Category Archives: Energy balance

Saturated fat, cholesterol, and carbohydrates

“You catch more flies with honey…”

^^^good policy in general, but especially for debating in the realm of nutritional sciences.

 

A short while back, Nina Teicholz discussed low carb ketogenic diets and plant-based diets with John Mackey.  Although I disagree with the dichotomy (keto vs. plant-based), it’s well-worth a watch:

 

 

Three topics that could not be avoided in such a discussion: saturated fat, cholesterol, and carbohydrates.

 

 

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Artificial light regulates fat mass: no bueno.

“despite not eating more or moving less”

We’ve seen this time and time again: LIGHT IS A DRUG.

 

above quote is extrapolated from this rodent study: “Prolonged daily light exposure increases body fat mass through attenuation of brown adipose tissue activity.”

 

Artificial light impacts nearly every biological system, and it doesn’t even take very much to have an appreciable effect (think: checking your smart phone or watching a television show on your iPad in bed at night).  In this study, adding 4 hours to the usual 12 hours of light slammed the autonomic nervous system, disrupting sympathetic input into brown adipose leading to a significant increase in body fat  “despite not eating more or moving less.”

 

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OmniCarb

Why Low Carb?

OmniCarb (Sacks et al., 2014)

Study design & results in a nutshell:

5 weeks, low(ish) vs. high carb (40 vs. 58%) with the calorie difference split between protein (23 vs. 16%) and fat (37 vs. 27%).  In other words, the low(ish) carb diet was higher in protein and fat.  And there was 2 versions of each diet —  a high and low glycemic index.  Lots of crossing over; all in all, weak intervention but decent study design & execution.

Aaaand nothing drastic happened.  Goal was insulin sensitivity, not weight loss.

 

glucose and insulin

 

Important points:

1) The participants were relatively healthy at baseline.  Anyone on meds was excluded.  Average BMI 32.  Mostly educated non-smokers.  This population is expected to respond reasonably well to any diet (wrt body weight… see next point).

2) “Calorie intake was adjusted to maintain initial body weight.”

^^^this really knocks the wind out of low carb. One of the big benefits of cutting carbs is spontaneous appetite suppression –- two points here: 1) this effect is most prominent in obese IR; and 2) it is more relevant to weight loss.  By not targeting insulin resistant and/or type 2 diabetics, and feeding specifically to prevent weight loss, I ask you this: Why Low Carb?

3) the biggest difference between the two diets was carbs (45% higher in low[ish] fat group), but the biggest difference from baseline, was protein in the LC group (53% increase).  In other words, the Low Carb group had their carbs decreased from 50 to 40% of calories. *meh*

4) Body composition wasn’t assessed; so even if LCHP induced nutrient partitioning and improved body comp, we wouldn’t know it.

5) Everyone was eating cereal or oatmeal for breakfast, bread with most meals, and pasta or rice for dinner.  What did you expect?  Really?

REALLY?

Prior posts in what seems to be developing into a series of rants:
2 New Diet Studies
CICO and rant 

 

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Circadian phase: role of diet

Circadian phase advance: going to bed earlier, waking up earlier.  Blue blockers at sunset, bright light at sunrise.  Flying east.  Autumn.

Circadian phase delay: staying up late, sleeping in.  Flying west.  Spring.  Using smart phones, tablets, and iPads in bed at night.  Light pollution.

Relative to adolescents, infants and children are circadian phase advanced.  This is part of what is fueling the movement to delay high school start times.  Kids are mentally better prepared to work later in the day.  With early school start times, performance is down in the morning, but they kill it on video games after school.  Delaying start time by an hour won’t totally fix this, but could help.

Edit: it seems like a similar movement is happening for adults, too – ie, starting work an hour later.

I’m not saying everything healthwise deteriorates with age, but the gradual circadian phase delay that occurs with aging and overusing blue light-emitting devices at night might not be a good thing.  If a particular diet can promote phase advance, why not? (at least it’d be countering the phase delay).

