Biological systems are self-maintaining. They have to be. We don’t have maintenance workers, mechanics, troubleshooters that can “take a look inside” and make sure everything’s running smoothly. Doctors perform a kind of biological maintenance, but even they are working blind from the outside.
No, for life to sustain itself, it has to perform automatic maintenance work on its cells, tissues, organs, and biological processes. One of the most important types of biological maintenance is a process called autophagy.
Autophagy: the word comes from the Greek for “self-eating,” and that’s a very accurate description: Autophagy is when a cell consumes the parts of itself that are damaged or malfunctioning. Lysosomes—members of the innate immune system that also degrade pathogens—degrade the damaged cellular material, making it available for energy and other metabolites. It’s cellular pruning, and it’s an important part of staving off the worst parts of the aging process.
In study after study, we find that impairment to or reductions of normal levels of autophagy are linked to almost every age-related degenerative disease and malady you can imagine.
- Cancer: Autophagy can inhibit the establishment of cancer by removing malfunctioning cellular material before it becomes problematic. Once cancer is established, however, autophagy can enhance tumor growth.
- Diabetes: Impaired autophagy enables the progression from obesity to diabetes via pancreatic beta cell degradation and insulin resistance. Impaired autophagy also accompanies the serious complications related to diabetes, like kidney disease and heart failure.
- Heart disease: Autophagy plays an important role in all aspects of heart health.
- Osteoporosis: Both human and animal studies indicate that autophagy dysfunction precedes osteoporosis.
- Alzheimer’s disease: Early stage Alzheimer’s disease is linked to deficits in autophagy.
- Muscle loss: Autophagy preserves muscle tissue; loss of autophagy begins the process of age-related muscle atrophy.
Okay, so autophagy is rather important. It’s fundamental to health.
But how does autophagy happen?
The way it’s supposed to happen is this:
Humans traditionally and historically lived in a very different food environment. Traditionally and historically, humans were feasters and fasters. While I don’t think our paleolithic ancestors were miserable, wretched, perpetually starving creatures scuttling from one rare meal to the next—the fossil records show incredibly robust remains, with powerful bones and healthy teeth and little sign of nutritional deficits—they also couldn’t stroll down to the local Whole Foods for a cart full of ingredients. Going without food from time to time was a fundamental aspect of human ancestral life.
They worked for their food. I don’t mean “sat in a cubicle to get a paycheck to spend on groceries.” I mean they expended calories to obtain food. They hunted—and sometimes came back empty handed. They dug and climbed and rooted around and gathered. They walked, ran, stalked, jumped, lifted. Movement was a necessity.
In short, they experienced energy deficits on a regular basis. And energy deficits, particularly sustained energy deficits, are the primary triggers for autophagy. Without energy deficits, you remain in fed mode and never quite hit the fasted mode required for autophagy.
Now compare that ancestral food environment to the modern food environment:
Almost no one goes hungry. Food is cheap and plentiful, with the tastiest and most calorie-rich stuff tending to be the cheapest and most widely available.
Few people have to physically work for their food. We drive to the store and walk a couple hundred steps, hand over some money, and—BOOM—obtain thirty thousand calories, just like that. Or someone comes to our house and delivers the food directly.
We eat all the time. Unless you set out to do it, chances are you’ll be grazing, snacking, and nibbling throughout the day. We’re in a perpetually fed state.
The average person in a modern society eating a modern industrial diet rarely goes long enough without eating something to trigger autophagy. Nor are they expending enough energy to create an energy deficit from the other end—the output. It’s understandable. If our ancestors were thrust into our current situation, many would fall all over themselves to take advantage of the modern food environment. But that doesn’t make it desirable, or good for you. It just means that figuring out how to trigger autophagy becomes that much more vital for modern humans.
Here are 7 ways to induce autophagy with regular lifestyle choices.
There’s no better way to quickly and reliably induce a large energy deficit than not eating anything at all. There are no definitive studies identifying “optimal” fasting guidelines for autophagy in humans. Longer fasts probably allow deeper levels of autophagy, but shorter fasts are no slouch.
2) Get Keto-Adapted
When you’re keto- and fat-adapted, it takes you less time to hit serious autophagy upon commencing a fast. You’re already halfway there.
3) Train Regularly
With exercise-related autophagy, the biggest effects are seen with lifelong training, not acute. In mice, for example, the mice who are subjected to lifelong exercise see the most autophagy-related benefits. In people, those who have played soccer (football) for their entire lives have far more autophagy-related markers of gene activity than people of the same age who have not trained their whole lives.
4) Train Hard
In studies of acute exercise-induced autophagy, the intensity of the exercise is the biggest predictor of autophagy—even more than whether the athletes are in the fed or fasted state.
5) Drink Coffee
At least in mice, both caffeinated and decaffeinated coffee induce autophagy in the liver, muscle tissue, and heart. This effect persists even when the coffee is given alongside ad libitum food. These mice didn’t have to fast for the coffee to induce autophagy.
Certain nutrients can trigger autophagy, too….
6) Eat Turmeric
Curcumin, the primary phytonutrient in turmeric, is especially effective at inducing autophagy in the mitochondria (mitophagy).
7) Consume Extra Virgin Olive Oil
The anticancer potential of its main antioxidant, oleuropein, likely occurs via autophagy.
Disclaimer: The autophagy/nutrient literature is anything but definitive. Most studies take place in test tube settings, not living humans. Eating some turmeric probably won’t flip a switch and trigger autophagy right away, but it won’t hurt.
Autophagy is a long game.
This can’t be underscored enough: Autophagy is a lifelong pursuit attained by regular doses of exercise and not overeating every time you sit down to a meal. Staying so ketotic your pee tests look like a Prince album cover, doing epic 7-day fasts every month, fasting every other day, making sure you end every day with fully depleted liver glycogen—while these strategies might be “effective,” obsessing over their measures to hit some “optimal” level of constant autophagy isn’t the point and is likely to activate or trigger neurotic behavior.
Besides, we don’t know what “optimal autophagy” looks like. Autophagy isn’t easy to measure in live humans. You can’t order an “autophagy test” from your doc. We don’t even know if more autophagy is necessarily better. There’s the fact that unchecked autophagy can actually increase existing cancer in some cases. There’s the fact that too much autophagy in the wrong place might be bad. We just don’t know very much. Autophagy is important. It’s good to have some happening. That’s what we have to go on.
Putting These Tips Into Practice
Autophagy happens largely when you just live a healthy lifestyle. Get some exercise and daily activity. Go hard every now and then. Sleep deeply. Recover well. Don’t eat carbohydrates you don’t need and haven’t earned (and I don’t just mean “earned through glycogen depleting-exercise”). Reach ketosis sometimes. Don’t eat more food than you need. Drink coffee, even decaf.
All those caveats aside, I see the utility in doing a big “autophagy session” a few times a year. Here’s how mine looks:
- Do a big training session incorporating strength training and sprints. Lots of intense bursts. This will trigger autophagy.
- Fast for two or three days. This will push autophagy even further.
- Stay busy throughout the fast. Take as many walks as possible. This will really ramp up the fat burning and get you quickly into ketosis, another autophagy trigger.
- Drink coffee throughout the fast. Coffee is a nice boost to autophagy. Decaf is fine.
I know people are often skeptical of using “Grok logic,” but it’s likely that most human ancestors experienced similar “perfect storms” of deprivation-induced autophagy on occasion throughout the year. You track an animal for a couple days and come up short, or it takes that long to make the kill. You nibble on various stimulants plucked from the land along the way. You walk a ton and sprint some, then lift heavy. And finally, maybe, you get to eat.
If you find yourself aging well, you’re on the right track. If you’re not progressing from obesity to diabetes, you’re good to go. If you’re maintaining and even building your muscle despite qualifying for the blue plate special, you’ve probably dipping into the autophagy pathway. If you’re thinking clearly, I wouldn’t worry. Obviously, we can’t really see what’s happening on the inside. But if everything you can verify is going well, keep it up.
That’s it for today, folks. If you have any more questions about autophagy, leave them down below and I’ll try to get to all of them in future posts.
Thanks for reading!
Yang ZJ, Chee CE, Huang S, Sinicrope FA. The role of autophagy in cancer: therapeutic implications. Mol Cancer Ther. 2011;10(9):1533-41.
Barlow AD, Thomas DC. Autophagy in diabetes: ?-cell dysfunction, insulin resistance, and complications. DNA Cell Biol. 2015;34(4):252-60.
Sasaki Y, Ikeda Y, Iwabayashi M, Akasaki Y, Ohishi M. The Impact of Autophagy on Cardiovascular Senescence and Diseases. Int Heart J. 2017;58(5):666-673.
Florencio-silva R, Sasso GR, Simões MJ, et al. Osteoporosis and autophagy: What is the relationship?. Rev Assoc Med Bras (1992). 2017;63(2):173-179.
Li Q, Liu Y, Sun M. Autophagy and Alzheimer’s Disease. Cell Mol Neurobiol. 2017;37(3):377-388.
Jiao J, Demontis F. Skeletal muscle autophagy and its role in sarcopenia and organismal aging. Curr Opin Pharmacol. 2017;34:1-6.
Schwalm C, Jamart C, Benoit N, et al. Activation of autophagy in human skeletal muscle is dependent on exercise intensity and AMPK activation. FASEB J. 2015;29(8):3515-26.
De oliveira MR, Jardim FR, Setzer WN, Nabavi SM, Nabavi SF. Curcumin, mitochondrial biogenesis, and mitophagy: Exploring recent data and indicating future needs. Biotechnol Adv. 2016;34(5):813-826.
Przychodzen P, Wyszkowska R, Gorzynik-debicka M, Kostrzewa T, Kuban-jankowska A, Gorska-ponikowska M. Anticancer Potential of Oleuropein, the Polyphenol of Olive Oil, With 2-Methoxyestradiol, Separately or in Combination, in Human Osteosarcoma Cells. Anticancer Res. 2019;39(3):1243-1251.
The post The Definitive Guide To Autophagy (and 7 Ways To Induce It) appeared first on Mark’s Daily Apple.
