Tag Archives: ketogenic

The current state of affairs in nutri-Twitter

Rant.

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1) It’s almost as if you’re either:

a red meat-eating 110% keto-advocate

or

you think red meat and a ketogenic diet is harmful.

 

If you don’t say the diet is magical, the zealots will try to trick you into, or outright accuse you of saying it’s harmful.

Further,

 

2. And the protein/kidney debate re-surfaced again recently. To be clear: no studies have shown direct harmful effects of protein on kidney function. The studies cited by KDOQI are observational and on end-stage renal disease. Not mild kidney disease or slightly impaired renal function. If I had ESRD, I’d rather play it safe and not enroll in one of Jose Antonio’s high protein diet studies (~4.4 g/kg lol).

I’m pro-LC and HP but not anti-LF. Humans have thrived on a wide variety of diets over time regardless of macronutrient composition. Food quality seems more important in this context.

3. If ketones are muscle-sparing, then…

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CARBOTOXICITY [screaming face emoji]

Noxious Effects of Exaggerated Carbohydrate Intake (Kroemer et al., 2018)

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This blog post is about the above mentioned article. Disclaimer (qualm #1): it is very pro-low carb and refused to include any neutral or negative points about low carb. For example, had it been within the scope of the article, the authors may have said despite excluding the majority of carbohydrate-containing foods, low carb diets actually aren’t restrictive at all. In other words, this is not an unbiased review article.

 

 

Qualm #2: the authors say people have long-recognized the problems of lipid excess and it even has a name, “lipotoxicity.” But these revolutionaries thought the problems of carbohydrate excess need to be recognized so they coined the term “carbotoxicity.” Are we to believe these dorks never heard of “glucotoxicity” even though it was coined before lipotoxicity even was?!

The review is about the molecular, cellular, and neuroendocrine mechanisms that link a prolonged energy surplus to disease and accelerated aging. It doesn’t really distinguish how the energy surplus is established, specifically, but every now and then they throw out there “carbz.” Ignoring that, there are actually some pretty good points.

The history of dietary carbs had three major, transformative steps. The first was the transition from hunter-gatherers to agriculture which shifted the carbs from fruits, seeds, tubers, nuts, roots, and bulbs to a range of cereals (in Europe), rice (in Asia), corn (in Mesoamerica), and potatoes (in South America). And in Weston Price fashion, this was associated with an increase in dental cavities (probably more cause than correlation here).

Acarbose blocks carb digestion, D-glucosamine blocks glycolysis.

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The Current Status of the Ketogenic Diet in Psychiatry

Here’s when it’s important to measure your ketones (Bostock et al., 2017). Actually, this is one of the cooler aspects of keto: you don’t need to rely on FFQ’s or diet diaries or other unreliable methods to determine adherence. You just measure ketones directly — if they’re there, you’re adhering to the diet. And while this isn’t really important for body recompositioning purposes, it may matter for neuropsychiatric applications where the ketones themselves may be part of the MOA directly.

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Major limitations in the published studies on this: NOT MEASURING KETONES. If keto didn’t work and they didn’t report ketones, it’s hard to know if keto really didn’t work or adherence failure.

One more point before diving into the studies: rigid, strict adherence is very important here. One study showed efficacy in mild cognitive impairment, but adherence worsened with disease severity. In other words, the people who potentially stood to benefit the most were the least able to stick to the diet. This is why I’m open to coconut oil or medium chain triglyceride-supplemented low(ish) carb diets or even ketone supplements.

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Watch the Clock, Not the Scale

I’ve been known to say intermittent fasting is #weaksauce because most of the human studies show little or no effect and people frequently report being hungry (yes, even if LCHF). Human studies, not “n=1’s.”

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Well, now we know why. Time-restricted feeding (TRF) only really works when the feeding window is early (eTRF), as demonstrated by the recent Sutton study which showed, miraculously, great benefits achieved sans weight loss. Calories were strictly controlled in that study to prevent weight loss. AND when the participants were on eTRF, they actually reported less hunger in the evening.

