For this week’s Dear Mark, I’m answering a question from a reader about a topic I thought I’d covered (so did they) already. A quick look through the archives (hey, I can’t remember absolutely everything I ever wrote) showed that I had not, so here we go. It’s all about whether fermented foods—sauerkrauts, kimchis, pickles, yogurts, and any other food that has been acted upon by probiotic bacteria—make eating meat healthier and more enjoyable. From the start, I suspected that they do, but I had to confirm it in the scientific literature.

Let’s find out:

Hi Mark,
I’m trying to find an article on why you should eat ferments with meat, (how it breaks down the fats) our mutual friend Hilary, AKA #thelunchlady ? and I are working on getting some of the high end butcher’s around LA to understand this, so they can help educate their customers. I was hoping to find info on your site, but now hoping you might write one for us

As for the effect you mention—fermented food breaking down the fat in meat—I’m unaware of any evidence. I am aware of a beneficial effect of fermented food on carbohydrate metabolism though. See, lactofermentation produces acetic acid as a byproduct. Acetic acid provides the “sour” flavor, the acidity of a batch of sauerkraut or pickles. It’s also what makes vinegar so sour, and there’s a long line of evidence showing that vinegar improves glucose tolerance and reduces the blood glucose load of high carb meals.

  • A 2017 review of the evidence found that vinegar was significantly effective at reducing both postprandial blood sugar and insulin levels.
  • It works in type 2 diabetics who eat vinegar with their high-carb meals, lowering the blood glucose response.
  • Research shows that acetic acid, rather than some other component in the vinegar, is the active component responsible for the effect on blood sugar. Anything with acetic acid should work, like food ferments.

That’s carbohydrate, and it’s good info, but you didn’t ask about carbs. You asked about meat. So, is fermented food pointless when eating meat? Not at all.

There are many examples of traditional cultures and cuisines making it a point to serve fermented foods with meats:

Koreans, kimchi, BBQ.

Germans, sauerkraut, sausage.

Japanese, pickles/natto/miso, meat/fish.

Indians, yogurt/pickles/chutneys, meat curry/tandoori chicken.

Italians, cheese, salami (itself a fermented meat).

They may not have “known” about the biochemistry. They weren’t citing PubMed studies. But over the many hundreds of years, these pairings emerged as combinations that just worked and made people feel good and the food go down more easily.

What could be going on here?

One thing I’ve stressed over the years is the importance of consuming foods high in polyphenols, not only for their isolated health benefits but for their ameliorative effects on the potential carcinogenicity of meats—particularly high-heat cooked meats (barbecue, grilling, searing). If you eat foods high in polyphenols, like blueberries or leafy greens, with your meat, that meal becomes healthier. It reduces the formation of carcinogenic compounds and reduces the peroxidative damage done to the fat.

And if you take a food high in polyphenols and subject it to fermentation, those polyphenols change and actually become more effective.

Red wine is one such fermented food that is higher in polyphenols than its non-fermented counterpart. The fermentation process alters the polyphenols already present in the grapes, making them more bioavailable and more effective, and creating entirely new compounds in the process. One reason red wine pairs so well with steak on a subjective level is that it actually reduces the formation of toxic lipid oxidation byproducts in “simulated digestion” studies that attempt to recreate the stomach environment after a meal, inhibits the absorption of those toxic lipid byproducts, and, when added to meat marinades, reduces the formation of heat-related carcinogens when you cook the meat, even over open flame. The responsible compound for these effects in red wine isn’t the alcohol, it’s the polyphenols. Grape juice doesn’t have the same effect.

This applies to everything. Fermentation of almost any other food, from beans to cabbage to garlic, also changes and improves the antioxidative capacity of the polyphenols. And the more polyphenols a food has, and the more effective they are at reducing oxidation, the healthier they’ll make any meat we eat.

Fermented foods also contain probiotic bacteria, and there’s some limited evidence that certain bacterial strains can actually enhance metabolism of cooked meat carcinogens.

So, in a roundabout way, fermented foods actually are improving the way we digest the fats in meat. They aren’t quite “breaking them down,” but they are allowing us to metabolize them in a healthier way that produces fewer toxic byproducts and inhibits our absorption of the toxic byproducts that do slip by.

This actually gives me a good idea for a post: A series of elevator pitches that inspired readers can use to lobby restaurant owners, butchers, doctors, and anyone else about the otherwise complicated health and nutrition topics we’ve bandied about on this blog for a decade. Most folks’ brains will glaze over when you start talking “omega-3s” or “peroxidized lipids” or “oxidized LDL particles” or “high heat carcinogens,” but it’s still important information. I think I’ll start putting that together in the next few weeks, starting with today’s topic, and I could really use your help. What other topics have you wanted to broach but can’t figure out how to make relatable, simplistic, or elegant enough to drop in casual conversation with professionals (or friends) who could help make a difference?

Let’s get a list going and try to knock this out.

That’s it for today, folks. Take care and be well. Thanks for reading!

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References:

Shishehbor F, Mansoori A, Shirani F. Vinegar consumption can attenuate postprandial glucose and insulin responses; a systematic review and meta-analysis of clinical trials. Diabetes Res Clin Pract. 2017;127:1-9.

Liatis S, Grammatikou S, Poulia KA, et al. Vinegar reduces postprandial hyperglycaemia in patients with type II diabetes when added to a high, but not to a low, glycaemic index meal. Eur J Clin Nutr. 2010;64(7):727-32.

Mettler S, Schwarz I, Colombani PC. Additive postprandial blood glucose-attenuating and satiety-enhancing effect of cinnamon and acetic acid. Nutr Res. 2009;29(10):723-7.

Gorelik S, Ligumsky M, Kohen R, Kanner J. The stomach as a “bioreactor”: when red meat meets red wine. J Agric Food Chem. 2008;56(13):5002-7.

Gorelik S, Ligumsky M, Kohen R, Kanner J. A novel function of red wine polyphenols in humans: prevention of absorption of cytotoxic lipid peroxidation products. FASEB J. 2008;22(1):41-6.

Kanner J, Gorelik S, Roman S, Kohen R. Protection by polyphenols of postprandial human plasma and low-density lipoprotein modification: the stomach as a bioreactor. J Agric Food Chem. 2012;60(36):8790-6.

