For today’s edition of Dear Mark, I’m answering three questions. First, what’s the deal with the new Harvard study claiming that eating more red meat increases the death rate? Does it actually prove this? Second, how about the one claiming that reduced carb diets also increase death? Should you worry? And finally, why do I recommend eating locally farmed farmer’s market produce, even if it isn’t organic?
What’s your take on this Harvard study? www.hsph.harvard.edu/news/press-releases/increasing-red-meat-consumption-linked-with-higher-risk-of-premature-death/
“those who increased their daily servings of red meat over an eight-year period were more likely to die during the subsequent eight years”
It’s total nonsense with very little applicability to MDA readers.
Red meat eaters were more likely to be smokers.
Red meat eaters weighed more.
What else did people change as they added or removed red meat from their diets over the eight years?
The study doesn’t say much.
What we know:
Those who ate more red meat as time wore on also ate more calories per day—roughly 400 more. Those who ate less red meat as time wore on tended to reduce their overall calorie intake.
Those who ate more red meat as time wore on also gained more weight.
The simplistic urge is to assign blame for these changes to the increase in red meat, since that’s what the study is studying and that’s what they keep mentioning throughout the paper. But there are a million other variables that could have caused it, that likely did cause it, because that’s how cause-and-effect works in this world. Or rather, causes-and-effect.
And remember: this wasn’t an interventional study where one group was told to avoid red meat and one group was told to eat more red meat. This was data pulled from two different studies done decades ago, gathered by asking people what they ate on a typical day and then following up with them at a late date to see who died, who got cancer, who gained weight. It wasn’t explicitly about red meat. So, this is a mishmash of remembrances of what some people think they might have eaten, and the researchers from today’s particular paper homed in on the red meat and tuned out everything else.
This isn’t about individual people. These are abstract numbers.
One of the more interesting notes in the discussion section of the paper was this line:
Unprocessed meat consumption was only associated with mortality in the U.S. populations, but not in European or Asian populations.
I’ll be revisiting that line in the near future. For now, though, any ideas what could be going on?
Mark, do low-carb diets increase all-cause mortality? Hearing from lots of people about this latest one…
He’s talking about this one.
This is another piece of nonsense. Instead of studying legitimate low-carb diets like keto, Atkins, or basic Primal Blueprint, it separated people into four tiers of “low-carb” intake.
- Tier one got 66% of their energy from carbohydrates.
- Tier two got 57% of energy from carbohydrates.
- Tier three got 49% of energy from carbohydrates.
- Tier four—the one with the highest mortality risk—got 39% of energy from carbohydrates.
Now, I could probably hit “send” and stop the post right now. I mean, that about says it all. In what world is 39% of calories from carbohydrates a low-carb diet? How is that the “lowest-carb” diet? Pure madness.
The study also didn’t discuss diet quality. What kind of fats, carbs, and protein are these people eating? What exactly are they omitting and including? How’s their omega-3 intake? They eating mostly chicken, mostly beef, or plants?
All we know, in addition to their macronutrient ratios, is that people in the “low-carb”/39% carb group:
- Smoked the second most.
- Ate the least saturated fat.
- Drank the most alcohol.
- Exercised the least.
Really what this study is saying is that eating the high-fat, high-carb Standard American Diet will increase your mortality. This is no surprise.
As I’ve said before, you should pick a macronutrient—fat or carbs—to focus on and go with it. Sure, Michael Phelps could eat 10k calories of McDonald’s and maintain optimal performance, body comp, and health because he’s burning through it all, but you’re not him and you’re not training at an Olympic level for five hours a day. Trying to hang out in no-man’s land where you’re kinda high-carb, kinda high-fat is a bad idea for most people. You could make a 39% carb diet “better” by going with Perfect Health Diet principles, sticking to healthy Primal sources of starches and fats, but that doesn’t work for everyone.
You mentioned going to Farmers Markets every week. I would love someone to explain to me the push for buying local and going to Farmers Markets. Every time I hear them mentioned I cringe a little. I certainly understand buying local, and I agree with that, IF the fruits and vegetables are organic. Usually they are not, so I stay away from local and avoid the toxins/pesticides.
I can only assume that those who buy local don’t mind the pesticides, and if they juice, drinking a glass of chemicals.
What am I missing here? I would love to buy local, but sadly it’s rarely organic. I’d rather buy non-local organic.
Have you ever talked to the supposedly non-organic farmers?
In my experience, the vast majority of vendors at the farmers markets are using organic methods even if they aren’t certified. Reason being, organic certification is quite stringent to attain. It’s a multi-year process.
They have to go chemical-free for years. If they’re at year three of the conversion to organic, they can’t advertise “organic” but for all intents and purposes they’re there.
It costs money. Farming is a hard way to make a living. Going legit might represent a big chunk of cash that they can’t quite justify at the moment.
Go to a market, and go frequently. Get to know the people there. Look the farmer in the eyes and ask how they grow. The majority of the ones I’ve met are doing things right. They’re small operations. They’ve got their kids pitching in and helping out. They’re using man/womanpower and precision and know-how. They aren’t flying crop dusters to carpet bomb the entire field with chemicals.
Another (big) advantage of local produce is the freshness. Fruit and vegetables that travel fifty miles after being picked the day before are a world of difference from produce picked last week and shipped halfway across the country (let alone world sometimes).
That’s it for today, folks. If you have any questions or comments about today’s questions and answers, write in down below.
The post Dear Mark: Increased Red Meat, Reduced Carb, Increased Death? appeared first on Mark’s Daily Apple.
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I left the pro athlete world a long time ago. I no longer compete. I don’t train with the intensity and volume it’d take to win races. But I do pay attention to what’s going on in that world, and I still have a lot of friends who never left it. Developments there often foreshadow developments in the rest of the health world. And after things like keto, MCT oil/ketones, and collagen, the performance hack that’s blowing up among elite athletes is CBD oil. Almost everyone I talk to who puts in serious training and competing time (in a variety of sports and pursuits) is dabbling with CBD.
What are they using it for?
There are two main claims when it comes to CBD and fitness.
- That it improves sleep.
- That it reduces pain, improves workout recovery, and helps you get back to training and competition.
Do their claims have any scientific support?
CBD and Sleep
A big review of CBD and sleep found that CBD increased sleep time and reduced the number of times people woke up during the night, improved sleep quality, reduced REM-related behavioral disorder (where you act out your dreams in your sleep), and improved sleep in anxiety patients.
