For today’s edition of Dear Mark, I’m answering three questions. First up, what can a person do to help their gut recover its barrier function after too many antibiotics? Are there any foods, supplements, or dietary strategies? Second, what can explain rapid fatigue during sprint sessions on a keto diet? Is this simply part of the deal, or are there modifications you can make? And finally, what do I do when I know I’m going to get a bad night’s sleep?

Let’s go:

Mark – any idea how to cure leaky gut caused by overuse of antibiotics. Tried raw dairy for a month to no avail.

First of all, check out my post on leaky gut. Read through it and follow my suggestions for preventing and treating intestinal permeability. It’s a great place to start.

Then, let’s look at some other interventions that have been shown to improve recovery from antibiotic therapy. While most of the studies referenced don’t explicitly describe antibiotic-induced leaky gut, anything that improves gut function and restores healthy gut bacteria will also normalize leaky gut—since it’s the eradication of native gut bacteria that causes antibiotic-induced leaky gut.

Fermented dairy. You tried raw dairy. What about fermented dairy? While raw dairy has its merits, it’s fermented dairy that just works for recovery from antibiotics. Yogurt is a good option to try, although the evidence is a bit inconsistentKefir is probably better; it’s been shown to improve patients’ tolerance to triple antibiotic therapy during treatment for H. pylori infection. This is even worth consuming during antibiotic therapy, as many of the probiotic bacteria found in fermented dairy show resistance to common antibiotics.

Fermented vegetables like sauerkraut are also must-eats. The fermented cabbage contains ample amounts of L. plantarum, a bacteria strain that’s been shown to prevent antibiotic-related diarrhea in piglets (another omnivorous mammal). Good options exist in stores (check the refrigerated section; shelf-stable pickles and kraut aren’t lactofermented), and even more are available in farmer’s markets, but the best way to get the most bacteria-rich vegetable ferments is to make your own.

Supplemental probiotics are fantastic here, too: large doses of the desired microorganisms delivered directly to your gut. Some of the strains used in Primal Probiotics, like B. clausii and S. boulardii, have been shown to be effective against antibiotic-related diarrhea, so that could be a good choice.

Don’t forget the food for your gut bugs: prebiotics. You need to eat fermentable fibers and other prebiotics like resistant starch to support the growth and maintenance of the helpful bacteria that improve gut barrier function. Consider eating cooked and cooled potatoes, unheated potato starch, leeks, garlic, onions, green bananas, apples, pears, berries, and pretty much any fruit or vegetable you can get your hands on. Plenty of them are low-carb enough to work on a keto diet, if that’s your desire. Oh, and dark chocolate is a great source of fiber and polyphenols, which have prebiotic effects in the gut.

Incorporate intermittent fasting. Going without food for a spell gives your gut a break and induces autophagy, which can help with tissue healing.

Get dirty, too, to introduce potentially helpful bacteria. Go out and garden. Go barefoot at the park (do your due/doo diligence, of course) and practice tumbling, or roughhouse with your kids (or friends). Don’t immediately rush to wash your hands all the time (unless you’ve been handling raw meat and/or dog poop).

Whatever you do, don’t stress too much about the antibiotics you had to takeStress is awful for gut health and you’ve already taken the antibiotics—which were probably necessary—so that ship has sailed.

If probiotics with prebiotics aren’t helping (or making things worse), you might want to try going the opposite direction—removing all plant foods and doing a carnivore diet for a few weeks. While I have doubts about the long term viability and safety of eschewing all plant foods, enough people have written to me about their great experiences resolving gut issues with a bout of carnivory that it’s worth trying.

When on a strict keto plan, why do I become so quickly fatigued while attempting a HIT sprint workout?

The first five seconds of a sprint are primarily powered by phosphocreatine (or creatine phosphate), a “quick burst” energy source that burns hot but disappears quickly. This is the stuff used to perform max effort Olympic lifts, short sprints, and other rapid expressions of maximum power. It doesn’t last very long and takes a couple minutes to replenish itself. A keto diet doesn’t affect our creatine phosphate levels. If anything, it should improve them if we’re eating meat.

After five seconds, anaerobic metabolism of muscle glycogen provides the lion’s share of your energy needs. The longer your sprint, the more glycogen you’ll burn. The less glycogen you carry in your muscles, the shorter your sprint. Because once you run out of creatine phosphate and glycogen, you’re left with aerobic metabolism—great for longer distances, not so great for max effort sprints.

