Dear Mark: What Breaks a Fast Followup

For today’s edition of Dear Mark, I’m answering a round of questions drawn from the comment section of the “What Breaks a Fast” post. You folks had tons of follow-up questions about whether other types of foods or compounds break a fast. Does a teaspoon of honey? Does elevated insulin from BCAAs? Does coconut milk? Does pure prebiotic fiber? What about longer fasts—are they recommended? And how about unsweetened cocoa powder? What explains my ability to predict your questions? Do sausages break a fast? Does liquor? How should you exercise?

Let’s dig right in:

Hey, what about honey? 1 tsp in morning tea?

A teaspoon or less of honey is fine and won’t negate the benefits of fasting. I alternate between doing collagen coffee and coffee with cream and teaspoon of sugar (which was my typical morning coffee for over a decade). No reasonable person should fear a teaspoon of sugar or honey.

For what it’s worth, honey isn’t “just” sugar. It elicits a more beneficial (or less negative) metabolic response than other forms of sugar.

I’m shocked about the BCAA. I used to fast and take BCAA’s (yes, to continue dynamic exercise). I used to find it extremely difficult to fast compared to now when I fast without taking them. Does that mean that the insulin response made fastic more difficult?

It’s possible. Insulin impairs lipolysis—the release of stored body fat into circulation for energy usage—and the success of fasting depends on lipolysis. Without lipolysis, you can’t access all that stored energy.

Thank you very much for this info!! I am a butter-coffee-for-breakfast drinker, and I always worry about the ingredients breaking a fast. Could you please comment on coconut milk (in the can)? I love putting that in my coffee/breakfast.
Thanks.

Coconut milk is a less concentrated source of medium chain triglycerides, or MCTs (as in MCT oil). MCTs convert directly to ketones, making MCT oil and to a lesser extent coconut oil or coconut milk a potential “boost” for fasting. Still, energy is energy, and any energy you take in is energy you won’t be pulling from your body.

I find MCTs and coconut to be more useful when someone is just getting the hang of fasting or ketosis—as a nice boost to get things moving in the right direction.

Keep your coconut milk under a tablespoon and you’ll be fine.

Does prebiotic (resistant starch) fiber break a fast? Acacia senegal or potato starch? Thanks!

No. If you’re worried, test your postprandial blood sugar after eating the fiber.

Great input Mark as someone 3days into a 7day water fast with electrolytes of course what’s your view on longer fasts.

Check out the post I wrote on long fasts. Potentially beneficial but the risks accumulate the longer you go. You just have to be even more careful and methodical.

How about unsweetened cocoa?

A tablespoon runs just over 12 calories (depending on the brand; some cocoa powders contain more fat and thus more calories), with around a gram of net carbs and a gram of fat. Also a nice source of potassium and magnesium, along with a ton of polyphenols which can have fasting-mimicking effects on their own.

Eating enough unsweetened cocoa powder to knock you out of your fast would be incredibly repulsive. Probably impossible.

Cocoa is definitely a nice addition.

Okay it’s almost creepy the way Sisson answers my questions before I even ask them! I was wondering about this yesterday and then this post popped up in my inbox.

How does he do that…? ?

Kraft-Heinz has a strong relationship with Google and Amazon, and the Kraft acquisition gave me access to Alexa/Google Home datasets and the ability to predict what my readers are wondering about.

Just kidding, though it’s scarily not out of the realm of possibility anymore.

What about a small snack of paleo sausages, smoked or dried? So meat and fat (beef, pork or lamb), and some spices. Maybe 100g worth.

Well, that’s a legit snack bordering on a small meal. That will break the fast, but it’s not all for naught. There is the whole “fasting-mimicking diet,” where you eating very few calories for several days out of the week and retain many if not most of the benefits of full-on fasting.

Let’s just say if you ate a small snack of paleo sausages on your “fasting” days, you’d still be way ahead of 99% of people.

But do try a full-on fast at least once. You might surprise yourself.

Great post! What about alcohol? Specifically, a shot or 2 of liquor. I would assume beer and wine would break a fast, but what about whiskey or tequila?

When alcohol enters the system, utilization of all other energy sources is suspended until the alcohol is burned. Back in 1999, researchers did a study where they gave fasting adult men the equivalent of a couple shots of liquor. They stopped releasing stored body fat, stopped burning body fat, and began burning way more acetate (a product of ethanol metabolism). They didn’t exactly “break” the fast, but all the metabolic trajectories we love about fasting took a big pause.

Good morning Mark,
How does one exercise in the morning while fasting? When to eat?

You can exercise any way you like, but I change how I train based on when I’m going to break the fast with food.

If I’m going to break the fast with a meal right after, I train any way I like. I’ll do sprints, HIIT, weights, anything.

If I’m going to keep fasting after the workout, I like to stick to strength training and low-intensity movement (walking, hiking, standup paddling). The strength training is essential during a fast because it’s an anabolic signal to your muscles—move it or lose it. Simply lifting heavy things during a fast can stave off muscle loss.

That’s it for today, folks. Stay tuned later this week for “What Breaks a Fast: Supplements Edition.”

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Dear Mark: Protein Efficiency in Seniors, Earned Carbs, Hardgainer with Limited Time

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.

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References:

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.

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Dear Mark: Fasting, Training, and Growth Hormone; Wear and Tear on the Arteries

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.

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Dear Mark: How Does LDL Even Penetrate the Arteries, New Zealand Farmed Salmon, Elevated Ferritin

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?

Let’s go:

My reading of this post by Malcolm Kendrick MD is that LDL particles cannot infiltrate the endothelial lining of our arteries:
https://drmalcolmkendrick.org/2018/08/16/what-causes-heart-disease-part-52/

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.

Moving on:

In atherosclerosis susceptible regions, reduced expression of eNOS and SOD leads to compromised endothelial barrier integrity (), 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!

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References:

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.

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