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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After almost a century of being outlawed, hemp—a form of cannabis with extremely low levels of psychoactive THC—is now legal in the United States. This is big news for people interested in the therapeutic effects of cannabidiol (or CBD) because—while hemp doesn’t contain enough THC, the compound that provides the “high” of cannabis, or any other psychoactive compounds—it does contain cannabidiol (CBD).
For years, all anyone talked about when they talked about cannabis was the THC content. Breeders focused on driving THC levels as high as possible and ignored the other compounds. Even pharmaceutical companies interested in the medical applications of cannabis focused on the THC, producing synthetic THC-only drugs that performed poorly compared to the real thing. It turns out that all the other components of cannabis matter, too, and foremost among them is CBD.
CBD doesn’t get you high, but it does have big physiological impacts. These days, researchers are exploring CBD as a treatment for epilepsy, anxiety, and insomnia. They’ve uncovered potential anti-inflammatory, anxiolytic, and immunomodulatory properties. And now that it’s quasi legal, hundreds of CBD-rich hemp oil products are appearing on the market.
What are the purported benefits of using CBD-rich hemp oil, and what does the evidence say?
Although CBD research is growing, it’s still understudied and I expect I’ll have to update this post in the near future with more information. But for now, here’s a rundown of what the research says.
The Health Benefits of CBD In Hemp Oil
CBD For Anxiety Reduction
Anxiety can be crippling. I don’t have generalized social anxiety, but I, like anyone else, know what it feels like to be anxious about something. It happens to everyone. Now imagine feeling that all the time, particularly when it matters most—around other people. The average person doesn’t consider the import and impact of anxiety on a person’s well-being. If CBD can reduce anxiety, that might just be its most important feature. Does it?
Before a simulated public speaking event, people with generalized social anxiety disorder were either given 600 mg of CBD or a placebo. Those who received CBD reported less anxiety, reduced cognitive impairment, and more comfort while giving the speech. Seeing as how people without social anxiety disorder claim public speaking as their biggest fear, that CBD helped people with social anxiety disorder give a speech is a huge effect.
This appears to be legit. A placebo-controlled trial is nothing to sniff at.
CBD For Sleep
A 2017 review provides a nice summary of the effects of CBD on sleep:
In insomnia patients, 160 mg/day of CBD increased sleep time and reduced the number of arousals (not that kind) during the night.
Lower doses are linked to increased arousals and greater wakefulness.
In preliminary research with Parkinson’s patients, CBD reduced REM-related behavioral disorder—which is when you basically act out your dreams as they’re happening.
More recently, a large case series (big bunch of case studies done at once) was performed giving CBD to anxiety patients who had trouble sleeping. Almost 80% had improvements in anxiety and 66% had improvements in sleep (although the sleep improvements fluctuated over time).
While its psychoactive counterpart THC has been embroiled in controversial links with psychosis and schizophrenia for decades, CBD may be an effective counterbalancing force for mental health.
In patients with schizophrenia, six weeks of adjunct treatment with cannabidiol resulted in lower rates of psychotic symptoms and made clinicians more likely to rate them as “improved” and made researchers more likely to rate them as “improved” and not “severely unwell.” There were also improvements in cognitive performance and overall function. It seems the “adjunct” part of this study was key, as other studies using cannabidiol as the only treatment mostly failed to note improvements.
This was placebo controlled, so it makes a good case for CBD hemp oil as adjunct treatment (in addition to regular therapy) in people with schizophrenia.
Among 11 PTSD patients who took an average of 50 mg of CBD per day for 8 weeks, 10 (90%) experienced a 28% improvement in symptoms. No one dropped out or complained about side effects. CBD seemed to particularly benefit those patients who had issues with nightmares.
This is promising but preliminary. This was an 11-person case study, not a placebo-controlled trial.
A recent review of four human trials lays out the evidence: More than a third of all epilepsy patients experienced 50% or greater seizure reductions with just 20 mg of CBD. The effect of CBD on seizure activity is so widely acknowledged and understood that the only FDA-approved CBD-based product is Epidiolex, a plant-based CBD extract used to treat seizures in patients with Dravet syndrome and Lennox-Gastaut syndrome.