Sleep is one of the biggest weak spots for many athletes. They sacrifice sleep for gym time. They train late at night under bright lights and come home energized and unable to get to bed. They focus on the workouts rather than the recovery. But here’s the thing: the more you train, the more sleep you need. The more performance you need to wring out of your body, the higher your sleep requirements are going to stack. There’s no getting around it. Sleep is one of the most important things to get right if you want to improve performance and make your hard work count for something.
But let’s get more granular. You want details?
Sleep deprivation ruins your posture and makes you more liable to make technique mistakes, get injured, and compromise movement quality and power. If you can’t coordinate your limbs, you won’t succeed in the gym or on the field (and you’ll probably make a critical mistake that gets you hurt).
Sleep deprivation kills your judgment. If you’re not thinking clearly, you’ll make silly mistakes and dangerous choices. Go for the last rep on the deadlift when your back’s about to give out, that sort of thing.
Sleep deprivation squanders your adaptation to training. Enjoy the insulin sensitivity and improved energy utilization training provides? Sleep loss blunts both. Like gaining muscle in response to lifting heavy things? Sleep loss inhibits muscle protein synthesis.
Sleep deprivation makes eating well harder. If you’re training for fat loss and body composition, you know that eating is well over half the battle. A single night of bad sleep makes you more vulnerable to the rewarding effects of junk food. It becomes harder to resist and more addictive.
Sleep deprivation causes muscle loss. A lack of sleep increases urinary nitrogen, a sign that the body is breaking down lean muscle mass.
So, is there a connection between sleep, CBD, and performance?
That hasn’t been directly tested. We know two things:
- CBD can help people who are having trouble sleeping get more sleep.
- Sleep is ergogenic. If you aren’t sleeping, you aren’t maximizing your performance in the gym and adaptation to your training.
That’s not to say you can’t get good sleep without CBD. It’s not a requirement for good sleep. But if CBD is helping athletes get better sleep than they would otherwise, it’s also giving them a performance and training boost.
CBD and Pain, Adaptation, and Recovery
One of the biggest quandaries an athlete faces is how to balance pain management, training adaptation, and workout recovery.
You can use ice baths to get back in the game quicker, but you might reduce training adaptations.
You can take two days off after a really tough workout and maximize the training effect, but you won’t be able to compete in the interim.
You can pound NSAIDs to reduce pain, but it might slow down your recovery and impair your adaptation to the exercise.
Everything has a tradeoff. And if you lean too far in one direction, you’ll pay the price. Back when I was competing, I leaned hard toward “getting back out there.” I ate ice cream and grains by the gallon to replenish the energy I expended, popped Tylenol like candy to dull the pain long enough to let me get through the next workout. It all worked out in the end (I wouldn’t be doing this if I hadn’t messed up so badly), but boy if I didn’t cut it close.
Where Does CBD Fit In?
CBD is a potent antioxidant and anti-inflammatory. It can block neurotoxicity from oxidative stress. It lowers inflammatory cytokines and raises anti-inflammatory cytokines. It may reduce a person’s reliance on opioids for pain control. It can even synergize with NSAIDs, reducing the amount you need to get the same effect. And it can do all this without causing liver damage. Sounds uniformly beneficial, right?
Be careful. Anti-inflammation can be a double-edged sword. After all, inflammation isn’t wholly pathogenic:
The inflammatory response is the healing response.
Training adaptations occur in response to the inflammatory effect of exercise.
The inflammatory reactive oxygen species that we’re all so worried about also serve as cellular messengers that provoke the creation of new mitochondria and the production of endogenous antioxidants like glutathione.
This is hormesis—the application of good stressors to make us healthier, stronger, and more resilient.
NSAIDs have many of the same effects, like blocking inflammatory cytokines, and have been used by athletes for decades to reduce pain, improve acute performance, and hasten the return to competition. They’ve also been shown to reduce muscle adaptations to resistance training and impair healing even as they reduce pain.
One of CBD’s anti-inflammatory effects is to blunt the release of interleukin 6 (IL-6), an inflammatory cytokine. This isn’t always helpful, as studies show. A hard training session spikes IL-6, and, at least in animal studies using IL-6 knockouts (mice who produce no IL-6 at all), lack of an IL-6 response tends to reduce muscle and adipose tissue adaptations to exercise. NSAIDs are another anti-inflammatory drug that block IL-6 and have been shown to impair muscle adaptations to resistance training in the young and improve them in the elderly. In other words, NSAIDs impair the hormetic stress effect of exercise in the young (who tend to have a lower stress burden and higher stress resilience) and enable it in the elderly (who tend to have lower stress resilience).
What Does This Mean For You?
Well, it depends on who you are and your situation.
High stress lifestyle? CBD can probably help you blunt some of your underlying stress to give the training a bigger effect. Low stress lifestyle? CBD might blunt it too much and render your training less adaptive.
As for CBD’s effect on pain means, there are a lot of unanswered questions that I trust will be answered in due time.
CBD may help mask the pain from injuries by exerting anti-inflammatory effects while slowing down healing. However, if your baseline inflammatory status is high, reducing inflammation may be just what you need to improve healing.
CBD may help reduce pain by speeding up the healing process. There’s even some evidence in rodents that CBD can speed up the healing process of a fractured bone. Does that happen in humans? Does that happen in other types of injuries? Maybe.
That said, if taking CBD before a workout is the only thing that lets you actually get through the workout without pain, it’s going to be better than not taking it. I know of a few people who swear by CBD for joint relief; they couldn’t do what they love without it.
We have a lot more to learn about CBD and training. The benefits for athletes who need help with sleep are clear and well-established. The benefits for athletes who need help with pain and recovery are murkier—we simply don’t know the details yet. It’s likely that CBD will help athletes recover in some situations and not in others. But for the most part, it’s relatively low-risk. Give it a shot and see what you notice. The beauty of it all is that even if CBD impairs your training adaptation, it’s not set in stone. The safety profile is good. The research is only growing. You can always drop it and keep training and regain your gains.
That’s it for today, folks. Have you used CBD to enhance your training? Did it work? Did it hurt? Tell us all about it down below!
Kozela E, Juknat A, Kaushansky N, Rimmerman N, Ben-nun A, Vogel Z. Cannabinoids decrease the th17 inflammatory autoimmune phenotype. J Neuroimmune Pharmacol. 2013;8(5):1265-76.