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For today’s edition of Dear Mark, I’m answering three questions. First, can LDL actually infiltrate the arteries, or is there more to the story? Malcolm Kendrick says there’s more to the story, so I dig into some literature to see if they corroborate his position. Second, is New Zealand farmed salmon good to eat? And finally, what should you do about elevated ferritin levels—and why else might they be elevated if not because of your iron?
My reading of this post by Malcolm Kendrick MD is that LDL particles cannot infiltrate the endothelial lining of our arteries:
Great read. Malcolm Kendrick is consistently fascinating, insightful, and enlightening.
He’s basically suggesting that LDL particles can’t manhandle their way into the artery wall, which are equipped with tight junctions—the same kind that regulate passage through our gut lining. Something has to “allow” them in. The something he finds most plausible is injury, trauma, or insult to the endothelial lining (artery wall, for lack of a better phrase).
A free public textbook available on PubMed since last month called The Role of Lipids and Lipoproteins in Atherosclerosis tackles the topic head on. In the abstract, they say:
Population studies have demonstrated that elevated levels of LDL cholesterol and apolipoprotein B (apoB) 100 [note: ApoB is a stand-in for LDL particle number, as each LDL-P has an ApoB attached to it], the main structural protein of LDL, are directly associated with risk for atherosclerotic cardiovascular events (ASCVE). Indeed, infiltration and retention of apoB containing lipoproteins in the artery wall is a critical initiating event that sparks an inflammatory response and promotes the development of atherosclerosis.
This seems to posit that infiltration of the LDL particle into the artery wall is a critical initiating event. But is it the critical initiating event? Does something come before it? How does the infiltration happen, exactly? Moving on:
Arterial injury causes endothelial dysfunction promoting modification of apoB containing lipoproteins and infiltration of monocytes into the subendothelial space. Internalization of the apoB containing lipoproteins by macrophages promotes foam cell formation, which is the hallmark of the fatty streak phase of atherosclerosis. Macrophage inflammation results in enhanced oxidative stress and cytokine/chemokine secretion, causing more LDL/remnant oxidation, endothelial cell activation, monocyte recruitment, and foam cell formation.
If I’m reading this correctly, they’re saying that “arterial injury” is another critical initiating event—perhaps the critical initiating event, since the injury causes “endothelial dysfunction,” which in turn modifies (or oxidizes) the LDL particles. But wait: so they’re saying the LDL particles are already there when the arterial injury occurs. They’ve already made it into the endothelial walls, and they’re just…waiting around until the arteries get injured. Okay, okay, but, just like Malcolm Kendrick points out, nowhere in the abstract have the authors actually identified how the LDL particles enter the endothelial lining. Maybe it’s “common knowledge,” but I’d like to see it explained in full.
In atherosclerosis susceptible regions, reduced expression of eNOS and SOD leads to compromised endothelial barrier integrity (Figure 1), leading to increased accumulation and retention of subendothelial atherogenic apolipoprotein B (apoB)-containing lipoproteins (low-density lipoproteins (LDL)) and remnants of very low-density lipoproteins (VLDL) and chylomicrons)
Ah ha! So, in regions of the arteries that are prone to atherosclerosis, low levels of nitric oxide synthase (eNOS)—the method our bodies use to make nitric oxide, a compound that improves endothelial function and makes our blood flow better—and superoxide dismutase—an important antioxidant our bodies make—compromise the integrity of the arterial lining. The compromised arterial lining allows more LDL particles to gain entry and stick around. So, are low levels of nitric oxide and impaired antioxidant activity the critical initiators? That’s pretty much what Malcolm Kendrick said in his blog post.
Still—high LDL particle numbers are a strong predictor of heart disease risk, at least in the studies we have. They clearly have something to do with the whole process. They’re necessary, but are they sufficient? And how necessary are they? And how might that necessariness (yes, a word) be modified by diet?
I’ll explore this more in the future.
In regards to the oily fish article (and more indirectly given the omega 6 concern- the Israeli Paradox) What do you think of NZ farmed salmon? I’m in Australia, & occasionally like a fresh piece of salmon- there are no wild caught available here sadly, but I am wondering how it measures up as an alternative?
Last year, I explored the health effects of eating farmed salmon and found that it’s actually a pretty decent alternative to wild-caught salmon, at least from a personal health standpoint—the environmental impact may be a different story.
I wasn’t able to pull up any nutrition data for New Zealand farmed salmon, called King or Chinook salmon. Next time you’re at the store, check out the nutritional facts on a NZ farmed salmon product, like smoked salmon. The producer will have actually had to run tests on their products to determine the omega-3 content, so it should be pretty accurate. Fresh is great but won’t have the nutritional facts available. I don’t see why NZ salmon would be any worse than the farmed salmon I discussed last year.
According to the NZ salmon folks, they don’t use any pesticides or antibiotics. That’s fantastic if true.
I used to eat a lot of King salmon over in California, and it’s fantastic stuff. Very fatty, full of omega-3s. If your farmed King salmon comes from similar stock, go for it.
ok can someone tell me how to reduce ferritin? Is is just by giving blood?
Giving blood is a reliable method for reducing ferritin. It’s quick, effective, simple, and you’re helping out another person in need. Multiple wins.
Someone in the comment board recommended avoiding cast iron pans in addition to giving blood. While using cast iron pans can increase iron intake and even change iron status in severe deficiency, most don’t have to go that far. Giving blood will cover you.
Ferritin is also an acute phase reactant, a marker of inflammation—it goes up in response to infections (bacterial or viral) and intense exercise (an Ironman will increase ferritin). In fact, in obese and overweight Pakistani adults, elevated ferritin seems to be a reliable indicator of inflammatory status rather than iron status.
Thanks for reading, everyone. Take care and be well!
Birgegård G, Hällgren R, Killander A, Strömberg A, Venge P, Wide L. Serum ferritin during infection. A longitudinal study. Scand J Haematol. 1978;21(4):333-40.
Comassi M, Vitolo E, Pratali L, et al. Acute effects of different degrees of ultra-endurance exercise on systemic inflammatory responses. Intern Med J. 2015;45(1):74-9.
The post Dear Mark: How Does LDL Even Penetrate the Arteries, New Zealand Farmed Salmon, Elevated Ferritin appeared first on Mark’s Daily Apple.
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The scientific literature is awash in correlations between a person’s health status and various biomarkers, personal characteristics, and measurements. As we hoard more and more data and develop increasingly sophisticated autonomous tools to analyze it, we’ll stumble across new connections between seemingly disparate variables. Some will be spurious, where the correlations are real but the variables don’t affect each other. Others will be useful, where the correlations indicate real causality, or at least a real relationship.
One of my favorite health markers—one that is both modifiable and a good barometer for the conditions it appears to predict—is grip strength.
The Benefits of Grip Strength
In middle-aged and elderly people, grip strength consistently predicts mortality risk from all causes, doing an even better job than blood pressure. In older disabled women, grip strength predicts all-cause mortality, even when controlling for disease status, inflammatory load, depression, nutritional status, and inactivity.
Poor grip strength is also an independent risk factor for type 2 diabetes across all ethnicities, and it can predict the presence of osteoarthritis in the knee. Among Korean adults, those with lower grip strength have a greater risk of clinical depression.
Even when hand grip strength fails to predict a disease, it still predicts the quality of life in people with the disease. The relative rate of grip strength reduction in healthy people is a good marker for the progression of general aging. Faster decline, faster aging. Slower (or no) decline, slower aging. Stronger people—as indicated by their grip strength—are simply better at navigating the physical world and maintaining independence on into old age.
Health and longevity aside, there are other real benefits to a stronger grip.
You command more respect. I don’t care how bad it sounds, because I agree. Historically, a person’s personal worth and legitimacy was judged by the quality of their handshake. Right or wrong, that’s how we’re wired. If you think you feel differently, let me know how you feel the next time you shake hands and the other person has a limp, moist hand. Who are you more likely to respect? To hire? To deem more capable? To befriend? To approach romantically? I’m not saying it’s right. I’m saying it’s simply how it is. We can’t avoid our guttural reaction to a strong—or weak—handshake. To me, that suggests we have a built-in sensitivity to grip for a very good reason.
So, how does one build grip?
10 Exercises To Build Grip Strength
Most people will get a strong-enough grip as long as they’re lifting heavy things on a consistent-enough basis.
Deadlifts are proven grip builders. Wide grip deadlifts are also good and stress your grip across slightly different angles.
2. Pullups and 3. Chinups
Both require a good grip on the bar.
Any exercise where your grip supports either your weight or an external weight (like a barbell, dumbbell, or kettlebell) is going to improve your grip strength. But there are other, more targeted movements you can try to really turn your hand into a vise. Such as:
4. Bar Hangs
This is pretty simple. Just hang from a bar (or branch, or traffic light fixture) with both hands. It’s probably the purest expression of grip strength. As it happens, it’s also a great stretch for your lats, chest, shoulders, and thoracic spine.
Aim to hit one minute. Progress to one-hand hangs if two-handers get too easy. You can use a lower bar and keep one foot on the ground for support as you transition toward a full one-handed hang.
5. Sledgehammer Work
Grab the heaviest sledgehammer you can handle and use it in a variety of ways.
If you had to pick just one sledgehammer movement to target your grip, do the bottoms up. Hold the hammer hanging down pointing toward the ground in your hand, swing it up and catch it with the head of the hammer pointing upward, and hold it there. Handle parallel to your torso, wrist straight, don’t let it fall. The lower you grip the handle, the harder your forearms (and grip) will have to work.
6. Fingertip Pushups
Most people who try fingertip pushups do them one way. They do them with straight fingers, with the palm dipping toward the ground. Like this. Those are great, but there’s another technique as well: the claw. For the claw, make a claw with your hand, like this, as if you’re trying to grab the ground. In fact, do try to grab the ground. This keeps your fingers more active, builds more strength and resilience, and prevents you from resting on your connective tissue.
