The relationship between stress and carbohydrates is confusing, with seemingly contradictory arguments bouncing around the online health sphere.

There are those who say high-carb diets cause stress, and that eating more fat and fewer carbs is the solution.

There are those who say high-fat diets increase stress and eating carbs ameliorates it.

Who’s right? They can’t both be right, can they?

Well…

You’d be surprised.

Let’s dig into four common carb questions and assertions.

“Stress Increases Carb Cravings.”

This is well-established. You have a terrible day at the office, your kids have appointments twenty miles apart within fifteen minutes of each other, the traffic is backed up to your driveway, you’re late for work, the dog needs a walk, you haven’t even thought about what to make for dinner, you slept four hours last night—it adds up. People deal with a lot. And in that moment, a carbohydrate-based snack really does seem to take the edge off.

Across millions of years of hominid evolution, the human stress response developed in the context of real-world, short-term, and infrequent but intense stressors: battles, hunts, freak injuries, dangerous animal encounters, interpersonal conflicts. These were situations that demanded heightened senses, available fuel, and a rapid heart rate to deliver everything to the tissues that needed to move and act. It makes perfect sense for your body to pump out adrenaline to increase fat burning and glucose in the blood—you need that fuel to deal with the situation. It also makes sense for your body to follow that up with a blast of cortisol, which makes you crave high-carb junk food to replace the fuel you utilized. The problem is that our modern stressors are too frequent, they aren’t physically demanding, we aren’t utilizing the fuel we mobilize, and we have no real need for the carb cravings that come after.

What happens when we eat too many carbs that we never actually needed?

We get fat. Cellular energy supply becomes overloaded, impairing our mitochondria’s ability to process energy efficiently. This degrades metabolic flexibility—the ability to switch between different fuel sources—preventing us from burning the fat on our bodies in between meals. We become reliant on those carbs, and when we don’t get them fast enough, our bodies perceive that as a major stressor.

So while giving in to carb cravings can reduce stress in the short-term, it sets us up for longer-term, more chronic stress.

“What About Gluconeogenesis? Isn’t That a Stress Response?”

It can be.

A primary goal of cortisol is to increase glucose availability. It does this through multiple avenues. One I just mentioned is to increase carb cravings. Another is to make you insulin resistant, thereby preventing insulin from sucking up blood glucose. Gluconeogenesis—the creation of glucose from amino acids and other substrates—is another.

If you’re a sugar-burner, stressful situations will increase carb cravings, induce gluconeogenesis, and may even make you insulin resistant. If you’re fat-adapted, the story shifts.

A fat-adapted person will have ketones and fatty acids available to provide energy in between meals. A fat-adapted person will have ketones and fatty acids available to provide energy in stressful situations. A fat-adapted person will be able to utilize those ketones and fatty acids during stressful situations—their mitochondria will literally be primed to utilize those fuels, not just glucose. A fat-adapted person is less likely to perceive carbohydrate shortages as stress shortages because they’ve got all this other fuel available to burn.

This adaptation doesn’t happen overnight. If your diet is low-carb or keto, but your body is still reliant on sugar, you will perceive reduced carb availability as a stressor. That’s one of the hallmarks of the keto flu, and it’s one reason why some people have extended keto flu—their bodies are still expecting and demanding glucose.

Some people never get over the carb cravings; they never fully adapt. This is the subset of the population that doesn’t function or perform well on a long-term ketogenic diet. The cause is unknown, at least for now (I suspect it has to do with recent ancestry and genetic proclivities), but what matters is that these people exist. For them, a long-term keto or very low carb diet approach will probably always be stressful. But even in these folks, spending some time in ketosis—through short term low-carb eating, intermittent fasting, or even extended low-level endurance activity that primarily burns fat—is a good idea that will reduce stress and improve overall resilience.

“But Carbs Make Exercise Less Stressful!”

Exercise is stressful to begin with. But then you adapt to the stress and overcome it—and end up stronger, fitter, and faster than before. Without the stress, working out doesn’t work. A legitimate method for increasing your work capacity is to train-low (carb), race-high (carb). Athletes have been doing this for decades—training in a low-carb state to get better at performing without ample muscle glycogen, then going into a race with full glycogen reserves and the ability to perform without glycogen. Exercising in that low-glycogen state is stressful, but that’s the whole point. It makes them better, stronger, faster, and it conserves glycogen for when they really need it.

