Category 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 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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Ketogenic diet as a metabolic therapy for mood disorders

Recent findings and current developments: where do we stand today?

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Great “Tl;dr:” figure ->

 

 

 

There is most definitely a multi-level bidirectional relationship between mood disorders and diet/lifestyle habits. Can diet cause or cure mood disorders? Can mood disorders cause you to eat/behave a certain way? Yes, yes, and yes. #Context.

That said, diet interventions present a unique and potentially useful treatment avenue for mood disorders.

Mood disorders are a significant source of mental capital loss with high rates of treatment resistance, in part, because we have no clue about the causes, full influence of their spectrums, or how exactly the effective pharmacotherapies work.

The ketogenic diet: why it should be explored ->

  1. Ketogenic diet has profound effects in multiple targets implicated in the pathophysiology of mood disorders, including glutamate/GABA transmission, monoamine levels, mitochondrial quantity and quality, neurotrophism, oxidative stress, insulin signaling, inflammation, etc., etc…
  2. Benign dietary ketosis is a very exclusive diet, immediately cutting out many of the potentially offensive foods.
  3. Malign dietary ketosis, while still technically ketosis, is full of unhealthy n6- and trans fat-rich oils, insufficient protein and fibre, etc. It’s basically the bacon-wrapped cheese dog version of keto.

Domains of depressive symptomatology of interest: anhedonia, rumination, suicidality, sleep disruption, appetite dysregulation, among others.

In this context, it may be perfectly legitimate to supplement a low carb diet with exogenous ketones or coconut oil.

BDNF BDNF BDNF!

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

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Scientifically, high protein breakfast FTW

It wasn’t even *that* high in protein (30g) but relative to skipping breakfast, everything got better (Gwin and Leidy, 2018).

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At 7 days, this study was longer than some but shorter than others. Breakfast was provided by the researchers. Participants were on their own for lunch and dinner. Ad lib, although 7 days isn’t really long enough to influence body weight and this wasn’t even a goal of the researchers. Their goals were hunger, satiety, fullness, and sleep quality.

RANDOMIZED CROSSOVER. BOOM.

 

 

Small sample size (n = 13), although based on previous findings & expected effect sizes, they needed 12 participants for an 80% chance of detecting a statistically significant difference if one truly existed. Bigger sample sizes are usually better, but when those resources can be better spent elsewhere, researchers use these power calculations to determine the fewest participants required…

moving on

On day 7, they assessed some brain stuff before lunch and then sent them home with party boxes loaded with an assortment of pre-weighed foods & snacks. The participants were instructed to eat as much of whatever they wanted, ad lib, and return the boxes the following day.

The brain stuff:

Just like #eTRF

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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. I recommend Lion’s Mane for the brain and Reishi for everything else

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

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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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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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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.”

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

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