies on the myriad processed, packaged Paleo food options, Pegan is not going to be easier. Changing your diet to focus on carefully sourced “real food” is still going to be a massive shift. It’s going to be much more expensive and time consuming to prepare your meals, and it will probably be incredibly burdensome at the beginning.

Sure, being able to include a small serving of gluten-free grains and legumes might make life a little easier for Paleo folks… but how much really? (For this reason I’d be skeptical if you’re considering using the Pegan diet to lose weight.) Are a lot of Paleo folks really falling off the wagon because they are feeling deprived of ½ cup of lentils? Dr. Hyman has said that his issue with Paleo is “some use the paleo philosophy as an excuse to eat too much meat and too few plant-based foods.” I’m not really seeing this pervasively in the Paleo/ancestral community, to be honest (intentional carnivore dieters notwithstanding). This strikes me as an attempt to solve a problem that didn’t need solving.

Truthfully, the things I like about Pegan are all the ways in which it is similar to Primal, which are many. Both Primal and Pegan have vegetables as the base of their food pyramids. They similarly emphasize the importance of choosing healthy fats and oils, avoiding grains and processed modern junk foods, and moderating carbohydrate intake (which Dr. Hyman frames as maintaining low glycemic load, but the effect is the same). Still, for many people the tighter Primal guidelines around carbs are probably better suited for weight loss and even weight maintenance.

Most days, if you were a fly on the wall in my kitchen, you’d see me eat a big-ass salad for lunch and a piece of meat with several types of vegetables on the side for dinner, and you wouldn’t be able to discern if I was Primal or Pegan. Then again, those nights when I tear into a giant steak would you most certainly be able to tell… and, trust me, I’m not giving those up any time soon.

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I have a confession to make: I, Mark Sisson, suffer from keto crotch.

It’s embarrassing, really. I thought maybe it was just the change in climate moving from Malibu to Miami—the humidity, the heat, the fact that I’m paddling and swimming more often now. There’s a whole lot of moisture down there. Perpetual steaminess.

But then I met up with my writing partner and good pal Brad Kearns, who’s been working with me on my upcoming book. Brad lives in Northern California, which is far from hot or humid right now. He’s also a staunch keto guy most of the time, and, well, let’s just say I could smell him before I could see him. We met up at a coffee shop and cleared out everyone in a fifteen foot radius. We sampled a new exogenous ketone product he’s been trying and not one, not two, but three separate individuals approached to inquire if we were salmon fishermen.

Okay, let’s get serious. Does “keto crotch” really exist? And, if it does, what can you do to prevent it?

I’m writing this not because of overwhelming demand from loyal followers of the Keto Reset plan. In fact, I hadn’t ever heard of “keto crotch” before last week. There’s a good chance almost no one heard of it before March 2019, if Google Trend data for “keto crotch” searches is any indication. I’m writing this post because the barrage of news articles, Twitter hashtag campaigns, and extremely serious warnings from people with lots of acronyms after their name has led people to ask me if it’s a legitimate phenomenon. A few acquaintances have brought it up in social situations. Our marketing director found herself fielding keto crotch questions at a dinner for Expo West last week.

So, are women following a ketogenic diet experiencing an epidemic of stinky vaginas?

Probably not.

Is Keto Crotch Even Physiologically Plausible?

Vaginal odor does change. It fluctuates naturally, and sometimes it can get worse. The most common cause of unpleasant changes to vaginal odor is bacterial vaginosis, which occurs when something upsets the balance between the beneficial lactobacilli bacteria that normally live in the vagina and pathogenic bacteria. What can upset the balance?

The vagina is supposed to be an acidic environment; that’s how the healthy lactobacilli thrive. If something upsets that pH balance, tilting it toward alkalinity, unhealthy bacteria gain a foothold and become predominant, and begin producing unpleasant-smelling amines like putrescine, tyramine, and cadaverine. This is bacterial vaginosis. As it turns out, the lactobacilli bacteria normally present in the vagina are instrumental in maintaining an acidic pH. They consume glycogen, spit out lactic acid, and exert antimicrobial and antifungal effects that block common vaginal pathogens like candida, e. coli, and gardnerella from taking hold and causing trouble.

The interaction between diet and vaginal biome is understudied. To my knowledge, there exist no direct controlled trials that address the issue. It’d be great to have a study take a cohort of women, split them up into different dietary groups, and follow them for a year,  tracking their vaginal pH and bacterial levels. Alas, we do not.

We do have a study that provides a hint. In 2011, researchers looked for correlations between dietary patterns and bacterial vaginosis in a cohort of nearly 2000 non-pregnant mostly African-American women aged 15-44. While there probably weren’t many keto dieters, and the diets as a whole were of the standard American variety, glycemic load—which basically boils down to carb load—was the strongest predictor of bacterial vaginosis. Other markers of food quality, like a person’s adherence to “healthy eating guidelines,” initially seemed to reduce the chance of bacterial vaginosis, but those relationships were almost abolished after controlling for other factors. Only glycemic load remained highly significant.

This connection between dietary glycemic load and bacterial vaginosis starts looking more causal when you realize that diabetes—a disease where one’s “glycemic load” is perpetually elevated and exaggerated—is another risk factor for bacterial vaginosis.

There’s also a 2007 study that found “high” intakes of dietary fat, particularly saturated and monounsaturated fat, were a significant predictor of bacterial vaginosis. In this study, “high fat” meant around 39% of energy from fat. That leaves 61% of energy from carbohydrate and protein, the kind of “high-fat, high-carb” Standard American No-Man’s-Land that’s landed the country in the current metabolic predicament. High-fat intakes in the presence of high-carb intakes may very well be bad for your vagina, but it says nothing about the likelihood of keto crotch.

At any rate, neither study was a controlled trial, so we can’t say anything about causality.

What about a yeast infection? The most common offender is candida, which usually favors sugar for fuel, but there’s also evidence that it can metabolize ketones. Could keto make a latent yeast infection worse and lead to smelly “keto crotch”?

Perhaps keto can make candida worse (that’s for another day), but that’s not the cause of “keto crotch.” Candida vagina infections don’t smell very much, if at all, and they certainly don’t smell “fishy.” That’s only caused by bacteria and the aforementioned amines they can produce.

Free glycogen levels in vaginal fluid are a strong predictor of bacterial vaginosis. If ample glycogen is available, the good lactic acid bacteria have plenty of food and produce plenty of lactic acid to maintain the acidic pH conducive to vaginal health. If inadequate glycogen is present, the lactic acid bacteria have less food and produce less lactic acid, increasing the chances of the pH tilting toward alkalinity. An alkaline vagina is a vagina where pathogenic bacteria—the ones that produce stinky amines—can establish themselves.