If you consistently perform glucose-intensive high-intensity anaerobic activity for extended periods of time—CrossFit style WODs done 3-5 times per week, for example—you will run up a glucose debt and should replenish some of the carbohydrates you expend or risk cortisol spikes. Fat-adaptation can improve your tolerance of anaerobic activity in a low-glucose state, but there’s a breaking point, a physiological limit.

Eat the carbs you earn. This is a subtle point I don’t often see made. The reverse is widely understood—don’t eat the carbs you don’t earn—because millions of obese and overweight people do that every day. It’s a big reason why we’re so overweight. But if you fail to eat the carbs you earn through intense, protracted physical activity, you’re creating an undeniable glycogen deficiency that your body may perceive as a stressor. It may turn out that fully fat- and keto-adapted athletes can perform intense medium-to-long-term activities at high levels, and there’s some indication that this is the case, but for the time being it appears that eating the carbs you earn can stave off the stress.

“Low-Carb Diets Are Stressful For Women.”

There’s a glimmer of truth here. Allow me to explain.

Women are inherently more sensitive to caloric fluctuations than men…on average. The reason is sheer biology. Human evolution is concerned with fertility and reproduction. Can you produce, foster, and support viable offspring? Awesome. Natural selection deems you fit.

To fulfill their biological role, men have to produce sperm. They can do so almost indefinitely. They don’t run out; they just make more. If a batch is damaged due to poor lifestyle or dietary choices, there’s more on the way. After a man gets someone pregnant, his biological involvement with the growing baby is done. What or when he eats has no impact on the survival of the growing baby.

To fulfill theirs, women have a finite number of eggs, or “chances.” Once an egg is gone, there’s no replacing it.

And so the body seeks to inculcate the egg from environmental insults.

When you are preparing to get pregnant, your body needs extra nutrients to build up a reserve and “prime the pump.”

When you are pregnant, the growing baby needs a reliable and constant stream of nutrients for almost a year.

After you’ve given birth, the growing newborn needs breastmilk. To make that milk requires additional calories and extra doses of specific nutrients. Modern technology allows us to skip nursing and go straight to the bottle, but your body doesn’t “know” that.

It all points to women being more finely attuned to caloric deficits. For example, women’s levels of ghrelin, the hunger hormone, are quicker to rise after meals. Even if you’re never going to have kids, your body is still wired to protect against these caloric fluctuations.

Where do carbs come in?

One’s carbohydrate consumption is uniquely hewed to our sense of caloric sufficiency. If carbs are plentiful, your body perceives that as a signal of environmental plenty: the weather is good, the plants are producing, the trees are bearing fruit, the men are bringing back lots of honey. Life is good. It’s the perfect time to get pregnant. Above all other macronutrients, carbohydrate consumption increases the short-term expression of leptin, a satiety hormone that signals the presence of incoming calories, caloric sufficiency, and environmental plenty.

There’s also the issue of extreme satiety. Low-carb diets often become low-calorie diets without you even trying. That’s why they work so well for fat loss, by inadvertently reducing the amount of food you eat and increasing satiety. But for some women, especially those at or approaching their ideal weight, going too low in calories can increase stress.

Summing Up…

Are you unable to access your own body fat in between meals for energy? Then you’ll be a ball of stress unless you can get those Jolly Ranchers unwrapped quickly enough. It’ll be a constant battle. And yeah, if you keep pumping yourself full of carbs to keep your blood glucose topped off, you’ll keep stress at bay—but you’ll always be teetering on that precipice.

Are you exercising? Then you should strike a balance between gaining the adaptive benefits of training in a low-carbohydrate state and eating the carbs you earn.

Are you a woman? Then you’re probably more sensitive to diet-induced stress and may benefit from occasional carbohydrate refeeds. You should watch out for excessive satiety on ketogenic diets, which is great for fat loss but can lead to stress issues down the line if calories get too low.

The relationship between carbohydrates and stress isn’t exactly straightforward, but it is navigable. Hopefully after today you have a better idea of where you stand in the relationship.

What’s been your experience with stress and carbohydrates? Has your tolerance for stress gone up or down since going low-carb or keto? Thanks for stopping in today.

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References:

Mcallister MJ, Webb HE, Tidwell DK, et al. Exogenous Carbohydrate Reduces Cortisol Response from Combined Mental and Physical Stress. Int J Sports Med. 2016;37(14):1159-1165.

Dirlewanger M, Di vetta V, Guenat E, et al. Effects of short-term carbohydrate or fat overfeeding on energy expenditure and plasma leptin concentrations in healthy female subjects. Int J Obes Relat Metab Disord. 2000;24(11):1413-8.