These are hard for most people. They’re quite hard on the connective tissue, which often goes underutilized in the hands and forearms. Don’t just leap into full fingertip pushups—unless you know you’re able. Start on your knees, gradually pushing your knees further back to add resistance. Once they’re all the way back and you’re comfortable, then progress to full pushups.
7. Active Hands Pushups
These are similar to claw pushups, only with the palm down on the floor. Flat palm, active “claw” fingers. They are easier than fingertip pushups.
8. Farmer’s Walks
The average person these days is not carrying water pails and hay bales and feed bags back and forth across uneven ground like they did when over 30% of the population lived on farms, but the average person can quickly graduate past average by doing farmer’s walks a couple times each week. What is a farmer’s walk?
Grab two heavy weights, stand up, and walk around. They can be dumbbells, barbells, kettlebells, or trap bars. You can walk up hill, down hill, or around in circles. You can throw in some shrugs, or bookend your walks with deadlifts or swings. The point is to use your grip to carry something heavy in both hands.
9. Pinch Grips
Grasp and hold weight plates between your thumb and each finger.
10. Hammer Curls
Next time you do some curls, throw in a few sets of hammer curls. These are identical to normal bicep curls, except you hold the weights in a hammer grip, with palms facing toward each other—like how you hold and swing a hammer. Make sure to keep those wrists as straight as possible.
The thing about grip is it’s hard to work your grip without getting stronger, healthier, and faster all over. Deadlifting builds grip strength, and it also builds back, hip, glute, and torso strength. Fingertip pushups make your hands and forearms strong, but they also work your chest, triceps, abs, and shoulders. That’s why I suspect grip strength is such a good barometer for overall health, wellness, and longevity. Almost every meaningful piece of physical activity requires that you use your hands to manipulate significant amounts of weight and undergo significant amounts of stress.
For that reason, the best way to train your grip is with normal movements. Heavy deadlifts and farmer’s walks are probably more effective than spending half an hour pinch gripping with every possible thumb/finger permutation, because they offer more full-body benefits. But if you have a few extra minutes throughout your workout, throw in some of the dedicated grip training.
Your grip can handle it. The grip muscles in the hands and forearm are mostly slow-twitch fiber dominant, meaning they’re designed to go for long periods of exertion. They’re also gross movers, meaning you use them all the time for all sorts of tasks, and have been doing so for decades. To make them adapt, you need to stress the heck out of them with high weight. Train grip with high reps, heavy weights, and long durations. This is why deadlifts and farmer’s walks are so good for your grip—they force you to maintain that grip on a heavy bar or dumbbell for the entire duration of the set with little to no rest.
Oh, and pick up some Fat Gripz. These attach to dumbbells and barbells and increase the diameter of the bar, giving you less leverage when grabbing and forcing you to adapt to the new grip conditions by getting stronger.
Now, will all this grip training actually protect you from aging, type 2 diabetes, osteoarthritis, and early all-cause mortality? Maybe, maybe not.
But it—and the muscle and fitness you gain doing all these exercises—certainly doesn’t hurt.
How’s your grip? How’s your handshake? How long can you hang from a bar without letting go?
Thanks for reading, everyone. Take care, be well, and go pick up and hold some heavy stuff.
Sasaki H, Kasagi F, Yamada M, Fujita S. Grip strength predicts cause-specific mortality in middle-aged and elderly persons. Am J Med. 2007;120(4):337-42.
Leong DP, Teo KK, Rangarajan S, et al. Prognostic value of grip strength: findings from the Prospective Urban Rural Epidemiology (PURE) study. Lancet. 2015;386(9990):266-73.
Rantanen T, Volpato S, Ferrucci L, Heikkinen E, Fried LP, Guralnik JM. Handgrip strength and cause-specific and total mortality in older disabled women: exploring the mechanism. J Am Geriatr Soc. 2003;51(5):636-41.
Van der kooi AL, Snijder MB, Peters RJ, Van valkengoed IG. The Association of Handgrip Strength and Type 2 Diabetes Mellitus in Six Ethnic Groups: An Analysis of the HELIUS Study. PLoS ONE. 2015;10(9):e0137739.
Wen L, Shin MH, Kang JH, et al. Association between grip strength and hand and knee radiographic osteoarthritis in Korean adults: Data from the Dong-gu study. PLoS ONE. 2017;12(11):e0185343.
Lee MR, Jung SM, Bang H, Kim HS, Kim YB. The association between muscular strength and depression in Korean adults: a cross-sectional analysis of the sixth Korea National Health and Nutrition Examination Survey (KNHANES VI) 2014. BMC Public Health. 2018;18(1):1123.
Lee SH, Kim SJ, Han Y, Ryu YJ, Lee JH, Chang JH. Hand grip strength and chronic obstructive pulmonary disease in Korea: an analysis in KNHANES VI. Int J Chron Obstruct Pulmon Dis. 2017;12:2313-2321.
Iconaru EI, Ciucurel MM, Georgescu L, Ciucurel C. Hand grip strength as a physical biomarker of aging from the perspective of a Fibonacci mathematical modeling. BMC Geriatr. 2018;18(1):296.
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This is a surprisingly common question.
To get it out of the way: Yes, it does. Bone broth contains calories, and true fasts do not allow calorie consumption. You eat calories, you break the fast.
However, most people aren’t fasting to be able to brag about eating no calories for X number of days. They fast for shorter (often intermittent) periods of time for specific health benefits. It’s entirely possible that bone broth “breaks a fast” but allows many of the benefits we associate with fasting to occur.
As is the problem with so many of these specific requests, there aren’t any studies addressing the specific question. The scientific community hasn’t caught up to the current trends sweeping the alternative health community. But we can isolate the most common benefits of fasting and see how bone broth—and the components therein—interact.
Common Benefits of Fasting: Does Bone Broth Help or Hinder?
Fasting is a quick and easy (or simple) way to get into ketosis. You have little choice in the matter. Since you’re not eating anything, and your body requires energy, you break down body fat for energy. And because you’ve only got fat “coming in,” you’ll quickly start generating ketone bodies. If bone broth stops ketosis, it’s probably breaking the fast.
Bone broth doesn’t contain any digestible carbohydrates. Common additions like tomato paste and carrots might add a few tenths of a gram of carbohydrate to your cup of broth, but not enough to throw you out of ketosis.
Bone broth is quite high in protein, especially if you make it right or buy the right kind, but if it’s the only thing you’re consuming during your fast, the overall caloric load won’t be enough for the protein in broth to stop ketosis.
I can’t point to a paper. I know for a fact that I’ve consumed bone broth without affecting my ketones.
Fat-burning is another important aspect of fasting. Since bone broth contains calories, you’ll probably burn slightly less fat drinking broth during a fast. But the calories come from protein, the macronutrient least associated with fat gain and most supportive of lean mass retention. And at any rate, your total calorie intake on a fasting+broth day will be under 100 calories—plenty low enough to promote fat loss.
Over the long term, fasting is an effective way to improve insulin sensitivity and glucose tolerance. Most things that make you better at burning fat and expending, rather than storing, energy—like exercise, low-carb diets, weight loss in general—tend to improve insulin sensitivity over time. But the sometimes counterintuitive piece to all this is that in the short term, fasting can reduce insulin sensitivity. This is a physiological measure the body takes to preserve what little glucose remains for the brain. All the other tissues become insulin resistant so that the parts of the brain that can’t run on ketones and require glucose get enough of the latter to function.
There’s also the matter of sleep, fasting, and insulin sensitivity to consider. Some people report sleep disturbances during fasts, especially longer fasts. This is common. If the body perceives the fast as stressful, or if you aren’t quite adapted to burning fat, you may interpret the depleted liver glycogen as dangerous and be woken up to refuel in the middle of the night. Some people just have trouble sleeping on low-calorie intakes in general, and a fast is about as low as you can get. If that’s you, and your fasting is hurting your sleep, it’s most likely also impairing your insulin sensitivity because a bad night’s sleep is one of the most reliable ways to induce a state of insulin resistance. There’s some indication that total sleep deprivation creates transient type 2 diabetes.
That’s where bone broth comes in. A big mug of broth is one of my favorite ways to ensure a good night’s sleep. It’s a great source of glycine, an amino acid that has been shown in several studies to improve sleep quality and reduce the time it takes to fall asleep. It may “break” the fast by introducing calories, but a broken fast is preferable to bad sleep and the hit to insulin sensitivity that results from it.
Things fall apart. Cars, tools, buildings, toy trucks, civilizations. That’s entropy, which dictates that all things are constantly heading toward disorder. And people aren’t exempt. Our cells and tissues are subject to entropy, too, only we can resist it. One of the ways our bodies resist entropy is through a process of cellular pruning and cleanup called autophagy. There’s always a bit of back and forth between autophagy and our cellular detritus, but it occurs most powerfully in periods of caloric restriction. Fasting enhances autophagy like nothing else because it’s a period of total caloric restriction. If bone broth destroys autophagy, that’d be a big mark against drinking it during a fast.
Amino acids tend to be anti-autophagy signaling agents. When we eat protein, or even consume certain isolated amino acids, autophagy slows. Bone broth is pure protein. It’s almost nothing but amino acids. The key is: Which amino acids are in bone broth, and have they been shown to impede autophagy?
The primary amino acids that make up the gelatin in bone broth are alanine, glycine, proline, hydroxyproline, and glutamine.
Let’s say you’re drinking a mug of strong, really gelatinous bone broth with 15 grams of gelatin protein. How do those amino acids break down?
- 5 grams of glycine. In piglets, dietary glycine activates mTOR, the pathway that triggers autophagy.
- 1.5 grams of alanine.
- 2.4 grams of proline.
- 2 grams of hydroxyproline.
- 1.75 grams of glutamine. 30 grams of glutamine inhibits autophagy.
So it’s a mixed bag. The most prominent amino acid in bone broth—glycine—seems to allow autophagy, but the less proinent amino acids may not. It’s unclear just how much of each amino acid it takes to affect autophagy either way. The absolute amounts found in bone broth are low enough that I’m not too concerned.
What Else To Know…
Okay, so while bone broth technically “breaks” the fast, it may preserve some of the most important benefits. Is there anything else related to bone broth and fasting that deserve mention?
