Tag Archives: diet

The carb/insulin model of obesity was tested again, and it fared better this time.

Effects of a low carbohydrate diet on energy expenditure during weight loss maintenance: randomized trial (Ebbeling et al., 2018)

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This is another NuSi study designed to evaluate certain aspects of the carb/insulin model of obesity. Understanding the design of this study is critical to being able to properly evaluate the results.

Very important:

 

1. All food was provided, all the diets were healthy, and most people complied.

2. This was a very expensive study. They used great methods.

Study design: during the “Run-in diet,” everyone followed the same diet (C/F/P: 45%/30%/25%) at 40% caloric restriction in order to lose about 10% of their initial body weight.

Importantly, insulin sensitivity was assessed and this may have influenced what happened next, in the weight maintenance phase. I used to put a lot of weight on this theory — eg, the top 25% most insulin sensitive people will do better on low fat whereas the bottom 25% insulin sensitive people (the most insulin resistant, ie) will do better on low carb — this theory has fared better or worse depending on which study you look at. In this study, it did pretty well.

 

 

In the end, we had 38 people in the entering into the high carb arm of the weight maintenance phase and 43 on low carb.

Remember, they all lost weight on the same diet. Now they’re being fed enough to maintain body weight (low carb, moderate carb, or high carb) and we’re measuring things.

Really exciting stuff!

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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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Study: protein & seafood. They work!

I liked this study for a couple reasons:

Effect of combined use of a low(ish)-carbohydrate, high-protein diet with omega-3 polyunsaturated fatty acid supplementation on glycemic control in newly diagnosed type 2 diabetes: a randomized, double-blind, parallel-controlled trial (Liu et al., 2018)

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There were FOUR groups: 1) high-carb, low protein (HCLP, aka CONtrol group); 2) LCHP; 3) HCLP+n3; and 4) LCHP+n3. So, instead of just taking a group of people, putting them on LCHP+n3 and comparing the results to baseline, they actually controlled for the variables independently.

 

 

All groups were assign 30% fat and the protein was either 17% or 28%. THIS WAS CONFIRMED with serum urea nitrogen and you know how much I like biomarkers! n3 status of the n3 groups were confirmed with plasma n3’s and you know how much I like biomarkers!

Some more details on the study design…

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New study: very low carb diets don’t impair high intensity interval training (Cipryan et al., 2018)

Effects of a 4-week very low-carbohydrate diet on high-intensity interval training responses (Cipryan et al., 2018)

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Relevant study design details: 18 young, healthy, moderately-trained males. First, this was a study on exercise performance. Had it been on glucose management in patients with type 2 diabetes or obesity, this is not the population they would have selected. Second, they needed at least a moderately-trained population otherwise both groups would’ve made big n00b gainz which may have out-weighed any differences incurred by ketoadaptation in 4 weeks.

 

 

Third, 4 weeks is a good duration for this kind of study because maximal ketoadaptation occurs in about 3 weeks and doesn’t get stronger thereafter (gains seen beyond 3 weeks are more associated with training effects).

On to the dietary protocols, results, and 2 other relevant new studies… but for that, head on over to Patreon! Five bucks a month gets you full access and there are many other options. It’s ad-free and you can cancel if it sucks 🙂

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Dopamine regulates systemic glucose metabolism in humans

In Four. EPIC. Experiments (ter Horst et al., 2018)

Tl;dr: sunlight & breakfast in the morning.

[FULL ARTICLE ON PATREON]

Dopamine receptors are downregulated in obese patients and are restored in long-term weight loss patients after bariatric surgery. It’s better to get your dopamine hit via sunlight than sugar duh.

This is some amazing science.

 

 

Experiment 1. 50-year old dude with severe OCD gets diagnosed with type 2 diabetes and is only able to get his glucose under control with metformin and 226 IU insulin. At 53, his OCD is treated with deep brain stimulation (DBS). His insulin requirements declined to 180 IU. He didn’t lose weight but went off quetiapine, so maybe coincidence because: 1. quetiapine is diabetogenic; and 2. DBS induces dopamine release.

Two-step hyperinsulinemic euglycemic clamp when DBS is turned off and turned on. BOOM! When it’s on, lower fasting insulin, and better insulin-induced suppression of liver glucose output, free fatty acids, & muscle glucose disposal! DBS improved insulin sensitivity in liver, adipose, and skeletal muscle.

For the rest of the discussion on these super-interesting experiments, head over to PatreonFive bucks a month for full access and there are many other options. It’s ad-free and you can cancel if it sucks 🙂

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

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Cycloset (bromocriptine)

 

 

Go for a walk.

And #eTRF.

 

Intermittent fasting is homeopathy-level #nothingsauce

From all of the published human studies and “n=1’s” I’ve seen on online forums, intermittent fasting is #nothingsauce. Don’t @ me.