The post 4 Misunderstandings About Carbs and Stress appeared first on Mark’s Daily Apple.

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Ready for some hormone talk? In this episode, we chat with hormone health educator Candace Burch, founder of Your Hormone Balance, a consulting and hormone testing practice that helps women of all ages correct hormone imbalances. Because, here’s something you might not realize:  hormones can wreak havoc on your health at any age. Hormones dictate our health in so many ways: mood, heavy periods, weight gain, adrenal fatigue, you name it. Candace’s mission is to educate and guide women toward a safe, natural approach to hormone balance so that they can live their healthiest life. Her own journey began with…

The post Podcast Ep 107: Candace Burch of Your Hormone Balance appeared first on Fit Bottomed Girls.

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For today’s edition of Dear Mark, I’m answering a couple of questions from the comment sections of the last couple weeks. First, it’s been established that fasting and exercise both raise growth hormone. What about fasted exercise—does that have an even stronger effect? And what about continuing to fast after your fasted workout? Then, I discuss the inevitability (or not) of wear and tear on the arteries from blood flow-induced shear stress. Is shear stress “bad,” or do certain factors make it worse?

Let’s dig in.

Marge asked:

So fasting raises growth hormone levels? Interesting. So does weight lifting. I’ll bet fasted weight workouts would be pretty powerful.

They do, and they are.

What’s even better is to work out in a fasted state and keep fasting after the workout. This keeps the GH spike going even longer. And in my “just so story” imagination—which is actually quite accurate, judging from real world hunter-gatherers—it mirrors the circumstances of our Paleolithic ancestors. You’d get up early to go hunting without having eaten. You’d expend a lot of energy on the hunt. You’d make the kill, procure the food. And then you’d bring it back to camp to finally eat. Maybe you’d pass the heart and liver around the circle before heading back. And sometimes, you just didn’t make the kill. You didn’t eat at all.

Makes sense, right? Fasting, doing something physical, and continuing to fast shouldn’t be a monumental undertaking. It should be well within the realm of possibility for the average person.

Now, I wouldn’t do this all the time. There is such a thing as too much of a good thing. A hormetic stressor can become a plain old stressor if it’s prolonged for too long. Instead, I would throw post-fasted-workout fasting in on an occasional basis.

Nor would I expect huge “gains” from this. Physiological growth hormone production won’t make you huge or shredded. In fact, workout-related increases in testosterone and growth hormone don’t actually correlate with gains in hypertrophy. Instead, I’d expect more intangible benefits, things you won’t notice right away. It’s important in cognition. It helps maintain bone health, organ reserve, and general cellular regeneration. It’s great for burning fat.

Growth hormone does way more than promote overt muscular growth.

Steve wrote:

In the linked article it says:

“Endothelial cell dysfunction is an initial step in atherosclerotic lesion formation and is more likely to occur at arterial curves and branches that are subjected to low shear stress and disturbed blood flow (atherosclerosis prone areas) (7,8). These mechanical stimuli activate signaling pathways leading to a dysfunctional endothelium lining that is barrier compromised, prothrombotic, and proinflammatory.

So it seems that endothelial disfunction comes first, triggered by blood flow stresses. It’s common wear and tear in exposed areas. The patched knees on jeans. Managing endothelial health and healing may slow or diminish rate of progression or is it mostly too late for that?

I’m not a doctor. This isn’t medical advice. This is just speculation.

I find it rather hard to believe that healthy arteries are inherently fragile and prone to damage and incapable of weathering the “stress” of blood flowing through them, even at the “susceptible” curves. I find it more likely that poor health, poor diets, and poor lifestyles make us more susceptible to otherwise normal stresses.

Do the mechanical stimuli weaken the endothelium in people with healthy levels of nitric oxide production? Or are we talking about people whose poor nitric oxide status is exacerbating the damaging blood flow patterns, leaving their endothelium vulnerable to atherosclerosis?

Think about how much context matters in our response to stimuli. If you’re shy around girls, a school dance will be a traumatic experience. If you’re comfortable around girls, a school dance will be a great experience. If you’re weak, lifting a barbell will be scary, and you may injure yourself. If you’re strong, lifting a barbell will be second nature, and you may get stronger. The baseline context determines the quality of the response.