The question then is if ketogenic diets lower free glycogen in the vaginal fluid. That’s a fair question. I wasn’t able to find any solid answers. I guess “ketosis effect on vaginal glycogen” isn’t the most lucrative avenue of scientific inquiry.

Should I Worry?

Even assuming this is a real phenomenon, it’s a rare one. The vast, vast majority of people following a ketogenic diet aren’t coming down with keto crotch. Other than a few Reddit posts from the past 5 years, I haven’t seen anyone at all in our neck of the woods complain.

Maybe people doing Primal keto are eating more nutrient-dense ketogenic diets than people doing conventional (or caricature) keto. Salads, steaks, eggs, and lots of non-starchy veggies are a great way to stay keto and obtain micronutrients. And there are links between micronutrient status and bacterial vaginosis. The most common relevant deficiencies include vitamin D (correcting the deficiency can cure the vaginosis) and folate. Hard to get adequate folate if your diet is based on salami and cream cheese.

We also know that the health of your skin biome tracks closely with that of your gut, and that eating plenty of non-starchy veggies, fermented foods (yogurt, kefir, sauerkraut, kimchi, etc), and colorful produce can provide prebiotic fiber, prebiotic polyphenols, and probiotic bacteria that nourish your gut biome. If the vaginal biome is also connected to the gut biome (and it is), tending to the latter should also have positive effects on the former.

The Primal brand of keto tends to emphasize micronutrients and gut health a bit more than some other types of keto I see floating around. If—and it’s a very big “if”—keto crotch is legit, that may explain some of the discrepancy.

Finally, be sure to check out this very interesting Twitter thread where the author lays out his suspicions that the whole “keto crotch” phenomenon might be a manufactured stunt designed to vilify the ascendant ketogenic diet. Nothing definitive, but it’s certainly food for thought.

If You’re Concerned…

Okay. Say you’ve recently gone keto and your vagina is smellier than usual. (And you’ve ruled out other, more obvious potential causes like changes in soaps, etc.) It’s hard to ignore, and I wouldn’t want you to. What can you do?

  • Confirm that you have bacterial vaginosis. Seriously, get it checked out.
  • Make sure you’re getting enough folate and vitamin D. Supplement if need be.
  • Eat prebiotics and probiotics. Fermented food and/or a good probiotic supplement.
  • Try a carb refeed. If ketosis depletes vaginal glycogen and increases pH, the occasional carb refeed could restore glycogen by 30-50 grams and should do the trick. Note that this is entirely theoretical; I’m not saying it’s a “problem” on keto.
  • Hang out in the keto zone. I’ve written about the keto zone—that metabolic state where you’ve reached full keto and fat-adaptation and find yourself shifting in and out of ketosis as you please due to increased metabolic flexibility. A few carbs here, a fasting day there, a few more days of keto. Again, if full keto is theoretically depleting vaginal glycogen, maybe relaxing your restrictions will solve the issue while maintaining your fat adaptation. This is actually where I hang out most of the time.

That’s it for today, folks. Do you have “keto crotch”? Do you know anyone who does? Or did your vaginal health improve on keto? I’m curious to hear what everyone’s experiences have been, so don’t be shy.

Take care and be well.

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References:

Thoma ME, Klebanoff MA, Rovner AJ, et al. Bacterial vaginosis is associated with variation in dietary indices. J Nutr. 2011;141(9):1698-704.

Kalra B, Kalra S. Vulvovaginitis and diabetes. J Pak Med Assoc. 2017;67(1):143-145.

Taheri M, Baheiraei A, Foroushani AR, Nikmanesh B, Modarres M. Treatment of vitamin D deficiency is an effective method in the elimination of asymptomatic bacterial vaginosis: A placebo-controlled randomized clinical trial. Indian J Med Res. 2015;141(6):799-806.

Dunlop AL, Taylor RN, Tangpricha V, Fortunato S, Menon R. Maternal vitamin D, folate, and polyunsaturated fatty acid status and bacterial vaginosis during pregnancy. Infect Dis Obstet Gynecol. 2011;2011:216217.

The post The Curious Phenomenon of “Keto Crotch” appeared first on Mark’s Daily Apple.

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We’ve all heard the story. Maybe we’ve even been the protagonist.

Person goes full keto. They lose a bunch of weight, normalize their pre-diabetic glucose numbers, resolve their high blood pressure readings, have more energy, feel great, and have nothing but high praise for the new way of eating.

Except for one thing, everything seems perfect: their cholesterol is sky-high. It throws a wrench into the whole operation, installs a raincloud over the procession, spoils their confidence.

“Could I be killing myself?”

“Are my health improvements just a mirage?”

In other words, are the apparent benefits of keto merely superficial if your cholesterol skyrockets?

The evidence is pretty clear that for the majority of adults who go keto, their cholesterol numbers improve.

In obese adults with type 2 diabetes, a ketogenic diet improved blood lipids and boosted fat loss compared to a low-calorie diet.

In lean, healthy adults without any weight to lose (and who didn’t lose any weight during the course of the diet), total cholesterol went up from 159 to 208 mg/dL and triglycerides fell from 107 to 79 mg/dL. A lipophobic doc might freak out at the rise in TC, but given that the triglycerides dropped, I bet the change reflects a rise in HDL and an overall positive, at worst-neutral effect.

Another study of lean adults with normal cholesterol numbers found that going keto improved their lipids, reducing triglycerides, increasing HDL, and leaving LDL unchanged. Those with small pattern B LDL particles (the “bad kind”) saw their LDL particle size increase, on average. All told, keto was beneficial.

But you aren’t everyone. You aren’t the average of a population. And, given the number of readers I have and the number of people trying a ketogenic diet, there are bound to be some people whose lipid profiles go in the other direction.

I don’t give medical advice here, and I always encourage people to partner with the physicians for health solutions. That said, let me share some thoughts on the keto-cholesterol question….

I’m not just talking about high total cholesterol or high LDL-C. I’m talking about what appears to be the real, legit risk factor for a cardiac event: elevated LDL particle number. According to experts like Dr. Peter Attia and Dr. Chris Masterjohn, atherosclerosis occurs when LDL particles infiltrate the endothelial lining of our arteries. Thus, it’s not high LDL cholesterol that increases the risk of atherosclerosis—LDL-C is the cholesterol found inside the particles— it’s a high number of LDL particles in circulation. The more LDL-P, the greater the chance of them becoming oxidized and infiltrating the arterial wall. There are many factors to consider, like oxidative stress, inflammation, and fatty acid composition of the LDL particles, but all else being equal, a greater number of LDL particles seems to increase the risk of a heart attack.