Lundberg TR, Howatson G. Analgesic and anti-inflammatory drugs in sports: Implications for exercise performance and training adaptations. Scand J Med Sci Sports. 2018;28(11):2252-2262.
Kogan NM, Melamed E, Wasserman E, et al. Cannabidiol, a Major Non-Psychotropic Cannabis Constituent Enhances Fracture Healing and Stimulates Lysyl Hydroxylase Activity in Osteoblasts. J Bone Miner Res. 2015;30(10):1905-13.
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Have you heard? There’s a new “red meat will kill you” study. This time, it’s colorectal cancer.
Here’s the press release.
Here’s the full study.
I covered this a couple Sundays ago in “Sunday with Sisson.” If you haven’t signed up for that, I’d recommend it. SWS is where I delve into my habits, practices, and observations, health-related and health-unrelated—stuff you won’t find on the blog. Anyway, I thought I’d expand on my response to that study here today.
How the Study Was Conducted
It’s the basic story you see with most of these observational studies. Around 175,000 or so people were asked to recall what they ate on a regular basis—a food frequency questionnaire. This is the exact questionnaire, in fact. The research team took the answers, measured some baseline characteristics of all the subjects—socioeconomic status, exercise levels, whether they smoked, education level, occupation, family history of colorectal cancer, and a few others—and then followed up with participants an average of 5.7 years later to see how many had developed colorectal cancer.
What the Study “Showed”
Those who had moderate amounts of red meat had a 20% higher chance of getting cancer.
And in the end, the increased risk was a relative risk. It wasn’t a 20% absolute increase in risk. It was a relative increase in risk. The subjects started with a 0.5% risk of getting bowel cancer. In those who ate the most processed meat and red meat, that risk increased 20%—to 0.6%!
From 0.5 to 0.6%. Sure, that’s an increase, but is it something to overhaul your entire diet for? To give up the best sources of zinc, iron, B vitamins, protein, carnosine, creatine? All that for a measly 0.1% that hasn’t even been established as causal?
Study Findings Most News Outlets Won’t Include
One head scratcher that leaps out: the link between unprocessed red meat and colon cancer was not actually statistically significant. Only processed meat was significantly linked to colon cancer.
Another head scratcher: red meat, whether processed or unprocessed, had no significant association with colorectal cancer in women. Why didn’t they highlight the fact that in women, eating red meat was completely unrelated? That’s half the world’s population. That’s you or your mom, your daughter, your grandmother, your girlfriend. And unless they were to look at the full study and read the fine print, they’d never know that red meat actually had the opposite relationship. You’d think the authors would want to mention that in the abstract or see that the press releases and media treatments highlighted that fact.
It’s probably because mentioning that red meat was neutral in women and had no statistically significant link to colon cancer in men and women would have destroyed their case for red meat as an independent carcinogen. See, carcinogens are supposed to be carcinogens. There are many meaningful differences between men and women, but a poison is a poison.
What’s the proposed mechanism for red meat triggering colon cancer in men but not in women? If they didn’t have one (and I imagine they wouldn’t have mentioned it if they did), then there’s probably something else going on.
Besides, the literature is far from unequivocal.
What Other Research Says About Red Meat and Bowel Cancer
In analyses that include consideration of cooking methods and other mitigating factors, red meat has no relationship with colon cancer.
Or what about this study, where colon cancer patients were more likely to eat red meat, but less likely to have type 2 diabetes? Should people avoid red meat and work toward getting diagnosed with type 2 diabetes?
Or how about this study, which found no difference in colorectal cancer rates between people who ate red meat-free diets and people who ate diets containing red meat? Shouldn’t the diet without any red meat at all have some effect?
Or this classic study, where rats on a bacon-based diet had the lowest rates of colon cancer. In fact, bacon protected them from colon cancer after they were dosed with a colon cancer promoter, while rats on normal “healthy” chow were not.
The Blind Spot In Red Meat Research
I don’t need to go into all the confounding factors that might predispose conventional red meat lovers to bowel cancer. Nor will I mention that it’s impossible to fully control for variables like the buns and bread and fries you eat the red meat with and the industrial seed oils it’s cooked in.
That last bit is crucial: the seed oils. It’s what nearly every cancer researcher misses. It’s not just a minor variable; it’s quite possibly the most important determinant of whether meat is carcinogenic in the colon or not. Heme iron—the compound unique to red meat that usually gets the blame for any increase in cancer—is most carcinogenic in the presence of the omega-6 fatty acid linoleic acid.
In one study, feeding heme iron to rats promoted colon cancer only when fed alongside high-linoleic acid safflower oil. Feeding MUFA-rich and far more oxidatively-stable olive oil alongside the heme prevented the colon carcinogenesis.
Another study had similar results, finding that meats containing medium to high amounts of heme—beef and beef blood sausage—promoted carcinogenic conditions in the colon when the fat sources were linoleic acid-rich corn and soybean oil.
And most recently is this paper. Mice were split into three groups. One group got heme iron plus omega-6 PUFA (from safflower oil). One group got heme iron plus omega-3 PUFA (from fish oil). The third group got heme iron plus saturated fat (from fully hydrogenated coconut oil, which contains zero PUFA). To determine the carcinogenicity of each feeding regimen, the researchers analyzed the effect the animals’ fecal water (which is exactly what it sounds like) had on colon cells. The fecal water of both PUFA groups was full of carcinogenic indicators and lipid oxidation byproducts, and exposing colonic epithelial cells to fecal water from PUFA-fed mice was toxic. The coconut oil-derived fecal water had no markers of toxicity or lipid oxidation.
I never see these (animal) studies cited in observational studies of meat and colon cancer. I think that’s a huge blindspot, and it’s one of the reasons I rarely put any stock in these scary-sounding studies.
That’s it for today, folks. Thanks for reading. Now go enjoy a steak.
Bylsma LC, Alexander DD. A review and meta-analysis of prospective studies of red and processed meat, meat cooking methods, heme iron, heterocyclic amines and prostate cancer. Nutr J. 2015;14:125.
Alsheridah N, Akhtar S. Diet, obesity and colorectal carcinoma risk: results from a national cancer registry-based middle-eastern study. BMC Cancer. 2018;18(1):1227.
Rada-fernandez de jauregui D, Evans CEL, Jones P, Greenwood DC, Hancock N, Cade JE. Common dietary patterns and risk of cancers of the colon and rectum: Analysis from the United Kingdom Women’s Cohort Study (UKWCS). Int J Cancer. 2018;143(4):773-781.