I’d argue that blood flowing through your arteries should be a commonplace occurrence. It shouldn’t be a traumatic experience. Now, maybe I’m wrong. Maybe it is stressful regardless of the baseline endothelial health and the amount of nitric oxide you produce. Maybe it’s just a matter of time. But:

  • We know that, as you quote, atherosclerosis tends to occur at bends and curves of the arteries—the places most likely to be subject to “disturbed flow” patterns.
  • We know that “laminar flow”—blood flowing smoothly through the artery—is protective of the endothelial wall, promoting anti-inflammatory effects and making the endothelium more resistant to damage.
  • We know that “disturbed flow” has an opposing effect on endothelial health, promoting inflammatory effects and rendering the endothelium more susceptible to damage. This increases atherosclerosis.
  • The question I’m wondering is if “disturbed flow” at the curves and bends of the arteries is inevitable or not. And if disturbed flow is always “bad.”
  • We know that hyperglycemia—high blood sugar—makes disturbed blood flow more damaging to arterial walls. Diabetics have higher rates of atherosclerosis because their elevated blood sugar interacts with disturbed blood flow patterns.
  • We know that nitric oxide increases vasodilation in response to shear stress—widening the arteries to accommodate the increased stress and mitigate the damage done. We know that people with hypertension don’t get the same vasodilatory benefits from nitric oxide.
  • We know that “functional increases” of shear stress attained via exercise increase nitric oxide and oxygen production and induce autophagy (cellular cleanup) in the endothelial walls.

That sounds like there are a lot of factors that increases and mitigate the effects of shear stress on the endothelial wall. It sounds like some factors make shear stress more damaging, and some factors make it less. There may even be factors, like exercise, that make shear stress healthy.

This topic is really pretty interesting to me. It deserves a deeper dive, don’t you think?

What about you, folks? What’s your take on fasted workouts and GH secretion? Ever try one?

And do you think your arteries are doomed to fall apart at the seams?

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References:

Nyberg F, Hallberg M. Growth hormone and cognitive function. Nat Rev Endocrinol. 2013;9(6):357-65.

Park SK, La salle DT, Cerbie J, et al. Elevated arterial shear rate increases indexes of endothelial cell autophagy and nitric oxide synthase activation in humans. Am J Physiol Heart Circ Physiol. 2019;316(1):H106-H112.

The post Dear Mark: Fasting, Training, and Growth Hormone; Wear and Tear on the Arteries appeared first on Mark’s Daily Apple.

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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?

  • Anxiety
  • Irritability
  • Loss of libido, vaginal atrophy
  • Night sweats
  • Hot flashes
  • Weight gain
  • Forgetfulness

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!

References:

Wu WH, Liu LY, Chung CJ, Jou HJ, Wang TA. Estrogenic effect of yam ingestion in healthy postmenopausal women. J Am Coll Nutr. 2005;24(4):235-43.

Murkes D, Lalitkumar PG, Leifland K, Lundström E, Söderqvist G. Percutaneous estradiol/oral micronized progesterone has less-adverse effects and different gene regulations than oral conjugated equine estrogens/medroxyprogesterone acetate in the breasts of healthy women in vivo. Gynecol Endocrinol. 2012;28 Suppl 2:12-5.

Ruiz AD, Daniels KR. The effectiveness of sublingual and topical compounded bioidentical hormone replacement therapy in postmenopausal women: an observational cohort study. Int J Pharm Compd. 2014;18(1):70-7.

Stephenson K, Neuenschwander PF, Kurdowska AK. The effects of compounded bioidentical transdermal hormone therapy on hemostatic, inflammatory, immune factors; cardiovascular biomarkers; quality-of-life measures; and health outcomes in perimenopausal and postmenopausal women. Int J Pharm Compd. 2013;17(1):74-85.

Zeng Z, Jiang X, Li X, Wells A, Luo Y, Neapolitan R. Conjugated equine estrogen and medroxyprogesterone acetate are associated with decreased risk of breast cancer relative to bioidentical hormone therapy and controls. PLoS ONE. 2018;13(5):e0197064.

Schiff I, Tulchinsky D, Ryan KJ, Kadner S, Levitz M. Plasma estriol and its conjugates following oral and vaginal administration of estriol to postmenopausal women: correlations with gonadotropin levels. Am J Obstet Gynecol. 1980;138(8):1137-41.

Scarabin PY. Hormone therapy and venous thromboembolism among postmenopausal women. Front Horm Res. 2014;43:21-32.

Espeland MA, Rapp SR, Manson JE, et al. Long-term Effects on Cognitive Trajectories of Postmenopausal Hormone Therapy in Two Age Groups. J Gerontol A Biol Sci Med Sci. 2017;72(6):838-845.