If you’re the type to train in a fasted state and eat right after, you might consider incorporating some bone broth right before the workout. Just like my pre-workout collagen smoothie does, bone broth (plus a little vitamin C to aid the effect) right before a workout improves the adaptations of our connective tissue to the training by increasing collagen deposition in the tendons, ligaments, and cartilage. You’ve already done most of the fast honestly. What’s shaving off a half hour of fasting time by drinking some broth or collagen, especially if you stand to improve your connective tissue in the process? Ask any older athlete and they’ll say they wish they could.
Some spices and herbs that are often added to bone broth can have effects similar to fasting. Take curcumin, found in turmeric. Research shows that it’s an independent activator of mTOR, which in turn can activate autophagy. Ginger and green tea (what, you haven’t tried steeping green tea in bone broth?) are other ones to try. 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!
That’s about it for bone broth and fasting. If you have any further questions, don’t hesitate to ask down below.
Xu X, Wang X, Wu H, et al. Glycine Relieves Intestinal Injury by Maintaining mTOR Signaling and Suppressing AMPK, TLR4, and NOD Signaling in Weaned Piglets after Lipopolysaccharide Challenge. Int J Mol Sci. 2018;19(7)
De urbina JJO, San-miguel B, Vidal-casariego A, et al. Effects Of Oral Glutamine on Inflammatory and Autophagy Responses in Cancer Patients Treated With Abdominal Radiotherapy: A Pilot Randomized Trial. Int J Med Sci. 2017;14(11):1065-1071.
Shaw G, Lee-barthel A, Ross ML, Wang B, Baar K. Vitamin C-enriched gelatin supplementation before intermittent activity augments collagen synthesis. Am J Clin Nutr. 2017;105(1):136-143.
Zhao G, Han X, Zheng S, et al. Curcumin induces autophagy, inhibits proliferation and invasion by downregulating AKT/mTOR signaling pathway in human melanoma cells. Oncol Rep. 2016;35(2):1065-74.
Hung JY, Hsu YL, Li CT, et al. 6-Shogaol, an active constituent of dietary ginger, induces autophagy by inhibiting the AKT/mTOR pathway in human non-small cell lung cancer A549 cells. J Agric Food Chem. 2009;57(20):9809-16.
Zhou J, Farah BL, Sinha RA, et al. Epigallocatechin-3-gallate (EGCG), a green tea polyphenol, stimulates hepatic autophagy and lipid clearance. PLoS ONE. 2014;9(1):e87161.
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Many of you have asked about prostate health in a Primal context. Men are interested because they know men have a decent chance of getting prostate cancer. Women are interested because they’re worried about the men in their lives getting prostate cancer. Today, I’m going to delve deep into the topic, exploring the utility (or lack thereof) of standard testing, the common types of treatment and their potential efficacy, as well as preventive and unconventional ways of reducing your risk and mitigating the danger of prostate cancer.
First, what does the prostate do, anyway? Most people only think about it in terms of prostate cancer.
It’s a gland about the size of a small apricot that manufactures a fluid called prostatic fluid that combines with sperm cells and other compounds to form semen. Prostatic fluid protects sperm against degradation, improves sperm motility, and preserves sperm genetic stability.
What Goes Wrong With the Prostate?
There are a few things that can happen.
Inflammation of the prostate, usually chronic and non-bacterial. A history of prostatitis is a risk factor for prostate cancer.
Benign Prostatic Hyperplasia
Non-cancerous enlargement of the prostate. As men age, the prostate usually grows in size. This isn’t always cancer but can cause similar symptoms.
What most of us are interested in when we talk about prostate health… After skin cancer, prostate cancer is the most common cancer among men and the sixth most common cause of cancer death among men worldwide. Yet, most men diagnosed with prostate cancer do not die from it; they die with it. The 5-year survival rate in the US is 98%.
That said, there is no monolithic “prostate cancer.” Like all other cancers, there are different grades and stages of prostate cancer. Each grade and stage has a different mortality risk:
- Low-grade prostate cancer grows more slowly and is less likely to spread to other tissues.
- High-grade prostate cancer grows more quickly and is more likely to spread to other tissues.
- Local prostate cancer is confined to the prostate. The 5-year relative survival rate (survival compared to men without prostate cancer) for local prostate cancer is almost 100%.
- Regional prostate cancer has spread to nearby tissues. The 5-year relative survival rate for regional prostate cancer is almost 100%.
- Distant prostate cancer has spread to tissues throughout the body. The 5-year relative survival rate for distant prostate is 29%. Distant prostate cancer explains most of the prostate-related mortality.
What Are Symptoms of Prostate Cancer?
The primary symptom is problems with urination. When the prostate gland grows, it has the potential to obstruct the flow of urine out of the bladder, causing difficulty urinating, weak urine flow, painful urination, or frequent urination. This can also be caused by benign prostatic hyperplasia, a non-cancerous enlargement of the prostate.
What Causes Prostate Cancer?
A big chunk is genetic. People with “knockout” alleles for BRCA, which codes for tumor suppression, have an elevated risk of some forms of prostate cancer. That’s the same one that confers added risks for breast cancer.
Ethnicity matters, too. Men of Sub-Saharan African descent, whether African-Americans in the U.S. or Caribbean men in the U.K., have the highest risk in the world for prostate cancer—about 60% greater than other ethnic groups. White men have moderate risks; South Asian, East Asian, and Pacific Islander men have lower risks.
Testosterone has a confusing relationship with prostate cancer. Conventional wisdom tends to hold that testosterone stimulates prostate cancer growth, and there’s certainly some evidence of a relationship, but it’s not that simple.
In one study, men with low free testosterone levels were less likely to have low-grade (less risk of spreading) prostate cancer but more likely to have high-grade (higher risk of spreading) prostate cancer.
In Chinese men, those who went into treatment with low testosterone were more likely to present with higher-grade localized prostate cancers.
Other studies have arrived at similar results, finding that “hypogonadism represents bad prognosis in prostate cancer.”
Many prostate cancer treatments involve testosterone deprivation, a hormonal reduction of testosterone synthesis. This can reduce symptoms and slow growth of prostate tumors during the metastatic phase, but prostate cancer tends to be highly plastic, with the ability to adapt to changing hormonal environments. These patients often see the cancer return in a form that doesn’t require testosterone to progress.
What About Testing?
If you have a prostate, should you get tested starting at age 40?
Not necessarily. The value of early testing hasn’t been established. Some researchers even question whether early testing is more harmful than ignoring it, and most of the research finds middling to nonexistent evidence in favor of broad testing for everyone. Early testing has a small effect on mortality from prostate cancer, but no effect on all-cause mortality.
PSA testing can also be inaccurate. PSA is prostate specific antigen, a protein produced by the prostate. It’s normal to have low levels of PSA present in the body, and while high levels of PSA are a good sign of prostate cancer—even years before it shows up in imaging or digital probes—they can also represent a false positive. Those two other common yet relatively benign prostate issues—benign hyperplasia and prostatitis—can also raise PSA levels well past the “cancer threshold.”
Other causes of high levels of PSA include:
- Urinary tract infections
- Recent sex or ejaculation
- Recent, vigorous exercise
- Certain medications.
In fact, if you have a PSA reading of 4 (the usual threshold), there’s still just a 30% chance it actually indicates cancer.
What About Treatment?
Let’s say you do have prostate cancer, confirmed by PSA and a biopsy (or two, or three, as needle biopsies often miss cancers). What next? Should you definitely treat it?
It’s unclear whether treatment improves survival outcomes. One study took men aged 50-69 with prostate cancer diagnosed via PSA testing, divided them among three treatment groups, and followed them for ten years. One group got active monitoring—they continued to test and monitor the status of the cancer. One group received radiotherapy—radiation therapy to destroy the tumor. And the last group had the cancer surgically removed. After ten years, there was no difference among the groups for all-cause mortality, even though the active-monitoring group saw higher rates of prostate cancer-specific deaths (8 deaths—in a group of 535 men— vs 5 in the surgery group and 4 in the radiotherapy group), cancer progression, and metastasis.
In another study of men with localized prostate cancer, removing the prostate only improved all-cause mortality rates among men with very high PSAs (more than 10). In men with lower PSAs, “waiting and seeing” produced similar outcomes as surgery.
Prostate removal also carries many unwanted side effects, like incontinence and sexual dysfunction. No one wants prostate cancer, but it’s no small thing to have problems with urination and sex for the rest of your life. Those are major aspects of anyone’s quality of life.
Before you make any decisions, talk to your doctor about your options, the relative mortality risk of your particular cancer’s stage and grade, and how the treatments might affect your quality of life.
How Can You Reduce the Risk of Prostate Cancer?
1. Inflammation is definitely an issue.
For one, there’s the relationship between prostatitis, or inflammation of the prostate, and prostate cancer that I already mentioned above.
Two, there’s the string of evidence linking anti-inflammatory compounds to reductions in prostate cancer incidence. For example, aspirin cuts prostate cancer risk. Low-dose aspirin (under 100 mg) reduces both the incidence of regular old prostate cancer and the risk of metastatic prostate cancer. It’s also associated with longer survival in patients with prostate cancer; other non-steroidal anti-inflammatories are not.
Third, anti-inflammatory omega-3 fatty acids (found in seafood and fish oil) are generally linked to lower rates of prostatic inflammation and a less carcinogenic environment; omega-6 fatty acids can trigger disease progression. A 2001 study of over 6,000 Swedish men found that the folks eating the most fish had drastically lower rates of prostate cancer than those eating the least. Another study from New Zealand found that men with the highest DHA (an omega-3 found in fish) markers slashed their prostate cancer risk by 38% compared to the men with the lowest DHA levels.
2. The phytonutrients you consume make a difference.
A series of studies on phytonutrient intake and prostate cancer incidence in Sicilian men gives a nice glimpse into the potential relationships:
The more polyphenols they ate, the less prostate cancer they got.
The more phytoestrogens they ate, the more prostate cancer they got. Except for genistein, an isoflavone found in soy and fava beans, which was linked to lower rates of prostate cancer. The Sicilians are eating more fava than soy, I’d imagine.