 

 

Possible role of diet

In the top half of the figure below, it’s mice fed a “normal diet (ND) (high carbohydrate)” (Oishi et al., 2012).  During normal “light dark (LD)” conditions, movement and feeding is concentrated in the active phase.  When the lights are permanently turned off in “dark dark (DD)” conditions, the free-running circadian clock begins to shift slightly forward (phase advance), but nothing drastic.

 

Phase advance high protein diet

 

In the bottom half of the figure, during normal LD conditions the mice are switched to a low carb, high protein diet.  Note how activity shifts leftward (phase advance) during the LD condition.  When low carb, high protein-fed mice are then switched to DD, we can see a clear circadian phase advance.

 

High protein metabolism

 

Low carb, high protein-fed mice ate more but didn’t get fat; physical activity and body temperature were unchanged.  But this post isn’t about that.  Gene expression of key circadian transcription factors in liver and kidney exhibited phase advances.

The next figure is study to the one above, although instead of switching to a low carb, high protein diet, the mice were switched to a low carb, high fat diet (Oishi et al., 2009).

Note the similarity of control (high carb diet) mice: gradual phase advance when switched to DD:

 

Ketogenic circadian phase

 

The phase advance is markedly enhanced in low carb, high fat-fed mice.

The circadian regulation of activity is similarly affected by low carb, high protein, and low carb, high fat diets.  What do those two diets have in common?

A bit of a stretch? carbohydrate restriction mimics some aspects of avoiding artificial light at night and being young: phase advance.  Whether the carbs are replaced with protein or fat doesn’t seem to matter in this aspect.

 

Wanna know what else can do this?  FOOD.  The food-entrainable oscillator (FEO) kickstarts circadian rhythms.  Rodent studies have shown that timed feeding, regardless of the actual time, consistently realigns the circadian expression of numerous genes (eg, Polidarova et al., 2011 and Sherman et al., 2012).

So what’s the hack?  Food: do more of it, earlier in the day.  Phase advance.  Kind of like avoiding artificial light at night or being young.

 

Oh, and mice exposed to dim light at night (who are pretty much metabolically screwed)? phase DELAYED (Fonken et al., 2010).

 

Dim light at night phase delay

 

 

 

calories proper

 

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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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Pharmaceutical-grade circadian enhancement?

Is it possible to improve the amplitude and resiliency of your circadian rhythms?  Is this desirable?  Yes and yes, I think.

Go the fuck to sleep.png

 

Introducing, the aMUPA mice (Froy et al., 2006).  What you need to know about ’em: they have very robust circadian rhythms.  How is this assessed?  Take some mice acclimated to their normal 12 hour light-dark cycle (LD) and place them in constant darkness (DD).  Then take liver biopsies and measure circadian genes to see how well they still oscillate throughout the dark day; this is also known as the free-running clock, and it craps out differently in different tissues depending on a variety of factors.  Most of the time, however, it’ll run for a few days in the absence of light.  Circadian meal timing also helps to hasten re-entrainment.

Note in the figure below: 1) there are two distinct lines of aMUPA mice; and 2) both exhibit a greater amplitude in circadian oscillations during free-running, or DD conditions.

strong circadian rhythms

 

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Evolution stole this dude’s circadian rhythm

I got a laugh out of this one; not for the actual content, but because of how the authors worded their findings.  They sure love their fishies.

We have two very closely related fish, both Mexican tetra, Astyanax mexicanus, one with eyes who lives on the surface, and another who’s blind and lives in dark caves (“Pachon”).  It’s thought that they were the same species one day; divergent evolution.