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Today’s post is about dry fasting. I’ve covered plenty of other aspects of intermittent fasting, including recommendations around longer fasts, but lately I’ve gotten enough questions about this particular angle that I thought I’d address it.
Dry fasting is going without both food and fluid. That means no coffee, no tea, no broth, and no water or liquid of any kind (except the saliva you manage to produce). It’s an extreme type of fast whose fans and practitioners are adamant that it can resolve serious health issues. But does it? Is it safe? And what kind of research is available on it?
Where Does the Idea of Therapeutic Dry Fasting Come From?
The main proponent of dry fasting is a Russian doctor named Sergei Filonov. Filonov is still practicing from what I can tell, somewhere in the Altai mountains that span Central Asia. I found a very rough English translation of his book—Dry Medical Fasting: Myths and Realities. Difficult to read in full because it’s not a professional translation, but manageable in small chunks.
His basic thesis is that dry fasting creates a competitive environment between healthy cells, unhealthy cells, and pathogens for a scarce resource: water. The dry fast acts as a powerful selective pressure, allowing the strong cells to survive and the weak and dangerous cells to die off. The end result, according to Filonov, is that the immune system burns through the weak cells for energy and to conserve water for the viable cells, leading to a stronger organism overall. He points to how animals in nature will hole up in a safe, comfortable spot and take neither food nor water when recovering from serious conditions, illness, or injuries that prevent them from moving around. But when they’re able to move while recovering from more minor issues, they’ll drink water and abstain from food. I’m partial to this naturalistic line of thought, but I don’t know if the claims about animal behavior during sickness are true.
Another claim is that dry fasting speeds up fat loss relative to fasts that include water. There may be something to this, as body fat is actually a source of “metabolic water”—internal water the body can turn to when exogenous water is limited. Burning 100 grams of fat produces 110 grams of water, whereas burning the same amount of carbohydrate produces just 50 grams of water.
Are There Any Dry Fasting Studies?
Unfortunately, we don’t have many long term dry fasting studies. In fact, we have one 5-day study in healthy adults. For five days, ten healthy adults refrained from eating food or drinking water. Multiple physiological parameters were tracked daily, including bodyweight, kidney function, heart rate, electrolyte status, and circumference of the waist, hip, neck, and chest.
Participants lost weight (over 2 pounds a day) and inches off of various circumferences, including waist, hip, neck, and chest. The drop in waist circumference was particularly large—about eight centimeters by day five. Blood pressure, heart rate, oxygen saturation, sodium and potassium levels, creatinine, and urea all remained stable throughout the study. Creatinine clearance—which can be a marker of muscle breakdown but also a normal artifact of fasting—increased by up to 167%.
The most voluminous research we have on dry fasting is the Ramadan literature. During the month of Ramadan, practicing Muslims complete a daily dry fast—from sunup to sundown—every single day. They eat no food and drink no fluids during daylight hours, which, in the countries where Islam originally arose, run about 15-16 hours. These are shorter dry fasts than the 5-day fast detailed above.
What happens to health markers during Ramadan? Mostly good things.
- Almost everyone loses body fat. Few lose muscle. There’s no sign of overt dehydration.
- In fatty liver patients, Ramadan fasting lowers blood glucose, insulin levels, inflammatory markers.
- In obese and overweight subjects, Ramadan fasting lowers inflammatory markers, body weight, and insulin resistance.
- In obese adults, Ramadan fasting improves the lipid profile.
- Athletic performance is compromised during Ramadan (like impaired maximal force production of the muscles), though not as much as you’d expect.
A 15- or 16- hour dry fast isn’t very extreme, even in the hot climates of the Near East. Two or three day-long dry fasts, particularly in hot weather, is another thing entirely. What works and is safe across 16 hours might not be safe or effective over three or four days.
I wonder if there’s a genetic component to dry fasting tolerance, too. Have populations who’ve spent thousands of years in hot, dry, desert-like climates developed greater genetic tolerance of periods without water? I find it likely, though I haven’t seen any genetic data one way or the other. It’s an interesting thing to ponder.
Is Dry Fasting Safe?
Obviously, skipping water can be dangerous. While we’ve seen people go without food for as long as a year (provided you have enough adipose tissue to burn, take vitamins and minerals, and are under medical supervision), going without water is a riskier proposal. The number I’ve always heard was three weeks without food, three days without water, though I’ve never really seen it substantiated or sourced.
One reason I’m skeptical of “three days” as a hard and fast rule is that most cases of people dying of dehydration occur in dire circumstances. People are lost out in the wilderness, hiking around in vain trying to find their way back to the trailhead. They’re thrown in jail after a night out drinking and forgotten by the guards for three days. They’re spending 24 hours dancing in a tent in the desert on multiple psychoactive drugs. These are extreme situations that really increase the need for water. Your water requirements will be much higher if you’re hiking around in hot weather bathing in stress-induced cortisol and adrenaline, or dancing hard for hours on end. Very rarely do we hear of people setting out to abstain from water on purpose for medical benefits, water on hand in case things go south, and ending up dehydrated. Part of the reason is that very few people are dry fasting, so the pool of potential evidence is miniscule. I imagine this last group will have more leeway.
Still, if you’re going to try dry fasting, you have to take some basic precautions.
6 Precautions To Take When Dry Fasting
1. Get Your Doctor’s Okay
Sure, most will be skeptical at best, but I’d still advise not skipping this step—particularly if you have a health condition or take any kind of medication. Diuretics (often used for blood pressure management), for one example, add another layer to this picture.
2. No Exercise
Avoid anything more intense than walking. For one, the hypohydration will predispose you to middling results, increasing cortisol and reducing testosterone. Two, the hypohydration may progress rapidly to dehydration. If you’re going to exercise during a dry fast, “break” the fast with water first and then train.
3. Keep It Brief
Yes, there was the 5-day study, but those people were being monitored by doctors every single day. I’d say 16-24 hours is a safe upper limit and probably provides most of the benefits (as Ramadan literature shows). Any longer, buyer beware. (And, of course, make sure you get fully hydrated in between any dry fasts you might do.)