What Could Be Causing LDL Elevations On Keto?

Weight Loss

I asked Dr. Cate Shanahan for her input on this topic, and she provided a beautiful explanation:

But when you stop eating so many carbs insulin politely steps aside, and your insulin levels plummet. Now your body fat can more easily and more often release its stores of fatty acids into your bloodstream.
When your body fat releases stored fatty acids, any unused fatty acids quickly get picked up by the liver and packed into VLDL lipoprotein. VLDL is a precursor to LDL. So in reducing your insulin levels and increasing your body’s use of fat, you will raise your VLDL, LDL and total cholesterol. You are simply trafficking in fat more often now. And now, because your body stabilizes fat carrying lipoproteins with cholesterol, there is a need for more cholesterol in your blood. These are not bad consequences. They are in fact happy signs your diet is doing what its supposed to be doing.

If you’re actively losing weight, you will probably experience a rise in cholesterol. This is the transient hypercholesterolemia of major weight loss, and it’s a well-known phenomenon. Once your weight stabilizes, cholesterol should normalize—although to a lesser extent than other diets, given Dr. Cate Shanahan’s explanation of increased “trafficking in fat.”

Low Thyroid Function

The thyroid is a barometer for your energy status. If you have plentiful energy to spare, thyroid function is normal. If your body perceives low energy availability, thyroid function may down-regulate. Since the thyroid plays a big role in regulation of LDL receptor activity, its downregulation can lower LDL receptor sites. Fewer LDL-receptors clear LDL particles from the blood. Folks with genetic predispositions to heart disease often have low LDL receptor activity, causing elevated LDL particles. Folks with genetic variants that increase the activity and expression of LDL receptors have lower heart disease rates. Although genes often have different effects that may affect disease risk via other pathways, that’s pretty strong evidence that LDL receptor activity regulates, at least in part, one’s LDL-P and heart disease risk.

Read this post for maintaining thyroid function on keto, and check out Elle Russ’ Paleo Thyroid Solution for an even deeper, more thorough dive into thyroid health.

Eating Too Damn Much

Some keto people pride themselves on gorging. Some are doing it for a good cause—a quest to find the fabled metabolic advantage. Some are doing it to show off and for keto cred—look how much salami I can eat! Some are using keto to deal with unresolved issues with food itself.

Everything I say about doing keto presupposes that you are eating like a normal person. You’re eating as much as you need to fuel your brain and daily activities, fitness and performance goals. You’re leaving the table satiated, not stuffed. For most people, this happens without even trying. It’s why keto is so effective for weight loss.

Genetic Variance

Genes aren’t destiny, but they do modify and regulate our response to a given environmental input.

Some people are dietary cholesterol hyper responders. Unlike the majority of the population, they absorb tons of dietary cholesterol and do not down-regulate their endogenous production to accommodate. The result is an increase in cholesterol synthesis and absorption, leading to a spike in blood cholesterol.

Some people are sensitive to saturated fat. In response to it, they produce elevated numbers of LDL particles. If your keto diet is high in saturated fat and you have a genetic sensitivity to it, your cholesterol will probably skyrocket.

Some people have genes that reduce the activity of their LDL receptors. This will necessarily boost LDL particle numbers.

This topic—genetic variance and how it affects keto—could be an entirely separate post, so I’ll leave it at that (and probably come back to it in the future).

Too Much Butter

Huh? Too much butter, Sisson? Is such a thing even possible?

Maybe. Subjecting cream to the butter-making process strips it of something called milk fat globule membrane (MFGM). And when you compare equal amounts of dairy fat through either cream (with MFGM intact) or butter oil (with MFGM absent), you get very different metabolic effects. Those who ate 40 grams of dairy fat through butter oil saw their lipids worsen, including ApoB, a surrogate for LDL particle number. Those who ate 40 grams of dairy fat through cream saw their lipids unchanged, and in the case of ApoB even improve.  That’s 4 tablespoons of butter compared to 4 ounces, or a half cup, of heavy cream.

Caveats apply here. The subjects weren’t eating a low-carb or ketogenic diet; they just added the butter or cream on top of their normal diet. But in keto people who are genetically susceptible, huge amounts of butter may be responsible for rising LDL-P.

I still love butter. It doesn’t affect my lipids like that. But your mileage may vary, and it’s something to think about if you’re in that situation.

For what it’s worth, whole food dairy like full-fat yogurt, kefir, and cheese do not have the same effect on lipids as butter. They also happen to be keto-friendly and more nutrient-dense.

So, What Can You Do If You See An Increase in LDL?

Start Chugging Soybean Oil

Kidding… It’s true that swapping out some of your animal fats for polyunsaturated seed oils will almost certainly lower your cholesterol levels. It does this by increasing LDL receptor activity, but, being far more unstable than other fats, omega-6 PUFAs also increase the tendency of the LDL particles to oxidize. And since oxidized LDL are the ones that end up wedging in the arterial walls and causing issues, loading up on PUFAs might not be the right path.

You know what just occurred to me? This is an aside, but maybe linoleic acid (the primary fatty acid in seed oils) up-regulates LDL-R activity because the body recognizes the inherent instability of linoleic acid-enriched LDL particles and wants to clear them out before they can cause trouble. I hope some researchers take this idea further.

Stop Being a Keto Caricature.

Half a package of cream cheese for a snack.

Dipping an entire stick of pepperoni into homemade alfredo sauce and calling it dinner.

I’m not saying cream cheese is bad. It’s great. Nor am I suggesting you never eat pepperoni, dipped in alfredo sauce or not. But the amounts are unreasonable. And turning those into regular meals is a bad idea. There’s no reason you can’t go keto while eating a hamburger patty or ribeye over a Big Ass Salad. Far more nutrients, far more micronutrients, and it tastes way better.

Eat Less

Maybe if you’re a nomadic horselord sweeping across Europe in the early Bronze Age, you need to eat an entire lamb intestine stuffed with marrow and organs, and you should wash it down with a quart of creamy mare milk. Such a meal would provide the calories you need to see your enemies driven before you and go great with the lamentations of their women. But you’re not a Yamnaya nomad. You’re you.

You probably don’t need that much food, that many calories, and that much fat—since there’s plenty of it on your body already, waiting to be liberated and converted into energy.  Therein lies the beauty of keto. That’s what this is all about: Getting better at burning your own body fat.