How about coffee, the richest source of polyphenols in many people’s daily diets? It doesn’t appear to reduce the incidence of prostate cancer, but it does predict a lower rate of fatal prostate cancer.
3. Your circadian rhythm and your sleep are important.
Like everything else in life, tumor suppression follows a circadian pattern. Nighttime melatonin—which is suppressed if your sleep hygiene is bad and optimal if your sleep hygiene is great—inhibits the growth of prostate cancer cells and reduces their ability to utilize glucose. One way to enhance nighttime melatonin is by getting plenty of natural, blue light during the day; this actually makes nighttime melatonin more effective at prostate cancer inhibition. On the other hand, getting that blue light at night is a major risk factor for prostate cancer.
4. Get a handle on your fasting blood sugar and insulin.
In one study, having untreated diabetic-level fasting blood sugar was a strong risk factor for prostate cancer. Another study found that insulin-lowering metformin reduced the risk, while an anti-diabetic drug that raised insulin increased the risk of prostate cancer. Metformin actually lowers PSA levels, which, taken together with the previous study, indicates a causal effect.
5. Keep moving, keep playing, keep lifting.
This has a number of pro-prostate effects:
It keeps you insulin sensitive, so neither fasting insulin, nor fasting glucose get into the danger zone.
Oh, and do some deadlifts. Men with prostate cancer who trained post-surgery had better control over their bodily functions, as long as they improved their hip extensor strength. If you don’t know, hip extension is the act of standing up straight, of moving from hip flexion (hip hinging, bending over) to standing tall. It involves hamstrings, glutes, and the entire posterior chain. Deadlifts are the best way to train that movement pattern.
The prostate cancer issue is frightening because it’s so common. Almost all of us probably know someone who has or had it, even unknowingly. But the good news is that most prostate cancers aren’t rapidly lethal. Many aren’t lethal at all. So whatever you do, don’t rush into serious treatments or procedures without discussing the full range of options in a frank, honest discussion with your doctor.
That’s it for today, folks. Thanks for reading. If you have any questions, comments, or concerns about prostate cancer, feel free to chime in down below. I’d love to hear from you.
Perletti G, Monti E, Magri V, et al. The association between prostatitis and prostate cancer. Systematic review and meta-analysis. Arch Ital Urol Androl. 2017;89(4):259-265.
Ilic D, Djulbegovic M, Jung JH, et al. Prostate cancer screening with prostate-specific antigen (PSA) test: a systematic review and meta-analysis. BMJ. 2018;362:k3519.
Brawer MK, Chetner MP, Beatie J, Buchner DM, Vessella RL, Lange PH. Screening for prostatic carcinoma with prostate specific antigen. J Urol. 1992;147(3 Pt 2):841-5.
Castro E, Eeles R. The role of BRCA1 and BRCA2 in prostate cancer. Asian J Androl. 2012;14(3):409-14.
Watts EL, Appleby PN, Perez-cornago A, et al. Low Free Testosterone and Prostate Cancer Risk: A Collaborative Analysis of 20 Prospective Studies. Eur Urol. 2018;
Neuzillet Y, Raynaud JP, Dreyfus JF, et al. Aggressiveness of Localized Prostate Cancer: the Key Value of Testosterone Deficiency Evaluated by Both Total and Bioavailable Testosterone: AndroCan Study Results. Horm Cancer. 2018;
Dai B, Qu Y, Kong Y, et al. Low pretreatment serum total testosterone is associated with a high incidence of Gleason score 8-10 disease in prostatectomy specimens: data from ethnic Chinese patients with localized prostate cancer. BJU Int. 2012;110(11 Pt B):E667-72.
Teloken C, Da ros CT, Caraver F, Weber FA, Cavalheiro AP, Graziottin TM. Low serum testosterone levels are associated with positive surgical margins in radical retropubic prostatectomy: hypogonadism represents bad prognosis in prostate cancer. J Urol. 2005;174(6):2178-80.
Banerjee PP, Banerjee S, Brown TR, Zirkin BR. Androgen action in prostate function and disease. Am J Clin Exp Urol. 2018;6(2):62-77.
Zhou CK, Daugherty SE, Liao LM, et al. Do Aspirin and Other NSAIDs Confer a Survival Benefit in Men Diagnosed with Prostate Cancer? A Pooled Analysis of NIH-AARP and PLCO Cohorts. Cancer Prev Res (Phila). 2017;10(7):410-420.
Russo GI, Campisi D, Di mauro M, et al. Dietary Consumption of Phenolic Acids and Prostate Cancer: A Case-Control Study in Sicily, Southern Italy. Molecules. 2017;22(12)
Russo GI, Di mauro M, Regis F, et al. Association between dietary phytoestrogens intakes and prostate cancer risk in Sicily. Aging Male. 2018;21(1):48-54.
Discacciati A, Orsini N, Wolk A. Coffee consumption and risk of nonaggressive, aggressive and fatal prostate cancer–a dose-response meta-analysis. Ann Oncol. 2014;25(3):584-91.
Dauchy RT, Hoffman AE, Wren-dail MA, et al. Daytime Blue Light Enhances the Nighttime Circadian Melatonin Inhibition of Human Prostate Cancer Growth. Comp Med. 2015;65(6):473-85.
Kim KY, Lee E, Kim YJ, Kim J. The association between artificial light at night and prostate cancer in Gwangju City and South Jeolla Province of South Korea. Chronobiol Int. 2017;34(2):203-211.
Murtola TJ, Vihervuori VJ, Lahtela J, et al. Fasting blood glucose, glycaemic control and prostate cancer risk in the Finnish Randomized Study of Screening for Prostate Cancer. Br J Cancer. 2018;118(9):1248-1254.
Haring A, Murtola TJ, Talala K, Taari K, Tammela TL, Auvinen A. Antidiabetic drug use and prostate cancer risk in the Finnish Randomized Study of Screening for Prostate Cancer. Scand J Urol. 2017;51(1):5-12.
Park JS, Lee KS, Ham WS, Chung BH, Koo KC. Impact of metformin on serum prostate-specific antigen levels: Data from the national health and nutrition examination survey 2007 to 2008. Medicine (Baltimore). 2017;96(51):e9427.
Galvão DA, Taaffe DR, Spry N, Joseph D, Newton RU. Combined resistance and aerobic exercise program reverses muscle loss in men undergoing androgen suppression therapy for prostate cancer without bone metastases: a randomized controlled trial. J Clin Oncol. 2010;28(2):340-7.
Ying M, Zhao R, Jiang D, Gu S, Li M. Lifestyle interventions to alleviate side effects on prostate cancer patients receiving androgen deprivation therapy: a meta-analysis. Jpn J Clin Oncol. 2018;48(9):827-834.
Uth J, Fristrup B, Haahr RD, et al. Football training over 5 years is associated with preserved femoral bone mineral density in men with prostate cancer. Scand J Med Sci Sports. 2018;28 Suppl 1:61-73.
Park J, Yoon DH, Yoo S, et al. Effects of Progressive Resistance Training on Post-Surgery Incontinence in Men with Prostate Cancer. J Clin Med. 2018;7(9)
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A Primal woman’s first reaction to the prospect of taking synthetic hormone replacements for menopause? Probably a healthy dose of skepticism. We in the ancestral health community, after all, tend to view pharmaceuticals as a last resort—interventions that are overprescribed by vested interests, create their own set of side effects, and may even do more harm than good. To suggest that we “need” this or that prescription raises our hackles.
Besides, it’s not like menopause is a product of modernity or an aberration our ancestors never experienced; it’s a physiological stage that evolution has protected and selected in humans. It’s perfectly natural. Rather than the debilitating, miserable experience many women report having, menopause should be easier. Graceful, even. But it often isn’t.
And nature unfortunately doesn’t care about that. Menopause is nature’s way of preventing undue discomfort and reducing genetic damage to the group. Your average 50-year-old woman has a lot to offer the tribe in terms of wisdom, child care, and general know-how, but natural selection has also determined that it’s better for everyone if middle-aged women don’t easily get pregnant. Menopause achieves this by down-regulating the hormones and weakening the tissues necessary for conception. The problem is that these same hormones and tissues also figure prominently in a woman’s enjoyment of life and overall health.
What can happen when Mother Nature decides to step in?
- Loss of libido, vaginal atrophy
- Night sweats
- Hot flashes
- Weight gain
Longer-term, menopause increases the risk of serious diseases like osteoporosis, heart disease, and breast cancer.
Those aren’t mere inconveniences. They can mar the beauty of what should be an enjoyable part of a woman’s life, interfering with her relationships, her productivity, her cognitive function, her sleep, and her basic ability to enjoy living.
Mother Grok didn’t take pharmaceutical hormone replacements, you might counter. She didn’t hit up the shaman for a compound blend of hormones, so why should you?
First of all, maybe she did. Pre-scientific peoples have been known to develop folk cures that seem primitive but end up getting scientific validation. Think of the medieval garlic-based concoction that we just found out can eliminate medication-resistant staph infections. Or the indigenous Amazonian tribes who somehow figured out if you brewed a certain vine with a certain leaf and drank the finished product you’d visit the spirit world, all without knowing the vine contained DMT and the leaf contained an MAO-inhibitor that made the DMT orally active. Or, to bring it back to menopause, the yam, which cultures have used for hundreds of years for menopause treatment without actually knowing it contains an estrogen mimetic with clinical efficacy.
Second of all, the basic Primal stance on pharmaceutical interventions is that they are useful and suitable when correcting a deficiency, a genetic proclivity, or an evolutionary mismatch—particularly when dietary and lifestyle interventions aren’t cutting it. If they can help us treat a condition that seriously impedes our life or pursuit of health, we should avail ourselves of the fruits of modern science. Hormone replacement therapy may very well qualify.
Philosophical qualms aside—does hormone replacement therapy (HRT) work? What factors play into its effectiveness—and safety?
First, Is It Safe?
This might just be the most contentious topic in medicine.
