For this week’s edition of Dear Mark, I’m answering three questions from readers. First, is the reduced protein efficiency in older adults due to inactivity, or is it something inherent to the aging process, or both? Second, how does a person know if they’ve actually “earned” any carbs? Does everyone on a keto diet earn carbs by virtue of exercising, or is there more to it? And finally, how can a hardgainer with a packed schedule all week long and limited gym time maintain what little muscle mass he’s managed to gain?
Let’s find out:
Interesting observation on protein needs and training in Sunday with Sisson – general consensus is that older folks need more protein as they age but maybe that’s because they are less active and not simply a result of aging.
That’s probably part of it, but it’s not all of it.
In studies where they compare resistance training seniors who eat extra protein with resistance training seniors who don’t, only the seniors eating extra protein gain muscle mass.
Now, it may be that a lifetime of inactivity degrades your ability to utilize protein, and if these older adults had always lifted weights they would have retained their protein efficiency. But maybe not. As it stands, all else being equal, an older adult needs more protein to get the same effect, even if he or she is lifting weights.
Enjoyable read. As someone who lives a ketogenic lifestyle, and who is athletically active, I am not sure exactly how to go about consuming the carbs I’ve “earned.” I rarely run into problems with athletic energy, at least not below anaerobic threshold. Not sure that eating more carbs will improve my performance. And, if they would improve my performance, how does one go about calculating earned carb replacement without losing the fat burning benefits of ketosis?
It sounds like you’re in a good place.
When I say “eat the carbs you earn,” I’m talking to the people who do run into problems with athletic energy, poor performance, insomnia, and other symptoms of exercise-induced stress. Typically, the people who “earn their carbs” are doing stuff like CrossFit, high volume moderate-to-high intensity endurance work, martial arts training, and team sports.
I doubt extra carbs will improve your performance if most of your training takes place in the aerobic zone. But if you wanted to experiment, you could try a small sweet potato immediately after a workout where you passed the anaerobic threshold.
That’s the best way to determine if you’ve earned carbs. Eat 20-30 grams after a workout and see if you enjoy performance gains without gaining body fat. There’s no consumer-friendly way to directly calculate carb debt; self-experimentation is it.
I recently took a job that has me out of bed at 4am and not home until 6pm Monday Through Friday. Is there an efficient way I can maintain muscle mass only lifting weights Saturday and Sunday? I’m a hardgainer at 5’10” and only 140lbs. I’m afraid giving up my 5 day split will ruin what muscle I’ve been able to gain.
Any hardgainer has to eat, and eat, and eat. Increase your food intake. Just eat. Stick to healthy Primal fare, but pack in the food. Meat, milk, veggies, potatoes, rice, eggs, avocados, fruit. Throw some liver in, too (old bodybuilder staple). It doesn’t sound like fat gain is an issue for you, so I’d take advantage of that and just consume calories.
As for training, get some exercise snacks in during the week.
As soon as you wake up, do a quick superset of pushups. Do as many pushups as you can. Wait 30 seconds. Do as many pushups as you can. Wait 30 seconds. Do as many pushups as you can. There you go. That shouldn’t take more than 5 minutes in the morning. Can you squeeze that in?
Repeat this every morning with a different exercise. Pullups, bodyweight rows, kettlebell swings, handstand pushups, dips, bodyweight squats, goblet squats, reverse lunges, reverse weighted lunges. Just choose one thing to do every morning, cram as many reps as you can using the same format (max reps, 30 s rest, max reps, 30 s rest, max reps). Buy any equipment you can if you choose to use weights.
When you get home at night, do the same thing with a different exercise. Morning pushups, evening KB swings, etc. That way, you get about 10 minutes per weekday of intense strength training without impacting your sleep or schedule in any real meaningful way.
Make sure your sleep hygiene is rock solid. Dim those lights at night, turn on f.lux or night mode, wear the blue blocking goggles, get to bed (ideally) by 8:30, 9 to give you 7 to 7.5 hours of sleep. Sleep is essential for gaining lean mass (and staying healthy in general).
On the weekend, hit the weights hard on both days, hitting the entire body. Go high volume/reps. If size is your goal, dropping the weight a bit and focusing on range of motion and a high rep count (10-15 per set) is very effective.
Food, sleep, reps. Good luck!
Thanks for stopping in today, everybody. Additional thoughts for these folks—or questions of your own? Share them below.
Tieland M, Dirks ML, Van der zwaluw N, et al. Protein supplementation increases muscle mass gain during prolonged resistance-type exercise training in frail elderly people: a randomized, double-blind, placebo-controlled trial. J Am Med Dir Assoc. 2012;13(8):713-9.
The post Dear Mark: Protein Efficiency in Seniors, Earned Carbs, Hardgainer with Limited Time appeared first on Mark’s Daily Apple.
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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.
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.
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?
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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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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Last week’s post on iron levels got a big response and garnered a ton of questions from you guys. Today, I’m going to clarify a few things and answer as many questions as I can. First, do iron and ferritin levels mean different things for men and women? If so, how do those differences manifest? What about premenopausal women vs postmenopausal women? Second, what do we make of the fact that ferritin is also increased in times of inflammation? Is there a way to distinguish between elevated ferritin caused by inflammation and elevated ferritin caused by high iron? Third, is desiccated liver a good option for liver haters? And finally, I share some exciting plague news.