Balance Your Fats

The overzealous and protracted drive to demonize all sources of saturated fat as evil has led to a vociferous backlash from the other direction. But just because the supposed experts got the saturated fat issue wrong doesn’t mean the opposite is true: That all the fat we eat should be as saturated as possible.

For one thing, eating nothing but saturated fat is very hard to do using whole foods. Very few animals exist in the world, past or present, with only saturated fat. The only exception I can recall is the coconut, a curious sort of beast that spends most of its time hanging from a tree impersonating a large hairy drupe. Your average slab of beef fat runs about 50% saturated fat, 45% monounsaturated fat, and 5% PUFA. That differs from cut to cut and depending on the diet of the animal, but not by much. It’s similar for other ruminants like bison and lamb. And the most prominent saturated fatty acid in ruminant fat is stearic acid, a fat that converts to monounsaturated oleic acid in the body and has an effect on cholesterol indistinguishable from MUFA or PUFA.

Or take the fatty acid composition of game meat—the type humans encountered and consumed for our entire history.

  • African kudu (antelope family): 35% SFA, 24% MUFA, 39% PUFA
  • African impala (antelope family): 51% SFA, 15% MUFA, 33% PUFA
  • Elk: roughly 40% SFA, 30% MUFA, 30% PUFA
  • Moose: roughly 33% SFA, 33% MUFA, 33% PUFA

I could go on, but you get the idea: Humans have been consuming a wide range of fatty acids for millennia. It probably makes sense to emulate that intake.

Once again, the folks whose cholesterol goes nuts on keto are outnumbered by those whose cholesterol improves. But if you’re one of the unlucky ones in the former category, try broadening your fatty acid intake (to, ahem, possibly include more nuts):

  • Focus on monounsaturated fats and fat from meat, rather than isolated sources of saturated fat like butter and coconut oil. You probably don’t have to eliminate those fats. Just don’t make them the centerpiece of your diet.
  • Eat more avocados, avocado oil, olives, olive oil, and mac nuts for monounsaturated fat. Salads are a great nutrient-dense way to incorporate high-MUFA foods.
  • Eat more fish. A couple portions of farmed Atlantic salmon were enough to improve LDL-P in overweight men and women. And compared to plain keto, keto + omega-3s from fish has a superior effect on inflammation and metabolic health.
  • Eat more kudu and impala (if you can get it). Sort of kidding. But really, eat them if you can.

They even have a version of keto called the Spanish ketogenic diet, which features a lot of extra virgin olive oil, olives, fish, and red wine. It works great and might be a good alternative for people whose cholesterol goes wild on saturated fat-heavy keto.

Are Traditional Lipid Markers Even Relevant for Keto Dieters?

Maybe, maybe not.

But be honest about it. You can’t oscillate between championing positive changes to blood lipids on a keto diet and pooh-poohing negative changes to blood lipids on a keto diet.

You can’t use positive changes to prove the efficacy and safety of the ketogenic diet, then turn around and claim that negative changes don’t count because keto dieters are understudied. What if those “positive” changes are actually negative in the context of a ketogenic metabolism? After all, keto dieters are largely understudied in both directions. If what’s unhealthy in a normal dieter might be healthy in a keto dieter, what’s healthy in a normal dieter may be unhealthy in a keto dieter.

I write these things as a strong proponent of spending a significant time in ketosis. As someone who frequently hangs out in a ketogenic state. As someone who wrote a book about keto and is writing another. But also as someone who insists on maintaining strict intellectual honesty and integrity.

We simply don’t know what very high cholesterol numbers mean in the subset of ketogenic dieters who experience them. I strongly suggest not being too flippant about them. 

True: There aren’t any perfect studies examining the utility of conventional cardiovascular risk factors in people eating the type of keto diets you see in the ancestral health space. Maybe your elevated LDL particle number doesn’t mean what it means in the average overweight adult eating the Standard American Diet. Maybe your inflammation is low enough that the risk of atherosclerosis and oxidative modification of LDL is low. But I wouldn’t take that risk, not until we have more data.

What do you think, folks? How did keto affect your blood lipids? Did you make any changes, and if so, did they work? Thanks for stopping in today.

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Note: This information isn’t intended as and shouldn’t be considered medical advice. Always consult your doctor in the management or treatment of any health issue.

References:

Hussain TA, Mathew TC, Dashti AA, Asfar S, Al-zaid N, Dashti HM. Effect of low-calorie versus low-carbohydrate ketogenic diet in type 2 diabetes. Nutrition. 2012;28(10):1016-21.

Phinney SD, Tang AB, Waggoner CR, Tezanos-pinto RG, Davis PA. The transient hypercholesterolemia of major weight loss. Am J Clin Nutr. 1991;53(6):1404-10.

Phinney SD, Bistrian BR, Wolfe RR, Blackburn GL. The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation. Metab Clin Exp. 1983;32(8):757-68.

Kleinveld HA, Naber AH, Stalenhoef AF, Demacker PN. Oxidation resistance, oxidation rate, and extent of oxidation of human low-density lipoprotein depend on the ratio of oleic acid content to linoleic acid content: studies in vitamin E deficient subjects. Free Radic Biol Med. 1993;15(3):273-80.

Rosqvist F, Smedman A, Lindmark-månsson H, et al. Potential role of milk fat globule membrane in modulating plasma lipoproteins, gene expression, and cholesterol metabolism in humans: a randomized study. Am J Clin Nutr. 2015;102(1):20-30.

Raatz SK, Johnson LK, Rosenberger TA, Picklo MJ. Twice weekly intake of farmed Atlantic salmon (Salmo salar) positively influences lipoprotein concentration and particle size in overweight men and women. Nutr Res. 2016;36(9):899-906.

De luis D, Domingo JC, Izaola O, Casanueva FF, Bellido D, Sajoux I. Effect of DHA supplementation in a very low-calorie ketogenic diet in the treatment of obesity: a randomized clinical trial. Endocrine. 2016;54(1):111-122.

Pérez-guisado J, Muñoz-serrano A. A pilot study of the Spanish Ketogenic Mediterranean Diet: an effective therapy for the metabolic syndrome. J Med Food. 2011;14(7-8):681-7.

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One thing I’ve realized being in this game for so long is that if you’re convinced that meat truly is deadly, you’re not going to stop looking for reasons why. They’ve tried blaming just about every part of meat over the years, including the protein itself, the saturated fat, the cholesterol, the methionine, the char on BBQ, and even the obscure compounds like TMAO or Neu5gc. The latest component of meat they’ve zeroed in on is iron—the essential mineral responsible for energy production and a host of other vital functions.