Hodis HN, Mack WJ, Henderson VW, et al. Vascular Effects of Early versus Late Postmenopausal Treatment with Estradiol. N Engl J Med. 2016;374(13):1221-31.

Santoro N, Allshouse A, Neal-perry G, et al. Longitudinal changes in menopausal symptoms comparing women randomized to low-dose oral conjugated estrogens or transdermal estradiol plus micronized progesterone versus placebo: the Kronos Early Estrogen Prevention Study. Menopause. 2017;24(3):238-246.

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.

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Back in June during the 21-Day Challenge, I asked you to share questions you had about my personal health routine, and I’m looking forward to answering those in the coming months. We talk a lot about generalities here, and for good reason. Research can and should drive principle, but oftentimes while we wait around for it (or have questions about the overall validity of what’s out there), n=1 self-experimentation can tell us a lot.

Over the years, I’ve gathered ideas for that experimentation by reading the studies and listening to others talk about the choices they make. All of it together has—and continues to—inform the routine I follow to live the life I want. Among the many questions you sent were inquiries about my supplement regimen. Today I’m sharing what I take, when I take it, and why.

As a former endurance athlete, supplements were tools of the trade. I fielded recommendations from coaches and specialists of course, but I also studied the subject intently on my own. To push my performance further, I even began developing my own formulas for training recovery back then. Though I’m not in the competitive athletic world anymore, I still feel the benefits of certain supplements in my personal health and performance, and I’ve continued to formulate those I wish to take.

Here’s a bit about my choices for supplementation and the changes I’ve made over the years in how I take them.

I’d love to hear your thoughts and any questions you have about what I take (or don’t take). And if you have other kinds of questions about my routine (or anything health-related of course), shoot me a message on the comment board. Thanks for stopping by, everyone.

Finally, for those who are curious about the supplements I’ve shared today, I have a deal on two of my favorites. Order Adaptogenic Calm today, and I’ll include a bottle of Primal Sun entirely free. Just add both Adaptogenic Calm and Primal Sun to the cart, and use the code FREESUN at checkout to redeem this offer. Valid on One-Time Purchases only. Offer expires 8/30 at midnight PDT.

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One of the biggest mistakes I see among people who exercise is they forget this core truth: we get fitter not from training, but from recovering from training. This doesn’t just occur in beginners either. Some of the most experienced, hardest-charging athletes I know fail to heed the importance of recovery. Hell, the reason my endurance training destroyed my life and inadvertently set the stage for creation of the Primal Blueprint was that I didn’t grasp the concept of recovery. I just piled on the miles, thinking the more the merrier.

It didn’t work.

What is recovery, anyway?

There’s short-term recovery. Your heart rate slows back down, your body temperature drops, your sweat dries, your muscles and lungs stop burning.

Long-term recovery is less conspicuous, more internal. You replace lost energy stores, repair damaged muscle, clear out waste products, and begin the process of adaptation to the training.

When both short- and long-term recovery happen together, you “feel ready” to go again.

Some portion of how quickly we recover from training is out of our direct control.

Genetics is one factor we can’t control. Researchers have found genetic variants of collagen-encoding genes that increase or decrease the rate at which we recover from exercise-induced muscle damage, muscle tissue genes that increase resistance to exercise-induced muscle soreness, immune genes that affect the speed of adaptation to training. But even many genetic variants purported to affect recovery act through decisions carriers make. A carrier of a genetic variant linked to muscle power experienced more muscle damage and required more recovery after a soccer match, but only because that carrier “performed more speed and power actions during the game.”

Age is another factor out of our direct control. Sure, living, eating, and training right can stave off many of the worst effects of aging. Sure, a sedentary 70-year-old will recover from a workout far more slowly (if he or she can be cajoled into training) than a 70-year-old master athlete. But time does tick on. Following training that fatigues but doesn’t damage the muscles, like easy cycling, light weight training, or a sub-aerobic threshold jog, older athletes recover muscle function and performance at similar rates to younger athletes. After intense exercises that damage the muscles, like sprints, heavy lifting, intervals, or longer race-pace runs, however, older athletes recover more slowly than younger athletes.

Other factors, while preventable and modifiable over the long haul, inexorably inhibit workout recovery once they’re in place:

If you’re sick, you won’t recover as quickly. Illness diverts some of the resources that would otherwise be used to recover from training.

If you have heart disease, you’ll recover more slowly. In one study, having heart disease was the greatest predictor of a slower rate of heart rate recovery after exercise.

If your hormones are out of whack, you’ll likely recover more slowly. Hormones are the messengers and managers that tell our cells what to do. That includes muscle repair, hypertrophy, fuel replenishment, inflammatory signaling, and every other cellular function related to recovery.