I’d love to see more info on iron levels as they relate to men and women differently. I recently had an iron infusion for low ferretin, not thinking much would change I actually experienced so many positive effects I didn’t even know were coming my way. I’m less cold, no more afternoon fatigue, less hair falling out, no more random palpitations, improved restless leg syndrome and the number one big change is it improved anxiety levels – in fact my anxiety is now gone. The last two are due to a connection between iron and dopamine. I learnt that children with mental health issues are often treated for low ferretin where possible, elevating levels to around 100 showing positive results (would love to see literature on this), for me my ferretin went from 20 to 130 and its changed my life, at 31 I haven’t felt this good in years. Yay iron!
That’s awesome to hear. Yes, it’s important to stress the very basic essentiality of iron. Without it, we truly cannot produce energy. And since energy is the currency for everything that happens in the body, an iron deficiency makes everything start to fall apart.
As for gender and iron, there’s a lot to discuss.
A good portion of women with hemochromatosis never actually express it phenotypically, meaning their lab tests don’t show evidence of dysregulated iron metabolism or storage. According to one study of hemochromatosis homozygotes (people who inherited the mutation from both of their parents), being a woman makes it 16x more likely that your hereditary hemochromatosis won’t actually present as iron overload.
Another study found that among mostly-age-matched men (42 years) and women (39 years) with hemochromatosis, 78% of the men had iron overload while just 36% of the women had it. Iron overload was defined as transferrin saturation over 52% combined with ferritin levels of 300 ng/mL for men and 200 ng/mL for women.
High iron levels are more of an issue for postmenopausal women than premenopausal women. The latter group regularly sheds blood through menstruation, and if anything, they’re at a higher risk of low iron. Plus, estrogen is a key regulator of iron metabolism. As menopause sets in and estrogen diminishes, that regulation suffers.
In postmenopausal Korean women, high ferritin levels predict metabolic syndrome and subclinical atherosclerosis.
High ferritin predicts metabolic syndrome in postmenopausal but not premenopausal women.
In premenopausal Korean women, higher ferritin levels predict better bone mineral density; menopause nullifies this relationship.
Remember that ferritin is actually a measurable protein bound to iron, so testing a ferritin level is technically an indirect way to measure iron. Why is this important? Another characteristic of ferritin (the protein) is that it is an ACUTE PHASE REACTANT. This means that ferritin levels can fluctuate with illnesses and other inflammatory states in the body that drive up a ferritin value that is not related to an actual iron level fluctuation. Don’t get ferritin checked when you are sick with a cold or other illness.
This is a great point.
Ferritin is marker of long term iron storage, but it’s also an acute phase reactant that up regulates in response to inflammation or oxidative stress.
If you want to be really careful, you should get a HS-CRP test—that measures your overall inflammatory status. If CRP is elevated, ferritin can be elevated without saying anything about your iron status.
Come to think of it, if elevated ferritin can be a marker of inflammation and oxidative stress, the inflammation could be responsible for some of the negative health effects linked to high ferritin. Or, if having too much iron in the body can increase oxidative damage, it may be that high iron levels are increasing inflammation which in turn increases ferritin even further. Biology gets messy. Lots of feedback loops. However, the fact that many studies cited in the previous iron post that use blood donation to treat high ferritin have positive results indicates that for most people, ferritin can be, in most situations, an accurate estimation of your iron status.
To make sure it’s an iron problem, get a transferrin saturation test as well. That indicates the amount of iron you’re absorbing, with below 20% being low and over 45% being high. People with high ferritin and high transferrin saturation do have high iron levels. People whose ferritin is artificially enhanced by inflammation will have normal transferrin saturation levels.
I have one last question on this. You say “Don’t stop eating liver every week.” If you can’t stand the taste of liver, what do you think about taking liver capsules made from grass-fed New Zealand beef every day instead?
That’s a great option. Go for it.
People should generally aim for 4-8 ounces of fresh liver a week. Note the amount of desiccated liver in your capsules and multiply by 3 to get the fresh liver equivalent, then take enough each day (or all at once) to hit 4-8 ounces over the week. I hear good things about this one.
Thank you for your article on HH. I carry the gene but have been managing my iron levels through phlebotomies. I am full Keto, meat and all and have found my iron levels have not been effected by going Keto. Early detection is the key and ongoing monitoring. Bring on the plague!!!
You joke about that now, but there’s a startup that’s breeding heritage rat fleas that produce a mild strain of the plague that evades the attention of the immune system and proliferates throughout the body to keep iron levels in check without killing you. I’m an early investor, have a couple swarms installed in my condo, and (knock on wood) so far have avoided anything worse than a sore throat and maybe a mild open sore or two. There’s actually a big rift forming between the techs who want to keep the fleas heritage and those who want to go ahead with CRISPR and engineer them. One variant has had a deer tick gene inserted that adds an anesthetic compound to the flea’s saliva. That way you can have a personal swarm on you and never feel any bites or itches.
I’m not sure about CRISPR just yet, but I gotta say it’s pretty nice to be covered in fleas and not feel the bites. Time will tell.
Ok, I’m joking.
That’s it for today, folks. I hope I’ve answered some of your concerns, and if not, let me know down below. Thanks for reading!