The experts’ track record with all the other “evil meat components” has many of my readers skeptical, so they asked me to weigh in on iron.

Iron is an essential mineral, integral in the production of energy and the creation of blood cells. If pregnant women don’t get it, they can’t deliver oxygen and nutrients to their growing babies. If kids don’t get it, they shortchange their mental and physical development. If adults don’t get it, their basic day-to-day physiological function falls apart. Without adequate iron, our antioxidant defenses, our immunity, and our metabolic function all suffer. Hell, most countries even mandate the fortification of refined flour with large amounts of iron to prevent these tragedies.

Iron also has a dark side. A large body of observational evidence links elevated iron levels to diseases and disease states like type 2 diabetesheart diseaseinsulin resistanceinflammation, Alzheimer’s disease, hypertension, fatty liver, hypothyroidism, arthritis, and cancer. You name it, it’s probably linked to elevated iron. And as much as I’d like to, I can’t dismiss these connections as non-causal.

For one, iron is inherently reactionary: The very same proclivity for electron exchange that makes iron so integral in biochemical reactions that address stress and support health means it can also create free radicals that damage DNA, cells, blood lipids, and increase stress and harm health.

Two, there’s a little something called hereditary hemochromatosis.

Hereditary hemochromatosis is a genetic condition increasing a person’s absorption and retention of dietary iron. This has benefits in certain contexts—carriers have a natural resistance to the bubonic plague, as one effect of hemochromatosis is to render white immune cells iron-deficient and thus resistant to the plague virus which feeds on iron—but it’s mostly negative in today’s relatively plague-free world. Most of the hemochromatosis literature focuses on homozygotes (carriers of two copies of the gene) and specific “iron overload-related diseases,” which include cirrhosis, liver fibrosis, liver cancer, elevated liver enzymes, “physician-diagnosed symptomatic hemochromatosis,” or finger arthritis. Those are bad conditions to have, to be sure, but that’s not even a complete list. Homozygous carriers of the mutation also have greater risks for diabetes, arthritis, fatigue, liver disease, and frailty and muscle loss. They’re more likely to experience neurodegenerative diseases like Parkinson’s and Alzheimer’s. Even heterozygous carriers (those who carry just one copy of the variant) have an elevated risk of iron overload compared to the general population.

Okay, okay. But couldn’t it be that the hemochromatosis gene is increasing disease risk through another, non-iron route? Perhaps high iron is just a marker of disease, not a cause. After all, most genes are pleiotropic—they have more than one effect.

Probably not. The most reliable treatment for hereditary hemochromatosis is phlebotomy. Literally removing iron from the body by draining blood is the first (and often only necessary) line of defense against hereditary iron overload. And it works really well.

Besides, phlebotomy may also be beneficial in people without clinical iron overload or hemochromatosis. It’s the most effective way to reduce iron stores and tends to increase insulin sensitivity. In insulin resistant men with fatty liver, blood donation normalized insulin sensitivity and liver enzymes. In meat eaters, blood donation reduced ferritin levels to match those of lacto-ovo-vegetarians and improved insulin sensitivity. One study even tested the effect of randomized phlebotomy on cancer incidence. After four and a half years, those subjects placed in the phlebotomy group lived longer, had less cancer, and had lower ferritin levels than the subjects who didn’t donate blood.

I can’t argue with the research, but the idea that a primary component of a food we’ve been eating for millions of years and to which we may even owe much of our brainpower—the iron in meat—still rankles. Is iron truly inherently “bad,” or is there anything about our modern environment that makes it so?

Possible Modern Influences On Iron Levels

Less Bleeding

One factor is that we don’t shed as much blood as before. Most men engage in far fewer bouts of direct violent conflict. Most people have fewer parasites feasting on their blood. And when’s the last time you exchanged blood oaths with anyone? We have fewer opportunities to bleed, in other words. That’s why regular phlebotomy can be such a useful tool for men (and some women) with too much iron in their bodies—it emulates all the bloodletting we used to do in a controlled, safe fashion.

Less Intense Activity

We use iron to generate energy. The more physical activity in which we engage, the more iron we utilize. This is usually couched in warnings for female athletes engaged in intense training, but it can also explain the beneficial effects of exercise in people with iron overload. There are even cases of “mild exercise” causing iron deficiency, so everything that increases energy expenditure—walking, gardening, hiking—will at least subtly reduce iron stores. More activity, less iron sitting around idle getting into trouble.

Too Many Seed Oils

I strongly suspect that the unprecedented dissemination of high-omega-6 seed oils throughout our food systems, our body fat, and our cellular membranes are exacerbating—if not causing—the relationship between excess iron and various diseases. Take the supposedly ironclad (pun intended) relationship between heme iron and colon cancer, which is mediated by iron’s peroxidative alteration of fatty acids in the colon. In animal studies that seek to show this relationship, you can’t get the colon cancer to “take” unless you feed the animal high-PUFA oils along with their heme iron. In one studyfeeding heme iron to rats promoted colon cancer only when fed alongside high-PUFA safflower oil. Feeding MUFA-rich and far more oxidatively-stable olive oil alongside the heme prevented the colon carcinogenesis. In another paper, only mice consuming fish oil-based and safflower oil-based diets exhibited carcinogenic fecal peroxides after eating heme iron; a coconut oil-based group of mice had no negative reaction to heme.

Among a cohort of US nurses, where PUFA intake is around 7% of calories and comes from seed oil, iron intake has moderate links to colon cancer. Among a cohort of Swedish women, where PUFA intake is under 5% of calories with a greater proportion coming from fish, the association is far weaker.

What To Do About All This?

First, men and postmenopausal women should figure out their hemochromatosis status. Both men and women with hereditary hemochromatosis have elevated risks of iron overload-related diseases, but they are much higher for men. (Premenopausal women have a handy built-in mechanism for shedding excess iron—menstruation.) Modern men and older women, with our absence of intestinal parasites and our lower tendency to engage in bloody hand-to-hand fighting, have few opportunities to shed iron. Your doctor will be able to order the test, or you can go through a genetic testing service and look for positive hits on C282Y and H63D.

Do it earlier rather than later. Studies indicate that one of the biggest predictors of whether someone with genetic iron overload develops liver cancer is their age at diagnosis of hemochromatosis. Those who wait risk incurring more damage.