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When people lose weight via IF, it’s because of caloric restriction. There’s no metabolic advantage, and if anything, maybe the opposite. Restricting your feeding window to a very short period = metabolic mayhem.

2000 kcals in one sitting?

*smh*

 

 

I believe “early Time-Restricted Feeding” #eTRF showed promise in that recent study because of the “early” part; no so much on the “TRF” part. I believe this, in part, because the large majority of our population suffers from some degree of circadian arrhythmia. Social jet lag, too much artificial light at night, skipping breakfast, etc., etc. An EARLIER feeding window is one way to re-align circadian rhythms.

 

 

It STARTS with Sleep. Wanna improve body comp and make mindlessly better food choices? Fix your circadian rhythms.

Now onto the one of the weirdest, but potentially most revealing human studies on time-restricted feeding…

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calories proper

 

 

The Fates of Pyruvate

As mentioned in the previous blog, obligatory glycolytic cells lack the apparatus (eg, mitochondria) to fully oxidize fuels down to CO2 and water. Thus, they can’t run on fatty acids, ketones, or beta-hydroxybutyrate. During prolonged starvation, there’s always some glucose in the blood, so they survive.

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Recommended textbook: Stipanuk or Gropper.

Glucose -> glycolysis -> pyruvate: then to lactate or the mitochondria, depending on the context. Skeletal muscle has mitochondria, but if you’re exercising hard, glycogen to lactate produces more energy faster than glycogen to pyruvate to mitochondria. Blood lactate increases in this context. During prolonged starvation, lactate is a valuable precursor for gluconeogenesis, so many tissues release lactate instead of oxidizing pyruvate.

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calories proper

 

Glucose dynamics during prolonged fasts

This is a somewhat complicated level of metabolism. Which tissues are producing what & how much, what are they burning & how much, etc., etc…

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After a few weeks, things begin to level out — we’ll pick it up there. Much of this is from a class I TA’d for in grad school, this book, and all the Cahill studies.

 

 

“The rate of glucose use at this time is around 90-100 g per day [remember, this is starvation, so all of that glucose comes from gluconeogenesis]. Of that, about 40 g is recycled via the Cori and glucose-alanine cycles and the remainder is ‘new’ glucose, ~18 g from glycerol and ~45 g from amino acids.”

Continue reading

Starvation ketosis and “priority” of brain fuels

“Priority” is a funny concept the fields of nutrition, metabolism, etc. For the brain, it is said to be glucose. It’ll use ketones when glucose is low and ketones are really high, like during starvation, but otherwise it’s just glucose. Why is this? One of my mentors had some great insights…

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“It seems that the loss of some energy as ketones in the urine is the price we pay to provide the brain with a suitable fuel. But there are a number of unanswered questions about brain fuel use. Why does the brain not use free fatty acids? The usual answer given is that they are not transported across the blood-brain barrier fast enough to be used as a major fuel and this is probably true. However, why did the brain not develop a suitable transport system, or localized store of glycogen for that matter.”

WHY NOT FATTY ACIDS?

Textbook: Biochemical, Physiological, and Molecular Aspects of Human Nutrition

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Also, I’m open to suggestions, so please don’t hesitate to leave a comment or contact me directly at drlagakos@gmail.com.

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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 eating them, Real Mushrooms makes great extracts. 10% off with coupon code LAGAKOS. recommend Lion’s Mane for the brain and Reishi for everything else.

calories proper

 

Metabolism of starvation/fasting =/= low carb diet

The Biology of Starvation (intro)

The Biology of Starvation: Renal Gluconeogenesis

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One of the major [obvious] differences in metabolism between fasting and low carb dieting is nitrogen metabolism… because you’re eating protein on a low carb diet, not so much while fasting. During fasting/starvation your body tries to downregulate the urea cycle because you can’t really afford to be ‘wasting’ amino acids/protein. I bet you never thought about the muscle-sparing effect of fat-derived fuels like that!

 

 

“Glucose production in starvation” is important because you need to make all of it and reduce the use of it.

 

For the rest of this article and more, head over to Patreon! Five bucks a month for full access and there are many other options.

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Also, I’m open to suggestions, so please don’t hesitate to leave a comment or contact me directly at drlagakos@gmail.com.

Affiliate links: still looking for a pair of hot blue blockers? Carbonshade and TrueDark are offering 15% off with the coupon codeLAGAKOS and Spectra479 is offering 15% off HERE.
If 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.

If you want the benefits of  ‘shrooms but don’t like eating them, RealMushrooms makes great extracts. 10% off with coupon code LAGAKOS. recommend Lion’s Mane for the brain and Reishi for everything else.

calories proper