Lainé F, Jouannolle AM, Morcet J, et al. Phenotypic expression in detected C282Y homozygous women depends on body mass index. J Hepatol. 2005;43(6):1055-9.
Qian Y, Yin C, Chen Y, et al. Estrogen contributes to regulating iron metabolism through governing ferroportin signaling via an estrogen response element. Cell Signal. 2015;27(5):934-42.
Seo SK, Yun BH, Chon SJ, et al. Association of serum ferritin levels with metabolic syndrome and subclinical coronary atherosclerosis in postmenopausal Korean women. Clin Chim Acta. 2015;438:62-6.
Cho GJ, Shin JH, Yi KW, et al. Serum ferritin levels are associated with metabolic syndrome in postmenopausal women but not in premenopausal women. Menopause. 2011;18(10):1120-4.
Chon SJ, Choi YR, Roh YH, et al. Association between levels of serum ferritin and bone mineral density in Korean premenopausal and postmenopausal women: KNHANES 2008-2010. PLoS ONE. 2014;9(12):e114972.
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For this week’s Dear Mark, I’m answering a question from a reader about a topic I thought I’d covered (so did they) already. A quick look through the archives (hey, I can’t remember absolutely everything I ever wrote) showed that I had not, so here we go. It’s all about whether fermented foods—sauerkrauts, kimchis, pickles, yogurts, and any other food that has been acted upon by probiotic bacteria—make eating meat healthier and more enjoyable. From the start, I suspected that they do, but I had to confirm it in the scientific literature.
Let’s find out:
I’m trying to find an article on why you should eat ferments with meat, (how it breaks down the fats) our mutual friend Hilary, AKA #thelunchlady ? and I are working on getting some of the high end butcher’s around LA to understand this, so they can help educate their customers. I was hoping to find info on your site, but now hoping you might write one for us
As for the effect you mention—fermented food breaking down the fat in meat—I’m unaware of any evidence. I am aware of a beneficial effect of fermented food on carbohydrate metabolism though. See, lactofermentation produces acetic acid as a byproduct. Acetic acid provides the “sour” flavor, the acidity of a batch of sauerkraut or pickles. It’s also what makes vinegar so sour, and there’s a long line of evidence showing that vinegar improves glucose tolerance and reduces the blood glucose load of high carb meals.
- A 2017 review of the evidence found that vinegar was significantly effective at reducing both postprandial blood sugar and insulin levels.
- It works in type 2 diabetics who eat vinegar with their high-carb meals, lowering the blood glucose response.
- Research shows that acetic acid, rather than some other component in the vinegar, is the active component responsible for the effect on blood sugar. Anything with acetic acid should work, like food ferments.
That’s carbohydrate, and it’s good info, but you didn’t ask about carbs. You asked about meat. So, is fermented food pointless when eating meat? Not at all.
There are many examples of traditional cultures and cuisines making it a point to serve fermented foods with meats:
Koreans, kimchi, BBQ.
Germans, sauerkraut, sausage.
Japanese, pickles/natto/miso, meat/fish.
Indians, yogurt/pickles/chutneys, meat curry/tandoori chicken.
Italians, cheese, salami (itself a fermented meat).
They may not have “known” about the biochemistry. They weren’t citing PubMed studies. But over the many hundreds of years, these pairings emerged as combinations that just worked and made people feel good and the food go down more easily.
What could be going on here?
One thing I’ve stressed over the years is the importance of consuming foods high in polyphenols, not only for their isolated health benefits but for their ameliorative effects on the potential carcinogenicity of meats—particularly high-heat cooked meats (barbecue, grilling, searing). If you eat foods high in polyphenols, like blueberries or leafy greens, with your meat, that meal becomes healthier. It reduces the formation of carcinogenic compounds and reduces the peroxidative damage done to the fat.
And if you take a food high in polyphenols and subject it to fermentation, those polyphenols change and actually become more effective.
Red wine is one such fermented food that is higher in polyphenols than its non-fermented counterpart. The fermentation process alters the polyphenols already present in the grapes, making them more bioavailable and more effective, and creating entirely new compounds in the process. One reason red wine pairs so well with steak on a subjective level is that it actually reduces the formation of toxic lipid oxidation byproducts in “simulated digestion” studies that attempt to recreate the stomach environment after a meal, inhibits the absorption of those toxic lipid byproducts, and, when added to meat marinades, reduces the formation of heat-related carcinogens when you cook the meat, even over open flame. The responsible compound for these effects in red wine isn’t the alcohol, it’s the polyphenols. Grape juice doesn’t have the same effect.
This applies to everything. Fermentation of almost any other food, from beans to cabbage to garlic, also changes and improves the antioxidative capacity of the polyphenols. And the more polyphenols a food has, and the more effective they are at reducing oxidation, the healthier they’ll make any meat we eat.
So, in a roundabout way, fermented foods actually are improving the way we digest the fats in meat. They aren’t quite “breaking them down,” but they are allowing us to metabolize them in a healthier way that produces fewer toxic byproducts and inhibits our absorption of the toxic byproducts that do slip by.
This actually gives me a good idea for a post: A series of elevator pitches that inspired readers can use to lobby restaurant owners, butchers, doctors, and anyone else about the otherwise complicated health and nutrition topics we’ve bandied about on this blog for a decade. Most folks’ brains will glaze over when you start talking “omega-3s” or “peroxidized lipids” or “oxidized LDL particles” or “high heat carcinogens,” but it’s still important information. I think I’ll start putting that together in the next few weeks, starting with today’s topic, and I could really use your help. What other topics have you wanted to broach but can’t figure out how to make relatable, simplistic, or elegant enough to drop in casual conversation with professionals (or friends) who could help make a difference?