Harbaum B, Hubbermann EM, Zhu Z, Schwarz K. Impact of fermentation on phenolic compounds in leaves of pak choi (Brassica campestris L. ssp. chinensis var. communis) and Chinese leaf mustard (Brassica juncea coss). J Agric Food Chem. 2008;56(1):148-57.

Kimura S, Tung YC, Pan MH, Su NW, Lai YJ, Cheng KC. Black garlic: A critical review of its production, bioactivity, and application. J Food Drug Anal. 2017;25(1):62-70.

Nowak A, Libudzisz Z. Ability of probiotic Lactobacillus casei DN 114001 to bind or/and metabolise heterocyclic aromatic amines in vitro. Eur J Nutr. 2009;48(7):419-27.

The post Dear Mark: How Do Fermented Food and Meat Interact? appeared first on Mark’s Daily Apple.

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For today’s edition of Dear Mark, I’m answering one eternal question: How do the Hadza tribespeople of Northern Tanzania eat so much honey and maintain their trim figures and pristine metabolic health? Are they eating keto whenever they’re not eating honey? Are they running hill sprints to burn through glycogen stores and improve their insulin sensitivity? Are they trading mongongo nuts for Metformin? Or is there something unique about honey that makes it different than sugar?

But before I get to the question, it’s a brand new year.

This New Year promises to be bigger and better than ever. Change is in the air, and not just in my own life. Everyone I talk to—all my friends, colleagues, family members, and random acquaintances—seems to be entering a period of great change. Their professional lives, their relationships, their health, their mindsets are all shifting. And for the better. The way I see it is that change happens regardless of what you do. It’s a far better idea to take the reins and make the change work in your favor than let yourself be swept away by powers and fate unseen.

Happy New Year to everyone! I hope 2019 is your best yet, and I’d love to hear your visions for it.

Okay, on to the question:

What are your thoughts on honey as the sweetener for the mulled wine? Given how the Hadza draw so many of their carbs from honey (especially given the particular sugars and micronutrients that it contains), I’m surprised it doesn’t appear more often in these recipes that call for sweetening.

In case readers are unaware of the reference, the Hadza are one of the few remaining hunter-gatherer groups on this planet. They inhabit northern Tanzania, and their lives haven’t changed much at all. They’ve resisted ethnic admixture from other groups. They still hunt and gather for the vast majority of their calories. Their hunting and foraging grounds have been condensed due to pressure from the state, and there are probably fewer game animals available, but they’re still in the same general area. According to their oral traditions, there’s even no indication that they came from somewhere else.

One of the more striking features of their diet is their utilization of honey.

Ask the average Hadza tribesperson what their favorite food is and “honey” will be the answer.

Catch the Hadza during the right month and they’ll get half their calories from honey. Averaged out across the year, they get 15% from honey.

They even use a bird called the honey guide to lead them to the choicest hives. After completing the harvest, they’ll burn or bury the remnants to keep their honey guide from getting too full for the next search.

The honey isn’t your store-bought, pristine golden syrup smelling faintly of HFCS. It’s straight up honeycomb, teeming with bees and larvae and pollen and the queenly secretions called royal jelly. In fact, studies tend to emphasize that the Hadza get 15-50% of their calories not from honey, but from “honey and bee larvae.”

Bee larvae, also known as bee brood, is packed with protein, vitamins, and minerals. It’s high in folate, B12, thiamine, pantothenic acid—pretty much all the B vitamins—and biotin, to name a few.

Whole hive eating also means eating the royal jelly, a potent, superconcentrated secretion used to feed larvae and queens. Think of it as colostrum, the potent milk mammals provide for their infants in the first few days of life. Royal jelly has shown potential activity (in humans, no less) against allergic rhinitisreduced the toxicity of cancer drugs in patients, lowered cholesterol in adults with high cholesterol (and women), and improved glycemic control and oxidative stress in diabetics.

How about the honey itself? I’ve written about honey as a sweetener and explored how its metabolic effects differ from plain white sugar. Suffice it to say, the evidence is clear that honey isn’t just sugar. Honey contains sugar—a lot of sugar—but it’s much more than that.

set of studies in humans compared the effects of honey, sham-honey (a mix of fructose and glucose), dextrose (which is just glucose), and sucrose on several health markers. Honey resulted in smaller blood glucose spikes (+14%) than dextrose (+53%). Sham honey increased triglycerides, while real honey lowered them along with boosting HDL and lowering LDL. After fifteen days of honey feeding, CRP and LDL dropped. Overall, honey improved blood lipids, lowered inflammatory markers, and had minimal effect on blood glucose levels, despite being similarly high in fructose in particular and sugar in general.

So, in some respects, the honey the Hadza eat like crazy isn’t the honey that most of us can easily obtain in stores or even farmer’s markets. Yet even standard honey is different from—and better than—white sugar.

This is a roundabout way of saying that a little honey will be just fine in your mulled wine. Extra points if you can throw some bee larvae and royal jelly in there, with maybe even a dash of Hadza fecal bacteria.

Of course, don’t eat 15% honey diets. You are not Hadza. You are not living like the Hadza. You don’t have the precise genetic makeup of the Hadza. It won’t work as well for the average Westerner reading blogs.

Do you eat honey? How do the metabolic effects compare to sugar in your experience?

That’s it for today, folks. Thanks for reading, and be sure to tell me your thoughts and New Year intentions down below.

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References:

Shaha A, Mizuguchi H, Kitamura Y, et al. Effect of Royal Jelly and Brazilian Green Propolis on the Signaling for Histamine H Receptor and Interleukin-9 Gene Expressions Responsible for the Pathogenesis of the Allergic Rhinitis. Biol Pharm Bull. 2018;41(9):1440-1447.

Osama H, Abdullah A, Gamal B, et al. Effect of Honey and Royal Jelly against Cisplatin-Induced Nephrotoxicity in Patients with Cancer. J Am Coll Nutr. 2017;36(5):342-346.

Chiu HF, Chen BK, Lu YY, et al. Hypocholesterolemic efficacy of royal jelly in healthy mild hypercholesterolemic adults. Pharm Biol. 2017;55(1):497-502.