For decades, HRT was the standard treatment for postmenopausal women. Not only was it given to treat the symptoms of menopause, it was billed as an antidote to many of the chronic diseases that increased in frequency after menopause like breast cancer, osteoporosis, and heart disease. Most of this was based on observational data and small pilot studies. That changed with the Women’s Health Initiative (WHI), a massive series of randomized controlled trials involving tens of thousands of postmenopausal women. Finally, the establishment would get the solid backing they needed to continue prescribing HRT to millions of women for prevention of chronic disease.
Except it didn’t turn out so well. Midway through, they stopped the trial because they weren’t getting the desired results.
There were two different HRT study groups. In one study, women without uteruses either got placebo or estrogen alone. In the other, women with uteruses got a combo of estrogen and progestin (a progesterone analogue) or placebo. The estrogen was Premarin, a conjugated estrogen. The progestin was Prempro, or medroxyprogesterone acetate.
The E/P combo increased the risk of heart disease, breast cancer, pulmonary embolism, and stroke, and reduced the risk of colorectal cancer and fractures (but not enough to offset the increased risks).
The estrogen alone had no effect on heart disease (contrary to their hypotheses), but it did appear to increase the risk of stroke while decreasing the risk of breast cancer and fractures.
Following the publication and wide dissemination of the WHI results, HRT use plummeted among women. Breast cancer cases subsequently dropped by 15-20,000 per year. Hormone replacement therapy developed a bad rap that it has yet to shake.
Is it deserved? Yes and no.
While the WHI results highlight some very real risks associated with HRT, they don’t tell the whole story. There are other variables to consider when deciding on HRT.
How Early You Start Taking HRT Matters
Most of the women in the WHI study began HRT when they were very post-menopause: older, in their 60s and upward. They got worse results.
A much smaller proportion of the women in the study were under 60 when they started HRT. They had better results. In fact, among those women who initiated HRT before age 60, total mortality actually dropped by 30%.
Another analysis of the Women’s Health Initiative data found that women who started taking HRT during early pre-menopause were less likely to see the negative effects, like increased breast cancer and heart disease.
Another study found that older post-menopausal women taking estrogen took hits to their working memory that remained after therapy cessation, while younger post-menopausal women had no such reaction.
Women who took oral estradiol 6 years after menopause saw their subclinical atherosclerosis slow down. Those who took it later (10 years after) did not.
A recent large Cochrane meta-analysis found that while in general postmenopausal women taking HRT had a moderately increased risk of heart disease, breast cancer, and other diseases, a subgroup of healthy, 50-59 year old (so, younger) HRT users only had a slightly increased risk of venous thromboembolism.
The longer you wait to initiate HRT after menopause, the more adverse effects occur. Start earlier, if you do start
How You Administer the HRT Matters
Oral hormones have different metabolic fates than transdermal hormones. When you swallow a hormone, it goes to the liver for processing. This creates various metabolites with different bioactivity. One example is oral estrogen. When you take estrogen orally, you raise CRP, a marker of inflammation. Transdermal estrogen has no effect on CRP.
Oral HRT has been shown across multiple studies to increase the risk of venous thromboembolism, while transdermal HRT does not. This is because oral HRT increases thrombin generation and clotting, while transdermal HRT does not.
In the Women’s Health Initiative that found negative effects, the HRT given to the subjects was oral. Perhaps this was the issue.
For local vaginal symptoms, local application is probably ideal, while oral application is suboptimal. In one study, vaginal estriol was far more bioactive than oral estriol, despite the latter resulting in higher serum levels of the hormone.
However, topical isn’t always best. In one study, sublingual users of bioidentical hormones saw relief from night sweats, irritability, hot flashes, anxiety, emotional lability, sleep, libido, fatigue, and memory loss, while topical users only saw relief from night sweats, emotional lability, and irritability.
The Type Of Hormone You Take Matters
Another factor the WHI failed to address was the composition of the medication itself. They used synthetic hormones—conjugated estradiol and medroxyprogesterone acetate. Could bioidentical hormones, exact replicas of endogenous hormones which exploded in popularity following the WHI, have a different effect?
The amount of research into conventional HRT dwarfs bioidentical hormone therapy (BHT) research, but what we have looks pretty compelling.
Breast cancer is a major concern for HRT users. Most breast cancers respond to estrogen, just over half respond to progesterone, and traditional HRT seems to increase their risk. Yet, at least in healthy postmenopausal women, a combination percutaneous estradiol gel (inserted into the skin) and oral micronized progesterone—both bioidentical to their endogenous counterparts—had no effect on epithelial proliferation of the breast tissue, while reducing activity of a protein that protects cancer from cell death. The conventional HRT had the opposite effect, increasing epithelial proliferation and breast volume (a risk factor for breast cancer). This wasn’t about cancer, but it’s suggestive.
In another study, postmenopausal women on BHT (which included estriol, estradiol, progesterone, testosterone, and DHEA) saw improvements across all measured cardiovascular, inflammatory, immune, and glucoregulatory biomarkers despite being exposed to high levels of life stress.
Then again, in a recent study, bioidentical hormones performed poorly compared to the pharmaceuticals equine estrogen and medroxyprogesterone acetate. The pharmaceutical hormones resulted in a lower risk of breast cancer, although the bioidentical hormones still reduced the risk compared to placebo.
Which Hormones You Take Matters
The vast majority of postmenopausal women take estrogen, progesterone, or some combination of the two. But there’s another hormone that, despite plummeting during menopause, gets ignored—testosterone.
Although testosterone is the “male hormone,” it also plays a vital role in female physiology, especially sexual function. Menopause reduces testosterone by about half, and studies indicate that topical testosterone replacement therapy can improve sexual function and desire (combined with estrogen) as well as musculoskeletal health and cognitive performance in postmenopausal women. More importantly, topical testosterone improves sexual function without causing any of the adverse effects commonly associated with testosterone usage in women, like hair loss, voice deepening, body hair growth, facial hair growth, breast pain or tenderness, or headaches.
Adding low-dose testosterone to a low-dose estrogen regimen may even be better at reducing somatic symptoms of menopause (sleep disturbances, hot flashes, and other physical symptoms) than a higher dose of estrogen alone.
Your Expectations Matter
Our big mistake was treating HRT as a panacea for the chronic conditions of aging. It’s not that smart hormone replacement can’t or won’t reduce the risk of certain diseases, like osteoporosis or heart disease. It’s that we’re still figuring it out.
A better, safer move is to focus on what we know HRT can treat: the symptoms of menopause.
Want to reduce hot flashes and get more sleep? HRT works.
Want to reduce anxiety? HRT works.
Want to improve cognitive function and your sense of smell? HRT works.
The use of bioidentical hormones may be safer or more effective against the bigger stuff. It remains to be seen. Until then, treat symptoms, not chronic disease—but keep in mind your overall risks and discern whether treating the symptoms is worth any additional risk for that bigger stuff.
Your Personal Context Matters
Women with a history of estrogen-responsive breast cancer (80% of breast cancers) should exhibit caution and check with their oncologist before taking any kind of HRT.
ApoE4 carriers should seriously look into taking HRT. In one recent study, postmenopausal ApoE4 carriers exhibited rapid cellular aging—except if they were taking HRT.
Whatever You Decide…
Don’t feel guilty if you decide to take some form of it. I myself take a small dose of testosterone to get my levels up to where they should be. My wife, Carrie, has taken bioidentical hormones in the past (a modest compound blend of estrogen, progesterone, and testosterone) to deal with the symptoms of menopause, including persistent brain fog that didn’t respond to any other herbal or alternative measure in her case. There’s no shame. This is restoration of what’s healthy and supportive of a good life.
Heck, I know women who are both aware of the potential long term risks—heart disease, breast cancer, and the like—and enthusiastic about the shorter-term, more immediate quality-of-life benefits they currently enjoy. They prefer the definite benefits over the small and uncertain absolute risk increases. Some have even said that feeling better day-to-day gives them the energy to continue living a healthy life in other ways.
I also know women who do the opposite, who either are lucky enough to not experience any profound symptoms in their transition or who prefer to use other methods and interventions to deal with their symptoms in order to avoid any increased long-term complications. (I’ll delve more into this in the future if there’s interest.) Regardless, it’s all a choice.
Hopefully after today you feel better equipped to make an informed one.
What about you, folks? I know I have thousands of readers who are facing this very question—or who have already faced it. What did you choose? How did you handle the HRT question?
Thanks for reading. Take care!
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Yazici K, Pata O, Yazici A, Akta? A, Tot S, Kanik A. [The effects of hormone replacement therapy in menopause on symptoms of anxiety and depression]. Turk Psikiyatri Derg. 2003;14(2):101-5.
Doty RL, Tourbier I, Ng V, et al. Influences of hormone replacement therapy on olfactory and cognitive function in postmenopausal women. Neurobiol Aging. 2015;36(6):2053-9.
Jacobs EG, Kroenke C, Lin J, et al. Accelerated cell aging in female APOE-?4 carriers: implications for hormone therapy use. PLoS ONE. 2013;8(2):e54713.
Kingsberg S. Testosterone treatment for hypoactive sexual desire disorder in postmenopausal women. J Sex Med. 2007;4 Suppl 3:227-34.
Davis SR, Wahlin-jacobsen S. Testosterone in women–the clinical significance. Lancet Diabetes Endocrinol. 2015;3(12):980-92.
Achilli C, Pundir J, Ramanathan P, Sabatini L, Hamoda H, Panay N. Efficacy and safety of transdermal testosterone in postmenopausal women with hypoactive sexual desire disorder: a systematic review and meta-analysis. Fertil Steril. 2017;107(2):475-482.e15.
Simon J, Klaiber E, Wiita B, Bowen A, Yang HM. Differential effects of estrogen-androgen and estrogen-only therapy on vasomotor symptoms, gonadotropin secretion, and endogenous androgen bioavailability in postmenopausal women. Menopause. 1999;6(2):138-46.
The post The Pros & Cons of Hormone Replacement Therapy for Primal Women 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?