Let’s get a list going and try to knock this out.
That’s it for today, folks. Take care and be well. Thanks for reading!
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Kimura S, Tung YC, Pan MH, Su NW, Lai YJ, Cheng KC. Black garlic: A critical review of its production, bioactivity, and application. J Food Drug Anal. 2017;25(1):62-70.
Nowak A, Libudzisz Z. Ability of probiotic Lactobacillus casei DN 114001 to bind or/and metabolise heterocyclic aromatic amines in vitro. Eur J Nutr. 2009;48(7):419-27.
The post Dear Mark: How Do Fermented Food and Meat Interact? appeared first on Mark’s Daily Apple.
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For today’s edition of Dear Mark, I’m answering one eternal question: How do the Hadza tribespeople of Northern Tanzania eat so much honey and maintain their trim figures and pristine metabolic health? Are they eating keto whenever they’re not eating honey? Are they running hill sprints to burn through glycogen stores and improve their insulin sensitivity? Are they trading mongongo nuts for Metformin? Or is there something unique about honey that makes it different than sugar?
But before I get to the question, it’s a brand new year.
This New Year promises to be bigger and better than ever. Change is in the air, and not just in my own life. Everyone I talk to—all my friends, colleagues, family members, and random acquaintances—seems to be entering a period of great change. Their professional lives, their relationships, their health, their mindsets are all shifting. And for the better. The way I see it is that change happens regardless of what you do. It’s a far better idea to take the reins and make the change work in your favor than let yourself be swept away by powers and fate unseen.
Happy New Year to everyone! I hope 2019 is your best yet, and I’d love to hear your visions for it.
Okay, on to the question:
What are your thoughts on honey as the sweetener for the mulled wine? Given how the Hadza draw so many of their carbs from honey (especially given the particular sugars and micronutrients that it contains), I’m surprised it doesn’t appear more often in these recipes that call for sweetening.
In case readers are unaware of the reference, the Hadza are one of the few remaining hunter-gatherer groups on this planet. They inhabit northern Tanzania, and their lives haven’t changed much at all. They’ve resisted ethnic admixture from other groups. They still hunt and gather for the vast majority of their calories. Their hunting and foraging grounds have been condensed due to pressure from the state, and there are probably fewer game animals available, but they’re still in the same general area. According to their oral traditions, there’s even no indication that they came from somewhere else.
One of the more striking features of their diet is their utilization of honey.
Ask the average Hadza tribesperson what their favorite food is and “honey” will be the answer.
Catch the Hadza during the right month and they’ll get half their calories from honey. Averaged out across the year, they get 15% from honey.
They even use a bird called the honey guide to lead them to the choicest hives. After completing the harvest, they’ll burn or bury the remnants to keep their honey guide from getting too full for the next search.
The honey isn’t your store-bought, pristine golden syrup smelling faintly of HFCS. It’s straight up honeycomb, teeming with bees and larvae and pollen and the queenly secretions called royal jelly. In fact, studies tend to emphasize that the Hadza get 15-50% of their calories not from honey, but from “honey and bee larvae.”
Bee larvae, also known as bee brood, is packed with protein, vitamins, and minerals. It’s high in folate, B12, thiamine, pantothenic acid—pretty much all the B vitamins—and biotin, to name a few.
Whole hive eating also means eating the royal jelly, a potent, superconcentrated secretion used to feed larvae and queens. Think of it as colostrum, the potent milk mammals provide for their infants in the first few days of life. Royal jelly has shown potential activity (in humans, no less) against allergic rhinitis, reduced the toxicity of cancer drugs in patients, lowered cholesterol in adults with high cholesterol (and women), and improved glycemic control and oxidative stress in diabetics.
How about the honey itself? I’ve written about honey as a sweetener and explored how its metabolic effects differ from plain white sugar. Suffice it to say, the evidence is clear that honey isn’t just sugar. Honey contains sugar—a lot of sugar—but it’s much more than that.
A set of studies in humans compared the effects of honey, sham-honey (a mix of fructose and glucose), dextrose (which is just glucose), and sucrose on several health markers. Honey resulted in smaller blood glucose spikes (+14%) than dextrose (+53%). Sham honey increased triglycerides, while real honey lowered them along with boosting HDL and lowering LDL. After fifteen days of honey feeding, CRP and LDL dropped. Overall, honey improved blood lipids, lowered inflammatory markers, and had minimal effect on blood glucose levels, despite being similarly high in fructose in particular and sugar in general.
So, in some respects, the honey the Hadza eat like crazy isn’t the honey that most of us can easily obtain in stores or even farmer’s markets. Yet even standard honey is different from—and better than—white sugar.
This is a roundabout way of saying that a little honey will be just fine in your mulled wine. Extra points if you can throw some bee larvae and royal jelly in there, with maybe even a dash of Hadza fecal bacteria.
Of course, don’t eat 15% honey diets. You are not Hadza. You are not living like the Hadza. You don’t have the precise genetic makeup of the Hadza. It won’t work as well for the average Westerner reading blogs.
Do you eat honey? How do the metabolic effects compare to sugar in your experience?
That’s it for today, folks. Thanks for reading, and be sure to tell me your thoughts and New Year intentions down below.
Shaha A, Mizuguchi H, Kitamura Y, et al. Effect of Royal Jelly and Brazilian Green Propolis on the Signaling for Histamine H Receptor and Interleukin-9 Gene Expressions Responsible for the Pathogenesis of the Allergic Rhinitis. Biol Pharm Bull. 2018;41(9):1440-1447.
Osama H, Abdullah A, Gamal B, et al. Effect of Honey and Royal Jelly against Cisplatin-Induced Nephrotoxicity in Patients with Cancer. J Am Coll Nutr. 2017;36(5):342-346.
Chiu HF, Chen BK, Lu YY, et al. Hypocholesterolemic efficacy of royal jelly in healthy mild hypercholesterolemic adults. Pharm Biol. 2017;55(1):497-502.
Lambrinoudaki I, Augoulea A, Rizos D, et al. Greek-origin royal jelly improves the lipid profile of postmenopausal women. Gynecol Endocrinol. 2016;32(10):835-839.
Pourmoradian S, Mahdavi R, Mobasseri M, Faramarzi E, Mobasseri M. Effects of royal jelly supplementation on glycemic control and oxidative stress factors in type 2 diabetic female: a randomized clinical trial. Chin J Integr Med. 2014;20(5):347-52.
Al-waili NS. Natural honey lowers plasma glucose, C-reactive protein, homocysteine, and blood lipids in healthy, diabetic, and hyperlipidemic subjects: comparison with dextrose and sucrose. J Med Food. 2004;7(1):100-7.
The post Dear Mark: How Do the Hadza Eat So Much Honey? and Happy New Year! appeared first on Mark’s Daily Apple.
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For today’s edition of Dear Mark, I’m answering a bunch of questions from comment sections. First, did I get AMPK and mTOR mixed up in a recent post? Yes. Second, I give a warning for those who wish to add ginger to their broth. Third, is it a problem that we can’t accurately measure autophagy? Fourth, how does coffee with coconut oil affect a fast? Fifth, is there a way to make mayonnaise with extra B12 and metformin? Actually, kinda. Sixth, should you feel awkward about proposing hypotheses or presenting scientific evidence to your doctor? No.
Great article, but a couple of amends are required with regards to mTOR. Firstly, you mention in the last paragraph that curcumin activates autophagy by activating mTOR. Reading the actual article abstract though, it states the opposite, ie the effect of curcumin “downregulating AKT/mTOR signaling pathway in human melanoma cells”.
Great catch. I’m not sure how I flipped that around. AMPK triggers autophagy, mTOR inhibits it.
What you say about curcumin goes for all the other broth ingredients I mentioned. Ginger, green tea, and curcumin all contain phytonutrients which trigger AMPK, which should induce autophagy, or at least get out of its way. What remains to be seen is whether the amino acids in broth are sufficient to inhibit fasting-and-phytonutrient-induced autophagy. I lean toward “yes,” but is it an on-off switch, or is autophagy a spectrum? Does inhibition imply complete nullification? I doubt it.
Regarding autophagy and health and longevity, it’s important to note the manner in which glycine, the primary amino acid found in broth and gelatin, opposes the effects of methionine, the primary amino acid found in muscle meat and a great stimulator of mTOR.
One notable study found that while restricting dietary methionine increased the lifespan of lab rodents, if you added dietary glycine, you could keep methionine in the diet and maintain the longevity benefits. That doesn’t necessarily speak to the effect of broth on autophagy during a fast, but it’s a good reminder that broth is a general good guy in the fight for healthy longevity.
Funny you mentioned ginger and turmeric as I add both, along with a whole lemon and/or lime, to my list of ingredients when cooking my broth. Here’s another great tip: I juice turmeric root, ginger & lemon together in my Omega juicer and freeze in ice cube trays. I add a cube to curries and other dishes.
That’s a great idea. One cautionary note about the raw ginger: it will destroy your gelatin.
Raw ginger has a powerful protease, an enzyme that breaks down protein. If you grate a bunch of ginger into a batch of finished broth, or juice a few inches and dump it in, there’s a good chance you’ll lose the gel. The amino acids will remain, but you’ll miss out on the texture, the mouthfeel, the culinary benefits of a good strong gelatinous bone broth.
Heating the ginger with the broth as it cooks, or even just reducing the amount of raw ginger you add, should reduce the protease activity.
The post Dear Mark: Broth, Fasting, Coffee, and Metformin (and More) appeared first on Mark’s Daily Apple.
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For today’s edition of Dear Mark, I’m answering a few questions from readers. First, the diabetes drug metformin looks like a “wonder” drug, even (or especially) for non-diabetics. Are there any known side effects? Is there anything we should watch out for?
Second, I address some of the concerns and criticisms shared in response to the Kraft Heinz announcement post.
Are there any adverse side effects to Metformin? It was mentioned in the fasting study.
Metformin is a diabetes drug that’s garnered a lot of attention from longevity seekers, health nuts, and low-carbers. I can see why. It appears to improve gut health (possibly because it impedes carbohydrate absorption, thereby increasing the amount of fuel available to our colonic bacteria), reduce cancer risk, lower blood glucose, improve insulin sensitivity, and increase fat loss. As far back as 2012, people I respect like Robb Wolf were suggesting metformin as a general all-purpose health enhancer.
Most of the interest in metformin from the general health crowd comes from its potential effect on longevity. It’s quite good at activating AMPK, the same pathway activated by exercise, fasting, and calorie restriction. There’s even some human research that hints at an effect—diabetics who take metformin actually live longer than non-diabetics who don’t take it. That’s a profound correlation.
But metformin does exert some of its effects via the hormetic pathway, which suggests it’s a stressor and may have a dark side. What could it be?
Well, there’s one main adverse side effect.
B12 depletion. Time and time again, studies show that metformin users are more likely to have B12 deficiency, whether they’re PCOS patients, Type 2 diabetes patients or others. Even when you age-match, health-match, and overall lifestyle-match your groups, the long-term metformin users have a higher chance of B12 deficiency. That certainly sounds causal, and even if it’s not, it’s a big risk. B12 plays a huge role in a host of physiological pathways. It protects against dementia, anxiety, depression, and fatigue. Its absence from vegan diets is one of the main reasons most vegans eventually flounder and have to turn to supplements or sneak into burger joints when no one’s watching. B12 is that important for overall health.
If you’re going to take metformin, make sure you’re tracking your B12 intake and status.
I’m not saying that’s the definitive answer. There may be more side effects. There probably are more. But on the whole, it’s a promising drug.
Now I’m going to address some of the concerns and questions from last week’s post on the Kraft Heinz acquisition. You guys made some good points and asked tough questions. I have answers.
On Disruption Of the Food Industry Being Hard or Impossible:
Believe me: We have disrupted the food industry. The ancestral movement is quite good at disruption. Take the fitness industry—just look at CrossFit and the thousands of small “functional fitness” gyms popping up everywhere. And the lighting industry—notice all the bulbs with warmer, less-blue lighting. And the tech industry—see the sudden development and adoption of “nightmode” to protect sleep and circadian health. Primal Kitchen disrupted the mayo, condiment, and dressing industry, not by upending or destroying it, but by highlighting the coming shift. That’s exactly why the acquisition occurred. They realized that things are changing and have changed, and that a growing number of people care about the quality of their packaged food and are willing to pay for it.
One thing that I didn’t realize until I got into this business—the packaged food business—is that smaller companies all eventually butt up against a ceiling. At some point, the smaller guys simply don’t have access to the same avenues of distribution as the larger guys. This isn’t negotiable. If you want to expand, you need access. From the beginning I wanted to put high-quality mayo, condiments, and dressings—the “extra” stuff that provides much of the added fat and sugar in the Western diet—in millions of homes. I couldn’t do that without access to those distribution channels, those industry connections, that capital. Now I can.
Some Worried About the Quality Of the Product. Will It Change?
I was adamant about maintaining product quality and integrity from the earliest of discussions with Kraft Heinz, and they were fully aligned with this from the beginning. It’s clear to me that Kraft Heinz sees that increasing numbers of people are flipping mayo jars around and scanning the labels. They know that the folks who buy Primal Kitchen products do so only because the ingredients we use are the best around, the very same ingredients you’d use if you were making mayo or dressing at home. If those ingredients change, you will stop buying. Business 101.
I know that. Kraft Heinz knows that.
On Extreme Skepticism:
We all have choices: do we let life unfold before us and respond accordingly, or do we fall prey to cynicism and assume the worst? I strongly recommend not being a cynic. It keeps many of us from ever fulfilling our potential and achieving our goals and dreams.
When I started Primal Nutrition, I left a well-paid, stable gig and put all my (borrowed) money and energy into the new venture. I had a wife and two small children at home, and the future was uncertain. It could have gone very wrong. But I did it just the same, because on some level I knew it would work. I left security and comfort and a steady paycheck for struggle and nerves and anxiety. My goal of changing how people eat and thrive kept increasing, from a million people, to ten million to a hundred million (I always think big). Now, with the leverage that Kraft Heinz brings, that goal of bringing healthier options to everyone is within reach.
On the Opportunity At Hand:
All across the U.S., in small towns and metropolises, rural communities and suburban sprawl, the vast majority of people are still eating way more seed oil and shifting the fatty acid ratio of their tissues accordingly than humans have ever done. I think of all the people dousing the salad their doctor said they should start eating in soybean oil-based dressing and buying “olive oil mayo” that was mostly just seed oil, and it frustrates me. Imagine if they switched? Imagine if they all switched? Imagine if we were able to shift the collective omega-6:omega-3 ratio back toward ancestral optimums. Longtime readers know how big a change a person can make in his or her health just by changing the fats you eat. Now imagine a population doing it.
It could be big.
That’s it for today, folks. Take care and share your thoughts below.
As always, thanks for reading.
Libby G, Donnelly LA, Donnan PT, Alessi DR, Morris AD, Evans JM. New users of metformin are at low risk of incident cancer: a cohort study among people with type 2 diabetes. Diabetes Care. 2009;32(9):1620-5.
Bannister CA, Holden SE, Jenkins-jones S, et al. Can people with type 2 diabetes live longer than those without? A comparison of mortality in people initiated with metformin or sulphonylurea monotherapy and matched, non-diabetic controls. Diabetes Obes Metab. 2014;16(11):1165-73.
De haes W, Frooninckx L, Van assche R, et al. Metformin promotes lifespan through mitohormesis via the peroxiredoxin PRDX-2. Proc Natl Acad Sci USA. 2014;111(24):E2501-9.
Esmaeilzadeh S, Gholinezhad-chari M, Ghadimi R. The Effect of Metformin Treatment on the Serum Levels of Homocysteine, Folic Acid, and Vitamin B12 in Patients with Polycystic Ovary Syndrome. J Hum Reprod Sci. 2017;10(2):95-101.
Pongchaidecha M, Srikusalanukul V, Chattananon A, Tanjariyaporn S. Effect of metformin on plasma homocysteine, vitamin B12 and folic acid: a cross-sectional study in patients with type 2 diabetes mellitus. J Med Assoc Thai. 2004;87(7):780-7.
The post Dear Mark: Metformin Side Effects, Kraft Heinz Deal Questions appeared first on Mark’s Daily Apple.
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Last week, Craig Emmerich graced us with a great post on the oxidative priority of various dietary fuel sources, namely fats, carbohydrates, and protein.
If you haven’t had the chance to read through Craig’s post, definitely do. The visuals really drive home the point of fuel priority. Visuals appeal to me. They have a way of sticking with you, and there’s a power in recalling them when you’re making daily choices.
Today, I’m going through and answering some of the questions you folks had in the comment board.
I’m actually answering a great series of questions from Gerard.
I’ve seen this analysis before, and always had the question – can we really lump “carbohydrates” together like this?
No, we can’t. Craig gave a great overview, a useful 30,000 foot view that’s sufficient for most people who just want to eat and metabolize their fuel better, but there are differences between different carbohydrates. I know he’d say as much, and he may have time to weigh in here, too. If his schedule allows, I’ll include his response later today. But back to the differences in carbohydrates…. I’ll save fructose versus glucose for my answers to Gerard’s next questions. What about others?
Think of fiber. Fiber the monolith is already different from more digestible carbohydrates like glucose and fructose in that we can’t extract very much (or even any) caloric energy from it. But you can go even further and look at the individual metabolic fates of the different types of fiber.
Fermentable fibers like inulin and resistant starch are fermented into short chain fatty acids like butyrate and propionate. These provide important cell signaling and are worth about 2 calories per gram, give or take. Others forms of fiber are not fermented and provide colonic bulk but not calories.
Certain carbohydrates are treated differently in different people. Lactose tolerance allows people to digest lactose with lactase and use it for fuel. Lactose intolerance prevents people from digesting lactose, instead diverting it to gut bacteria to ferment and cause terrible digestive distress. FODMAP intolerance is similar. Those with FODMAP intolerance ferment carbs like sugar, lactose, and others in the gut, producing gas but not calories; those without it digest the carbs, producing useable energy.
Are fructose and glucose metabolized differently for this purpose?
There are definitely differences. For one, glucose stimulates insulin production, while fructose does not. But the differences may not be as stark as we often think.
When scientists attached isotopes to fructose, had healthy sedentary people eat it, then tracked the metabolic fate of the fructose molecules, they found:
- 50% ended up as glucose, converted by the liver to be used elsewhere in the body.
- 25% ended up as lactate, converted by the liver.
- 17% ended up as liver glycogen.
- 2-3% was converted to fat in the liver via de novo lipogenesis.
- The rest was oxidized and expelled as CO2.
According to the study authors, this is quite similar to the metabolic fate of glucose. Even if you’re talking about de novo lipogenesis, often considered the sole province of fructose overfeeding, research shows that overfeeding with glucose also provokes the creation of new fat.
As far as burning/oxidizing of ingested glucose and fructose, there are differences. At rest, people tend to burn fructose faster than glucose. During exercise, people tend to oxidize glucose faster than fructose. However, when you give someone both fructose and glucose together, they burn them faster than either fuel source alone. In one study, subjects were either given 100 grams of fructose, glucose, or fructose+glucose. The fructose group burned through 43.8% of their dose, the glucose group burned through 48.1% of theirs, while the fructose+glucose group burned through 73.6% of their dose.
Is the storage capacity for energy from fructose and glucose equivalent (i.e., liver vs muscle glycogen)?
There’s actually a misconception about fructose and glycogen repletion. Here’s the story you may have heard: Fructose can only contribute to liver glycogen, while glucose only contributes to muscle glycogen.
It’s not quite accurate. I believed it for awhile, too, until I actually checked it out. It turns out that both fructose and glucose are able to contribute toward both liver and muscle glycogen. Fructose is about half as efficient as glucose at replenishing muscle glycogen, as it first must be converted into glucose in the liver before being sent out, but it will eventually get the job done.
One big difference is that there’s a lot more room in your muscles than in your liver. The average person can store about 300 grams of glycogen in their muscles but only 90 grams in their liver. Even if the metabolic fates are ultimately pretty similar in a vacuum, in the real world there’s simply less room for liver glycogen, and, thus, less room for fructose in the diet without overstepping the bounds and incurring metabolic dysfunction.
So, if you’re talking about an overweight, sedentary person walking around with full glycogen stores eating a hypercaloric diet, fructose will behave differently than glucose. In the healthy, lean, eucaloric, and active, whole foods-based fructose isn’t a big deal and may not have a drastically different metabolic effect compared to glucose.
At any rate, discussing isolated fructose and isolated glucose may not even be very relevant to real world results. You’re eating fruit, not quaffing cola. You’re enjoying a sweet potato, not a bag of Skittles smothered in agave nectar. You’re eating both glucose and fructose together in the context of a meal, of a whole food. Don’t get too bogged down in the effects of isolated nutrient-poor sugars unless you’re consuming them that way.
To what extent is fructose metabolized in a manner that is more similar to alcohol than carbohydrate?
Fructose is metabolized in the liver. Alcohol is metabolized in the liver.
Fructose gets taken up by the liver without insulin. Alcohol ends up in the liver without insulin rising.
But after that, according to Richard Feinman, the similarities stop. Alcohol is a toxin with known toxic metabolites. There may be some benefit to low level exposure to alcohol, but it remains a toxin. Fructose can be situationally toxic, as in the obese guy with glycogen-replete fatty liver and full-blown diabetes, but we are physiologically capable of handing normal amounts without producing toxic metabolites. Feinman considers it more of a rhetorical device than a statement of facts.
That’s it for today, folks. Thanks for reading and if you have any further questions on the topic, let me know down below and I’ll do my best to get to them.
Tappy L, Lê KA. Metabolic effects of fructose and the worldwide increase in obesity. Physiol Rev. 2010;90(1):23-46.
Sun SZ, Empie MW. Fructose metabolism in humans – what isotopic tracer studies tell us. Nutr Metab (Lond). 2012;9(1):89.
Blom PC, Høstmark AT, Vaage O, Kardel KR, Maehlum S. Effect of different post-exercise sugar diets on the rate of muscle glycogen synthesis. Med Sci Sports Exerc. 1987;19(5):491-6.
Mcdevitt RM, Bott SJ, Harding M, Coward WA, Bluck LJ, Prentice AM. De novo lipogenesis during controlled overfeeding with sucrose or glucose in lean and obese women. Am J Clin Nutr. 2001;74(6):737-46.
Rosset R, Lecoultre V, Egli L, et al. Postexercise repletion of muscle energy stores with fructose or glucose in mixed meals. Am J Clin Nutr. 2017;105(3):609-617.
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A commenter wrote a great comment that got me wondering:
As far as “the more exercise the better” study I wonder if folks who had to drop out of long distance cardio training due to injuries or cortisol driven exhaustion are considered in the equation? In other words, if you can tolerate chronic cardio you may live longer, otherwise it might break you down. Everyone has a sweet spot for exercising is my gut feeling and you have to “listen to your body”. I still like the primal mantra along the lines of (if I may be so presumptuous as to paraphrase Mark) “walk a lot, do sprints once a week, lift heavy things once or twice a week, spend time outdoors, take part in sports or recreational activities that are fun for you”.
What do I think is going on? How do the results of this paper jibe with my take on Chronic Cardio?
First off, we have to acknowledge the basic structure of the study.
This study didn’t actually measure “hours spent training.” They gave subjects treadmill tests (stress tests) to determine their cardiovascular fitness, then divided everyone into different tiers of fitness based on the results. In fact, the authors of the study criticized the shortcomings of previous studies which used self-reported training data instead of objective measurements of cardiorespiratory fitness like the treadmill test. This makes the study far more accurate and useful. It also means you can’t make any ironclad proclamations about the connections between hours spent training and longevity. You can certainly make inferences—people who had better cardio fitness probably spent more time training to get it—but there are other interpretations. All you can say for certain is that higher levels of cardio fitness predict greater longevity.
I don’t see how anyone could argue with that. Of course being fitter is better.
But my criticism of chronic cardio isn’t a criticism of cardiovascular fitness. It’s a criticism of how most people go around obtaining that fitness—by destroying their bodies.
That doesn’t have to happen anymore. Tons of top guys these days are finally figuring out that you don’t have to log as many laps/miles/etc as possible to maximize your performance, but that wasn’t always the case. I grew up convinced that the more miles I ran, the healthier I’d be. That’s how I did it back in my marathon and triathlon days, and it almost destroyed me and an entire generation of my peers.
You can train twice as much as the next guy yet have worse fitness, either because you’re not training intelligently, you’re overtraining and hampering the adaptive process, or you’re not sleeping. That’s chronic cardio. You can train less and get better results, if you’re optimizing your recovery, nutrition, and sleep. That’s Primal Endurance.
As for these subjects, there is some serious genetic confounding occurring. Those dudes with elite fitness levels well into their 70s are often a different breed. They’re hard to kill. They’re tough. They can withstand the discomfort of grueling mile after mile. What other types of discomfort can they bear and even grow from? They’re just more robust than the average 70-year-old. It may not be the elite training itself that’s making them resist death. It’s just as likely they have the genetic capacity to excel in endurance training, and even if they didn’t exercise they’d still live longer than average.
There’s also the healthy user bias. The kind of lifestyle regular exercisers follow emphasizes sleep, plenty of rest and recuperation, smart supplementation and nutrition, and all sorts of other things that are also linked to longer, better health.
This paper makes a strong case for using something like Primal Endurance to build great cardiorespiratory fitness without risking chronic cardio territory.
Thanks for writing and reading, folks. Take care!
The post Dear Mark: Is There No Upper Limit to Endurance Training? appeared first on Mark’s Daily Apple.
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