Lambrinoudaki I, Augoulea A, Rizos D, et al. Greek-origin royal jelly improves the lipid profile of postmenopausal women. Gynecol Endocrinol. 2016;32(10):835-839.

Pourmoradian S, Mahdavi R, Mobasseri M, Faramarzi E, Mobasseri M. Effects of royal jelly supplementation on glycemic control and oxidative stress factors in type 2 diabetic female: a randomized clinical trial. Chin J Integr Med. 2014;20(5):347-52.

Al-waili NS. Natural honey lowers plasma glucose, C-reactive protein, homocysteine, and blood lipids in healthy, diabetic, and hyperlipidemic subjects: comparison with dextrose and sucrose. J Med Food. 2004;7(1):100-7.

The post Dear Mark: How Do the Hadza Eat So Much Honey? and Happy New Year! appeared first on Mark’s Daily Apple.

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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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For today’s edition of Dear Mark, I’m answering a few questions from readers. First, the diabetes drug metformin looks like a “wonder” drug, even (or especially) for non-diabetics. Are there any known side effects? Is there anything we should watch out for?

Second, I address some of the concerns and criticisms shared in response to the Kraft Heinz announcement post.

Are there any adverse side effects to Metformin? It was mentioned in the fasting study.

Metformin is a diabetes drug that’s garnered a lot of attention from longevity seekers, health nuts, and low-carbers. I can see why. It appears to improve gut health (possibly because it impedes carbohydrate absorption, thereby increasing the amount of fuel available to our colonic bacteria), reduce cancer risk, lower blood glucose, improve insulin sensitivity, and increase fat loss. As far back as 2012, people I respect like Robb Wolf were suggesting metformin as a general all-purpose health enhancer.

Most of the interest in metformin from the general health crowd comes from its potential effect on longevity. It’s quite good at activating AMPK, the same pathway activated by exercise, fasting, and calorie restriction. There’s even some human research that hints at an effect—diabetics who take metformin actually live longer than non-diabetics who don’t take it. That’s a profound correlation.

But metformin does exert some of its effects via the hormetic pathway, which suggests it’s a stressor and may have a dark side. What could it be?

Well, there’s one main adverse side effect.

B12 depletion. Time and time again, studies show that metformin users are more likely to have B12 deficiency, whether they’re PCOS patients, Type 2 diabetes patients or others. Even when you age-match, health-match, and overall lifestyle-match your groups, the long-term metformin users have a higher chance of B12 deficiency. That certainly sounds causal, and even if it’s not, it’s a big risk. B12 plays a huge role in a host of physiological pathways. It protects against dementia, anxiety, depression, and fatigue. Its absence from vegan diets is one of the main reasons most vegans eventually flounder and have to turn to supplements or sneak into burger joints when no one’s watching. B12 is that important for overall health.

If you’re going to take metformin, make sure you’re tracking your B12 intake and status.

I’m not saying that’s the definitive answer. There may be more side effects. There probably are more. But on the whole, it’s a promising drug.

Now I’m going to address some of the concerns and questions from last week’s post on the Kraft Heinz acquisition. You guys made some good points and asked tough questions. I have answers.

On Disruption Of the Food Industry Being Hard or Impossible:

Believe me: We have disrupted the food industry. The ancestral movement is quite good at disruption. Take the fitness industry—just look at CrossFit and the thousands of small “functional fitness” gyms popping up everywhere. And the lighting industry—notice all the bulbs with warmer, less-blue lighting. And the tech industry—see the sudden development and adoption of “nightmode” to protect sleep and circadian health. Primal Kitchen disrupted the mayo, condiment, and dressing industry, not by upending or destroying it, but by highlighting the coming shift. That’s exactly why the acquisition occurred. They realized that things are changing and have changed, and that a growing number of people care about the quality of their packaged food and are willing to pay for it.

One thing that I didn’t realize until I got into this business—the packaged food business—is that smaller companies all eventually butt up against a ceiling. At some point, the smaller guys simply don’t have access to the same avenues of distribution as the larger guys. This isn’t negotiable. If you want to expand, you need access. From the beginning I wanted to put high-quality mayo, condiments, and dressings—the “extra” stuff that provides much of the added fat and sugar in the Western diet—in millions of homes. I couldn’t do that without access to those distribution channels, those industry connections, that capital. Now I can.

Some Worried About the Quality Of the Product. Will It Change?

I was adamant about maintaining product quality and integrity from the earliest of discussions with Kraft Heinz, and they were fully aligned with this from the beginning. It’s clear to me that Kraft Heinz sees that increasing numbers of people are flipping mayo jars around and scanning the labels. They know that the folks who buy Primal Kitchen products do so only because the ingredients we use are the best around, the very same ingredients you’d use if you were making mayo or dressing at home. If those ingredients change, you will stop buying. Business 101.

I know that. Kraft Heinz knows that.

On Extreme Skepticism:

We all have choices: do we let life unfold before us and respond accordingly, or do we fall prey to cynicism and assume the worst? I strongly recommend not being a cynic. It keeps many of us from ever fulfilling our potential and achieving our goals and dreams.

When I started Primal Nutrition, I left a well-paid, stable gig and put all my (borrowed) money and energy into the new venture. I had a wife and two small children at home, and the future was uncertain. It could have gone very wrong. But I did it just the same, because on some level I knew it would work. I left security and comfort and a steady paycheck for struggle and nerves and anxiety. My goal of changing how people eat and thrive kept increasing, from a million people, to ten million to a hundred million (I always think big). Now, with the leverage that Kraft Heinz brings, that goal of bringing healthier options to everyone is within reach.

On the Opportunity At Hand:

All across the U.S., in small towns and metropolises, rural communities and suburban sprawl, the vast majority of people are still eating way more seed oil and shifting the fatty acid ratio of their tissues accordingly than humans have ever done.  I think of all the people dousing the salad their doctor said they should start eating in soybean oil-based dressing and buying “olive oil mayo” that was mostly just seed oil, and it frustrates me. Imagine if they switched? Imagine if they all switched? Imagine if we were able to shift the collective omega-6:omega-3 ratio back toward ancestral optimums. Longtime readers know how big a change a person can make in his or her health just by changing the fats you eat. Now imagine a population doing it.