4. Fast While You Sleep
Ramadan-style probably isn’t ideal from a pure physiological standpoint. The length (16 hours) is great, but the eating schedule is not. Those who observe Ramadan fasting ritual often wake up before sunrise to fit in food. They may stay up late to eat more. They go to sleep in a well-fed state, never quite taking advantage of the 8 hours of “free” fasting time sleep usually provides (and, of course, that’s not what their fasting practice is about). For a health-motivated dry fast, on the other hand, you should take advantage of it.
5. Take Weather Into Account
Hot, humid weather will generally cause the most water loss. Cold, dry weather will cause the least. Adjust your dry fasting duration accordingly.
6. Listen To Your Body
I’ve said this a million times, but it’s especially worth saying here. If you’re not feeling well during the dry fast, listen to your instinct rather than your agenda. (And don’t begin a dry fast when you’re ill. That should go without saying.) This is an optional tool. There are hundreds of other ways to serve your health and well-being. Don’t lose the forest through the trees because you’re drawn to a practice that feels more radical. Approach it smartly, but let your body’s intuition be the final arbiter.
That’s it for me. I haven’t done any dry fasting, not on purpose at least, and I’m not particularly interested in it for myself, but I am interested in your experiences. Do any of you do dry fasting? What have you noticed? What do you recommend?
As always, if you have any questions, direct them down below. Thanks for reading!
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Fernando HA, Zibellini J, Harris RA, Seimon RV, Sainsbury A. Effect of Ramadan Fasting on Weight and Body Composition in Healthy Non-Athlete Adults: A Systematic Review and Meta-Analysis. Nutrients. 2019;11(2)
Fahrial syam A, Suryani sobur C, Abdullah M, Makmun D. Ramadan Fasting Decreases Body Fat but Not Protein Mass. Int J Endocrinol Metab. 2016;14(1):e29687.
Aliasghari F, Izadi A, Gargari BP, Ebrahimi S. The Effects of Ramadan Fasting on Body Composition, Blood Pressure, Glucose Metabolism, and Markers of Inflammation in NAFLD Patients: An Observational Trial. J Am Coll Nutr. 2017;36(8):640-645.
Unalacak M, Kara IH, Baltaci D, Erdem O, Bucaktepe PG. Effects of Ramadan fasting on biochemical and hematological parameters and cytokines in healthy and obese individuals. Metab Syndr Relat Disord. 2011;9(2):157-61.
Saleh SA, El-kemery TA, Farrag KA, et al. Ramadan fasting: relation to atherogenic risk among obese Muslims. J Egypt Public Health Assoc. 2004;79(5-6):461-83.
Gueldich H, Zghal F, Borji R, Chtourou H, Sahli S, Rebai H. The effects of Ramadan intermittent fasting on the underlying mechanisms of force production capacity during maximal isometric voluntary contraction. Chronobiol Int. 2019;36(5):698-708.
Shephard RJ. Ramadan and sport: minimizing effects upon the observant athlete. Sports Med. 2013;43(12):1217-41.
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It seems every “keto for women” forum abounds with stories about menstrual cycles gone wild in the first few months of keto. Irregular cycles, breakthrough bleeding, and periods lasting much longer than normal are common complaints. Sometimes these stories are cited as evidence that keto isn’t good for women, at least not premenopausal women, and that we need carbs for healthy hormones. Yet, many women don’t notice any changes in their menstrual cycles at all, while others report improvement in PMS symptoms and cycle regularity from the get-go.
What gives? Why do some women’s cycles apparently become wacky when they start keto, while others feel like keto is the key to period bliss? Can keto “mess up” the menstrual cycle?
We know that diet—what and how much we eat—can profoundly affect our hormones. This is true for both women and men. One of the reasons people are so excited about ketogenic diets is specifically because keto shows promise for helping to regulate hormones and improve cellular sensitivity to hormones such as insulin and leptin.
At the same time, women’s hormones are especially sensitive not only to dietary changes but also to downstream effects such as body fat loss. Furthermore, one of the ways women’s bodies respond to stressors is by turning down the dial on our reproductive systems. It’s reasonable to hypothesize, then, that women might have a tougher time adapting to or sustaining a ketogenic diet. Keto can be stressful depending on one’s approach, and that might negatively impact women’s reproductive health. But do the data actually bear that out, or is so-called “keto period” more misplaced hype than genuine fact?
Note that throughout this post, I’m going to use the term “reproductive health” to refer to all aspects of women’s menstrual cycle, reproductive hormones, and fertility. Even if you aren’t interested in reproducing right now, your body’s willingness to reproduce is an important indicator of overall health. When your reproductive health goes awry—irregular or absent periods (amenorrhea) or hormone imbalances—that’s a big red flag. Of course, post-menopausal women can also experience hormone imbalances that affect their health and quality of life (and low-carb and keto diets can be a great option for them).
Menstrual Cycle 101
Let’s briefly review what constitutes a normal, healthy menstrual cycle, understanding that everybody’s “normal” will be a little different. A typical cycle lasts from 21 to 24 days on the short end to 31 to 35 days on the long end, with 28 days being the median. Day 1 is the first day of your period and begins the follicular phase, which lasts until ovulation. Just before ovulation, levels of luteinizing hormone (LH), follicle stimulating hormone (FSH), and estradiol (a form of estrogen) spike. Next comes the luteal phase covering the approximately 14 days from ovulation to menses. LH, FSH, and estradiol drop, while progesterone rises. Estradiol bumps up again in the middle of the luteal phase. If a fertilized egg is not implanted, menstruation commences, and the whole cycles starts over again. All this is regulated by a complex communication network under the hypothalamic–pituitary–gonadal (HPG) axis, which is closely tied to the actions of the adrenal (the A in HPA axis) and thyroid glands.
Across the cycle, fluctuations in body weight are common as fluid is retained and then released along with shifts in estrogen and progesterone. Changes in blood glucose are also normal, and insulin-dependent diabetics often find that they need to adjust their dose at different times of their cycles to keep their blood sugar in check. The most common pattern is higher blood glucose readings in the pre-menstrual period (the second half of the luteal phase), and lower readings after starting your period and before ovulation. This is generally attributed to the fact that progesterone, which is highest during the luteal phase, is known to reduce insulin sensitivity. However, different women experience different patterns, which can also be affected by other factors such as oral contraceptive use.
Normal fluctuations in insulin resistance and blood glucose can mean that women get lower ketone readings at certain times of the month than others. When these occur premenstrually—and so they tend to coincide with a period of (transient) weight gain and food/carbohydrate cravings—women often feel as though they are doing something wrong. Rest assured that these variations reflect normal physiology.
