Tag Archives: calories

Meal frequency, intermittent fasting, and dietary protein

Dietary protein “requirements” are some of the most context-dependent nutrient levels to decipher, and depend largely on energy balance and even meal frequency.

An objective look at intermittent fasting (Alan Aragon, 2007)

Meal frequency and energy balance (Lyle McDonald, 2008)

New study: “Increased meal frequency attenuates fat-free mass losses and some markers of health status with a portion-controlled weight loss diet” (Alencar et al., 2015)

This wasn’t well-received in social media because bro-science & many low carb advocates say grazing is no longer in vogue — “it’s much better/healthier/whatever to eat once or twice daily, because intermittent fasting and all that jazz” …however, this may be problematic when it comes to meeting overall protein needs, which is particularly important when you’re losing weight.

 

 

The study: 2 vs. 6 meals per day, crossover.  

Conclusion: “On average, fat-free mass (FFM) decreased by -3.3% following the 2 meals/d condition and, on average, and increased by 1.2% following the 6 meals/d condition (P<.05).”  

 

fat-free mass

 

In other words, 6 meals per day was better for body composition than 2 meals per day.  But context is everything, and this hypothesis has been tested from a variety of different angles, so what does it mean?  

The relevant context here: 1) big energy deficit (1200 kcal/d for obese women is a pretty low calorie intake); and 2) “adequateTM” protein intake (75 g/d).

The standard dogma says that in the context of an adequate protein hypocaloric diet, meal frequency matters a LOT, whereas with high protein, it doesn’t matter as much.  Theory being that with an “adequate” (read: too low?) overall protein intake, the fasting periods are simply too long with only two meals per day; you need either: 1) higher protein intake; 2) increased meal frequency; or 3) more calories (ie, smaller energy deficit).  

In this study, BOTH diets suppressed insulin and induced weight loss, but the increased protein feeding frequency skewed the weight loss to body fat while preserving fat-free mass.   I actually agree with a lot of the bro-science in this case, and also think that 75 grams of protein is not enough in the context of a big energy deficit (if body composition is a goal).    




 

Historical precedence?

 

Meal frequency and weight reduction of young women (Finkelstein et al., 1971)

Relevant context:  6 vs. 3 meals per day (3 meals per day may not seem like that many more than 2, but it significantly cuts down on the duration of time spent with no food or protein).

Smaller energy deficit: 1700 kcal/d in overweight patients is less of a deficit than 1200 kcal/d in obese patients.

Higher protein intake: 106 – 115g/d.

Result: nitrogen balance (a surrogate for the maintenance of muscle mass) and fat loss were similar in both groups.  This study fixed two problems in the abovementioned study: 1) 3 meals is better than 2 in the context of an energy deficit; and 2) protein intake was higher.

 

And again here, with 3 vs. 6 meals per day (Cameron et al., 2010), just to make the point that 3 meals per day is better than 2 for preserving lean mass in the context of an energy deficit.

 

The effect of meal frequency and protein concentration on the composition of the weight lost by obese subjects (Garrow et al., 1981)

This study tested the opposite extremes: super-low calorie intake (800 kcal/d), much lower protein intakes (20g – 30g/d), and 1 vs. 5 meals per day.

Result: “a diet with a high-protein concentration, fed as frequent small meals, is associated with better preservation of lean tissue than an isoenergetic diet with lower-protein concentration fed as fewer meals.”

It basically confirmed all of the above.

 

Protein feeding pattern does not affect protein retention in young women (Arnal et al., 2000)

1 vs. 4 meals per day; and 70 grams of protein but no energy deficit (~2000 kcal/d isn’t very hypocaloric for lean young women).  In this study, no effect of meal frequency was seen, likely because 70 grams of protein isn’t inadequate when energy intake isn’t restricted.

 

 

 

1. PROTEIN “NEEDS” ARE HIGHLY CONTEXT-DEPENDENT

2. NEED =/= OPTIMIZATION

3. MEAL FREQUENCY & meal timing and peripheral circadian clocks > “MACRONUTRIENTS”

 

If you’re losing weight (ie, in an energy deficit), then intermittent fasting is cool if protein intake is high (above “adequateTM“)… the bigger the energy deficit, the more protein is necessary to optimize changes in body composition.