It could be big.

That’s it for today, folks. Take care and share your thoughts below.

As always, thanks for reading.

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References:

Libby G, Donnelly LA, Donnan PT, Alessi DR, Morris AD, Evans JM. New users of metformin are at low risk of incident cancer: a cohort study among people with type 2 diabetes. Diabetes Care. 2009;32(9):1620-5.

Bannister CA, Holden SE, Jenkins-jones S, et al. Can people with type 2 diabetes live longer than those without? A comparison of mortality in people initiated with metformin or sulphonylurea monotherapy and matched, non-diabetic controls. Diabetes Obes Metab. 2014;16(11):1165-73.

De haes W, Frooninckx L, Van assche R, et al. Metformin promotes lifespan through mitohormesis via the peroxiredoxin PRDX-2. Proc Natl Acad Sci USA. 2014;111(24):E2501-9.

Esmaeilzadeh S, Gholinezhad-chari M, Ghadimi R. The Effect of Metformin Treatment on the Serum Levels of Homocysteine, Folic Acid, and Vitamin B12 in Patients with Polycystic Ovary Syndrome. J Hum Reprod Sci. 2017;10(2):95-101.

Pongchaidecha M, Srikusalanukul V, Chattananon A, Tanjariyaporn S. Effect of metformin on plasma homocysteine, vitamin B12 and folic acid: a cross-sectional study in patients with type 2 diabetes mellitus. J Med Assoc Thai. 2004;87(7):780-7.

The post Dear Mark: Metformin Side Effects, Kraft Heinz Deal Questions appeared first on Mark’s Daily Apple.

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Last week, Craig Emmerich graced us with a great post on the oxidative priority of various dietary fuel sources, namely fats, carbohydrates, and protein.

If you haven’t had the chance to read through Craig’s post, definitely do. The visuals really drive home the point of fuel priority. Visuals appeal to me. They have a way of sticking with you, and there’s a power in recalling them when you’re making daily choices.

Today, I’m going through and answering some of the questions you folks had in the comment board.

I’m actually answering a great series of questions from Gerard.

I’ve seen this analysis before, and always had the question – can we really lump “carbohydrates” together like this?

No, we can’t. Craig gave a great overview, a useful 30,000 foot view that’s sufficient for most people who just want to eat and metabolize their fuel better, but there are differences between different carbohydrates. I know he’d say as much, and he may have time to weigh in here, too. If his schedule allows, I’ll include his response later today. But back to the differences in carbohydrates…. I’ll save fructose versus glucose for my answers to Gerard’s next questions. What about others?

Think of fiber. Fiber the monolith is already different from more digestible carbohydrates like glucose and fructose in that we can’t extract very much (or even any) caloric energy from it. But you can go even further and look at the individual metabolic fates of the different types of fiber.

Fermentable fibers like inulin and resistant starch are fermented into short chain fatty acids like butyrate and propionate. These provide important cell signaling and are worth about 2 calories per gram, give or take. Others forms of fiber are not fermented and provide colonic bulk but not calories.

Certain carbohydrates are treated differently in different people. Lactose tolerance allows people to digest lactose with lactase and use it for fuel. Lactose intolerance prevents people from digesting lactose, instead diverting it to gut bacteria to ferment and cause terrible digestive distress. FODMAP intolerance is similar. Those with FODMAP intolerance ferment carbs like sugar, lactose, and others in the gut, producing gas but not calories; those without it digest the carbs, producing useable energy.

Are fructose and glucose metabolized differently for this purpose?

There are definitely differences. For one, glucose stimulates insulin production, while fructose does not. But the differences may not be as stark as we often think.

When scientists attached isotopes to fructose, had healthy sedentary people eat it, then tracked the metabolic fate of the fructose molecules, they found:

  • 50% ended up as glucose, converted by the liver to be used elsewhere in the body.
  • 25% ended up as lactate, converted by the liver.
  • 17% ended up as liver glycogen.
  • 2-3% was converted to fat in the liver via de novo lipogenesis.
  • The rest was oxidized and expelled as CO2.

According to the study authors, this is quite similar to the metabolic fate of glucose. Even if you’re talking about de novo lipogenesis, often considered the sole province of fructose overfeeding, research shows that overfeeding with glucose also provokes the creation of new fat.

As far as burning/oxidizing of ingested glucose and fructose, there are differences. At rest, people tend to burn fructose faster than glucose. During exercise, people tend to oxidize glucose faster than fructose. However, when you give someone both fructose and glucose together, they burn them faster than either fuel source alone. In one study, subjects were either given 100 grams of fructose, glucose, or fructose+glucose. The fructose group burned through 43.8% of their dose, the glucose group burned through 48.1% of theirs, while the fructose+glucose group burned through 73.6% of their dose.

Is the storage capacity for energy from fructose and glucose equivalent (i.e., liver vs muscle glycogen)?

There’s actually a misconception about fructose and glycogen repletion. Here’s the story you may have heard: Fructose can only contribute to liver glycogen, while glucose only contributes to muscle glycogen.

It’s not quite accurate. I believed it for awhile, too, until I actually checked it out. It turns out that both fructose and glucose are able to contribute toward both liver and muscle glycogen. Fructose is about half as efficient as glucose at replenishing muscle glycogen, as it first must be converted into glucose in the liver before being sent out, but it will eventually get the job done.

One big difference is that there’s a lot more room in your muscles than in your liver. The average person can store about 300 grams of glycogen in their muscles but only 90 grams in their liver. Even if the metabolic fates are ultimately pretty similar in a vacuum, in the real world there’s simply less room for liver glycogen, and, thus, less room for fructose in the diet without overstepping the bounds and incurring metabolic dysfunction.

So, if you’re talking about an overweight, sedentary person walking around with full glycogen stores eating a hypercaloric diet, fructose will behave differently than glucose. In the healthy, lean, eucaloric, and active, whole foods-based fructose isn’t a big deal and may not have a drastically different metabolic effect compared to glucose.

At any rate, discussing isolated fructose and isolated glucose may not even be very relevant to real world results. You’re eating fruit, not quaffing cola. You’re enjoying a sweet potato, not a bag of Skittles smothered in agave nectar. You’re eating both glucose and fructose together in the context of a meal, of a whole food. Don’t get too bogged down in the effects of isolated nutrient-poor sugars unless you’re consuming them that way.

To what extent is fructose metabolized in a manner that is more similar to alcohol than carbohydrate?

Fructose is metabolized in the liver. Alcohol is metabolized in the liver.

Fructose gets taken up by the liver without insulin. Alcohol ends up in the liver without insulin rising.

But after that, according to Richard Feinman, the similarities stop. Alcohol is a toxin with known toxic metabolites. There may be some benefit to low level exposure to alcohol, but it remains a toxin. Fructose can be situationally toxic, as in the obese guy with glycogen-replete fatty liver and full-blown diabetes, but we are physiologically capable of handing normal amounts without producing toxic metabolites. Feinman considers it more of a rhetorical device than a statement of facts.

That’s it for today, folks. Thanks for reading and if you have any further questions on the topic, let me know down below and I’ll do my best to get to them.

Take care!

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References:

Tappy L, Lê KA. Metabolic effects of fructose and the worldwide increase in obesity. Physiol Rev. 2010;90(1):23-46.

Sun SZ, Empie MW. Fructose metabolism in humans – what isotopic tracer studies tell us. Nutr Metab (Lond). 2012;9(1):89.

Blom PC, Høstmark AT, Vaage O, Kardel KR, Maehlum S. Effect of different post-exercise sugar diets on the rate of muscle glycogen synthesis. Med Sci Sports Exerc. 1987;19(5):491-6.

Mcdevitt RM, Bott SJ, Harding M, Coward WA, Bluck LJ, Prentice AM. De novo lipogenesis during controlled overfeeding with sucrose or glucose in lean and obese women. Am J Clin Nutr. 2001;74(6):737-46.

Rosset R, Lecoultre V, Egli L, et al. Postexercise repletion of muscle energy stores with fructose or glucose in mixed meals. Am J Clin Nutr. 2017;105(3):609-617.

The post Dear Mark: Oxidative Priority Followup appeared first on Mark’s Daily Apple.

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Yesterday, I linked to a study showing that the beneficial effects of high levels of cardiorespiratory fitness—the kind you build with cardio/endurance training, HIIT, and sprints—have no upper limit. At first glance, this study appears to bust the “myth” of chronic cardio and the U-shaped curve of endurance training and prove that the more you train, the longer you’ll live. This appears to run counter to some of my central claims—that too much mid-to-high intensity endurance exercise leads to burnout, health issues, and diminishing returns.

A commenter wrote a great comment that got me wondering:

As far as “the more exercise the better” study I wonder if folks who had to drop out of long distance cardio training due to injuries or cortisol driven exhaustion are considered in the equation? In other words, if you can tolerate chronic cardio you may live longer, otherwise it might break you down. Everyone has a sweet spot for exercising is my gut feeling and you have to “listen to your body”. I still like the primal mantra along the lines of (if I may be so presumptuous as to paraphrase Mark) “walk a lot, do sprints once a week, lift heavy things once or twice a week, spend time outdoors, take part in sports or recreational activities that are fun for you”.

What do I think is going on? How do the results of this paper jibe with my take on Chronic Cardio?

First off, we have to acknowledge the basic structure of the study.

This study didn’t actually measure “hours spent training.” They gave subjects treadmill tests (stress tests) to determine their cardiovascular fitness, then divided everyone into different tiers of fitness based on the results. In fact, the authors of the study criticized the shortcomings of previous studies which used self-reported training data instead of objective measurements of cardiorespiratory fitness like the treadmill test. This makes the study far more accurate and useful. It also means you can’t make any ironclad proclamations about the connections between hours spent training and longevity. You can certainly make inferences—people who had better cardio fitness probably spent more time training to get it—but there are other interpretations. All you can say for certain is that higher levels of cardio fitness predict greater longevity.

I don’t see how anyone could argue with that. Of course being fitter is better.

But my criticism of chronic cardio isn’t a criticism of cardiovascular fitness. It’s a criticism of how most people go around obtaining that fitness—by destroying their bodies.

That doesn’t have to happen anymore. Tons of top guys these days are finally figuring out that you don’t have to log as many laps/miles/etc as possible to maximize your performance, but that wasn’t always the case. I grew up convinced that the more miles I ran, the healthier I’d be. That’s how I did it back in my marathon and triathlon days, and it almost destroyed me and an entire generation of my peers.

You can train twice as much as the next guy yet have worse fitness, either because you’re not training intelligently, you’re overtraining and hampering the adaptive process, or you’re not sleeping. That’s chronic cardio. You can train less and get better results, if you’re optimizing your recovery, nutrition, and sleep. That’s Primal Endurance.

As for these subjects, there is some serious genetic confounding occurring. Those dudes with elite fitness levels well into their 70s are often a different breed. They’re hard to kill. They’re tough. They can withstand the discomfort of grueling mile after mile. What other types of discomfort can they bear and even grow from? They’re just more robust than the average 70-year-old. It may not be the elite training itself that’s making them resist death. It’s just as likely they have the genetic capacity to excel in endurance training, and even if they didn’t exercise they’d still live longer than average.

There’s also the healthy user bias. The kind of lifestyle regular exercisers follow emphasizes sleep, plenty of rest and recuperation, smart supplementation and nutrition, and all sorts of other things that are also linked to longer, better health.

This paper makes a strong case for using something like Primal Endurance to build great cardiorespiratory fitness without risking chronic cardio territory.

Thanks for writing and reading, folks. Take care!

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The post Dear Mark: Is There No Upper Limit to Endurance Training? appeared first on Mark’s Daily Apple.

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For today’s edition of Dear Mark, I’m answering two questions from readers. First, is it possible to become deficient in omega-6 fats as an adult? What would that even look like, and is there anything that might make omega-6 more important?

Second is a question related to last week’s feature on prostate health. Is saw palmetto an effective supplement for prostate issues? It depends on the issue.

Let’s go:

I have a question for “Dear Mark”
Here it is:

I am completely and totally primal for 10 years now. Can I become O6 deficient ? Since 90% of my fat intake is saturated or O3.