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:
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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A few months ago, I explored the benefits and applications of cold therapy. Today, I’m going to talk about the benefits and applications of heat therapy—one of the most ubiquitous and ancestral therapies in the history of humankind. You name a culture and—as long as they didn’t live in perpetual tropical heat—they probably had some form of heat therapy. Native Americans had the sweat lodge, those of Central America the temazcal. The Romans had the thermae, which they picked up and refined from the Greeks. Other famous traditions include Finnish saunas, Russian banyas, Turkish hammams, Japanese sentó (or the natural spring-fed onsen), and the Korean jjimjilbang. People really like the heat.
Right off the bat, that’s one major benefit to heat therapy compared to cold: It’s an easy sell. “You can luxuriate in a sauna for half an hour or lower your naked body, genitals first, into a bathtub filled with ice water. Your choice.” People are far more likely to sit in the hot room for 20 minutes than they are to sit in an ice bath for 3 minutes or even take a cold shower. Short-term heat exposure is generally regarded as pleasant. Cold exposure is generally regarded as torture. If heat therapy offers legit health benefits, this is a major point in its favor. So, does it?
In a recent review of the available observational studies, controlled trials, and interventions, researchers found evidence that sauna usage has an impressive array of beneficial effects on health and wellness:
- Increased lifespan and decreased early mortality.
- Reduced cardiovascular disease.
- Lowered blood pressure.
- Improved cognitive function and reduced the risk of neurodegenerative disease.
- Improved arthritis symptoms.
What’s going on here? How could sitting in a hot room do so many good things?
Stress, in a word. One of the coolest things about us is that encountering, facing down, and then growing resistance to one type of stress tends to make us better at dealing with stress from other sources. A 30-minute sauna session at 174 ºF/80 ºC raises body temperature by almost 1 degree C, spikes your flight-or-flight hormones, raises cortisol, and triggers a powerful hormetic response by the rest of your body. That’s a stressor. After such a session, subjects report feeling “calm” and “pleasant.” This isn’t a surprise. Intense exercise also raises cortisol in the short term. And like regular exercise, longer term sauna usage (daily for four weeks in one study) actually reduces stress hormones. It’s a classic hormetic response, where acute doses of the stressor increase oxidative stress enough to provoke a compensatory adaptation by the organism.
What does this sauna-induced hormetic stress do for us?
Benefits of Heat Therapy
It reduces oxidative stress. Short term, it increases stress (that’s why we see the transient spike in cortisol and other stress hormones). Long term, it reduces oxidative stress. Long-term sauna use has an inverse association with levels of C-reactive protein (CRP), a “catch-all” biomarker for oxidative stress and inflammation. The more often you use the sauna, the lower your CRP.
It may reduce mortality. The more frequently a person visits the sauna, the lower his risk of premature death from heart attack and all causes. There is a dose-response relationship happening here, which has me leaning toward “causal.” Those using the sauna two to three times a week had a 23% lower risk of fatal heart attack compared to men who used it just once a week. Men who used the sauna four to seven times a week had a 48% reduced risk of fatal heart attack compared to once-a-weekers. The more frequently men used the sauna, the greater the protection (for other causes of mortality, too).
It improves vascular function. A single bout of sauna (or exercise, for that matter) reduces vascular resistance—the amount your blood vessels “resist” blood flow—in hypertensive patients for up to two hours.
It’s good against type 2 diabetes. Sauna use has been shown to improve almost every marker related to type 2 diabetes, including insulin sensitivity, fasting blood sugar, glycated hemoglobin, and body fat levels.
It can improve depression scores. Patients with depression who underwent heat therapy saw improvements in their Hamilton Depression Rating.
If you’re an athlete, or exercise at all, you should try the sauna. Training magnifies the benefits of the sauna.
Finally, pairing exercise and heat therapy together is a boon for cardiovascular health. For instance, people who frequent the sauna and the gym have a drastically lower risk of heart attack death than people who do either alone. That combo also reduces 24-hour blood pressure in hypertensive patients and confers special protection against all-cause mortality above and beyond either variable alone.
Post-workout sauna sessions improve endurance performance in runners: For three weeks, endurance runners sat in 89° C (+/- 2° C) humid saunas for 31 minutes following training sessions. This amounted to an average of 12.7 sauna sessions per runner. Relative to control (no sauna), sauna use increased time to exhaustion by 32%, plasma cell volume by 7.1%, and red cell volume by 3.2% (both plasma cell and red cell volume are markers of increased endurance performance).
Post-workout sauna use increases plasma volume in male cyclists: Following training sessions, cyclists sat in 87° C, 11% humidity saunas for 30 minutes. Just four sessions were sufficient to expand plasma volume. This is important because increasing plasma volume improves heat dissipation, thermoregulation, heart rate, and cardiac stroke volume during exercise.
Post-workout sauna—either dry or steam—can also alleviate muscle fatigue.
How About Pre-Workout?
The effects are more mixed. In one study, pre-workout sauna reduced strength endurance and 1 rep max leg press, had no effect on 1 rep max bench press, and improved maximum power (vertical leap). Another study found that in female athletes but not in males, maximum power decreases after sauna use. It’s possible that these performance disturbances are caused by dehydration rather than the heat itself, so make sure you rehydrate if you’re planning on training after a sauna session.
If you want to apply heat pre-workout without overdoing it, I’ve always liked a nice hot bath to help limber up, mobilize my joints, and clear out any stiffness for the coming workout session.
Oh, and It Can Help You Detox
I was going to write the full word “detoxification,” but I figured I’d write “detox” just to trigger the hardcore skeptics reading this…. Heat exposure can augment your natural detoxification capacities by at least two mechanisms.
First, exposure to extreme heat increases something called heat shock proteins, or HSPs. HSPs are responsible for many of the benefits of heat therapy, including enacting beneficial hormetic effects on our detoxification capacity. They trigger compensatory adaptations and activate antioxidant defenses in the blood of healthy volunteers. They even increase regeneration of the body’s main detoxifying organ—the liver—after it’s been damaged.
Second, contrary to popular belief, sweating can aid detoxification. Sweat itself contains bioaccumulated toxins, including BPA—even when it doesn’t show up in the blood or urine. Sweat also contains certain phthalate compounds and their metabolites, none of which we want. Sweat also contains arsenic and lead in people exposed to high levels of the metals. Sweating may even improve the function of another important detoxification organ—the kidney—by restoring nitrogen excretion in people with kidney disease. In one study, police officers with chronic illnesses caused by exposure to high levels of meth lab chemicals experienced major improvements after sauna therapy.
What If You Don’t Have Access To a Sauna?
There are other options.
Steam rooms work. Only problem with them is it’s difficult to remain in one long enough to trigger the necessary stress response. Saunas, with their dry heat, are easier to stick with. Steam rooms feel different enough that I wonder if there’s something unique about them. Not enough evidence to go on, unfortunately. Perhaps I can revisit this later.
Jacuzzis and hot baths work. A recent paper found that taking regular hot baths at home improved insulin sensitivity and increased nitric oxide synthase activity about as much as working out. Another found that, compared to showering, bathing improved mood, perceived stress, blood flow, and accumulation of metabolic waste products.
You could probably sit in a black car on a hot day with the windows rolled up and get an effect.
Just get hot, as hot as you can stand. Then stay a little longer. (As always, be sure to talk to your doctor. Certain conditions and scenarios, like pregnancy, require extra caution with saunas or other forms of heat therapy.)
Have you used the sauna? Are you a regular attendee? Or do you use other means of heat therapy? I’m curious to hear your experiences, tips, and stories below.
Laukkanen JA, Laukkanen T, Kunutsor SK. Cardiovascular and Other Health Benefits of Sauna Bathing: A Review of the Evidence. Mayo Clin Proc. 2018;93(8):1111-1121.
Leppäluoto J. Human thermoregulation in sauna. Ann Clin Res. 1988;20(4):240-3.
Sutkowy P, Wo?niak A, Rajewski P. Single whole-body cryostimulation procedure versus single dry sauna bath: comparison of oxidative impact on healthy male volunteers. Biomed Res Int. 2015;2015:406353.
Laukkanen JA, Laukkanen T. Sauna bathing and systemic inflammation. Eur J Epidemiol. 2018;33(3):351-353.
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.
Krause M, Ludwig MS, Heck TG, Takahashi HK. Heat shock proteins and heat therapy for type 2 diabetes: pros and cons. Curr Opin Clin Nutr Metab Care. 2015;18(4):374-80.
Laukkanen JA, Laukkanen T, Khan H, Babar M, Kunutsor SK. Combined Effect of Sauna Bathing and Cardiorespiratory Fitness on the Risk of Sudden Cardiac Deaths in Caucasian Men: A Long-term Prospective Cohort Study. Prog Cardiovasc Dis. 2018;60(6):635-641.
Kunutsor SK, Khan H, Laukkanen T, Laukkanen JA. Joint associations of sauna bathing and cardiorespiratory fitness on cardiovascular and all-cause mortality risk: a long-term prospective cohort study. Ann Med. 2018;50(2):139-146.
Gayda M, Paillard F, Sosner P, et al. Effects of sauna alone and postexercise sauna baths on blood pressure and hemodynamic variables in patients with untreated hypertension. J Clin Hypertens (Greenwich). 2012;14(8):553-60.
Hedley AM, Climstein M, Hansen R. The effects of acute heat exposure on muscular strength, muscular endurance, and muscular power in the euhydrated athlete. J Strength Cond Res. 2002;16(3):353-8.
Gutiérrez A, Mesa JL, Ruiz JR, Chirosa LJ, Castillo MJ. Sauna-induced rapid weight loss decreases explosive power in women but not in men. Int J Sports Med. 2003;24(7):518-22.
Genuis SJ, Birkholz D, Rodushkin I, Beesoon S. Blood, urine, and sweat (BUS) study: monitoring and elimination of bioaccumulated toxic elements. Arch Environ Contam Toxicol. 2011;61(2):344-57.
Genuis SJ, Beesoon S, Birkholz D, Lobo RA. Human excretion of bisphenol A: blood, urine, and sweat (BUS) study. J Environ Public Health. 2012;2012:185731.