Even if you’re negative for hereditary hemochromatosis, you can still have iron overload. Determine this by asking your doctor for a ferritin test. According to the Mayo Clinic, for men, the ferritin reference range is 24 to 336 ng/ml, and for women, it is 11 to 307. That is a wide range, and levels that your doctor would probably classify as technically normal have been associated with insulin resistance, atherosclerosis, and reduced telomere length (a marker of aging).

From what I can tell, levels approaching 200 ng/ml in men should definitely be classified as “high.” And lower may be even better. In one study, egg-and-dairy-eating vegetarian men had ferritin levels of 35 ng/ml and better insulin sensitivity than meat-eating men with ferritin levels of 72 ng/ml. After donating enough blood to hit 35 ng/ml, the meat eaters insulin sensitivity improved.

Dr. F. S. Facchini has used blood donation to induce “near iron deficiency”—the lowest body iron store that allows normal red blood cell production—in his gout patients, clearing them of gout attacks for as long as they maintained it. His patients at high risk for heart disease also saw major benefits from hitting very low ferritin levels (“to levels commonly seen in premenopausal females”), including increased HDL and lower blood pressure, even if they started with normal ferritin.

What seems safe is to stay on the low end of normal—say, from 50-150 ng/ml—as long as no symptoms of low iron arise.

As for women? Higher levels don’t seem to correlate with the same health issues in women. Lucky.

Now, say you have high iron, whether it’s hereditary hemochromatosis or just high normal ferritin levels….

What Should You Do About High Iron Levels?

Donate Blood

The quickest, safest way that also does the most social good (if you care about that sort of thing) is to donate blood. When you donate blood, your body must upregulate hemoglobin production to replace the lost blood. That requires iron, which is taken from body stores.

Don’t Manage Iron Overload With Diet

By that I mean stuff like:

  • Don’t give up red meat.
  • Don’t stop eating liver every week.
  • Keep eating oysters.
  • Don’t religiously adhere to reverse-kosher (only eating meat in the presence of dairy to inhibit iron absorption).

If you make dietary iron the focal point, you’ll miss out on all the incredible nutrients iron-rich foods like red meat and liver can offer. Besides, you’ll run yourself ragged following even more food restrictive rules that increase the chance of other nutrient deficiencies.

Don’t Manage an Iron Overload That Doesn’t Exist

I’ve seen people go down the rabbit hole of iron obsession without actually confirming they even had too much iron. They started giving blood (even self-administered), trying to reduce iron absorption by pairing dairy and calcium with their iron-rich foods, avoiding iron-rich foods—totally blind. Iron is an important nutrient. Deficiency is real. Anemia is no joke. Get tested before you start messing around with iron.

Follow a Healthy Primal Eating Plan

Whether it’s keto, low-carb, moderate-carb, or even vegetarian, going Primal will mitigate many of the potential effects of high iron by:

  • Avoiding Seed Oils and Excess Omega-6 Fats. Seed oils almost certainly make the “iron overload problem” worse, and may even be responsible for its negative effects and link to various diseases.
  • Including Phytonutrient-rich Fruits, Vegetables, Herbs, Teas, and Coffee. Polyphenols both inhibit iron absorption and reduce the oxidative interaction between iron and lipids.

So to sum up, get tested and be aware of the iron issue, but don’t let it rule you. It’s iron overload, not overlord.

Take care, everyone. What do you think of iron? Ever get tested? Ever give blood? See any benefits?

Let me know down below!

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References:

Tamosauskaite J, Atkins JL, Pilling LC, et al. Hereditary Hemochromatosis Associations with Frailty, Sarcopenia and Chronic Pain: Evidence from 200,975 Older UK Biobank Participants. J Gerontol A Biol Sci Med Sci. 2019;

Burke W, Imperatore G, Mcdonnell SM, Baron RC, Khoury MJ. Contribution of different HFE genotypes to iron overload disease: a pooled analysis. Genet Med. 2000;2(5):271-7.

Allen KJ, Gurrin LC, Constantine CC, et al. Iron-overload-related disease in HFE hereditary hemochromatosis. N Engl J Med. 2008;358(3):221-30.

Nowak A, Giger RS, Krayenbuehl PA. Higher age at diagnosis of hemochromatosis is the strongest predictor of the occurrence of hepatocellular carcinoma in the Swiss hemochromatosis cohort: A prospective longitudinal observational study. Medicine (Baltimore). 2018;97(42):e12886.

Larsson SC, Rafter J, Holmberg L, Bergkvist L, Wolk A. Red meat consumption and risk of cancers of the proximal colon, distal colon and rectum: the Swedish Mammography Cohort. Int J Cancer. 2005;113(5):829-34.

Liu B, Sun Y, Xu G, et al. Association between Body Iron Status and Leukocyte Telomere Length, a Biomarker of Biological Aging, in a Nationally Representative Sample of US Adults. J Acad Nutr Diet. 2018;

The post Is Iron the New Cholesterol? appeared first on Mark’s Daily Apple.

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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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It appears that we’re well into “outrageous media frenzy over terrible or misleading claims by nutrition scientists” season….

Last week I covered the “low-carb” and mortality study, and for this week’s edition of Dear Mark I’m covering the (latest) coconut oil controversy. A Harvard professor recently launched a dramatic harangue against coconut oil, calling it “pure poison.” Is it true this time? Are we indeed killing ourselves?

Let’s find out:

Speaking of fat, I’d be interested in Mark’s take regarding the latest attempt to put the kibosh on consumption of coconut oil–specifically, a Harvard professor saying it’s pure poison, probably because it’s so heavily saturated.

I can’t stand the stuff, personally. I don’t like anything made with coconut, and it doesn’t like me either, possibly because I’m sensitive to the overload of lauric acid. However, this and many other websites tout coconut products as being super healthful.

So is there any truth to these new claims that coconut oil is actually bad for us? Is there any hard evidence that points to related health issues? Or is this just more of the same-old, same-old that we saw with eggs, red meat, etc.?

Here’s what Shary’s talking about.

I won’t even talk about the Tokelau, a Pacific Island people who obtained most of their calories from coconut. Or the Kitavans, who ate a relatively low-fat diet but got most of their fat from coconuts. Both showed pristine metabolic health, and in the case of the Tokelau, they actually got incredibly unhealthy after switching from their coconut-rich diet to one rich in mainland foods, including seed oils.

Nor will I talk too much about the animal studies, most of which have found favorable effects on health as a result of eating coconut oil.

Let’s just focus on the human trials—the intentional studies in which actual living humans ate coconut oil and then underwent lab tests to determine the health effects. Concrete, objective effects. If coconut oil is as toxic as this Harvard professor claims, the evidence should be overwhelmingly negative. A Harvard professor would never misrepresent the evidence, right?