Keto dieters tend to walk around with less glycogen in their muscles. If that’s the case, longer sprints will be harder.

If you want to keep sprinting:

Do shorter sprints. Try a 10-second hill sprint rather than a 20-second one. Really go hard. Heck, you can even do 5-second sprints and derive major benefits; just do more of them and make sure to recover in between. There’s no rule saying you have to sprint for 20-30 seconds.

Take longer rest periods. Give your muscles a chance to replenish more creatine phosphate (and take creatine or eat red meat and fish, which are the best sources of dietary creatine).

Eat 20-30 grams of carbs 30 minutes before a sprint session. See if it helps. Alternatively, you can eat the 20-30 grams of carbs after the sprint session to replenish lost glycogen stores (without really impacting your ketone adaptation, by the way).

Most people figure out their sprinting sweet spot while doing keto. They may have to play around with the dosages, durations, and rest periods, but you can usually make it work. Be open to trying new permutations.

If you knew you were going to have a poor nights sleep, what measures would you take to reduce some of the damage?

I would exercise hard that night. Normally, a bad night’s sleep tanks your insulin sensitivity the next day, giving you the insulin resistance and glucose tolerance of a diabetic. A good hard interval session the night before a bad night’s sleep, however, counters the next-day insulin resistance.

I would make the most of it. Don’t dawdle. Don’t beat yourself up because of the impending sleep deprivation. It’s going to happen. You have to accept it, not let it destroy you.

Enjoy it. A little-known acute treatment for depression is sleep deprivation. That’s right: a single night of sleep deprivation has been shown to ameliorate depression in patients with clinical depression. Sometimes the effect lasts up to several weeks. It’s not a long term or sustainable fix for clinical depression, obviously, and you can’t do it every single night—chronic sleep deprivation is a major risk factor for developing depression—but it can improve your mood if you give in to it.

I would set out a jar of cassia cinnamon. I always add cassia cinnamon to my coffee in the morning after bad sleep; cassia cinnamon the day after a bad night’s sleep attenuates the loss of insulin sensitivity and glucose tolerance.

That’s it for today, folks. Thanks for writing in and reading! If you have any input on today’s round of questions, let me know down below.

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References:

De vrese M, Kristen H, Rautenberg P, Laue C, Schrezenmeir J. Probiotic lactobacilli and bifidobacteria in a fermented milk product with added fruit preparation reduce antibiotic associated diarrhea and Helicobacter pylori activity. J Dairy Res. 2011;78(4):396-403.

Bekar O, Yilmaz Y, Gulten M. Kefir improves the efficacy and tolerability of triple therapy in eradicating Helicobacter pylori. J Med Food. 2011;14(4):344-7.

Erginkaya Z, Turhan EU, Tatl? D. Determination of antibiotic resistance of lactic acid bacteria isolated from traditional Turkish fermented dairy products. Iran J Vet Res. 2018;19(1):53-56.

Yang KM, Jiang ZY, Zheng CT, Wang L, Yang XF. Effect of Lactobacillus plantarum on diarrhea and intestinal barrier function of young piglets challenged with enterotoxigenic Escherichia coli K88. J Anim Sci. 2014;92(4):1496-503.

Jitomir J, Willoughby DS. Cassia cinnamon for the attenuation of glucose intolerance and insulin resistance resulting from sleep loss. J Med Food. 2009;12(3):467-72.

The post Dear Mark: Antibiotic Recovery, Sprinting on Keto, Preparing for Bad Sleep 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?

Probably not.

Is Keto Crotch Even Physiologically Plausible?

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

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

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

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

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

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

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

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

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

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

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

Should I Worry?

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

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

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

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

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

If You’re Concerned…

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

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

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

Take care and be well.

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References:

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

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

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

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

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

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Here are Fit Bottomed Eats, we’re lucky in that we get the scoop on new healthy foods before they hit the shelves. And, lately, we’ve seen some big trends that are starting to pop. Here are the five hottest food trends we’ve got our eyeballs on — and think you should, too! The Hottest Food Trends of 2019 1. All the functional drinks. You’ve probably already noticed that the drink aisle at your natural grocery store is like a million miles long, but prepare for it to get even longer in the New Year. From more kombuchas and fermented drinks…

The post The Hottest Food Trends of 2019 appeared first on Fit Bottomed Girls.