It’s technically possible to become deficient in omega-6 fatty acids. The early rat studies that discovered the essentiality of Omega-6s found that their complete removal made the subjects consume more food (without gaining weight), drink more water (without peeing more than rats on a normal diet), develop scaly skin, lose fur, urinate blood, go infertile, grow weird tails, and die early. All this despite eating an otherwise nutrient-dense diet with all the fat-soluble vitamins (they even removed the fat from cod liver oil and gave the vitamins), B vitamins, and other nutrients a rat could ever want. The only thing missing was a source of omega-6 fats.

Once they discovered the issue—a lack of omega-6—how’d they fix it?

Coconut oil didn’t work, for obvious reasons. It’s almost pure saturated fat.

Butter worked, but you had to use a lot. The omega-6 fraction of butter is quite low.

Cod liver oil worked, but it didn’t fully cure the deficiency disease.

Lard worked well, as did corn oil, liver, flax oil, and olive oil. All of those fat sources fully resolved the issue and eliminated the symptoms. They were all good to decent sources of omega-6 fatty acids.

They also tried pure linoleic acid (the shorter-chained omega-6 PUFA found in nuts and seeds and the animals that eat them) and arachidonic acid (the long-chain omega-6 PUFA found in animal foods). Both worked, but AA worked best.

Throughout all these trials, exactly how much omega-6 fat did the rats require in their diets to cure deficiency symptoms?

When they used lard to cure it, the rats got 0.4% of calories from omega-6 PUFA. If the numbers hold true for humans, and you’re eating 2500 calories a day, that’s just 10 calories of omega-6, or about a gram and a half of pure arachidonic acid to avoid deficiency.

When they used liver to cure it, the rats got 0.1% of calories from omega-6 PUFA. If the numbers hold true for humans, and you’re eating 2500 calories a day, that’s just 2.5 calories of omega-6, or about a third of a gram of arachidonic acid to avoid deficiency.

The truth is that omega-6 deficiency is extremely hard to produce, even when you’re trying your hardest. Way back in the 1930s, the early omega-6 researchers tried to induce deficiency in an adult by giving him a 2 grams fat/day diet for months. Nearly all fat was removed, particularly the omega-6 fats, and the rest of the diet was fat-free milk, fat-free cottage cheese, orange juice, potato starch, sugar, and a vitamin/mineral supplement. Maybe not the ideal Primal diet, but better than some.

He ended up improving his health, not hurting it. There was no sign of deficiency.

Omega-6 fats are everywhere in the food environment, even if you’re actively avoiding concentrated sources of them. No one is developing a deficiency these days. However, certain conditions might increase the tolerable or beneficial upper limits of omega-6 intake.

If you’re strength training with the intent to gain lean mass, a little extra arachidonic acid can improve your results. The dose used was 1.5 grams per day. Average intake through food runs about 250-500 mg, though Primal eaters heavy on the animal foods are probably eating more.

If you’re recovering from injury or healing a wound, a little extra arachidonic acid can speed it up. AA is an important co-factor in the inflammatory response necessary for tissue healing.

Well done, Mark. My doc just prescribed saw palmetto to reduce multiple nighttime visits to the bathroom, though the research I’m looking at says there’s no clinical evidence to support saw palmetto for prostate problems. Your take?

It depends on the problem.

Large observational trials have found no connection between saw palmetto supplementation and prostate cancer risk. It neither helps nor harms.

Saw palmetto does seem to help benign prostatic hyperplasia, a non-cancerous growth of the prostate. This won’t cause serious health issues directly, but it can impede the flow of urine and lead to multiple nighttime bathroom visits. Saw palmetto is quite effective at reducing nighttime urination. If that’s what your doc is trying to help, I’d say give it a shot.

You might ask about combining saw palmetto with astaxanthin. It’s been shown to reduce the conversion of testosterone into estradiol that can sometimes result from plain old saw palmetto supplementation.

That’s it for today, folks. Take care and be well. Chime in down below if you have any questions or comments.

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References:

Mitchell CJ, D’souza RF, Figueiredo VC, et al. Effect of dietary arachidonic acid supplementation on acute muscle adaptive responses to resistance exercise in trained men: a randomized controlled trial. J Appl Physiol. 2018;124(4):1080-1091.

Oh SY, Lee SJ, Jung YH, Lee HJ, Han HJ. Arachidonic acid promotes skin wound healing through induction of human MSC migration by MT3-MMP-mediated fibronectin degradation. Cell Death Dis. 2015;6:e1750.

Bonnar-pizzorno RM, Littman AJ, Kestin M, White E. Saw palmetto supplement use and prostate cancer risk. Nutr Cancer. 2006;55(1):21-7.

Saidi S, Stavridis S, Stankov O, Dohcev S, Panov S. Effects of Serenoa repens Alcohol Extract on Benign Prostate Hyperplasia. Pril (Makedon Akad Nauk Umet Odd Med Nauki). 2017;38(2):123-129.

Vela-navarrete R, Alcaraz A, Rodríguez-antolín A, et al. Efficacy and safety of a hexanic extract of Serenoa repens (Permixon ) for the treatment of lower urinary tract symptoms associated with benign prostatic hyperplasia (LUTS/BPH): systematic review and meta-analysis of randomised controlled trials and observational studies. BJU Int. 2018;

Angwafor F, Anderson ML. An open label, dose response study to determine the effect of a dietary supplement on dihydrotestosterone, testosterone and estradiol levels in healthy males. J Int Soc Sports Nutr. 2008;5:12.

The post Dear Mark: Omega-6 Deficiency and Saw Palmetto appeared first on Mark’s Daily Apple.

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For today’s edition of Dear Mark, I’m answering four questions. First, is air-frying gentler than deep-frying? Does it produce less acrylamide? Second, what do I think of a reader’s Primal-style plant-based way of eating? It’s actually quite good. Third, why didn’t I mention the Perfect Health Diet in last week’s post on top trending diets? And last, did I make a typo or grammatical error when I wrote “bad rap”?

Let’s find out:

Russian squat thing is great.

Anyone know if air frying potatoes creates acrylamide to the same degree normal deep frying does?