First, there is 2017’s Effect of a Diet Enriched with Fresh Coconut Saturated Fats on Plasma Lipids and Erythrocyte Fatty Acid Composition in Normal Adults. Healthy adults either added coconut oil or peanut fat to their diet for 3 months, and researchers examined how the different fat sources affected their biomarkers. Coconut oil increased HDL levels and the proportion of an anti-inflammatory lipid subfraction in red blood cell membranes. All told, coconut oil had a neutral to beneficial effect on health.

2017 also had Physical Form of Dietary Fat Alters Postprandial Substrate Utilization and Glycemic Response in Healthy Chinese Men. As far as coconut oil’s toxicity goes, this one was a dud. Whether the men ate coconut oil or sunflower oil made no difference in their metabolic response to meals (though when the fats were in gel form, there was an effect).

Oh, but this one sounds negative: Coconut Oil Has Less Satiating Properties Than Medium Chain Triglyceride Oil. Finally! We’ve found a kink. Unfortunately, this one isn’t bad for coconut oil either. Although MCTs proved more satiating than coconut oil, the latter was still more satiating than the control oil—vegetable oil. This is actually a strong counter to the Harvard professor’s main contention that coconut oil is bad because it’s so high in saturated fat; MCTs are pure saturated fat and performed very well here. Also, most MCT oil products come from coconut oil.

Next is The Impact of Virgin Coconut Oil and High-Oleic Safflower Oil on Body Composition, Lipids, and Inflammatory Markers in Post-Menopausal Women.  There were no differences in body composition. Coconut oil raised total cholesterol, HDL, and LDL, but it was a wash. Both groups ended up with the same TC/HDL ratio (one of the best markers of overall heart health we have). One person had increased inflammation due to coconut oil, but most of the others had lower inflammation. Overall, though, the “impact of VCO and SO on other [inflammatory] cytokines varied on an individual basis.” The implication is that different people had different responses to the different oils. This is known, and it’s good to see researchers admit that people are different and the individual response arguably matters more than the statistical average of the responses.

In 2016, this came out: Postprandial serum endotoxin in healthy humans is modulated by dietary fat in a randomized, controlled, cross-over study. At first glance, it doesn’t look good for coconut oil. Compared to fish oil (which reduced it) and high omega-6 oil (which was neutral), coconut oil eaten with the meal increased the levels of serum endotoxin. Endotoxins are produced by bacteria in our guts and tend to increase systemic inflammation when they make it into our bodies. Coconut oil was pretty good at helping endotoxin make it past the gut and into the body. The good news is that this did not increase systemic inflammation—but keep in mind that these were “healthy humans.” An increase in serum endotoxins may have stronger effects on inflammation in unhealthy or obese humans. Another bit of good news is that pairing coconut oil with, say, fatty fish should mitigate any rise in serum endotoxins.

There’s also A Randomized Study of Coconut Oil Versus Sunflower Oil on Cardiovascular Risk Factors in Patients with Stable Coronary Heart DiseaseThe title tells it: patients with heart disease added either coconut oil or sunflower oil to their diets for two years. Researchers tracked basic risk factors and the number of “events,” or heart attacks. Despite people with actual heart disease eating the “worst” oil possible, “there was no statistically significant difference in the anthropometric, biochemical, vascular function, and in cardiovascular events after 2 years.” No difference.

Heck, according to 2016’s The Effect of Coconut Oil Pulling on Streptococcus Mutans Count in Saliva in Comparison to Chlorexidine Mouthwash, the coconut oil “myth” all the “experts” love to malign—that swishing coconut oil in your mouth can reduce harmful bacterial colonization—is actually true.

It’s obvious just from looking at these very recent studies, even some of the ones with negative or neutral effects, that coconut oil is far from poison. “Experts” do themselves no credit when they ignore and misrepresent the evidence like this.

Luckily, we can read for ourselves. And we can try for ourselves.

Thanks for reading, everyone. Thoughts on this coconut oil controversy—or other health related media hype? Other studies you’d like me to look at? Have a great week.

References:

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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.

Hi Mark,

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:

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.

References:

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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Interest in the ketogenic diet is at an all-time high, and for good reason. It’s a great way to lose body fat, gain steady energy throughout the day, increase fat-burning capacity at rest and during exercise, reduce inflammation, and improve cognitive function. Keto also has a number of promising medical applications, including seizure control, enhanced efficacy of chemotherapy, and abatement of age-related cognitive impairment.

But going keto takes work. You have to overhaul your diet, restrict certain classes of foods, and pay close attention to what you eat. People prefer to avoid work if they can. They like shortcuts. Exogenous ketone supplements promise a shortcut—swallow this pill or mix this powder into your water and see your ketones skyrocket without changing the rest of your diet.

Although I’ve discussed exogenous ketones in the past, I’ve had many readers ask for a straightforward primer and takeaway recommendations for exogenous ketones. Here it is. Before I evaluate the proper role of ketone supplements, let’s dig into some basic questions.

What Are Exogenous Ketones?

There are two main types: ketone esters and ketone salts.

Ketone esters are ketone bodies bonded to an alcohol molecule. They taste terrible but are more potent than ketone salts. The rise in ketones after ketone ester supplementation is more pronounced but doesn’t last as long.

Ketone salts are ketone bodies bonded to a salt, such as sodium, magnesium, or potassium. They taste better (but not good) but are less potent than esters. The rise in ketones after ketone salt supplementation doesn’t get as high but lasts longer.

Do They Work?

Exogenous ketones increase blood, urine, and breath levels of ketone bodies. In that sense, they “work.”

Are they an effective substitute for actually following a ketogenic diet? Probably not.

First, there’s something unnatural about having elevated levels of ketones and glucose together. It’s really hard to make that happen using traditional whole foods. The closest natural approximation you could get to it would be the traditional coconut-rich diets of the Kitava people in the South Pacific, where the medium chain triglycerides (MCT) in the coconut fat increased ketone production alongside the carbs in the fruit and tubers they ate. They had excellent metabolic health, but they weren’t anywhere close to a ketogenic diet. Coconut fat isn’t as ketogenic as purified MCT oil, let alone exogenous ketones.

That alone gives me pause. The evolutionary novelty raises my hackles.