Now I’ve got bad news and good news. Everything else that slows down workout recovery is under your direct control.

Factors We Can Control

Stress

Stress is stress. Traffic is a stressor. A job you hate is a stressor. Procrastinating until you absolutely must get working is a stressor. And yes, exercise is a stressor. Too much of the psychological, lifestyle, or mental stress we all face impairs our ability to recover from exercise-induced stress.

Recent research confirms that “mental stress” impairs workout recovery, and it doesn’t speak in generalities. Thirty-one undergrads were assessed for stress levels using a battery of psychological tests, then engaged in a heavy lower body strength workout. At an hour post-workout, students in the high stress group had regained 38 percent of their leg strength, while students in the low stress group had regained 60 percent of their strength.

I developed my anti-stress supplement Primal Calm (now, Adaptogenic Calm) back in the chronic cardio days as a way to improve my training recovery. That’s what gave the product so much momentum in the endurance community—it turns out that beating back stress of all kinds quickened recovery from a very specific type of training stress.

Some stress is unavoidable. But most of us create additional stress in our lives and fail to do enough to counter or manage it. Stop making unforced errors.

Poor Sleep

Sleep debt impairs exercise recovery primarily via two routes: by increasing cortisol, reducing testosterone production, and lowering muscle protein synthesis; and by disrupting slow wave sleep, the constructive stage of slumber in which growth hormone secretion peaks, tissues heal, and muscles rebuild. That’s probably why sleep deprivation has been linked to muscular atrophy and increased urinary excretion of nitrogen, and why the kind of cortisol excess caused by sleep deprivation reduces muscle strength.

Additionally, sleep loss can increase the risk of injuries by decreasing balance and postural control. If you trip and fall, or throw out your back due to poor technique, you won’t even have a workout to recover from.

Most people think bad sleep is unavoidable. It happens to the best of us from time to time, but a night of bad sleep here and there isn’t going to slow down recovery. The real recovery killer is chronically bad sleep, and that’s the kind most of us can avoid by sticking to a good sleep hygiene regimen.

Nutrient Deficiencies

Since every physiological function requires a micronutrient substrate—vitamin, mineral, hormone, neurotransmitter, etc.—and physiological functions increase with exercise and recovery, active people require more micronutrients in their diet. “More of everything” is a safe bet, but there are a few key nutrients that working out especially depletes:

Zinc: Exercise, especially weight training, works better with plenty of testosterone on hand to build muscle and develop strength. Zinc is a key substrate for the production of testosterone, and studies show that exercise probably increases the need for zinc. In fact, one study found that exhaustive exercise depleted testosterone (and thyroid) hormones in athletes, while supplementing with zinc restored it.

Magnesium and Other Electrolytes: Magnesium is required for a number of physiological processes related to workout recovery, including oxygen uptake by cells, energy production, and electrolyte balance. Unfortunately, as one of the main electrolytes, lots of magnesium is lost to sweat during exercise. The same could be said for other electrolytes like calcium, sodium, and potassium, but most people get plenty of those minerals from a basic Primal eating plan. Getting enough magnesium, however, is a bit tougher, making magnesium deficiency a real issue for people trying to recover from workouts.

Iron: Intense exercise depletes iron, which is instrumental in the formation of red blood cells and oxygen delivery to your tissues during training and the immune response after it. They even have a name for it—exercise-induced anemia.

Soreness

Post-workout delayed onset muscle soreness, or DOMS, is no joke. While many of you folks reading this probably enjoy DOMS and take it as feedback for a job well done, it’s a hurdle that many beginners never move past. They join a gym, d0 a workout, feel great, go to bed feeling awesome, sleep like a baby, then wake up and find they have the bipedal capacity of a three-month-old. They can barely walk. Lifting their arms to brush their teeth is agony. Walking downstairs is out of the question. Some will move past the DOMS and get back into the gym. Many will not.

Low Fuel Availability

Working out expends energy. That energy must be replenished before you’re fully recovered and prepared to do another workout. Unless you’re trying to increase efficiency by training in a state of low fuel availability, like the “train low-carb, race high-carb” method, you should recover what’s been lost. What you replenish is conditional on the type of exercise you did. If you went for a long hike or easy bike ride that burned primarily body fat, you don’t need to—and probably shouldn’t—”replenish what you lost.” If you’re coming off a 30-minute full body CrossFit session that left you gasping on the ground in a puddle of sweat, you probably have some glycogen stores to refill.