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Are you looking to get more more pre- and probiotics in your life? Do you even know the difference? Well, we have you covered in this enlightening interview with nutritionist extraordinaire Ellie Krieger. Ellie is also a spokesperson for Renew Life and shares with us all of the essentials to get your whole self (not just your gut!) healthier. (She likes to think of probiotics as amazing house guests for your body!) Ellie also dishes on what items you will always find in her fridge and pantry, her favorite go-to meals, the sheer loveliness of chewing, and the one food…

The post Podcast Ep 102: Nutritionist Ellie Krieger appeared first on Fit Bottomed Girls.

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For today’s edition of Dear Mark, I’m answering a bunch of questions from comment sections. First, did I get AMPK and mTOR mixed up in a recent post? Yes. Second, I give a warning for those who wish to add ginger to their broth. Third, is it a problem that we can’t accurately measure autophagy? Fourth, how does coffee with coconut oil affect a fast? Fifth, is there a way to make mayonnaise with extra B12 and metformin? Actually, kinda. Sixth, should you feel awkward about proposing hypotheses or presenting scientific evidence to your doctor? No.

Let’s go:

Great article, but a couple of amends are required with regards to mTOR. Firstly, you mention in the last paragraph that curcumin activates autophagy by activating mTOR. Reading the actual article abstract though, it states the opposite, ie the effect of curcumin “downregulating AKT/mTOR signaling pathway in human melanoma cells”.

Great catch. I’m not sure how I flipped that around. AMPK triggers autophagy, mTOR inhibits it.

What you say about curcumin goes for all the other broth ingredients I mentioned. Ginger, green tea, and curcumin all contain phytonutrients which trigger AMPK, which should induce autophagy, or at least get out of its way. What remains to be seen is whether the amino acids in broth are sufficient to inhibit fasting-and-phytonutrient-induced autophagy. I lean toward “yes,” but is it an on-off switch, or is autophagy a spectrum? Does inhibition imply complete nullification? I doubt it.

Regarding autophagy and health and longevity, it’s important to note the manner in which glycine, the primary amino acid found in broth and gelatin, opposes the effects of methionine, the primary amino acid found in muscle meat and a great stimulator of mTOR.

One notable study found that while restricting dietary methionine increased the lifespan of lab rodents, if you added dietary glycine, you could keep methionine in the diet and maintain the longevity benefits. That doesn’t necessarily speak to the effect of broth on autophagy during a fast, but it’s a good reminder that broth is a general good guy in the fight for healthy longevity.

Funny you mentioned ginger and turmeric as I add both, along with a whole lemon and/or lime, to my list of ingredients when cooking my broth. Here’s another great tip: I juice turmeric root, ginger & lemon together in my Omega juicer and freeze in ice cube trays. I add a cube to curries and other dishes.

That’s a great idea. One cautionary note about the raw ginger: it will destroy your gelatin.

Raw ginger has a powerful protease, an enzyme that breaks down protein. If you grate a bunch of ginger into a batch of finished broth, or juice a few inches and dump it in, there’s a good chance you’ll lose the gel. The amino acids will remain, but you’ll miss out on the texture, the mouthfeel, the culinary benefits of a good strong gelatinous bone broth.

Heating the ginger with the broth as it cooks, or even just reducing the amount of raw ginger you add, should reduce the protease activity.

“Bone broth with turmeric, green tea, and ginger might actually combine to form a decent autophagy-preserving drink during a fast. Only one way to find out!” You say this as if there is a way for us to try this and see. Since we cannot measure autophagy, this statement makes no sense.

Touché.

Although it will all shake out in the end, or towards it. If things seem to be “going good” for you as you get older, if your doctor is always pleasantly surprised at your test results, if you maintain your vim and vigor as your peers degenerate, maybe it worked. Maybe it’ll add a few months or years to your life, and you’ll never quite know because you don’t have an alternate life in which you didn’t add the turmeric, green tea, and ginger to your broth for comparison.

At any rate, the mix tastes really, really good. That’s reason enough to drink the stuff.

What about drinking a cup of black coffee with one tablespoon of coconut oil blended in? What effect does that have on fasting?

You’ll burn less body fat (because you’re eating 14 grams of it).

Autophagy will be maintained (because fat has little to no effect on autophagy).

You may have better adherence. The fast might “feel” easier, although you might not be “fasting as hard.”

I often have cream in my coffee during a “fast,” and I see no ill effects. Although as I alluded to in the previous answer, these things are hard to definitively measure. Much of it is a mix of speculation, hope, intuition, and faith that our health practices are helping us and improving our outcomes.

Read my post on coffee during a fast for more information.

Can you make a Mayo with metformin and increased B12? Thanks

You know what? Let’s try to make this happen.

Start with your favorite mayo recipe. Then, swap out the chicken egg yolks for two duck egg yolks. Each duck egg contains almost 4 micrograms of B12—more than the daily requirement. For comparison’s sake, the average chicken egg has about 0.5 micrograms.

At the end, add in a few drops of barberry extract—barberry is a good natural source of berberine, an alkaloid whose effects are similar to metformin’s. I don’t know if the extract will affect the emulsion of the mayo, but it shouldn’t be too much of a hindrance. Barberry is said to be bitter, so perhaps add a few pinches of a natural sweetener like stevia or monk fruit to counteract it.

I recently read a PubMed article that possibly ties Metformin use in diabetic patients with MTHFR mutation (in particular C677T) causing Vitamin B12 deficiency leading to Hyperhomocysteinemia which then may increase risk of vascular thrombosis. I have also read many articles/opinions that convey there is nothing to worry about with MTHFR mutations. My Mom is a Metformin treated (several years) diabetic who has the C677T mutation and has had one blood clot in her leg and, now while on blood thinners, has been experiencing severe swelling in lower extremities. I’m trying to figure out if we should be looking into this combination of Metformin and MTHFR mutation as the cause behind this or if the docs will think I’m just another wack-a-doo who diagnoses things via the internet, especially since I’ve already self-diagnosed Hereditary Hemochromatosis in myself earlier this year! Genes are fascinating! ?

Wack a doos make the world go round. Some of the greatest thinkers, creators, and doers throughout human history were considered by many to be insane.

And hey, this is your mother. There’s no shame in helping your kin.

A wack a doo would ask her doc about the potential for crystals to heal her tumor. A wack a doo would bring a printout of a random Reddit post to the appointment and use it as proof of her hypothesis. A wack a doo would ask the staff dietitian for a Breatharianism protocol. Bringing a legitimate medical article discussing a specific mutation that has been shown to induce B12 deficiencies in people taking the very same medication your mother is taking along with genetic results showing she has the mutation is far from crazy. Do it.

Besides, you’re totally right. A vitamin B12 deficiency (and the resultant elevated homocysteine levels) is a known risk factor for blood clots.

That’s it for today, folks. Take care and be sure to leave your comments and questions down below. Thanks for reading!

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References:

Joel BrindVirginia MalloyInes AugieNicholas CaliendoJoseph H VogelmanJay A. Zimmerman, and Norman Orentreich Dietary glycine supplementation mimics lifespan extension by dietary methionine restriction in Fisher 344 ratsThe FASEB Journal 2011 25:1_supplement528.2-528.2 

The post Dear Mark: Broth, Fasting, Coffee, and Metformin (and More) appeared first on Mark’s Daily Apple.

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inline Fiber.jpegThe tricky thing about fiber is that it’s not a monolith. There are dozens of varieties. Some of them perform similar functions in the body, but others have extremely unique effects. Some rend your colonic lining to stimulate lubrication. Some turn into gelatinous slurries. But we can’t talk about fiber without understanding that the word describes a variety of compounds. As such, anyone making declarative statements about “fiber” without differentiating between the different types and their effects isn’t being accurate (except for me in that exact sentence).

This leads to a lot of confusion. People make blanket statements that might be true for some types of fibers and incorrect for others. 

Today’s post will attempt to illuminate the bulk of the matter. I’ll go through some of the most common misconceptions and myths about fiber from all corners of the dietary world. Whether you’re keto, low-carb, vegan, carnivore, or breatharian, you’ll find something to love and hate in today’s post.

1) “Fiber makes you full.”

This is theoretically sound. Mechanoreceptors in the gut respond to physical fullness by triggering satiety hormones. Big loads of insoluble fiber increase intestinal bulk, while some soluble fibers can gel up and increase the size of the stuff moving through your gut. Both result in added pressure on gut mechanoreceptors.

How does it work in practice?

A review found that while soluble fiber reduced appetite more than insoluble fibers, the overall effect on body weight was quite small, unimpressive, and inconsistent. More recently, a soluble fiber supplement failed to have any effect on satiety hormones, appetite, and subsequent food intake for the first 150 minutes after eating in healthy adults. The plucky researchers aren’t giving in, however, promising “further research… to quantify how soluble fiber influences appetite several hours after consumption.”

