I’m totally cool with keto, honestly! but still don’t really like seeing stuff like the above graphic and people interpreting it to mean “KETO IS MUSCLE-SPARING.”
Warning: this post isn’t #Paleo Certified™. It’s more about convenience, choosing the lesser evil.
Quest Nutrition led the charge in low carb, high protein, fibre-rich bars. “Fibre-rich” is really the key in allowing a bona fide “low carb” bar with shelf-stability and decent texture. Sugar alcohols have also been used in some, but due to the high incidence of maltitol-induced GI discomfort, ymmv. But in general, you need one or the other to provide bulk and keep it together (except Epic Bars, which use black magic).
For the most part, the new bars have basically copied Quest’s formula with some new flavors.
Disclaimer #1: I’m a whole foods guy. Not really #Paleo™, but when it comes to people’s actual lifestyles, I recognize convenience is a huge factor… and selecting the lesser evil is frequently the best option — eg, you can store a couple LC protein bars in your office, car, etc.; not so much with hard-boiled eggs or other protein-rich foods… and these options are WAY better than many other snacks or “fast-foods” out there.
Disclaimer #2: yeah, I keep a few of these bars in my office, just in case…
Quest recently switched from isomaltosaccharides to soluble corn fibre (SCF), which will likely impact GI effects. YMMV! Isomaltosaccharides are cool, but I’m not prepared to say they’re superior to SCF for everyone, in every #context (personally, for the ‘biome, I prefer brassicas, alliums, the gristly bits, galactooligosaccharides, et al.).
[it’d awesome if Bi2Muno would collaborate with one of these companies]
In these n00bs to the protein bar market, some of the biggest differentiating factors are cost, net carbs, ratio of fibre to sugar alcohols, flavor profiles, etc.
I came across a recent study on a mouse model of Angelman Syndrome (an epigenetic disorder), and wasn’t surprised to learn there’s a strong circadian component to it. Epigenetics are one of the main ways circadian rhythms are programmed.
In this case, the circadian connection is more direct.
Angelman Syndrome (AS): you inherit 2 pairs of each gene, one from Mom and one from Dad. In some cases, one of the copies is silenced via epigenetics and you’re basically just hoping the other one is in good shape. In the genetically relevant region in AS, the paternal copy is silenced and the maternal copy does all the heavy lifting, but in AS, the maternal copy is mutated or absent, so none of the genes in this region are expressed.
Interestingly, scientists found that one of the genes, Ube3a (an ubiquitin ligase), is involved in regulating Bmal1, a core circadian gene (Shi et al., 2015) . And mice with a silenced paternal Ube3a and mutant maternal Ube3a exhibit many of the same circadian symptoms of children with AS. They don’t mimic all of the symptoms as there are many other genes in this region. But both show circadian abnormalities.
Prader-Willi Syndrome (PWS) is the epigenetic opposite: same region of DNA, but silenced maternal copy and mutant or absent paternal copy. This disorder is characterized by massive obesity and low muscle mass (among other things).
While reading about this disorder, I was taken aback with how the obesity was explained.
“Insatiable appetite” (Laurance et al., 1981), although from what I can gather, these children would develop massive obesity even if they were fed cardboard. Some studies even showed no change in food intake and/or energy expenditure (eg, Schoeller et al., 1988), which led some researchers to publish entire papers about how these children must be lying and/or stealing food (eg, Page et al., 1983) .
Further, other researchers even explained their obesity was due to an inability to vomit (Butler et al., 2007).
THEY’RE OBESE BECAUSE THEY’RE NOT BULEMIC.
AYFKM?
When these kids gain weight, it’s nearly all fat mass; when they lose weight, it’s nearly all muscle [shoulda been a BIG hint]… this even led some researchers (who detected no change in fat mass after significant weight loss) to conclude that their techniques to assess body composition must not be valid in this population because: surely, they must’ve lost some fat mass like normal people do.
THEY FAILED TO CONSIDER THIS IS AN EXTREME CIRCADIAN MISMATCH DISORDER IN NUTRIENT PARTITIONING
It was actually painful to read: these kids are being accused of stealing food and not vomiting because that’s the only way to explain it.
NO IT’S NOT, SCIENCE.
They can be forced into losing fat while maintaining some muscle with an extreme protein-sparing modified fast (eg, Bistrian et al., 1977)…
A few research groups have considered the possibility it’s a hormonal disorder, and some fairly long-term studies with GH replacement have shown promising results (eg, Carrel et al., 1999).
Prader-Willi Food Pyramid. Wait, wut? O_o
Some have even speculated involvement of leptin (eg, Cento et al., 1999), although this hasn’t been followed-up on.
Disclaimer: I don’t know the cure or best treatment modality for Prader-Willi, although given the strong circadian component in its sister condition, Angelman’s Syndrome, I strongly believe this avenue should be explored (in combination with the seemingly necessary hormonal corrections, which have been the only successful interventions yet). “Diet” doesn’t work; these kids aren’t obese because they’re stealing food or failing to vomit. Interventions strictly targeting CICO have massively failed this population.
