We evolved on Earth, with regular 24-hour “circadian” cycles; abandoning them is incompatible with survival. Natural Selection does not look upon this favorably.
The first time this was discussed, HERE, they ablated the master circadian clock, the SCN, which made the animals arrhythmic with a bollixed circadian period:
resulting in significantly increased predation in the wild:
Posted in angiotensin, Bromocriptine, Cabergoline, chronopharmacology, circadian
Tagged circadian rhythm, melatonin, mortality, Paleo, sleep
Over the course of human evolution, diets varied widely over time, seasons, geography, etc., ie, we can obviously thrive on many different dietary patterns… but the light/dark cycle was there the entire time. Why is this not the most important talking/debating point? Why do people think humans need one particular diet but can ignore circadian rhythms?
Because everyone’s still fussing about carbz and what we are “designed to eat”
*smh*
see also: “Lights Out!” by T.S. Wiley
Posted in Advanced nutrition, angiotensin, Bromocriptine, Cabergoline, chronopharmacology, circadian, diet, Dopamine, Ketosis, melatonin, sleep, Sun, vasopressin
Tagged calories proper, carbs, circadian rhythm, diet, insulin, ketosis, nutrition, Paleo
This study was pretty interesting.
Three groups of women:
1) normal weight
2) gynoid obesity (stores more fat in hips & butt), defined by WC/HC < 0.85
3) android obesity (stores more fat in belly, which is rare in women), defined by WC/HC > 0.85
First, we get confirmation that insulin sensitivity (IS) is better in morning than evening. But then we get these interesting glucose tolerance curves:
Fat stored in your hips & butt is thought to be healthier than that stored in your belly region. This is confirmed here. Gynoid obesity, while exhibiting an attenuated AM/PM difference, was able to restore euglycemia by the end of the experiment at both time points. Ie, gynoid obesity selectively improved IS in the evening.
Android obesity, which is more nefarious than gynoid (also confirmed here), had a similar though not as robust effect in the evening but deteriorated IS in the morning.
One potential interpretation: it’s better to have a little extra fat stored in your hips and butt than to be lean or have belly fat. However, I have a qualm with that interpretation. Healthy people show a robust circadian difference in glucose tolerance. Just as insulin resistance (IR) is an accepted physiological phenomenon observed in some ketogenic dieters, I view this circadian difference, also, as physiological.
Posted in Advanced nutrition, chronopharmacology, circadian, diabetes, diet, Dietary fat, Dopamine, insulin, liver, muscle, TPMC
Tagged Atkins, body composition, calories proper, carbs, circadian rhythm, diabetes, insulin, ketosis, nutrition, obesity
This article isn’t about alcohol tolerance. It’s about your liver.
Tl;dr: with a basic knowledge about alcohol metabolism and ketoadaptation, drinking on keto gives me pause.
It might be nothing, but it gives me pause.
Alcohol is metabolized primarily by alcohol dehydrogenase, producing acetaldehyde and reducing equivalents as NADH. This pathway produces energy.
Or more specifically, ketone monoesters and carbs. Literally, this study was a high-dose ketone monoester supp sans caloric or carb restriction. I know, weird right?
Non sequiter nutrition notes, #context, etc.:
1) ketone esters =/= ketone salts. Ketone salts are either sodium or potassium-dominant. Ketone esters are essentially salt-free. Possibly helpful background reading here.
2) nutritional ketosis =/= starvation ketosis =/= ketone supp ketosis. Because #context.
Starvation ketosis, but not nutritional ketosis, is muscle-sparing. Ketone supps sans carb restriction might be.
3) the theory of ketone supps for sport is: 1) ketones are an energetically favorable fuel; and 2) they’ll spare glycogen, theoretically allowing prolonged duration of moderate-to-high intensity performance. Adding in carbs will likely further this.
4) I have no studies to support this, but the idea of ketone supps in the #context of high carb doesn’t sit will with me. Seems like high levels of both substrates = mitochondrial overload and oxidative stress. Maybe.
5) there’s a gradient of fuel use during exercise:
-explosive power: creatine, anaerobic
-high intensity: glycogen, anaerobic
-low intensity: fatty acid oxidation, aerobic
But it’s a gradient with a lot of overlap, and ketoadaptation further blurs the lines.
Posted in Advanced nutrition, Dietary fat, endurance, Energy balance, Exercise, fat, insulin, Ketosis, muscle, Protein, TPMC
Tagged calories proper, carbs, diet, energy balance, exercise, fat, insulin, ketogenic, ketones, ketosis, muscle, nutrition, sugar
The circadian proteins Bmal and casein kinase (CK) enhance and degrade Period (PER), respectively, by completely different mechanisms. Both are necessary, but at different times of day… #context
Gross oversimplification: the Bmal party is kicked off in the morning by LIGHT, and acts to increase PER by night (among many, many other things). As the day progresses, REV-ERB the Repressor slowly shuts down Bmal, so that peak PER occurs in the evening and doesn’t carry over until the next morning. GSK3b activates REV-ERB the Repressor. Lithium puts the system in fast forward, leading to phase advance* and ZZZ’s when timed right, at night… I think
Posted in angiotensin, Bromocriptine, Cabergoline, chronopharmacology, circadian, diabetes, Dopamine, insulin, melatonin, mortality, Sun, vasopressin, Vitamin D
Tagged carbs, circadian rhythm, insulin, ketosis, melatonin, nutrition
Recent comments about FASTER have upgraded this study to “the only long-term study on fat-adaptation.” Needless to say, I disagree. Again.
Side note: FASTER had no randomization or intervention (ie, confounded by selection bias, among others); they basically recruited long-term low carb & high carb ultra-endurance runners and measured the stuffings out of ’em.
Ultimately, they showed a very high maximal fat oxidation rate in low carb ultra-runners, 1.5 grams per minute. This is important because MAXIMAL HUMAN FAT BURNING CAPACITY
In previous studies on SAD (Standard Athletic Diet haha), maximal fat oxidation at similar VO2max% has been reported to be much lower, <1 g/min (eg, Hetlid et al., 2015 and Volek et al., 2016).
Dr. Johnson’s recent paper is nothing short of a monster. They did a TON of experiments. Here, I only want to focus on one aspect.
The insulin-obesity hypothesis in a nutshell (very oversimplified): more insulin = more fat mass and vice versa.
I know I know, it was mice fed standard rodent chow, but also included models relevant to human biology like reduced insulin and caloric restriction, which may reflect certain aspects of ketogenic diets and intermittent fasting… and some of the results actually do reflect what happens to humans. Some.
Posted in Advanced nutrition, diet, empty calories, Energy balance, insulin, Ketosis, Leptin, TPMC
Tagged body composition, calories, carbs, diet, energy balance, energy expenditure, insulin, ketogenic, nutrition, obesity
Study: a handful of average-bodied Crossfitters in their mid-30’s were recruited and told to either: 1) keep doing what they’re doing; or 2) go full keto. Crossfit 4x/week. Strength testing before and after 6 weeks (Gregory et al., 2017).
I’ll start with the best part: KETOADAPTATION IS A REAL TRUE THING THAT WORKS (P<0.05). Otherwise, this group’s performance would’ve plummeted. It is known.
The performance test was time to complete a 500-meter row, 40 body weight squats, 30 abdominal mat sit-ups, 20 hand release pushups, and 10 pull-ups.
Tl;dr: both groups knocked about a half a minute off their time!
The key here is duration: 6 weeks of ketogenic dieting is adequate to restore performance back to baseline. <3 weeks is not.
Here’s the downside (sort of):
Basically, the keto group dropped carbs and failed to compensate by upping other calories. I know I know, spontaneous ad lib appetite reduction, but this is a study on PHYSICAL PERFORMANCE.
And in further support of “muscle growth sans carbs,” keto dieters upped protein by 15% and this still wasn’t enough to compensate for the reduction in carbs/insulin: they still lost a bit of lean mass (NS). Imagine if they hadn’t increased the brotein? yikes
so basically, they lost body fat because CICO and retained lean mass because exercise and protein haha jk
Admittedly, it was cool to see the body comp changes, but we know fat loss eventually plateaus and people start eating maintenance calories again (maybe a bit more if Ebbeling can be believed). And this is where they remain for the rest of their lives (hopefully). So at 6 weeks, they were still losing weight, nowhere near where they’re going to be for the rest of their lives, but THAT’s where I’d like to see performance testing (ie, at a stable body weight). Don’t get me wrong, I hate myself in advance for making this critique: the researchers should’ve pushed more calories in the keto dieters bc this is a confounder in a study on PHYSICAL PERFORMANCE… but this doesn’t really matter in the big scheme of things because Blackburn’s group did that and showed the results were the same haha
On another note, I don’t think people should expect an additional performance boost from being more ketoadapted (or more fat-adapted or whatever), primarily because whether the study is 3 weeks or 6, performance never really gets better than baseline in experienced athletes. With more advanced training techniques, sure (and I think this is common), but not more keto- or fat-adaptation.
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Posted in Advanced nutrition, diet, Dietary fat, Energy balance, Ketosis, muscle, Protein, TPMC
Tagged Atkins, body composition, calories proper, carbs, energy balance, energy expenditure, exercise, insulin, ketogenic, ketones, ketosis, muscle, nutrition, protein
Basically, this much is pretty obvious now: LIGHT and food in the morning + darkness after sunset = proper circadian entrainment. But the how is pretty cool; LIGHT affects different biochemical pathways at different times of the day, which is how it can either advance or delay your circadian phase.
LIGHT entering the eyes is perceived by ipRGCs which then dish out glutamate and PACAP. These mediators go on to activate receptors in the SCN (the “Master Clock”).
Depending on the time of day, glutamate and PACAP affect different pathways.
Posted in Advanced nutrition, angiotensin, Bromocriptine, Cabergoline, chronopharmacology, circadian, Dopamine, Ketosis, Leptin, melatonin, nicotine, Sun, vasopressin, Vitamin D
Tagged circadian rhythm, melatonin