Resistant starch, an indigestible type of starch that colonic bacteria ferment, on the other hand does appear to increase satiety in humans, reducing food intake by 15%.

2) “Every diet needs the same amount of fiber.”

As it turns out, fiber becomes more critical the more carbohydrates you eat.

Soluble fiber slows down digestion, reducing the rate at which energy is absorbed. This can be helpful for people with glucose intolerance or type 2 diabetes by slowing the release of glucose into the blood. 

The byproducts of fiber fermentation in the colon by gut bacteria often have beneficial effects on carbohydrate metabolism. Eating resistant starch, for example, lowers the postprandial blood glucose spike. This reduction may also extend to subsequent meals, indicating it’s honing your ability to handle glucose. Everyone can benefit from better glucose management, but it’s far more critical for people eating significant amounts of glucose.

3) “All the healthiest people studied eat fiber!”

Observational studies are fun and all, but they’re not a good way to prove the healthfulness of fiber. Looking at fiber intake is just about the best way to capture the “healthy user”—that person who does everything right, like walk daily, exercise regularly, abstain from tobacco, avoid binge drinking, and eat whole foods rather than refined ones. It doesn’t say anything definitive about the health effects of the specific dietary variable they’re observing.

That said, the fact that most healthy populations eat whole foods containing fiber indicates that fiber probably isn’t actively harmful.

4) “Fiber is just roughage for big impressive poops. No functional use.”

That’s mostly true of insoluble fiber, which is pure waste material that shreds your intestinal lining and increases stool volume.

There’s considerable evidence that people with type 2 diabetes can really benefit from prebiotic fiber supplementation:

  • Chicory-derived inulin, a potent prebiotic fiber, reduces liver enzymes and HbA1c, improves blood pressure and fasting glucose, and increases calcium homeostasis.
  • Inulin improves immune markers and glycemic control.
  • Resistant starch lowers insulin resistance and inflammation.

A review of studies found that while the prebiotic inulin reduces LDL-C (an imperfect biomarker of dubious utility) in all populations, only in type 2 diabetics does inulin improve HDL and blood glucose control. 

Prebiotic fiber may also help certain patients with non-alcoholic fatty liver disease (NAFLD). The usual therapy for NAFLD patients is weight loss. You lose enough body fat elsewhere and the fat you’ve accumulated in the liver starts to disappear, too.

What about lean NAFLD patients without any real weight to lose?

In lean patients with NAFLD, a synbiotic—blend of prebiotic fiber with probiotic bacteria—reduces liver fat and fibrosis by improving inflammatory markers. Pre-emptive consumption of prebiotics may even protect against the development of NAFLD.

Another function of fiber that occurs in everyone is the production of short chain fatty acids by gut bacteria. When gut bacteria ferment prebiotic fiber, they produce short chain fatty acids, many of which have beneficial metabolic effects.

Butyrate is the most important short chain fatty acid. It fuels colon cells and may prevent colon cancer. Its relationship with existing colon cancer cells is more controversial. Read more about that here.

One interesting line of research is studying the interaction between the ketone body beta-hydroxybutyrate and the short chain fatty acid butyrate. Initial indications suggest that the two may have synergistic effects on cognition, inflammation, and overall health. That alone may be a reason to make sure you get prebiotic fiber on your ketogenic diet, just to hedge your bets.

Now, might a low-carb or ketogenic diet work better for people with type 2 diabetes than adding fiber to their normal diet? Sure. Could such a diet reduce the need for fiber? Yeah, I could see it. The same goes for NAFLD—low carb diets are also excellent in this population. And perhaps people who aren’t eating so many carbs don’t need the short chain fatty acids to improve their metabolic function and insulin sensitivity. But the evidence for fiber in type 2 diabetes and NAFLD stands, and I suspect short chain fatty acid production matters even in low carb or keto dieters.

5) “Fiber cures constipation.”

It depends.

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.

A 2012 review found that while fiber may increase stool frequency, it doesn’t improve stool quality, treatment success, or painful defecation. Similarly, glucomannan, a soluble fiber, moderately improves defecation frequency in constipated kids, but has no effect on stool quality or overall treatment success.

However, galactooligosaccharides, a class of prebiotic fiber, do appear to improve idiopathic constipation. And inulin, another prebiotic fiber, improves bowel function and stool consistency in patients with constipation.

6) “Fiber aggravates gut issues.”

Some say fiber cures gut issues like IBS and IBD. Others say fiber aggravates them. Who’s right? Maybe both.