Khodarev VN, Zhemchuzhnova NL, Olempieva EV, Kuz’menko NV. [The influence of general infrared sauna on the antioxidant systems in the blood of volunteers]. Vopr Kurortol Fizioter Lech Fiz Kult. 2013;(5):10-3.
Shi Q, Dong Z, Wei H. The involvement of heat shock proteins in murine liver regeneration. Cell Mol Immunol. 2007;4(1):53-7.
Mccarty MF, Barroso-aranda J, Contreras F. Regular thermal therapy may promote insulin sensitivity while boosting expression of endothelial nitric oxide synthase–effects comparable to those of exercise training. Med Hypotheses. 2009;73(1):103-5.
Goto Y, Hayasaka S, Kurihara S, Nakamura Y. Physical and Mental Effects of Bathing: A Randomized Intervention Study. Evid Based Complement Alternat Med. 2018;2018:9521086.
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There’s good news and bad news. The bad news is that kids aren’t getting enough physical activity.
Inadequate amounts of physical activity are a strong risk factor for obesity and metabolic dysfunction in kids. It’s most likely causal, too, because as much as people question the usefulness of only exercising to lose weight, there’s no question that exercise and physical activity in general is important for preventing obesity from occurring.
Kids are getting so obese that a new RCT came out showing metformin can help them lose weight and normalize metabolic biomarkers.
It’s not just that inadequate physical activity is destroying the physical vitality, body weight, and metabolic health of children. It’s also ruining their movement skills and general athleticism. I don’t work with kids directly, but I have many friends who do. And all of them, from gymnastics coaches to running coaches to basketball/base/football coaches report that the athleticism of the beginners has degraded over the years. Fewer kids are coming into practice for the first time with that raw movement ability. They’re clumsier, clunkier, and more confused than ever before.
Childhood is a big window, but it’s a crucial one. All that time spent throwing a ball—or sitting on the couch manipulating an Xbox controller so that the character onscreen throws a ball—establishes neural pathways. Do you want those pathways to enable efficient, competent throwing (a skill that may have required our big brains and allowed humans to conquer the world), or do you want those pathways to enable skillful button and joystick maneuvering?
The good news is that kids love to move. Even the ones who don’t look it. Go down to a park, the beach, or walk through the city square on a hot day when the fountains are flowing and kids of all shapes and sizes will be moving frequently at slow, moderate, and fast paces. They’re playing tag. They’re roughhousing. They’re jumping from ledges twice their height. They’re all over the place.
And that’s how it works: Get even the most screen-obsessed kid in a fun, physical environment with plenty of opportunities for movement and he or she will move. The innate desire for physicality and play exists in all children.
Overweight kids aren’t too far gone either, and exercise can work wonders. According to a 2015 meta-analysis, there’s “moderate” evidence that exercise by itself is an effective way to reduce bodyweight in overweight and obese children. Another study concluded that strength training and aerobic exercise are more effective at lowering children’s BMI than either alone. I imagine you could optimize a kid’s training regimen even further and get even better results.
How Much Exercise Do Kids Need?
Ethnographic studies have found that, by and large, kids in hunter-gatherer groups play all day long with little to no supervision (PDF). They don’t have scooters and Laser Tag, or barbells and kettlebells, but they also don’t have smartphones and televisions. For these kids, play is movement and movement is play. There’s no other way. Of course, contemporary hunter-gatherer groups are a very rough approximation of our hunter-gatherer ancestors. The former have been pushed onto marginalized land by better-armed and more numerous city folk; the latter ranged across an untouched world teeming with large game. Even still, they’re the best model we have for ancestral childhood physical activity.
But we don’t even have to go back to the paleolithic to illustrate the amount of physical activity the average kid should be getting. Just talk to an elderly neighbor. Talk to an older colleague. Or heck, search within your own memory bank. What were summers like as a kid for you? I for one was out all day long if school was out, exploring the neighborhood, roaming the woods, getting into trouble. And I rarely stopped moving.
Anecdotes and personal memories not enough? The data tells the same story. The parents of today’s children got over 8 hours a week of outdoor play (which is still too little). Today’s children get under four. That trend is likely to continue as you go back in time, with outdoor play doubling in frequency and lack of supervision with each previous generation.
These are averages, of course. Some kids get quite a lot. Others don’t.
Kids in Denmark aged 6-12 average 90 minutes of moderate-to-vigorous physical activity (MVPA) per day. It’s highest in the six-year-olds and declines by 3.5 minutes each year.
Elementary school kids in Qatar average around 28 minutes of MVPA per day, with a large discrepancy along gender lines. By age 9, for example, boys are getting over 40 minutes a day and girls are getting just 23 minutes.
Even the Danes aren’t doing enough, in my book.
Kids should be moving all day. I won’t mince words. Look, my kids probably could have moved more, and I knew about this stuff. It’s hard. I get it. But that doesn’t negate that the ideal situation is for kids to be constantly moving. After all, kids have fatigue-resistant muscles akin to elite athletes’. That’s why they can run all day without getting tired, and that’s a fairly strong indicator they’re meant to move all day.
That’s not in the cards, though, so what should kids aim for?
To stave off overweight/obesity, 60 minutes of MVPA (moderate-to-vigorous physical activity) with at least 15 minutes of genuinely vigorous physical activity each day is the absolute minimum. That’s not optimal. That’s barebones.
Kids should be:
- Running (sprinting rather than jogging)
- Squatting (the movement pattern more than heavy weight)
- Lifting/hip hingeing
- Supporting their own bodyweight
- Playing, ideally using all the skills and movements I just mentioned
Ideas To Get Kids Moving
What are some ideas? How can we get kids to get enough exercise while having fun and developing skill? Many need a little nudge. There are innumerable ways to unlock what’s already inside. I’ll throw out 30 of them right here.
- Walk to School. If you can make it work, walking to and from school will contribute a good amount of MVPA to a kid’s life. Extra points for getting into trouble on the way.
- Swim underwater as far as you can.
- Dive for Objects. Give kids a goal, make it a game. Throw a handful of quarters into the pool; see if they can get them all in with one breath. Toss a kettlebell into the deep end and have them bring it back up.
- Biggest Splash Contest. Who can make the biggest splash into the pool? Encourage different dives, cannonballs, jackknives, and other jumps.
- Water Polo. An excellent training stimulus. One of the hardest sports around.
- Lift Weights. Real ones. In Germany, 11-year-old soccer players and 12-year-old Olympic weightlifters are safely front squatting their bodyweight.
- Race the Dog (with a Head Start). Tell your kid to make a break for it, hold your dog for a few seconds, then release.
- Play Catch. Great way to practice throwing and catching, the latter of which is particularly tricky (and useful to learn).
- Barefoot Hike. Your kid will thank you when she’s all grown up and thinks nothing of walking across gravel.
- Creek Walk. Jump from rock to rock, climb over logs, balance on fallen trees, take a little dip.
- Check Out the local rec center schedule. You’d be surprised at the quality of some of these classes. Gymnastics, dance, martial arts are all good options for building good movement skills.
- Get a pullup bar in the house. Place it at a level your kid can reach. Start with hanging, swinging, and various holds, but work your way up to pullups. Give incentives (“do 5 pullups and I’ll give you $20”).
- Get the dog they’ve always wanted, with the stipulation being they have to walk it and play with it.
- Set up an obstacle course. It doesn’t have to be fancy. Just give them things to climb under/over, crawl under/through/, leap over.
- Hill Sprints. If you want a killer workout, sling that kid over your shoulder in between his sprints and run some of your own.
- Gymnastics. Great foundation for movement later in life. Just stop short of elite competition unless it’s something they really want to commit to.
- Have them race. If you catch kids at the right age, they love races without being attached to the outcome. They’ll just let it rip and go all out, all smiles. Winner and loser both have fun.
- Roughhouse. Roughhousing is a lost art that helps kids establish boundaries and limits, learn what hurts and what doesn’t, grasp when something is “too rough.” Plus, it’s fun.
- Try Parkour. Parkour isn’t something a seven year old just leaps into (go to a parkour gym for formal instruction),but they can certainly start playing around on manmade structures. Visit a business park for good climbing and play.
- Animal Impersonations. Crawl like a bear. Hop like a rabbit. Leap like a frog. Slither like a snake. Walk like a duck. These are very difficult modes of transportation that make for great exercise. To keep things fresh and playful, come up with other animals to emulate.
- Play Fetch. Throw the ball, they go chase it and bring it back. Same concept as running your dog.
- Reverse Box Jumps. That cool Persian tot aside, it makes more sense for small children to practice jumping down from tall objects than trying to jump up them. Besides, landing is where the danger lies later.
- Trampoline. Studies indicate they’re responsible for a large number of emergency visits, but a properly set-up trampoline enclosed by a protective net can be a great place to learn how to jump with good form. And again, fun.
- Keep a scooter/bike/skateboard around. Kids love zooming around on wheels.
- Chore Duty. Give them a standing order to help with bags/groceries/trash. There’s always something they can carry, and every little bit helps make them stronger and more resilient.
- Kettlebell Challenge. Keep a kettlebell in the living room and have him or her lift it every day. Marvel at the perfect deadlift form.
- Build forts, then destroy them.
- Try conventional sports. Although specialization isn’t advised at such an early age (it can actually increase the risk of overuse injuries and inhibit the athletic growth of children), sports are fun and do offer a great path to overall athletic development.
- Build up to a mile run. Start by walking it. Throw in some quick sprints in the middle. Then a full on mile run. Then unleash the offer: “I’ll give you [x] if you can run a mile in [x-amount of time].”
- Set a good example. If you fail to embrace physical culture while demanding your child do the opposite, that’s a strong nudge in the wrong direction. Make sure you’re moving, too.
That’s it for today, folks. I’d love to hear from you.
What kinds of games, sports, and other activities do you use to increase your children’s physical activity and help them develop a positive relationship with exercise? What’s worked, what hasn’t, and what’s the most unconventional activity you’ve had success with?
Take care all.
The post How Much Exercise Do Kids Need? Plus, 30 Activities to Get Them Moving appeared first on Mark’s Daily Apple.
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