 

How much is ‘enough?’  Sorry, can’t give you a gram or even gram per pound of body weight answer… but if you’re losing weight and seeing no discernible effect on body composition (muscle vs. fat mass), then it may be prudent to consider eating more protein-rich foods… and paying more attention to sleep quality (which also greatly impacts nutrient partitioning).

No amount of protein will help you if circadian rhythms aren’t intact!!!

 

 

further reading:

Yes, it’s a high protein diet (Tom Naughton, 2015)

Protein requirements, carbs, and nutrient partitioning

Dietary protein, ketosis, and appetite control 

 

 

calories proper

 

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Non-celiac gluten sensitivity

Gluten is protein, not carbs.  A gluten-free diet is frequently low-carb, because most dietary gluten comes in the form of bread (and wheaty foods).  But believe it or not, bread is an incredibly complex food… many different proteins, carbohydrates, and nutrients that could be problematic for some people (more on this later).

Gluten is not a FODMAP, but most gluten-containing foods are.  Gluten is actually very rich in the amino acid glutamine.  Gluten, not bread.

So we have three studies on purified “gluten,” asking if it’s the gluten, FODMAPs, or something else in wheaty food that is problematic.

Study #1. No effects of gluten in patients with self-reported non-celiac gluten sensitivity after dietary reduction of FODMAPs (Biesiekierski et al., 2013)

Strong study design; patient population was people who thought they were gluten sensitive (but definitely not celiac).

This is the study which led journalists to claim non-celiac gluten sensitivity doesn’t exist, and it’s really sensitivity to FODMAPs, in part, because of this:

 

 

low FODMAPs and gluten free

 

 

Baseline = low gluten diet
Run-in = low gluten and low FODMAPs

 

Here’s the fly in the ointment:

 

symptoms returned in all participants

 

After the run-in period, subjects still followed their gluten-free diets but also received either 16g relatively pure gluten/d (High gluten), 2g gluten + 14g whey protein (Low gluten), or 16g whey protein (placebo).  GI symptoms returned in all participants.  So, low FODMAPs worked for about a week, but then symptoms returned regardless of whether they were eating gluten or not.  In other words, neither low FODMAPs nor low/no gluten worked very well in this study.

But this study may have introduced a brilliant new confounder: food intake was strictly controlled — the experimental diets were different from their normal diets.  Restricting gluten and FODMAPs may have provided some transient benefit, but if the new experimental diet introduced something else that caused problems, then that may explain the gradual return of symptoms…

bollixed?

 

 

Study #2. Small Amounts of Gluten in Subjects with Suspected Nonceliac Gluten Sensitivity: a Randomized, Double-Blind, Placebo-Controlled, Cross-Over Trial (Di Sabatino et al., 2015)

It was another high quality study design: “Randomized, Double-Blind, Placebo-Controlled, Cross-Over.”  And it was addressing a basic question: do people who strongly suspect they have non-celiac gluten sensitivity (NCGS) really have NCGS?  Alternatively, is NCGS real?

Intervention was strong:

1) 4.375 grams of gluten or placebo (rice starch) daily for a week.  This is roughly equivalent to two slices of bread (note: this is way more than enough gluten to destroy the intestines of a patient with bona fide celiac disease).

2) important: they defined the what they would classify as NCGS prior to starting the trial.  A priori.

61 patients strongly suspected of NCGS started the trial, and one withdrew due to gluten-related symptoms in both the gluten and placebo groups.

 

Results:  regardless of whether they were assigned to gluten or placebo FIRST (prior to the crossover), most patients reported gluten-related symptoms.  More importantly, 3 of the 59 patients exhibited significantly worse symptoms on gluten relative to placebo according to the endpoint they defined prior starting the trial.  In one sense, this could be interpreted to mean 5% of people who strongly believe they have NCGS actually have NCGS.

 

gluten sensitive patients

 

Two patients reacted just as selectively strongly to the placebo as the three “real” NCGS patients did to gluten.  Rice-starch sensitivity?