The many factors that affect your cycle and the levels of your sex hormones include: other hormones, gut health and microbiome, metabolic health (e.g., insulin sensitivity), environmental toxins, stress, sleep, immune health, nutrient deficiencies, activity level and energy expenditure, and age. Each affects the others, and all (except age of course) can be affected by diet. It’s no surprise, then, that it can be extremely difficult to pin down a root cause of menstrual changes or reproductive issues.
What the Research Tells Us About Keto and Menstruation
As I said at the outset, there are lots of anecdotes, both positive and negative. In my experience, most women whose cycles seem to go crazy when they start keto find that things get back to normal—and often a better version of normal—after a few months.
First, it’s tricky to determine the effects of keto per se, since many people combine a ketogenic diet with calorie restriction (intentionally to lose weight or unintentionally due to the appetite suppressing effects of keto) and with fasting (intermittent and/or extended). Each of these can independently impact the factors listed above, lead to weight loss, and affect the menstrual cycle and reproductive health.
So, is there any evidence that keto itself causes changes to menstruation?
The scientific evidence is scant….
The one statistic you’ll see floating around the interwebs is “45% of (adolescent) females experience irregular menstrual cycles on keto.” This statistic comes from one small study of adolescent girls using a therapeutic ketogenic diet to treat epilepsy. Six of the twenty girls reported amenorrhea (loss of period) and three were diagnosed with delayed puberty. However, the ketogenic diet used for epilepsy is different and usually much stricter than an “everyday” keto diet needs to be, and epilepsy is frequently associated with menstrual dysfunction regardless of diet.
To extrapolate the findings of this study and argue that nearly half of teenage girls (or women generally) are likely to experience menstrual problems from going keto is a huge leap.
The fact is, I’m unable to find any studies done in healthy human females (or mice for that matter) demonstrating that otherwise normal menstrual cycles are disturbed by going keto.
5 Ways Keto-Related Factors *Might* Affect Your Menstrual Cycle
With the limited amount of research looking directly at keto and menstruation, let’s look first at whether there are direct effects of carbohydrate restriction or elevated ketone production on the menstrual cycle. Those are the defining characteristics of keto and what differentiates keto from other ways of eating. Then we can examine indirect effects that occur due to factors such as weight loss. These are not unique to keto, though they might be more likely on a ketogenic diet compared to other ways of eating.
There is no real body of evidence that looks at ketogenic levels of carb restriction and menstruation, but there are some clues. In this small study, functional hypothalamic amenorrhea (FHA) was associated with dietary fat restriction; women with FHA actually ate non-significantly more carbs than matched controls and nearly identical total calories. Likewise, in this small study, FHA was associated with lower fat intake but no significant difference in carb intake.
This meta-analysis looked at the effect of low-carb (not keto) diets on markers of reproductive health among overweight women. The researchers found four studies that examined effects on menstruation; all showed improved menstrual regularity and/or ovulation rates. Of six studies that looked at levels of reproductive hormones, five reported significant improvements.
Carb restriction also results in decreased insulin production. Hyperinsulinemia and insulin resistance are frequently associated with polycystic ovarian syndrome (PCOS), one of the leading causes of female infertility and a frequent cause of menstrual irregularity. There is currently a lot of interest in using keto to treat PCOS, but only one small study has so far directly tested the effectiveness of a ketogenic diet to treat PCOS, with positive results.
No studies have looked at the direct effects of ketones on menstruation.
Of course weight loss is not unique to keto, but keto can be very effective for weight loss. Some women experience rapid weight loss when first starting a keto diet. Weight loss in and of itself can impact menstruation through a variety of pathways. A key way is by reducing the hormone leptin. Leptin’s main job is to communicate energy availability to the hypothalamus—high levels of leptin tell the hypothalamus that we have enough energy on board, which also means we can reproduce. Low leptin can disrupt the menstrual cycle and is linked to hypothalamic amenorrhea.
Body fat loss can also affect estrogen levels since estrogen is both stored and produced in adipocytes (fat cells). While fat loss in the long term will decrease estrogen production, it is possible that rapid fat loss might temporarily raise estrogen levels and can also affect estrogen-progesterone balance. These transient changes in estrogen levels might underlie some of the menstrual irregularities women report.
Stress can impact the menstrual cycle in myriad ways. Cortisol acts on the hypothalamus and pituitary glands, affecting hormone levels, sleep, immune function, and gut health, to name a few. Diets can be a source of stress, both at the physiological and psychological levels. Keto has a reputation for being especially stressful because it is more restrictive than other low-carb diets, but this can be mitigated by following the Keto Reset tips for women.
Thyroid dysregulation is another common cause of menstrual irregularities, and there remains a pervasive belief that keto is bad for thyroid health. Indeed, the thyroid is sensitive to nutrient deficiencies and caloric restriction, and thyroid hormones, especially T3, do frequently decline on keto. However, as Mark has discussed in a previous post, changes in T3 levels might not be a problem, especially in the absence of other problematic symptoms. Moreover, many practitioners now use keto as a cornerstone in their treatment of thyroid disorders.
What Should I Take From These Findings?
The first takeaway: there just isn’t much direct evidence about how keto might affect your menstrual cycle, positively or negatively. We have some studies suggesting that low-carb diets improve some aspects of menstruation and reproductive health, but keto is more than just another low-carb diet. Ketones themselves have important physiological properties, such as being directly anti-inflammatory, which might positively impact women’s reproductive health.
Second, the ways that keto is likely to (negatively) affect menstruation aren’t unique to keto, they’re common to any diet: hormone shifts mediated by energy balance, stress, and weight loss.
Furthermore, since keto is so often combined with caloric restriction, time-restricted eating, and fasting, even the anecdotal evidence might not be able to tell us all that much. If a woman is eating ketogenically, in a big caloric deficit, and doing OMAD (one meal a day), and her leptin plummets, how are we to know what really caused it? We don’t have good evidence that otherwise healthy women start a well-executed ketogenic diet and end up messing up their menstrual cycles.
That said, women do need to be cognizant of the sum total of the signals they are sending their bodies when it comes to energy availability and stress. A lot of women come to the keto diet with a history of adrenal, thyroid, metabolic, and reproductive issues. It’s important that they’re extra careful about how they approach keto. Done correctly, it might be just what the doctor ordered. I encourage any woman who’s dealing with other hormonal issues to work with a medical practitioner to tailor a keto diet to her unique needs.