Wasn’t it? It’ll obviously never happen around here, and it would raise all sorts of civil rights issues if adopted across the board, but man would it be effective.

Turns out that air-frying is way more gentle on potatoes than deep-frying. Compared to deep-frying, air-frying potatoes reduced acrylamide formation by 90%.

And if you “pre-treated” the potatoes with a solution of nicotinic acid, citric acid, glycine, and salt, you’d get a further reduction of 80-90%.

I don’t know. The initial 90% sounds good enough that I’d hold off on that strange pre-treatment. In fact, I bet you could get a decent approximation of the benefits with a simple marinade on the potatoes. Maybe lemon juice and thyme?

Great round up Mark!

I’m just wondering what you think of a very ‘primal’ 95% vegan like diet?

I have Chron’s disease, but despite the data showing a carnivorous diet helps IBD I have found through a lot of trial and error I cannot handle cooked muscle or organ meat of any kind without a lot of pain.

I eat a vast variety of gently cooked vegetables, massaged salads, cooked and cooled legumes (also potatoes) Seaweed, some cooked and cooled buckwheat & rice, plus the occasional raw dozen oysters or fresh sashimi (Around once a week, expensive & I find it feels like enough). I only use olive oil (I have a Mediterranean background and find I tolerate it better than Butter or coconut oil)

I feel best on this, but wouldn’t really quantify it as any of the above diets.

Anything you think I could be missing out on eating this way? I’m a slim female with a high glucose tolerance if that helps.

Cheers Sophie

That’s a solid way to vegan. It’s quite close to what I recommend plant-based dieters do. You’re eating real food. You’re eating actual plants, not plant-based junk food. You’re avoiding seed oils. You’re eating oysters and raw fish—that’s huge. You’re treating your legumes right, and you don’t appear to be overly reliant on grains. Rice is one of the more innocuous grains, and buckwheat is actually a pseudo-cereal (and quite a nutrient-dense one at that).

A few suggestions:

Supplement creatine. It’s only found in red meat and fish, and most vegans are deficient. Correcting the deficiency tends to improve cognitive function. Since you eat fish once a week, you won’t be quite as deficient as others, but it’s still a good idea (and really inexpensive) to take 5 grams a day. Here’s a good creatine supplement.

Supplement carnosine and taurine. These are two other nutrients found primarily/only in animal foods. They act as antioxidants in the brain and play big roles in health and disease. Here’s a good carnosine supplement. Here’s a good taurine supplement.

Eat some raw egg yolks. I love a handful of raw egg yolks. One of my favorite ways to get choline, a true nootropic. It’s a decent, gentle source of uncooked high quality animal protein, too, which you can probably use.

How could you not mention the Perfect Health Diet?

The Perfect Health Diet is a great way to eat. Back in 2012, I even wrote the foreword to The Perfect Health Diet book. The problem is that it doesn’t qualify as a “popular diet trend.” It should be. I’d love for Dr. Oz to plug the PHD, for Oprah to include it in her book club. The world would be a much healthier place. But that’s not where we are.

The article was designed to inform newcomers to the diet scene while still providing enough meat for the more advanced readers. There just aren’t all that many newcomers looking for info on the Perfect Health Diet.

Speaking of which, if you guys have noticed a dearth of activity on Paul Jaminet’s part, it’s for good reason: He and his wife have been developing a new cancer drug that, according to his preliminary animal research, looks to be effective against every tumor they tested. Even the really malignant ones. Phase 1 human trials are set to begin in 2020. I really, really hope it all works out.

Typo heads-up…
You said: “Atkins gets a bad rap”. It should be Atkins gets a bad “rep”. The correct word (rep) is short for reputation. Thought you might like to know. Loved the post though!

Thanks for the tip!

I actually intended to use “rap,” though, in the sense of “criticism.” Think of the “rap sheet,” a list of a person’s crimes or offenses. Or “rap” as in “sharp blow,” sort of a physical manifestation of criticism or reprimand.

That’s it for today, folks. Thanks for reading and be sure to comment down below if you have any input or additional questions.

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References:

Sansano M, Juan-borrás M, Escriche I, Andrés A, Heredia A. Effect of pretreatments and air-frying, a novel technology, on acrylamide generation in fried potatoes. J Food Sci. 2015;80(5):T1120-8.

Antioxidant activity of carnosine, homocarnosine, and anserine present in muscle and brain. Proceedings of the National Academy of Sciences. 1988;85(9):3175.

Yamori Y, Taguchi T, Hamada A, Kunimasa K, Mori H, Mori M. Taurine in health and diseases: consistent evidence from experimental and epidemiological studies. J Biomed Sci. 2010;17 Suppl 1:S6.

The post Dear Mark: Air-Frying, “Primal” Vegan-ish, Perfect Heath Diet, and Bad Rep or Rap appeared first on Mark’s Daily Apple.

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For today’s edition of Dear Mark, I’m answering three questions from readers. There was some good feedback after last week’s sauna post, and I want to address a few of the comments. First, does the fact that Finns don’t live as long as some of the other more storied “blue zone” populations despite using saunas negate the utility of the sauna? Second, what should we make of the recent study showing negative effects of sauna on sperm health? And third, isn’t it more “natural” and Primal to seek out smaller ambient temperature fluctuations, rather than brief exposures to extreme temperatures?

Let’s go:

Lots of Finnish references but the Fins are not one of the Blue Zone populations. Of the 5 BZ populations, the Okinawans may use a sauna/hot springs – not sure about the the other 4 though.

Finnish men do have the lowest life expectancy among Nordic countries. It’s still pretty good globally—84 years for women, 79 for men—but for being in one of the more developed areas of the world, it’s not great. Yet they use saunas, a supposedly life-extending practice. What gives?

The biggest killers of Finnish men are diabetes, heart disease, and alcohol. Some combination of diet, genes, environment, and lifestyle are contributing to those deaths—that’s what the Finns are up against. Most of the Blue Zones don’t have these issues:

They tend to be in milder climates with better access to sunshine.

They have lower levels of social isolation than Nordic countries like Finland.

They have more “longevity genes” than other areas. The Blue Zone Sardinians, for example, are the subjects of a major ongoing study into the genetics of longevity.