 

 

We know from the studies by Jacobs and Hirsh that under ad lib AND isocaloric conditions, people lose more weight eating all their food for breakfast than those eating all their food for dinner.

 

 

That’s cuz metabolism is gimped at night. Lower metabolic rate and greater propensity to store fat.

Melatonin sensitizes the system, preparing it to optimally partition nutrients in the morning.

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The neuroprotective properties of ketone bodies.

There is some overlap between the metabolic effects of calorie restriction (CR) and ketogenic diets (Maalouf et al., 2009). A lot of the underlying mechanisms are related to mitochondrial quality and quantity, anti-apoptotic factors, and neurotrophic factors (eg, BDNF induced by ketosis).

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The influence of ketones on intermediary metabolism

Two studies: one on infusion of D-b-hydroxybutyrate at three different level producing up to 2 mM at the highest level (Mikkelsen et al., 2014); and one on ingestion of a ketone monoester (R-3-hydroxybutyl-R-3-hydroxybutyrate) producing ~3.2 mM (Myette et al., 2018). Both studies were relatively small (n = 6 and 20, respectively) yet interesting.

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Mikkelsen: mainly justified the use of exogenous ketones in T2DM because of their ability to suppress hyperglycemia and hyperlipidemia. And justified ’em in CNS disorders because adherence is poor in this population and goes downhill with increasing disease severity. They’re anti-ketone salts because: 1) the GI distress and salt load with doses required to get into the 2-3 mM range; and 2) they’re often racemic mixtures of D- and L-b-hydroxybutyrate (“D” is the endogenous one).

 

 

As expected, increasing the infusion dose linearly increased plasma bHB:

Further, as expected, brain uptake increased in parallel to plasma levels:

Interestingly, muscle uptake seemed to become saturated and not increase much further… this may be related to the “muscle-sparing effect of fat-derived fuels,” in other words, muscle is sparing ketones for the brain like it does during late starvation.

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ketones inhibit lipolysis

 

 

 

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Low carb diet. NAFLD.

An integrated understanding of the rapid metabolic benefits of a carbohydrate-restricted diet on hepatic steatosis in humans (Mardinoglu et al., 2018)

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Critique and analysis.

They did two very small (n=10 & n=7) 2-week long studies of low carb, high protein. Carb/fat/protein was 4/72/24 compared to 20/42/18 at baseline. There was no control group, so the results were compared to baseline.

 

 

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Isocaloric MCT-supplemented ketogenic diet may improve cognition in Alzheimer’s patients

Two-thirds of the time, it works half of the time 🙂

Yes, we all pretend to know the mechanism how ketones may improve cognition in MCI/Alzheimer’s, but we don’t. Nobody does.

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-Preferred fuel? kinda meaningless

-Niacin receptor? if so, where are the studies on niacins or even nicotinamide riboside (the latter is kind of unrelated, but should yield some niacin in vivo) (P.S. blog post on NR in the works).

-Epigenetics? Idk. Of those, I’d say probably all contribute somehow.

Ketogenic Diet Retention and Feasibility Trial #KDRAFT (Taylor et al., 2017)

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Ketone supps and physical performance

We’ve had a couple more studies on the various ketone supps: two esters (D-b-hydroxybutyrate-R 1,2-Butanediol Monoester and R,S-Butanediol Diacetoacetate) and one beta-Hydroxybutyrate sodium and potassium salts (KetoForce). We’ll call them Clarke, Burke, and Stewart so I don’t get Carpal Tunnel Syndrome typing them out each time. Technically, b-hydroxybutyrate isn’t really a ketone, but whatevs.

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“Clarke”

 

“Burke”

 

“Stewart” (this is actually a blend of the sodium “Na” and potassium “K” [not shown] salts)

 

Two studies on Stewart

Nutritional ketone salts increase fat oxidation but impair high-intensity exercise performance in healthy adult males (O’Malley et al., 2017)

“Ten healthy, recreationally active men.” The participants did a brief warm-up then a 150 km cycling time trial after receiving 24 g Stewart or salt-matched placebo.  Controlling for salt was cool, but Stewart has about as 5 kcal/g, so the placebo could’ve controlled for that somehow, with either fat or carb, or something… (probably wouldn’t have mattered anyway)

Results: blood beta-hydroxybutyrate reached about 1 mM, power output declined 7% and it took the keto group about 45 seconds longer to complete the time trial.

Oral beta-hydroxybutyrate salt fails to improve 4-minute cycling performance following submaximal exercise (Rodger et al., 2017)

“Highly trained cyclists.” Similar study design as McSwiney’s — drain the tank with 90 minutes cycling at 80% max then 4 minute maximal performance test. Same dose as above in 2 divided doses. Same issue with the control group.

Results: blood beta-hydroxybutyrate reached ~0.6 mM and there was a trivial (non-significant) increase in power. This is actually in line with my interpretation of McSwiney regarding the decline in power output before and after draining the tank; ketoadaptation and all that jazz.

 

One study on Burke

Ketone diester ingestion impairs time-trial performance in professional cyclists (Leckey et al., 2017)

“Internationally competitive elite cyclists.” Two doses of 20 g Burke then a 20-minute warm-up followed by a 31 km time-trial. Non-caloric placebo control, whereas Burke is estimated 4.7 kcal/g. They were well-fed and caffeinated.

Results: beta-hydroxybutyrate reached ~1.1 mM, time-trial took 2% longer, and power was reduced 3.7%.

 

One study on Clarke

Nutritional ketosis alters fuel preference and thereby endurance performance in athletes (Cox et al., 2016)

“High performance athletes.” This study was different: one group got a drink that was 40% Clarke and 60% carbs (by calories), the other drink was 100% carbs. Calorie-controlled. They cycled for an hour at 75% max (to drain the tank), then 30-minute time trial.

Results: this is the first one that worked. beta-hydroxybutyrate reached 2-3 mM and they made it 2% further during the time-trial.

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If you want the benefits of  ‘shrooms but don’t like eating them, Real Mushrooms makes great extracts. 10% off with coupon code LAGAKOS.

For my interpretation of these studies and an  explanation why I think the different keto supps had different effects (or if you just like what I do and want to support it), head over to Patreon! Five bucks a month for full access and there are many other options. It’s ad-free and you can cancel if it sucks 🙂

Also, I’m open to suggestions so feel free to leave a comment or email me directly at drlagakos@gmail.com.

Affiliate discounts: if you’re still looking for a pair of hot blue blockers, Carbonshade is offering 15% off with the coupon code LAGAKOS and Spectra479 is offering 15% off HERETrueDark is running a pretty big sale HEREIf you have no idea what I’m talking about, read this then this.

20% off some delish stocks and broths from Kettle and Fire HERE

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As if we needed another study about breakfast. Or 4.

Exhibit A. Participants were given ~30 grams of whey, casein, or carbs 30 minutes before bed (Kinsey et al., 2014). [side note: the closer it is to bedtime, the less food is needed to mess up your rhythms. Worded another way, if you’re gonna have a big dinner, the earlier the better]. The following morning, you guessed it, they weren’t hungry for breakfast. And they had higher insulin levels. FFS. Worded another way, light early dinner -> lower insulin and more hungry for breakfast, in the morning.

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Dopamine and breakfast.

Light and food in the morning.

Metabolism is gimped at night.

Exhibit B1. Expecting mothers: “Across the whole cohort, night-time, but not day-time, carbohydrate intake was positively associated with glucose concentrations after the glucose load and inversely associated with early phase insulin secretion (P < 0.05)” (Chandler-Laney et al., 2016).

 

 

Evening is not the best time to carb… but it’s not just carbs… and it affects infants, too.

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20% off some delish stocks and broths from Kettle and Fire HERE

If you want the benefits of  ‘shrooms but don’t like the taste, Real Mushrooms makes great extracts. 10% off with coupon code LAGAKOS.

For full access to all articles and more (or if you just like what I do and want to support it), head over to Patreon! It’s only three bucks a month and there are many other options. It’s ad-free and you and you can cancel if it sucks 🙂

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Sunlight, Meal Timing, and Circadian Rhythms.

we’re talking some serious epigenetics

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