 

See here for a more detailed description of the statistics involved in this study.  I’m willing to accept the “5%” rate, despite the strength of the placebo-responders, whereas the author of that blog post is not.  That’s fair, imo.

And here is another article which questions the legitimacy of NCGS based on this study.  I don’t think that’s totally fair.

And Raphael’s post, where he humorously concludes: “[Gluten-free] does not include advice to sport a gas mask when walking past bakeries.”

 

 

Study #3. Effect of gliadin on permeability of intestinal biopsy explants from celiac disease patients and patients with non-celiac gluten sensitivity (Hollon et al., 2015)

 

 

gluten increases intestinal permeability

 

 

“Delta TEER” is basically the amount of intestinal permeability in intestinal explants exposed to media + gluten (experimental condition) minus those exposed to plain media (control condition).  A better control condition, imo, would’ve been something like they did above: substitute gluten with another protein like whey protein.

 

NC: healthy people
RCD: celiac patients in remission
ACD: celiac patients with active disease
GS: non-celiac gluten sensitivity

 

Active celiac samples responded significantly worse than those in remission, which is good as it functions as a positive control for the experimental protocol.

 

However, gluten sensitive samples responded significantly worse than celiac remission samples; actually, they responded just as badly as celiac samples with active disease.  Celiac disease is supposed to be a million times worse than non-celiac gluten sensitivity… and statistically speaking, even permeability the normal samples declined as much as NCGS samples.

 

This led some to conclude that gluten is bad for EVERYONE.  I’d say it means the assay is bollixed.  Occam’s razor?

 

 

My advice: don’t be anti-science, but don’t use bad science to justify diet choices.  We simply need better studies on non-celiac gluten sensitivity and FODMAPs.

If bread doesn’t work for you, don’t eat bread.  You’re not missing much.

 

calories proper

 

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Carbs: Low vs. Lower

 

 

This was met with much backlash from the low carb cavalry, because, well, if low is good then lower must be better

I’m not anti-keto; but I’m not anti-science.  FACT.  

 

“…some people are not genetically equipped to thrive in prolonged nutritional ketosis.” –Peter Attia

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CICO and rant

“Wait… what?  nutrient partitioning?”

Calories In, Calories Out should not be interpreted as “eat less, move more,” but rather kept in its more meaningless form of: “if you eat less than you expend, you’ll lose weight.”  At least then, it’s correct… meaningless, but correct.  Eating less and moving more is no guarantee of fat loss, in part, because total energy expenditure isn’t constant and there’s that whole thing with nutrient partitioning.

For obese insulin resistant folks, this is Low Carb’s strong suit: it causes “eat less, move more”spontaneously.

For some obese insulin sensitive patients, for whatever reason, their adherence and success is greater with Low Fat.  You might say, “yeah, but those suckers had to count calories.”  To that, I’d counter with: “it doesn’t matter, THEY WERE MORE SUCCESSFUL COUNTING CALORIES ON LOW FAT THAN NOT COUNTING ON LOW CARB.”  The spontaneous reduction in appetite obviously didn’t cut it.  Do not be in denial of these cases.

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Protein “requirements,” carbs, and nutrient partitioning 

One way to determine protein requirements is the nitrogen balance technique.  If all of the nitrogen from dietary protein intake is equivalent to that lost via feces, urine, and sweat, then one is in nitrogen balance.  Growing children and pregnant women are usually in positive nitrogen balance, because much of the nitrogen is being invested in the growth of new tissue.  Cachectic cancer patients and sarcopenic elderly may be in negative nitrogen balance, because they’re losing lean mass.

Protein requirements to maintain nitrogen balance are largely dependent on total energy intake.  More calories in, less protein needed.  For people in negative energy balance (losing weight), this usually means more protein is required else muscle will be wasted.

Exercise lowers, not raises, protein “requirements,” because exercise is a potent anabolic stimulus; it helps preserve nitrogen at any level of dietary protein.  That’s not to say more won’t improve functional outcomes; just that it’s not “necessary” to prevent muscle loss.

Need =/= optimization.

Lastly, total grams, not percent of calories, is the most relevant way to talk about protein requirements in the context of nutrient partitioning and body composition.  This is just how protein operates.

Part 2.  The poor, misunderstood Randle Cycle

“The glucose-sparing effect of fat-derived fuels” …when you’re body starts burning more fat (and fat-derived fuels; ie, ketones), it’s use of glucose declines.  Thus, it’s “glucose-sparing” (spares glucose for the brain and obligatory glycolytic tissues, yada yada yada).

During starvation, much of that glucose comes from amino acids from skeletal muscle proteins, so it can also be phrased as: “the muscle-sparing effect of fat-derived fuels,”  which is equally biologically relevant, because similar to zeroglycemia, an unabated loss of muscle is incompatible with survival.

That is, in starvation, where the “protein” is skeletal muscle, not dietary (because starvation)… but what about when following a low carb or ketogenic diet – do ketones (fat-derived fuels) exert a muscle-sparing effect in this context?

One study compared the impact of two isonitrogenous diets, low carb (Diet A) vs. high carb (Diet B), on nitrogen balance and showed that, except at very high levels of energy intake, nitrogen balance was consistently better on high carb.

carbs vs protein req

 

However, 51 kcal/kg is the textbook number of kcals “required” for young, moderately active adults.  With this understanding, it could be interpreted to mean that nitrogen balance is better with low carb (Diet A) for people in energy balance; and better with high carb (Diet B) if energy deficit.

edit: 51 kcal/kg is for athletes; probably about 20-25% less for non-athletes.

Or not: in another study, a low carb diet promoted better nitrogen retention albeit less weight loss than an isocaloric low fat diet.  The low carb group lost slightly more fat mass, which, combined with nitrogen balance data, suggest modestly improved body composition.  The differences were small, because this was a “non-ad lib” isocaloric diet study.  In the absence of large differences in intake, the most we can expect from such studies are subtle alterations in nutrient partitioning (which are usually difficult to detect).

Cancer cachexia is a condition of severe muscle wasting, and one study set out to determine, more directly, if ketones spared muscle in this context.  The study only lasted one week, but I suspect a certain degree of expedited ketoadaptation because: 1) it was very low in carbohydrate; 2) the fat was primarily MCTs; 3) they supplemented oral ketones; and 4) energy expenditure is elevated in this population.  Both the control and ketogenic diets were modestly hypercaloric, but nitrogen balance was more favorably improved by the high carb diet, in contrast to the above studies.

Thus, ketones don’t work in the context of a hypercaloric diet; however, pharmacologically elevating ketones via intravenous infusion in fasting subjects does work (because it’s more like starvation).

The muscle-sparing effect of fat-derived fuels is conceptually and physiologically more relevant to starvation, not nutritional ketosis.

Part 3.  Protein “requirements”

Effects of high-protein diets on fat-free mass and muscle protein synthesis following weight loss: a randomized controlled trial (Pasiakos et al., 2013) 

Protein intake was 1x, 2x, or 3x the RDA; fat was 30% of calories, and carbs made up the rest; on a weight maintenance diet and again on 30% calorie restriction (it was technically a 40% energy deficit, because they tried to ramp up energy expenditure with exercise).

RDA

All groups lost weight, but the ratio of fat to muscle loss was significantly higher in the 2x and 3x RDA groups, which amounted to ~120 and 185 grams of protein per day, respectively.  The 3x group didn’t fare as well, possibly, because that much protein induces a high degree of satiety – this group ended up consuming significantly fewer calories than the 2x group.  So the interplay between energy intake and protein requirements is back on the table: the added energy deficit apparently increased protein requirements to some level above 185 grams per day.  Not much, given the small difference in muscle loss, but increased none the less.

Side note: be cautious when interpreting a study about the amount of protein required for xyz endpoint, because such studies usually only measure one of many important markers, and they don’t report absolute changes in size, strength, etc.  Also, context matters.