This is a common issue for folks trying to lose weight through diet and exercise. Inadequate calorie intake coupled with intense exercise sends a “starvation” signal to the body, causing a down-regulation of anabolic hormones. Instead of growing lean mass and burning body fat, starvation (whether real or simulated) promotes muscle atrophy and body fat retention. Either alone can be somewhat effective, but combining the two for too long will only impair recovery.

Alcohol

Drinking directly impairs muscle protein synthesis, the essential step in muscle recovery and adaptation to training. Moderate or “social” drinking is probably safe (just don’t use alcohol as a post-workout recovery drink), but even just a single day per week of binge drinking is linked to 4x the risk of sarcopenia, or muscle-wasting. It’s hard to recover from your workouts if your muscles are atrophying.

Oddly, drinking directly after a training session also increases testosterone levels. One theory is that testosterone levels rise after drinking because it becomes less bioavailable; your muscle cells’ resistance to testosterone goes up, so it just circulates and gives “false” readings.

Things You Can Try

The obvious thing to try is the opposite of all the modifiable and preventable recovery-inhibitors mentioned above. Get good sleep, don’t drink too much (especially post-workout), get a handle on your stress, eat enough food, eat enough protein, get your micronutrients. What else?

Watermelon

L-citrulline is an amino acid found in watermelon that shows a significantly ameliorative effect on post-workout muscle pain, or delayed onset muscle soreness (DOMS). You can also supplement directly with L-citrulline, which may work, but watermelon is so good right now with a little salt, lime juice, and cayenne pepper, and it’s actually lower in carbs than you probably think (about 10 grams per cup of watermelon). I recommend fresh watermelon over pasteurized juice, as heat treatment reduces the effect.

Beets

Beets (and beet juice) aren’t only good for exercise performance. They also reduce DOMS. Nitrates have been posited as the primary constituent responsible for the effect, but beet juice works better than pure sodium nitrate.

Tart Cherry Juice

Tart cherry juice is best used to recover during competition, when your primary concern is to get back out there and perform. Its extreme effectiveness at killing muscle pain, reducing local and systemic inflammation and exercise-induced muscle damage suggests it may hamper training adaptations, however. It does also improve sleep, which should translate into better adaptations.

Massage

Massage feels great, and the evidence shows that it’s great for recovery from exercise. It alleviates DOMS. It speeds up the recovery of muscle strength and enhances proprioception. It improves central nervous system parasympathetic/sympathetic balance, even if the masseuse is one of those weird back massage machines.

Compression Garments

These aren’t just for show. A recent meta-analysis of the available research concluded that compression garments enhance muscle recovery after strength training and improve next-day cycling performance.

Whey

Compared to other proteins, whey protein accelerates muscle adaptation to eccentric exercise.

Creatine

Although we get creatine from red meat and fish, supplementary creatine can boost our recovery from exercise via a couple mechanisms. First, it increases muscle content of phosphocreatine. That’s the stuff we use for quick bursts of maximal effort, so carrying a little extra can do wonders for our ability to perform. Second, it enhances muscle glycogen replenishment without increasing insulin.

Fish Oil (or Fatty Fish)

Adding fish oil to a recovery drink reduced post-workout muscle soreness without affecting performance. Fish oil may also enhance muscle recovery from and adaptation to strength training.

Cold Water

A cold water plunge after training enhances the recovery of muscle function. However—and this is a big “however”—post training cold water plunges also seem to impair long term muscular adaptations to resistance training. In other words, a cold plunge might help you get back in the game for the short term at the cost of long-term adaptations.

More Carbs

I always say “Eat the carbs you earn.” While that often means eating fewer carbs than before, it can also mean eating more if you’ve trained hard enough to warrant them. This even applies to keto folks; depleting glycogen through exercise creates a “glycogen debt” that you can repay without inhibiting ketosis or fat-adaptation too much. The carbs—which you don’t need much of—go into muscle glycogen stores for recovery and later use without disrupting ketosis.

Don’t take this final section as a blanket recommendation, however. Before taking ice baths, dropping $500 on massages every week, taking a long list of expensive supplements, and walking around in a full body compression suit, make sure you’re sleeping, eating enough food, and giving yourself enough time between workouts. Quite often, handling the basics will be enough.

What have you found to be the best way to recover from your training? What are the biggest roadblocks? Let me know down below, and thanks for reading!

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The post What Causes Slow Post-Workout Recovery—and What Can You Do About It? appeared first on Mark’s Daily Apple.