 

note: eyeless

note: eyeless

The blind ones are circadian arrhythmic (Moran et al., 2014).  Surface-dwellers are more active during the day than night (blue line, left figure below), and their free-running circadian clock maintains this in the absence of photic input (blue line, right figure).  The blind ones, on the other hand, exhibit no circadian rhythm in the light or dark (orange lines):

 

Circadian rhythm metabolism

 

Cave-dwellers are circadian arrhythmic.  This is both in their natural photoperiod (ie, darkness) and in light-dark conditions (which is technically an environmental mismatch, but since they’re eyeless, it doesn’t really matter).

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“Afternoon diabetes” and nutrient partitioning

Don’t exacerbate afternoon diabetes with afternoon carbs.

Skeletal Muscle
As discussed previously [at length], insulin sensitivity in skeletal muscle follows a circadian pattern: starts out high in the morning and wanes throughout the day.

Diurnal variation in oral glucose tolerance: blood sugar and plasma insulin levels, morning, afternoon and evening (Jarrett et al., 1972)

 

impaired circadian glucose tolerance in the morning

 

Diurnal variation in glucose tolerance and insulin secretion in man (Carroll and Nestel, 1973)

Circadian variation of the blood glucose, plasma insulin and human growth hormone levels in response to an oral glucose load in normal subjects (Aparicio et al., 1974)

Adipose Tissue
And insulin sensitivity of adipose tissue goes in the opposite direction: starts out low, and increases as the day progresses.

Diurnal variations in peripheral insulin resistance and plasma NEFA: a possible link? (Morgan et al., 1999)
The studies were standardized for a period of fasting, pre-test meal, and exercise… Following insulin, NEFA fell more slowly in the morning (149 uM/15 min) than in the evening (491 uM/15 min).

Diurnal variation in glucose tolerance: associated changes in plasma insulin, growth hormone, and non-esterified fatty acids (Zimmet et al., 1974)
Adipose tissue insulin sensitivity is greater in the evening.  FFA are higher, and get shut down more rapidly, after a carb meal in the evening.

Summary: to minimize blood glucose excursions and proclivity for fat storage, eat more calories earlier in the day; this is circadian nutrient timing.  And according to the Alves study, a low-carb protein-rich dinner best preserves lean tissue during weight loss.

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2 New Diet Studies

*ugh* journalists

I’m talking to you, Mandy Oaklander!

Regarding the new low carb vs low fat study, she writes: “Popular diets are pretty much the same for weight loss, study finds.

Effects of low-carbohydrate and low-fat diets: a randomized control trial (Bazzano et al., 2014)

Further, “An earlier study in Annals of Internal Medicine did find that low-carb dieters lost slightly more weight than low-fat dieters after one year. The study today reached similar conclusions, but the differences in weight loss were not significant.”

Perhaps Mandy just doesn’t realize there’s a difference between significant, as in “meaningful,” and significant, as in “P<0.05.”  Pro-tip: you can tell them apart relatively easily, because the latter is usually accompanied by a cute little asterisk.  For example, the differences in weight loss were quite statistically significant (P<0.05):

Bazzano BW
She goes on to say “After a year follow-up, some of those pounds crept back for people on both diets…”

To that I say: yeah, but fat mass continued to decline in those on the low carb diet, meaning some of that weight re-gain was muscle:

Bazzano FM

So, between 6 and 12 months, carbs and calories were creeping up in the LC group, yet fat mass was still declining.  Perhaps this way of eating improved their metabolism, or restored the ability to effectively partition nutrients.

***in real-time: at this point, I realize that Mandy was actually talking about the other study, which she was covering accurately.  Sorry, Mandy!***

Bazzano PA

…so maybe the low-carb (LC) diet improved muscle mass because it was also high protein? …perhaps, but 19% vs 24% (71 vs 85 grams) isn’t a very big difference.  Alternatively, since the LC group really just maintained absolute protein intake (86 grams at baseline, 85 at month 12), whereas low-fat (LF) dieters decreased (86 grams at baseline, 71 at 12 months); perhaps this is why LF lost muscle mass..?  Still, those changes in protein intake are small, and I think people can be too quick to chalk up the benefits of LC to “high protein.”