But I’m Telling You, Keto Made My Period Go Haywire!
Ok, I believe you, really! But changes do not necessarily equal dysfunction. It is normal to experience hormone fluctuations when you make a massive—or even a relatively small but important—shift in your nutrition. Sometimes those fluctuations are unpleasant or unwanted, such as a period that lasts 14 days or one that arrives a week before you planned while you’re on vacation. However, that doesn’t make them bad from a health perspective. We need to respect that our bodies are dynamic systems. Changing the input will invariably change the output, and the system might need a few months to adapt to a new normal.
If your cycle goes wonky but you’re otherwise feeling good, give it a few months to sort itself out. If after a few months it’s still all over the place (or definitely if you’re having other disruptive symptoms), enlist help. In the meantime, check to make sure you’re not short-changing yourself nutritionally or calorically. Scale back on fasting efforts, and consider shifting more toward a traditional Primal way of eating.
At the end of the day, if you go keto and experience negative effects, stop. Keto is super hyped right now, but if your body is sending you clear signals that keto is not a good approach for you at this time, don’t do it. You can always try again later. It might be that your first attempt at keto didn’t work, but with a few adjustments and some experimentation over time you can find a version of keto that works for you.
Thanks for reading, everyone. Do you have comments, questions, or feedback? Let me know below.
Comninos AN, Jayasena CN, Dhillo WS. The relationship between gut and adipose hormones, and reproduction. Human Reproduction Update 2014; 20(2): 153–174.
Fontana R, Della Torre S. The Deep Correlation between Energy Metabolism and Reproduction: A View on the Effects of Nutrition for Women Fertility. Nutrients. 2016;8(2):87.
Klok MD, Jakobsdottir S, Drent ML. The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review. Obesity Reviews 2007;8(1):21-34.
Meczekalski B, Katulski K, Czyzyk A, Podfigurna-Stopa A, Maciejewska-Jeske M. Functional hypothalamic amenorrhea and its influence on women’s health. J Endocrinol Invest. 2014;37(11):1049–1056.
Tena-Sempere M. Roles of Ghrelin and Leptin in the Control of Reproductive Function. Neuroendocrinology 2007;86:229-241.
The post Keto and the Menstrual Cycle: Is There Reason To Worry? appeared first on Mark’s Daily Apple.
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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.
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?
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.
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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.
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?
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.
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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.
The post What’s the Pegan Diet? (And How Does It Compare To Primal?) appeared first on Mark’s Daily Apple.
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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?
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.
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.
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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?
I asked Dr. Cate Shanahan for her input on this topic, and she provided a beautiful explanation:
But when you stop eating so many carbs insulin politely steps aside, and your insulin levels plummet. Now your body fat can more easily and more often release its stores of fatty acids into your bloodstream.When your body fat releases stored fatty acids, any unused fatty acids quickly get picked up by the liver and packed into VLDL lipoprotein. VLDL is a precursor to LDL. So in reducing your insulin levels and increasing your body’s use of fat, you will raise your VLDL, LDL and total cholesterol. You are simply trafficking in fat more often now. And now, because your body stabilizes fat carrying lipoproteins with cholesterol, there is a need for more cholesterol in your blood. These are not bad consequences. They are in fact happy signs your diet is doing what its supposed to be doing.
If you’re actively losing weight, you will probably experience a rise in cholesterol. This is the transient hypercholesterolemia of major weight loss, and it’s a well-known phenomenon. Once your weight stabilizes, cholesterol should normalize—although to a lesser extent than other diets, given Dr. Cate Shanahan’s explanation of increased “trafficking in fat.”
Low Thyroid Function
The thyroid is a barometer for your energy status. If you have plentiful energy to spare, thyroid function is normal. If your body perceives low energy availability, thyroid function may down-regulate. Since the thyroid plays a big role in regulation of LDL receptor activity, its downregulation can lower LDL receptor sites. Fewer LDL-receptors clear LDL particles from the blood. Folks with genetic predispositions to heart disease often have low LDL receptor activity, causing elevated LDL particles. Folks with genetic variants that increase the activity and expression of LDL receptors have lower heart disease rates. Although genes often have different effects that may affect disease risk via other pathways, that’s pretty strong evidence that LDL receptor activity regulates, at least in part, one’s LDL-P and heart disease risk.
Read this post for maintaining thyroid function on keto, and check out Elle Russ’ Paleo Thyroid Solution for an even deeper, more thorough dive into thyroid health.
Eating Too Damn Much
Some keto people pride themselves on gorging. Some are doing it for a good cause—a quest to find the fabled metabolic advantage. Some are doing it to show off and for keto cred—look how much salami I can eat! Some are using keto to deal with unresolved issues with food itself.
Everything I say about doing keto presupposes that you are eating like a normal person. You’re eating as much as you need to fuel your brain and daily activities, fitness and performance goals. You’re leaving the table satiated, not stuffed. For most people, this happens without even trying. It’s why keto is so effective for weight loss.
Genes aren’t destiny, but they do modify and regulate our response to a given environmental input.
Some people are dietary cholesterol hyper responders. Unlike the majority of the population, they absorb tons of dietary cholesterol and do not down-regulate their endogenous production to accommodate. The result is an increase in cholesterol synthesis and absorption, leading to a spike in blood cholesterol.
Some people are sensitive to saturated fat. In response to it, they produce elevated numbers of LDL particles. If your keto diet is high in saturated fat and you have a genetic sensitivity to it, your cholesterol will probably skyrocket.
Some people have genes that reduce the activity of their LDL receptors. This will necessarily boost LDL particle numbers.
This topic—genetic variance and how it affects keto—could be an entirely separate post, so I’ll leave it at that (and probably come back to it in the future).
Too Much Butter
Huh? Too much butter, Sisson? Is such a thing even possible?
Maybe. Subjecting cream to the butter-making process strips it of something called milk fat globule membrane (MFGM). And when you compare equal amounts of dairy fat through either cream (with MFGM intact) or butter oil (with MFGM absent), you get very different metabolic effects. Those who ate 40 grams of dairy fat through butter oil saw their lipids worsen, including ApoB, a surrogate for LDL particle number. Those who ate 40 grams of dairy fat through cream saw their lipids unchanged, and in the case of ApoB even improve. That’s 4 tablespoons of butter compared to 4 ounces, or a half cup, of heavy cream.