CBD for epilepsy is legit. Side note: I wonder how CBD would combine with ketogenic dieting for epilepsy control.
By far the biggest draw for medical consumers of CBD is its supposed ability to nullify pain.
In one study, researchers induced arthritis in rats with intra-articular injections, then gave them CBD. Rats given CBD were able to put more weight on their joints and handle a heavier load before withdrawing. Local CBD reduced nerve damage.
That’s great for pet rats. What about people?
There actually isn’t a lot of strong data on pain management using CBD by itself. Far more robust is the evidence for using CBD with THC for pain. According to this group of researchers, the two compounds exert “constituent synergy” against neuropathic pain. One study found that low doses of each were more effective combined than high doses of either alone in neuropathic cancer-related pain. Another gave a THC/CBD oromucosal spray to otherwise treatment-resistant neuropathy patients, finding that the spray reduced pain, improved sleep, and lessened the severity of symptoms.
Anecdotal evidence for pain relief and other benefits with CBD is vast. Chris Kresser, a practitioner and researcher I trust, swears by it. I have employees who use it quite frequently, reporting that it improves their sleep, hones their focus, reduces pain, speeds recovery, and reduces anxiety. These things are always hard to evaluate, but I can say that my people do great work, and I have zero reason to distrust them.
In later posts, I’ll probably revisit some of these other, more theoretical or anecdotal potential benefits to see if there’s any evidence in support.
Is It Safe?
A recent study gave up to 6000 mg of CBD to healthy subjects, finding it well tolerated and the side effects mild and limited to gastrointestinal distress, nausea, somnolence, headaches, and diarrhea. For comparison’s sake, keep in mind that a typical dose of CBD is 20 mg.
Mouse research indicate that extended high-dose CBD (15-30 mg/kg of bodyweight, or 1200-2400 mg per day for an 80 kg man) might impair fertility. Male mice who took high-dose CBD for 34 days straight experienced a 76% reduction in testosterone, reduced sperm production, and had dysfunctional weird-looking sperm. In the 30 mg/kg group, the number of Sertoli cells—testicular cells where sperm production takes place and sperm is incubated—actually dropped. Male mice taking CBD also were worse at mounting females and had fewer litters.
Those are really high doses. For epilepsy, a common dose is 600 mg/day, and that’s for a severe condition. Most other CBD therapies use much smaller doses in the range of 20-50 mg/day. Long term safety may still be an issue at these lower doses, but we don’t have any good evidence that this is the case.
There’s some evidence that the dosages of CBD required to achieve anti-inflammatory effects are also high enough to induce cytotoxicity in healthy cells, though that’s preliminary in vitro (petri dish) research and as of yet not applicable to real world applications. Time will tell, though, as the legal environment opens up and we accumulate more research.
Is Isolated CBD the Same As Whole Plant Extracts?
As we’ve learned over the past dozen years of reading about nutrition and human health, whole foods tend to be more effective than isolated components. Whole foods have several advantages:
They contain all the components related to the compound, especially the ones we haven’t discovered and isolated. Supplements only contain the isolated compounds we’ve been able to quantify.
They capture all the synergistic effects of the multiple components working together. Isolated supplements miss that synergy unless they specifically add it back in, and even then they’ll probably miss something.
It’s likely that whole plant hemp extracts high in CBD are superior to isolated synthetic CBD for the same reason. Is there any evidence of that?
A high-CBD cannabis whole plant extract reduces gut inflammation and damage in a mouse model of inflammatory bowel disease. Purified CBD does not.
Even at a 2:1 CBD:THC ratio, co-ingesting isolated CBD with isolated THC using a vaporizer fails to reduce the psychotic and memory-impairing effects of THC. In another study, however, smoking cannabis naturally rich in both CBD and THC completely prevented the memory impairment.
And as we saw in the pain section above, THC combined with CBD seems more effective against pain than either alone.
That’s not to say isolated (even synthetic in some cases—see note below) CBD isn’t helpful. We saw it improve joint pain and reduce nerve damage in arthritic rats. It’s just that full-spectrum hemp oil containing multiple naturally-occurring compounds is probably ideal for general health applications. Specific conditions requiring high doses may be another question entirely. Again, we’ll find out as more research comes out.