Both IBS-D (irritable bowel syndrome with diarrhea) and IBS-C (irritable bowel syndrome with constipation) patients can benefit from soluble fiber (psyllium) while insoluble fiber (bran) is far less effective.

Wheat bran works okay for IBS, if the patients can tolerate it. They tend to tolerate something like hydrolyzed guar gum much better.

For IBD, the evidence is mixed. One survey of Crohn’s patients found that those eating more fiber (23 grams/day) had fewer flareups than those eating less (10 grams/day), while colitis patients reported no difference in symptoms based on fiber intake.

On the other hand, studies indicate that a low-FODMAP diet, which eliminates most sources of fiber, especially fermentable prebiotic fiber, is an effective treatment for IBS and IBD. Low-FODMAP diets have been shown to reduce bloating, abdominal pain, quality of life, and overall symptoms in intestinal disorders.

These contrary results may not even be contradictory. If your gut’s messed up, one solution could be to add back in the fibers you’re missing. Another could be to take all the fiber out and start from scratch.

7) “Fiber reduces nutrient absorption.”

For a long time, the consensus was that fiber tends to bind with minerals in the gut and thus reduce their absorption. These days, researchers understand that many of these fiber-bound minerals become available after fermentation in the colon.

Another wrinkle is that dietary fiber often comes with phytic acid, which binds minerals and prevents their absorption. Take wheat bran. Often deemed “wheat fiber” and lambasted for its tendency to bind minerals, wheat bran isn’t just fiber. It’s also a significant source of mineral-binding phytic acid.

Prebiotics increase absorption of magnesium, heme iron, and calcium. This makes sense. Even if the prebiotics are binding minerals, they release them once they reach the colon for fermentation by gut bacteria.

Fiber may reduce absorption of plant polyphenols, however.

8) “No one needs fiber.”

On the surface, this appears to be a sound conclusion. The human host digestive system cannot digest it. The majority of the fiber we eat gets pooped out as literal waste material. Certain classes of fiber may improve our gut health, but no one is keeling over from a lack of fiber in their diet.

Some have argued that a sterile gut is ideal if you have the right diet, that employing vast hordes of gut bacteria is just an adaptive measure taken to deal with a substandard diet full of roughage. The problem is that most people throughout history and prehistory have eaten that roughage, employed those gut bacteria, utilized the metabolites those bacteria produce. I suspect thinking long and hard before you consider it immaterial to human health.

If that were true, why would breast milk—the only food specifically designed for human consumption—contain loads of indigestible oligosaccharides that feed the growing gut biome? Even if it turns out that feeding the gut biome is only vital during infancy, that’s still a population of humans who truly need fiber.

Here’s where I come down: Fiber is an intrinsic part of many whole plant foods (and even whole animal foods, if it turns out that our gut bacteria can utilize “animal fibers” like other top carnivores). The Primal-friendly plants, the ones our ancestors grew up eating approximations of, like fruits, vegetables, roots, and tubers, are mostly higher in soluble fiber and lower in insoluble fiber. The only way to get huge doses of insoluble fiber these days is with supplementation or by eating grains. I don’t suggest eating grains or supplementing with insoluble fiber. I do suggest eating fruits, vegetables, roots, and tubers (while managing your carbs).

As for the carnivore issue, I’m open to the possibility that a properly-constructed carnivorous diet (which may, remember, include gristly animal fiber) obviates the need for plant fiber, prebiotic or otherwise. I’m not confident enough to try it myself, though.

Do I think everyone should be supplementing with prebiotic fiber? No. I add inulin to my Primal Fuel protein powder, mostly to improve mouth-feel but also to feed beneficial microbes and increase butyrate production. I add prebiotic cassava fiber to my collagen bars, again to improve texture and feed gut bacteria. And I’ll sometimes use raw potato starch for its considerable resistant starch content, often just mixing it into sparkling water and drinking it straight. But for the most part, the fiber I eat is incidental to the foods I consume. Berries, non-starchy vegetables, jicama, garlic, onions, green bananas, nuts—these are all foods rich in fiber, particularly prebiotic fiber, and I eat a fair amount of them while remaining low-carb and often keto.

As you can see, the fiber story isn’t simple. At all. There are many variables to consider. If you’re confused and unsure of how to think about fiber, you’re on the right track.

What do you think, folks? How has fiber helped or harmed you? I’d love to hear from everyone.

Take care and be well.

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