Caveats apply here. The subjects weren’t eating a low-carb or ketogenic diet; they just added the butter or cream on top of their normal diet. But in keto people who are genetically susceptible, huge amounts of butter may be responsible for rising LDL-P.
I still love butter. It doesn’t affect my lipids like that. But your mileage may vary, and it’s something to think about if you’re in that situation.
So, What Can You Do If You See An Increase in LDL?
Start Chugging Soybean Oil
Kidding… It’s true that swapping out some of your animal fats for polyunsaturated seed oils will almost certainly lower your cholesterol levels. It does this by increasing LDL receptor activity, but, being far more unstable than other fats, omega-6 PUFAs also increase the tendency of the LDL particles to oxidize. And since oxidized LDL are the ones that end up wedging in the arterial walls and causing issues, loading up on PUFAs might not be the right path.
You know what just occurred to me? This is an aside, but maybe linoleic acid (the primary fatty acid in seed oils) up-regulates LDL-R activity because the body recognizes the inherent instability of linoleic acid-enriched LDL particles and wants to clear them out before they can cause trouble. I hope some researchers take this idea further.
Stop Being a Keto Caricature.
Half a package of cream cheese for a snack.
Dipping an entire stick of pepperoni into homemade alfredo sauce and calling it dinner.
I’m not saying cream cheese is bad. It’s great. Nor am I suggesting you never eat pepperoni, dipped in alfredo sauce or not. But the amounts are unreasonable. And turning those into regular meals is a bad idea. There’s no reason you can’t go keto while eating a hamburger patty or ribeye over a Big Ass Salad. Far more nutrients, far more micronutrients, and it tastes way better.
Maybe if you’re a nomadic horselord sweeping across Europe in the early Bronze Age, you need to eat an entire lamb intestine stuffed with marrow and organs, and you should wash it down with a quart of creamy mare milk. Such a meal would provide the calories you need to see your enemies driven before you and go great with the lamentations of their women. But you’re not a Yamnaya nomad. You’re you.
You probably don’t need that much food, that many calories, and that much fat—since there’s plenty of it on your body already, waiting to be liberated and converted into energy. Therein lies the beauty of keto. That’s what this is all about: Getting better at burning your own body fat.
Balance Your Fats
The overzealous and protracted drive to demonize all sources of saturated fat as evil has led to a vociferous backlash from the other direction. But just because the supposed experts got the saturated fat issue wrong doesn’t mean the opposite is true: That all the fat we eat should be as saturated as possible.
For one thing, eating nothing but saturated fat is very hard to do using whole foods. Very few animals exist in the world, past or present, with only saturated fat. The only exception I can recall is the coconut, a curious sort of beast that spends most of its time hanging from a tree impersonating a large hairy drupe. Your average slab of beef fat runs about 50% saturated fat, 45% monounsaturated fat, and 5% PUFA. That differs from cut to cut and depending on the diet of the animal, but not by much. It’s similar for other ruminants like bison and lamb. And the most prominent saturated fatty acid in ruminant fat is stearic acid, a fat that converts to monounsaturated oleic acid in the body and has an effect on cholesterol indistinguishable from MUFA or PUFA.
Or take the fatty acid composition of game meat—the type humans encountered and consumed for our entire history.
- African kudu (antelope family): 35% SFA, 24% MUFA, 39% PUFA
- African impala (antelope family): 51% SFA, 15% MUFA, 33% PUFA
- Elk: roughly 40% SFA, 30% MUFA, 30% PUFA
- Moose: roughly 33% SFA, 33% MUFA, 33% PUFA
I could go on, but you get the idea: Humans have been consuming a wide range of fatty acids for millennia. It probably makes sense to emulate that intake.
Once again, the folks whose cholesterol goes nuts on keto are outnumbered by those whose cholesterol improves. But if you’re one of the unlucky ones in the former category, try broadening your fatty acid intake (to, ahem, possibly include more nuts):
- Focus on monounsaturated fats and fat from meat, rather than isolated sources of saturated fat like butter and coconut oil. You probably don’t have to eliminate those fats. Just don’t make them the centerpiece of your diet.
- Eat more avocados, avocado oil, olives, olive oil, and mac nuts for monounsaturated fat. Salads are a great nutrient-dense way to incorporate high-MUFA foods.
- Eat more fish. A couple portions of farmed Atlantic salmon were enough to improve LDL-P in overweight men and women. And compared to plain keto, keto + omega-3s from fish has a superior effect on inflammation and metabolic health.
- Eat more kudu and impala (if you can get it). Sort of kidding. But really, eat them if you can.
They even have a version of keto called the Spanish ketogenic diet, which features a lot of extra virgin olive oil, olives, fish, and red wine. It works great and might be a good alternative for people whose cholesterol goes wild on saturated fat-heavy keto.
Are Traditional Lipid Markers Even Relevant for Keto Dieters?
Maybe, maybe not.
But be honest about it. You can’t oscillate between championing positive changes to blood lipids on a keto diet and pooh-poohing negative changes to blood lipids on a keto diet.
You can’t use positive changes to prove the efficacy and safety of the ketogenic diet, then turn around and claim that negative changes don’t count because keto dieters are understudied. What if those “positive” changes are actually negative in the context of a ketogenic metabolism? After all, keto dieters are largely understudied in both directions. If what’s unhealthy in a normal dieter might be healthy in a keto dieter, what’s healthy in a normal dieter may be unhealthy in a keto dieter.
I write these things as a strong proponent of spending a significant time in ketosis. As someone who frequently hangs out in a ketogenic state. As someone who wrote a book about keto and is writing another. But also as someone who insists on maintaining strict intellectual honesty and integrity.
We simply don’t know what very high cholesterol numbers mean in the subset of ketogenic dieters who experience them. I strongly suggest not being too flippant about them.
True: There aren’t any perfect studies examining the utility of conventional cardiovascular risk factors in people eating the type of keto diets you see in the ancestral health space. Maybe your elevated LDL particle number doesn’t mean what it means in the average overweight adult eating the Standard American Diet. Maybe your inflammation is low enough that the risk of atherosclerosis and oxidative modification of LDL is low. But I wouldn’t take that risk, not until we have more data.
What do you think, folks? How did keto affect your blood lipids? Did you make any changes, and if so, did they work? Thanks for stopping in today.
Note: This information isn’t intended as and shouldn’t be considered medical advice. Always consult your doctor in the management or treatment of any health issue.
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