To say nothing of the diet differences.

Sauna usage may very well be keeping life expectancy higher than it should be, given the other risk factors. Research indicates that using a sauna 4-7 times per week confers a 40% reduction in all-cause mortality and even greater reductions in heart related deaths among middle aged Finnish men, which is the cohort most at risk of dying. These numbers, coupled with the numerous protective mechanisms outlined in the last sauna post, lead me to believe that saunas are helping, not hurting Finnish mortality.

Stefan pointed out:

One conundrum is that daily sauna use will sabotage your ballsack precisely because of the heat. Check this old nut-of-a-study:
https://academic.oup.com/humrep/article/28/4/877/653255

Sadly, yes. This is a real issue.

What happened in this study?

10 men were recruited to participate. They were in their 30s, generally healthy, and, at baseline, had normal sperm parameters. For 3 months, they each used the sauna at 80-90?C twice a week for 15 minutes per session. Sperm parameters were tested at the start of the sauna use, after 3 months of sauna, and at 3- and 6-months post sauna. They included:

Sex hormones (testosterone, estradiol, FSH, LH, sex hormone binding globulin)

Sperm count (absolute number of sperm)

Sperm motility (ability of sperm to move independently and perform necessary functions)

Sperm histone/protamine ratios (indicative of sperm quality; smokers’ sperm more likely to have dysfunctional ratio, for example)

Sperm mitochondrial function

After three months of sauna, almost every parameter was negatively affected. Sex hormones remained the same, but sperm count and motility were greatly reduced. The proportion of sperm with dysfunctional histone/protamine ratios increased. Sauna increased the number of sperm with poor mitochondrial function. Luckily, everything returned to normal 6 months after sauna use stopped. But still, that’s a big effect.

This seems like a strong mark against using saunas when you’re trying to conceive. The doses were realistic (15 minutes a day, twice a week) and the effects significant. Not only do saunas appear to lower sperm count and motility, they may decrease the genetic fitness and quality of the surviving sperm. This could increase the risk of miscarriage and even have long term effects on the offspring,

If you’re an older guy uninterested in conceiving, this study shouldn’t affect your sauna habits. Sauna doesn’t affect your sex hormones, which have an outsized effect on the quality of your life. It just reduces the viability of your sperm.

If you’re a younger guy interested in having kids, don’t ignore these results. Avoiding saunas for 3-6 months before trying to conceive might be a good idea.

So, in the name of being seasonal and living naturally, what about just getting out in the heat (and not having an air conditioner–but yet cooking a lot) in the summer and being out in the cold in the winter and keeping the house temp low? Is that enough heat/cold exposure to have beneficial effects? (Might be harder to study.) Instead of taking the time to do something extra that takes up natural resources to create, get the exposure through living. Spend half the year hot and half the year cold. (Plus the cold exposure of going to the grocery store in hardly any clothes in the summer, and the heat exposure of going to someone’s house or the local school dressed for cold in the winter.) (Of course this only works in places that have different weather in the seasons.) Isn’t that more along the lines of Grok-ness?

This is ideal, yes. It’s a great point.

There’s actually some evidence that exposing oneself to cold and hot ambient temperatures, rather than maintaining a steady 70º at all times, is good for us.

As I pointed out in an older post, the general trend is that the more people are exposed to predictable, constant ambient temperatures through central heating, the more likely they are to gain weight. In mice, keeping all other variables (diet, activity, etc) the same while switching to a “thermoneutral” ambient temperature (the temperature at which organisms can maintain body temperature without expending any extra energy) triggered inflammation, increased atherosclerosis, ruined blood lipids, and made the mice obese.

Mild cold exposure (just a few degrees’ worth) was enough to activate brown fat (the metabolically active form that kicks in to keep us warm, burning calories in the process) in people. They achieved it by setting the thermostat a bit lower than normal—nothing extreme like ice baths.

I see saunas and cold baths as extreme stressors that address extreme deficiencies. Just like intense workouts can mitigate the effects of sitting around all the time and failing to get the constant low-level movement our physiologies expect, intense heat or cold exposure can mitigate the effects of indoor climate control. But they’re probably not enough. It’s probably better—and certainly more Primal—to also keep the heat down in the house, walk around in the cold in short sleeves, and get comfortable with hot weather.

One thing I’ve been experimenting with is limiting the amount of time I use the AC. I’m trying to just deal with hot days, whether by walking around in as little clothing as possible or creating air flow with open doors and windows. AC has always felt”stale” and “artificial.” I still use it when it’s unavoidable, but I’m beginning to almost enjoy the sensation of low level heat.

That’s it for today, folks. What’s your take on all this? Anyone conceive despite using the sauna? Anyone else trying to vary the ambient temperature in their life? Let me know down below.

Thanks for reading!

Tanskanen J, Anttila T. A Prospective Study of Social Isolation, Loneliness, and Mortality in Finland. Am J Public Health. 2016;106(11):2042-2048.

Laukkanen T, Khan H, Zaccardi F, Laukkanen JA. Association between sauna bathing and fatal cardiovascular and all-cause mortality events. JAMA Intern Med. 2015;175(4):542-8.

Garolla A, Torino M, Sartini B, et al. Seminal and molecular evidence that sauna exposure affects human spermatogenesis. Hum Reprod. 2013;28(4):877-85.

Giles DA, Ramkhelawon B, Donelan EM, et al. Modulation of ambient temperature promotes inflammation and initiates atherosclerosis in wild type C57BL/6 mice. Mol Metab. 2016;5(11):1121-1130.

Chen KY, Brychta RJ, Linderman JD, et al. Brown fat activation mediates cold-induced thermogenesis in adult humans in response to a mild decrease in ambient temperature. J Clin Endocrinol Metab. 2013;98(7):E1218-23.

The post Dear Mark: Saunas and Finnish Longevity, Saunas and Sperm, What About Ambient Temperature? appeared first on Mark’s Daily Apple.

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

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

Let’s find out:

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

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

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

Here’s what Shary’s talking about.

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

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

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

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

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

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

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

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

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

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

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

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

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

References:

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The post Dear Mark: Is Coconut Oil Pure Poison? appeared first on Mark’s Daily Apple.

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