In sum, this is actually one of the more “pro” LC studies.  And it wasn’t even a huge difference in carbs: 198 vs 127 grams/d at month 12 (54% vs 34%).  Big difference in fat mass; and CRP, a marker of inflammation, even declined in the LC group.

Low fat diet advocates have been giving me headaches for years… the low fat diet caused headaches (P<0.05):

Adverse Events 1

 

 

Adverse Events 2

The study Mandy was actually talking about: Comparison of weight loss among named diet programs in overweight and obese adults: a meta-analysis (Johnston et al., 2014)

It was a meta-analysis, which is just about the only type of study capable of taking down LC.

 

 

…but at least it had this cool chart (modified):

cool chart (modified)

cool chart (modified)

 

*ugh* scientists

crap

The macro’s in “Low fat” overlap with “Moderate,” implying “Low carb” is “EXTREME”  …the authors’ bias is subtle, I’ll give ‘em that, but I’m getting too old for this.

Dear Obesity Researchers,

If you want to design a study showing a low fat diet is as good as low carb for fat loss, here’s your best bet: recruit young, exercise-tolerant overweight patients who aren’t on any meds.  PROOF (see Ebbeling study).  Or find 10 similar ones and write up a pro-LF meta.

If you want to show low carb is better, recruit patients with obesity.

 

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Cyclical ketosis, glycogen depletion, and nutrient partitioning

Meal & exercise timing in the contexts of “damage control” and nutrient partitioning are frequent topics on this blog.  I generally opt for a pre-workout meal, but nutrient timing hasn’t panned out very well in the literature.  That’s probably why I’m open to the idea of resistance exercise in the fasted state.  A lot of pseudoscientific arguments can be made for both fed and fasted exercise, and since a few blog posts have already been dedicated to the former, this one will focus on the latter.

The pseudoscience explanation is something like this: since fatty acids are elevated when fasting, exercise in this condition will burn more fat; and chronically doing so will increase mitochondria #.  The lack of dietary carbs might enhance exercise-induced glycogen depletion, which itself would bias more post-workout calories toward glycogen synthesis / supercompensation.  Much of this is actually true, but has really only been validated for endurance training (eg, Stannard 2010, Van Proeyen 2011, & Trabelsi 2012; but not here Paoli 2011)… and the few times it’s been studied in the context of resistance exercise, no effect (eg, Moore 2007 & Trabelsi 2013).  However, there are some pretty interesting tidbits (beyond the pseudoscience) which suggest how/why it might work, in the right context.

Exercising fasted or fed for fat loss?  Influence of food intake on RER and EPOC after a bout of endurance training (Paoli et al., 2011)

John Kiefer, an advocate of resistance exercise in the fasted state, mentioned: “the sympathetic nervous system responds quicker to fasted-exercise. You release adrenaline faster. Your body is more sensitive particularly to the fat burning properties of adrenaline and you get bigger rushes of adrenaline.”

Much of this is spot on.  That is, ketogenic dieting and glycogen depletion increase exercise-induced sympathetic activation and fat oxidation (eg, Jansson 1982, Langfort 1996, & Weltan 1998).

The question is: can this improve nutrient partitioning and physical performance?  Magic 8-Ball says: “Signs point to yes.”  I concur.

Contrary to popular beliefs, glycogen depletion per se doesn’t harm many aspects of physical performance.  A lot of fuel systems are at play; you don’t need a full tank of glycogen.

Effect of low-carbohydrate-ketogenic diet on metabolic and hormonal responses to graded exercise in men (Langfort et al., 1996)

High-intensity exercise performance is not impaired by low intramuscular glycogen (Symons & Jacobs, 1989)

Increased fat oxidation compensates for reduced glycogen at lower exercise intensities (eg, Zderic 2004), and ketoadaptation may do the same at higher intensities.

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