Second, there are inherent metabolic differences between boosting ketones via diet and boosting ketones via supplements. On a ketogenic diet, ketones go up because you’re converting body and dietary fat into ketone bodies. A rise in endogenous ketones means you’re burning fat and building the requisite machinery to metabolize the new energy source. On exogenous ketones, ketones go up because you ate some ketones; conversion of body and dietary fat into ketone bodies goes down if anything.

Take this study where human volunteers drank either ketone ester or ketone salt beverages alongside their normal diet. It worked. They got into ketosis, showed elevated levels of ketone bodies, and did this without changing their diet. Their conclusion says it all: “exogenous ketone drinks are a practical, efficacious way to achieve ketosis.”

Another effect of the ketone drinks was to lower blood glucose, free fatty acids, and triglyceride levels. This sounds great. Elevated levels of all those markers are harbingers of disease, particularly if they remain chronically elevated. But think about what this means. If free fatty acids go down, that means adipose tissue isn’t being liberated for burning.

That’s exactly what ketones do: inhibit lipolysis, the breakdown of body fat into triglycerides and free fatty acids for burning. In normal conditions where ketones are produced endogenously, this is expected and beneficial. If homemade ketones increased lipolysis, you’d end up with ketoacidosis. You’d make ketones which released more body fat which got turned into more ketones which released more body fat which became more ketones. And on and on. It simply wouldn’t stop.

But if you’re taking exogenous ketones to lose weight, you’re going to be disappointed.

Although they aren’t officially classified as a macronutrient, they are a source of energy. If you’re consuming exogenous ketones, you’re burning less of another energy source. And you’re making less ketones.

That’s not to suggest that exogenous ketones are useless. They have many potential uses, as I’ll explain. They just aren’t the same as getting into ketosis using diet or fasting.

What Are Their Practical Benefits?

Exogenous ketones can lower appetite during a fast. After an overnight fast, normal weight human subjects either drank a ketone ester supplement or a calorie-matched glucose drink. Compared to the glucose drinkers, the ketone drinkers had lower insulin, lower ghrelin, greater satiety, and less hunger. This can be useful for people trying to extend their fast who don’t want to or can’t yet deal with the hunger. You’re still taking in energy, but the metabolic profile remains similar to that of a fasted person.

Exogenous ketones can acutely improve the glucose response. After an overnight fast, healthy, normal weight humans drank a ketone ester supplement which spiked their ketone levels up to 3.2 and remained elevated throughout the oral glucose tolerance test. This reduced their blood glucose response and increased their insulin sensitivity.

Exogenous ketones can suppress expression of an inflammatory pathway linked to several disease states, including arthritis.

As it stands now, there are two areas where exogenous ketones show great potential.

Where Do Exogenous Ketones Make the Most Difference?

Medical Applications

For whatever reason, many patients won’t attempt a ketogenic diet—even if the evidence is clear that it could help. Doctors are often hesitant to recommend dramatic dietary shifts—even if they believe in their efficacy—to patients who are already dealing with difficult health issues. If you’ve got a picky kid with epilepsy, a pickier adult with Alzheimer’s, or a cancer patient who refuses to give up the familiar-yet-non-ketogenic foods that give him some small manner of comfort in this trying ordeal, exogenous ketones could make a big difference.

The human studies aren’t quite there yet, but it seems likely that they’d help. A recent human case study found that ketone esters added to the regular diet improved Alzheimer’s symptoms. Animal studies indicate that adding exogenous ketones to a regular lab (read: not ketogenic) diet can reduce seizure activity and improve overall symptoms in epilepsy animal models, reverse early neuronal hyperactivity in Alzheimer’s animal models, and reduce anxiety in rats.

High Performance Endurance Athletics

Alongside a normal high-carb athlete’s diet, the provision of exogenous ketones before a race increased performance over carbohydrate alone. It increased fat utilization and preserved glycogen reserves until the later part of the race—just like fat-adapted training, only with carbs in the diet.

Exogenous ketones don’t seem to improve high-intensity, glucose-intensive exercise, increasing fat burning during steady state exercise but dropping top-end high-intensity performance. Another study found that ketone dieters reduced 50-minute time trial performance in cyclists, though another group of researchers have criticized the methods. Even when a ketone ester didn’t improve performance in the shuttle run to exhaustion and 15 meter sprint repeats, it did reduce the drop in brain function following the exercise.

There’s a lot more research coming down the pike in this area, but there’s clearly some efficacy in endurance athletics, and maybe athletics in general.

Suggestions for Purchasing Exogenous Ketone Supplements

Ketone supplement choices include a variety of products with beta-hydroxybutyrate or those containing medium-chain triglycerides (liquid or powder), which will help boost liver ketone production if you’re already following a keto dietary approach. Products with beta-hydroxybutyrate often include additional agents like amino acids or minerals.

As for MCT oil (and oil powders), powder formulations tend to cause less digestive distress (e.g. probiotics), but some folks object to the additional ingredients like sunflower lecithin or soluble corn fiber). Even if you’d like to eventually settle on an oil, I’d recommend starting with a powder to see how you respond and to give your body the chance to adapt over time.

Over the past couple years, I’ve tried a number of ketone supplements, generally to enhance a longer fast or to offer an edge before one of my Ultimate Frisbee evenings. This Kegenix variety is one I’d recommend. I’ve also used Quest Nutrition MCT oil powder with good results as well, but there are plenty of other solid formulations to choose from.

Are There Side Effects?

The most common side effect is GI distress. In my experience, it’s urgent GI distress. If you decide to try an exogenous ketone supplement, do so slowly. Space out your doses. Remain close to a trusted bathroom.

They also taste terrible, although that’s improving. If you don’t think “tastes bad” is a side effect worth mentioning, you haven’t take a shot of ketone esters.

If you take exogenous ketones, use them for something of substantial benefit:

  • Seizure cessation.
  • Cognitive improvement in dementia.
  • Increased fasting tolerance.
  • High-end performance, especially endurance training.

But don’t sit around and take ketone esters or salts because you want to “bump your ketones up” for some vague reason. Or because you think they’ll be a miracle weight loss supplement (they won’t be). Have a purpose. Give those ketones something to do. Have a specific, appropriate, research-affirmed job for them.

Finally, don’t expect them to be a replacement for regularly spending time in an endogenously-ketogenic state. Living keto is considerably more effective than trying to supplement your way to it.

Thanks for stopping in, everybody. I’d love to hear your thoughts and questions. As I mentioned, I intended this as a basic primer for beginners and visitors to the site. (Welcome, by the way!) If questions warrant, I’ll do a follow-up post that gets more granular.

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The post What Are Exogenous Ketones and Who Should Take Them? appeared first on Mark’s Daily Apple.

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