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Even after I fixed my diet, ditched the chronic cardio, and cleaned up my overall lifestyle to be more in line with our evolutionary upbringing, one big problem remained: my response to stress.

This had always been an issue for me. Part of it was that I kept a full plate at all times. Whether it was my training load, my businesses, my overall type A personality, stress was simply unavoidable, I thought.

How did I approach the situation and manage my stress differently over time?

First, I agonized over the existence of stress. My entire modus operandi throughout life had been to handle problems when they arose. I didn’t let things fester, I didn’t accept bad situations and learn to deal. I took care of things. If a problem didn’t resolve quickly , I assumed I was doing something wrong. Applied to stress, though? Man, what a disaster. I quickly realized that it was impossible to avoid stress, or eliminate it altogether. I needed a new approach.

So the first major step was admitting that stress is a fact of life, that stressors would arise, and what mattered was how I responded to them. My response could make the stress worse, or it could make it more manageable.

The first way I figured out how to improve my stress response was with smart supplementation. When I was still competing and doing the chronic cardio training required to succeed, I developed a supplement you might recognize by its old Primal Calm label and now called Adaptogenic Calm—designed to mitigate the negative effects of all that training stress. Both Brad Kearns and I used it, and it actually became an underground hit in the endurance scene. Athletes of all kinds were taking it and seeing great results. Of course, most of us just used it to allow our bodies to train even more and accumulate even more stress, which was one of the problems that got me into this mess in the first place.

The next step was realizing that even if I couldn’t eliminate stress entirely, I could eliminate unnecessary stress. First on the list was my training. You’ve heard the story before, so I won’t get too deeply into it. Suffice it to say, I was engaged in way too much endurance training—what I call chronic cardio—and spending way too much time out of the aerobic zone in the no-man’s land of moderately high-intensity that leads to sugar-burning and depresses fat-burning. This training was killing me, taking up all my time, necessitating an inflammatory high-carb, high-sugar diet that led to chronic GI distress and joint pain, and getting in the way of living.  If any of you can identify a big stressor upstream of a bunch of things going wrong in your life, take action and eliminate it. Changing how I trained led to the development of the Primal Blueprint and the resolution of most of my health problems.

Meditation always intrigued me. Even before it became an Internet sensation and every podcaster/blogger/CEO/coach out there credited their success to their morning meditation routine, I was surrounded by meditators. My wife, Carrie, has done it for decades. Lots of my athlete friends used it to—you guessed it—fight stress. And Malibu, CA, where I lived until a few months ago, is no stranger to yoga studios, health food stores, and other similar hives of mindfulness. I tried it. But it didn’t work for me. My mind was too active to become aware of its (lack of) self. Still, the science was convincing and I didn’t want to give up on what looked to be a potent anti-stress tool:

If sitting meditation didn’t work, maybe there was another way to get to a similar mindstate.

In a post I wrote about meditation alternatives, I gave 15 options and readers followed up with dozens of awesome suggestions in the comments. Standup paddling, hikes (or just hanging out) in nature, and guided meditations were my alternatives. They help me achieve the hyper-present flow state I’d only had glimpses of during “real” meditation. And sure enough, stress melts away as I’m doing the activity, I’m far less reactive to stressors (I have an extra split second or two to decide how I want to respond) throughout the week, and I appear to have greater resistance to stress. It’s almost an adaptogenic effect: rather than blunt or eliminate the stress response across the board, I’m able to call forth cortisol when the situation is serious. A car honking at me doesn’t trigger it, in other words.

Where am I today?

Stress is still there. It won’t ever go away, and I’m okay with that. I’ve got a growing food and supplement business, I’m as busy as ever with the writing, I just moved to Miami.

Meditation has gotten easier, but I’m still not a “meditation guy.” I don’t expect to be doing a 10-day silent retreat anytime soon.

Adaptogenic Calm remains a staple for me. The nutrients it contains are supraphysiological responses to the supraphysiological doses and durations of stress we receive in the modern world.

I welcome stress. If I align myself with the things I truly find meaningful and maintain active participation in life and avoid becoming a passive character in someone else’s storyline, the stressors become obstacles that make the narrative of my life more interesting. They propel me forward. Without stressors, I’m not living. I’m not doing anything. Stressors indicate action. They mean you’re bouncing up against reality and testing its mettle (and it, yours).

What’s your stress response journey? I’d love to hear how you’ve handled stress in the past, what you’ve learned along the way, and how you handle it now. Thanks, everybody.

I’ve got a contest coming up later this morning, so be sure to check back.

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