For example, Moore and colleagues (2014) showed that 0.24 g/kg (17 grams for a 70 kg adult) was enough to maximally stimulate myofibrillar fractional synthetic rate (mFSR):

mFSR

However, in the contexts of three square meals and energy balance (or deficit), 0.72 g/kg (50 g/d) is woefully inadequate.  Point being: mFSR (in this case) is only one measurement and shouldn’t be extrapolated to total daily requirements.  Perhaps you could eat six 17 g servings in order to fully maximize 24-hour mFSR, or you could realize that going above what saturates mFSR isn’t a bad thing, or wasteful.  mFSR is just one of many measurements of muscle protein balance.

My opinion

For those who need exact numbers, hopefully one point I’ve made is that there’s no answer to this question.  I’d guess that most people “need” 100+ grams of protein per day (more if losing weight), and 100 grams is probably too much in one sitting.  Also, need =/= optimization, and context matters.

Nutritional ketosis doesn’t appear to reduce the amount of dietary protein necessary to maintain lean mass.  The muscle-sparing of fat-derived fuels works during starvation; in other contexts, all bets are off.

calories proper

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Paleo Plants and Carnivory

From what I gather, it’s been difficult to pinpoint the role of plants in the diet of our ancestors for a variety of reasons.  For example, evidence of plants on cooking tools and dental remains is suggestive but doesn’t disprove the possibility that said evidence came from preparing the plants for some other purpose (eg, tools, weapons, or medicine), or that the stomach contents of an herbivore was ingested (which gets partial credit).

That said, after reviewing a few studies on the topic (see below), it’s safe to say that plants were eaten, probably frequently, and the types & quantities varied seasonally & geographically.  Collectively, the data suggest we aren’t carnivores.

…you had to have something to hold you over until the next fish fell prey to your deadly hunting spear…  

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Skipping meals, intermittent fasting, grazing, etc.

or… Circadian Meal Timing!

They say if you’re going to [intentionally] skip a meal, it should be breakfast – and hey, that’s probably the easiest meal to skip.  However, a recent study showed skipping dinner FTW (well, not exactly).  I’ve never seen a proper study directly comparing the effects of skipping different meals, but here are a few that come close.  The findings may surprise you.

omelette

note: with the exception of Fernemark (Exhibit B), these studies are mostly macronutrient-controlled. That is, protein, fat, and carbs are similar between the groups; the only thing that differs is when they were ingested.  This can be tricky and/or very nuanced in some instances, like if dinner was smaller (fewer calories) but more protein-rich, for example… but in order to include 5 relevant studies and not bore you to death, you’ll have to check the full texts for those details.

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Nutrient Partitioning: …a *very* high protein diet.

Or: what happens when you eat a ton of protein?

RDA: 0.8 g/kg

Active individuals: 1.2-2.0 g/kg (via ISSN)
Comment (1): I think sedentary, physically inactive, and non-exercisers should be in this range to offset disuse atrophy.  And they should exercise.
Comment (2): Do athletes really need more protein than non-athletes?  They have exercise, a powerful anabolic stimulus.  More protein may improve performance or body composition, but they might not *need* it, in terms of nitrogen retention… there’s probably a study on this.

NEED =/= OPTIMIZATION

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Melatonin is the chemical expression of darkness.

Melatonin is secreted from the pineal gland, the seat of the soul, the third eye.   Pinealectomy induces circadian arrhythmia and has interesting effects on adipose tissue biology.

Exhibit A.  In 2004, Alonso-Vale and colleagues showed that 6 weeks after pinealectomy, [melatonin-deficient] rats subjected to fasting exhibited an impaired energy conservation response.  That is, they lost more weight and significantly depleted their adipocytes:

pinealectomy

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Pharmaceutical-grade circadian manipulation.

BMAL1 and CLOCK, ‘positive’ regulators of circadian gene expression, activate transcription of the negative regulators Per, Cry, and Rev-erb.  PER and CRY inhibit BMAL1 and CLOCK, whereas Rev-erb inhibits Bmal1.  It is said that Rev-erb is “an important link between the positive and negative loops of the circadian clock.”  You don’t really need to know any of that to follow this blog post.

circadian genes

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