A word about synthetics: this is fodder for a follow-up, but it appears there may be additional concerns with synthetic CBD, and even supposedly “natural” CBD companies have in some cases allegedly added ingredients to their formulas without letting consumers know.
Is It Legal?
CBD-rich hemp oil lies in a legal grey area. The recently passed Farm Bill allows people to grow and make products from industrial hemp, as long as it contains less than 0.3% THC. That means CBD derived from industrial hemp is legal at a federal level. But because the Farm Bill has provisions that allow states to set their own rules, legality at a state level is more complicated.
States where hemp is still illegal—South Dakota, Idaho, and Nebraska—do not permit the sale or use of hemp-derived CBD oil.
In states that permit recreational cannabis—California, Vermont, Massachusetts, Maine, Oregon, Colorado, Washington, Nevada, Michigan, and Alaska—CBD derived from both hemp and psychoactive cannabis is legal.
In all other states, hemp-derived CBD is legal.
The FDA has yet to approve of CBD, so most of the big online retailers like Amazon and Walmart don’t allow CBD products to be advertised. However, Amazon sells a ton of “hemp extract” tinctures and oils with “hemp extract content” listed in milligram dosages—a workaround for listing the CBD content.
If you’re looking for CBD-rich hemp oil, watch out for culinary hemp oil, which comes in larger quantities and has no discernible CBD content. CBD-rich hemp oil will come in dropper bottles, not liters.
You can also buy directly from manufacturers online who proudly advertise their CBD content. I’ve heard good things about Ojai Energetics and Sabaidee, though I haven’t used either.
Many health food stores sell it. Surprisingly, I’ve seen it in every pet store I’ve entered in the last half year.
Word of Caution: Because it isn’t regulated by the FDA yet, there’s no telling exactly what you’re getting. Choose a product with verifiable lab tests. Many CBD hemp oil products have far less CBD than advertised. In addition to CBD content, the most reputable manufacturers also test for pesticides, heavy metals, mycotoxins, and bacteria and advertise their results.
CBD-rich hemp oil is a hot topic these days, and it’s only going to get hotter. I think the compound shows great promise in promoting health and wellness, and I’ll look forward to doing more research as it unfolds.
For now, what about you? Do you use CBD? Have you noticed any benefits? Any downsides? Share your questions and feedback down below.
Thanks for reading, everyone. Take care.
Bergamaschi MM, Queiroz RH, Chagas MH, et al. Cannabidiol reduces the anxiety induced by simulated public speaking in treatment-naïve social phobia patients. Neuropsychopharmacology. 2011;36(6):1219-26.
Lattanzi S, Brigo F, Trinka E, et al. Efficacy and Safety of Cannabidiol in Epilepsy: A Systematic Review and Meta-Analysis. Drugs. 2018;78(17):1791-1804.
Elms L, Shannon S, Hughes S, Lewis N. Cannabidiol in the Treatment of Post-Traumatic Stress Disorder: A Case Series. J Altern Complement Med. 2018;
Serpell M, Ratcliffe S, Hovorka J, et al. A double-blind, randomized, placebo-controlled, parallel group study of THC/CBD spray in peripheral neuropathic pain treatment. Eur J Pain. 2014;18(7):999-1012.
Silva RL, Silveira GT, Wanderlei CW, et al. DMH-CBD, a cannabidiol analog with reduced cytotoxicity, inhibits TNF production by targeting NF-kB activity dependent on A receptor. Toxicol Appl Pharmacol. 2019;368:63-71.
Carvalho RK, Souza MR, Santos ML, et al. Chronic cannabidiol exposure promotes functional impairment in sexual behavior and fertility of male mice. Reprod Toxicol. 2018;81:34-40.
Morgan CJA, Freeman TP, Hindocha C, Schafer G, Gardner C, Curran HV. Individual and combined effects of acute delta-9-tetrahydrocannabinol and cannabidiol on psychotomimetic symptoms and memory function. Transl Psychiatry. 2018;8(1):181.
Morgan CJ, Schafer G, Freeman TP, Curran HV. Impact of cannabidiol on the acute memory and psychotomimetic effects of smoked cannabis: naturalistic study: naturalistic study [corrected]. Br J Psychiatry. 2010;197(4):285-90.
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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 almostno 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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