Side note: in the Angelman Syndrome mouse model, *unsilencing* the paternal copy worked… maybe the same could work in PWS (and/or other forms of obesity)…?
Evidence supporting potential circadian-related treatment modalities for PWS:
A Prader-Willi locus IncRNA cloud modulates diurnal genes and energy expenditure (Powell et al., 2013)
Magel2, a Prader-Willi syndrome candidate gene, modulates the activities of circadian rhythm proteins in cultured cells (Devos et al., 2011)
Circadian fluctuation of plasma melatonin in Prader-Willi’s syndrome and obesity (Willig et al., 1986)
And the connection with LIGHT:
Artificial light at night: melatonin as a mediator between the environment and the epigenome (Haim and Zubidat, 2015)
Circadian behavior is light re-programmed by plastic DNA methylation (Azzi et al., 2014)
PWS is much worse than just nutrient partitioning (seriously, just spend a few minutes on any Prader-Willi support forum or this; maybe it is an appetite disorder, but given the data on weight gain [mostly fat mass] and weight loss [mostly muscle mass], it seems far more likely a circadian disorder of nutrient partitioning),
but that component jumped out at me; more specifically, despite the only positive results coming from non-dietary interventions, researchers were still all “#CICO.”
“Lean meat, sugar-free Jello, and skim milk”
FFS
Circadian biology, hormone replacement [where appropriate], and figure out if any specific diets help. PMSF/CR doesn’t work unless “refrigerators and cabinet pantries are locked shut.”
Maybe this applies to other forms of obesity, too.
Maybe.
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Affiliate links: KetoLogic for keto-friendly shakes, creamers, snacks, etc. And get 15% off your ketone measuring supplies HERE.
Still looking for a pair of hot blue blockers? TrueDarkis offering 10% off HERE and Spectra479is offering 15% off HERE. If you have no idea what I’m talking about, read this then this.
If you want the benefits of ‘shrooms but don’t like eating them, Real Mushrooms makes great extracts. 10% off with coupon code LAGAKOS. I recommend Lion’s Mane for the brain and Reishi for everything else.
Similar to the glycemic index, which is an estimate of the rise in blood glucose after eating a particular food, the insulin index is an estimate of the rise in insulin after eating a particular food. In general, these indices are obvious: processed carbs have high glycemic and insulin indices, whereas whole foods are lower. Some exceptions are things like dairy and lean meat, which induce more insulin than you’d expect given to their low carbohydrate content…
STORY TIME
When some protein-rich foods were discovered to induce insulin secretion, people thought this information might help type 1 diabetics more accurately calculate their insulin dose. Interesting rationale, worth testing.
Tl;dr: it didn’t work very well.
More of the protein-derived amino acids may have been incorporated into lean tissue, but the extra insulin load ended up causing hypoglycemia more often than not. Hypoglycemia is acutely more harmful than hyperglycemia, and is still quite harmful in the long-term. Some studies on incorporating the insulin index for type 1 diabetics are mixed, ie, increased or no change in risk of hypoglycemia, but no studies show it reduces the risk.
Intermittent fasting (IF) is not a universal panacea, regardless of whether you’re not eating anything at all for a few days each week/month or just restricting your feeding window to a few hours per day.
Some protocols, eg, 20h fasting every second day, significantly improve insulin sensitivity in adipose tissue (Halberg et al., 2005). This is expected to make fat gain easier, and while this wasn’t meant to be a study on body composition per se…
After just a few weeks, things weren’t changing in a good way (NS).
^^^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.
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.”
Dietary protein “requirements” are some of the most context-dependent nutrient levels to decipher, and depend largely on energy balance and even meal frequency.
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.
@CaloriesProper Really? Drawing conclusions based on a 2 week study of 11 pts?
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).”
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).
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.
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.”
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.
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).
Affiliate links: KetoLogic for keto-friendly shakes, creamers, snacks, etc. And get 15% off your ketone measuring supplies HERE.
Still looking for a pair of hot blue blockers? TrueDarkis offering 10% off HERE and Spectra479is offering 15% off HERE. If you have no idea what I’m talking about, read this then this.
If you want the benefits of ‘shrooms but don’t like eating them, Real Mushrooms makes great extracts. 10% off with coupon code LAGAKOS. I recommend Lion’s Mane for the brain and Reishi for everything else.
Is it possible to improve the amplitude and resiliency of your circadian rhythms? Is this desirable? Yes and yes, I think.
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.
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
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):
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).
led the charge in low carb, high protein, fibre-rich bars. “Fibre-rich” is really the key in allowing a bona fide “low carb” bar with shelf-stability and decent texture. Sugar alcohols have also been used in some, but due to the high incidence of maltitol-induced GI discomfort, ymmv. But in general, you need one or the other to provide bulk and keep it together (except 
, which use black magic).
would collaborate with one of these companies]
(an epigenetic disorder), and wasn’t surprised to learn there’s a strong circadian component to it. Epigenetics are one of the main ways circadian rhythms are programmed.
(PWS) is the epigenetic opposite: same region of DNA, but silenced maternal copy and mutant or absent paternal copy. This disorder is characterized by massive obesity and low muscle mass (among other things).
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:
