Category Archives: coconut

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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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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Ketosis in an evolutionary context

Humans are unique in their remarkable ability to enter ketosis.  They’re also situated near the top of the food chain.  Coincidence?

During starvation, humans rapidly enter ketosis; they do this better than king penguins, and bears don’t do it at all.

Starvation ketosis

 

Starvation ketosis

Humans maintain a high level of functionality during starvation.  We can still hunt & plan; some would even argue it’s a more finely tuned state, cognitively.  And that’s important, because if we became progressively weaker and slower, chances of acquiring food would rapidly decline.

Perhaps this is why fasting bears just sleep most of the time: no ketones = no bueno..?

Observation: chronic ketosis is relatively rare in nature. This doen’t mean animals evolved a protective  mechanism against ketosis.

 

 

Animals with a low brain/carcass weight ratio (ie, small brain) don’t need it. Babies and children have a higher brain/carcass weight ratio, so they develop ketosis more rapidly than adults. Is this a harmful process? No, more likely an evolutionary adaptation which supports the brain.

ketones age

The brain of newborn babies consumes a huge amount of total daily energy, and nearly half comes from ketones.  A week or so later, even after the carbohydrate content of breast milk increases, they still don’t get “kicked out of ketosis” (Bourneres et al., 1986).  If this were a harmful state, why would Nature have done this?  …and all those anecdotes, like babies learn at incredibly rapid rates… coincidence?  Maybe they’re myths.  Maybe not.




 

Ketosis in the animal kingdom

Imagine a hibernating bear: huge adipose tissue but small brain fuel requirement relative to body size and total energy expenditure.  No ketosis, because brain accounts for less than 5% of total metabolism.  In adult humans, this is around 19-23%, and babies are much higher (eg, Cahill and Veech, 2003Hayes et al., 2012).

 

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Non sequiter dietary fats

Tl;dr: SFA and DHA

Essential fatty acids?  Well, there’s really only one, DHA, and we really only need a gram or two.  In other words, our entire requirement for dietary fat can be met by about 2% of total calories (plus a few extra grams to accommodate fat-soluble vitamins) (plus DHA is never the sole fat in a food, so you’d be getting a few more grams of other fats, too).  But still, a very low fat diet!  But impractical and probably not very palatable or healthy.

On average, dietary fat comprises about a third of calories, roughly equally divided between SFA, MUFA, and PUFA (slightly less PUFA).

Major sources of SFA are pizza and desserts – no wonder SFA gets a bad rap!

 

cheese-crust-pizza

 

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Alcohol on keto

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.

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Ketone supps

1st Generation: ketone salts.  Only problem is the huge dose of salt limits how much you can take without adverse effects… but these are the ones on the market.

 

2nd Generation: ketone esters.

Advantage: no salt, and probably “slow-release.”

Disadvantage: gonna be WAY more expensive than the salts (which are still pretty expensive).

 

 

~40 grams of (R)-3-hydroxybutyl (R)-3-hydroxybutyrate (a ketone ester) (from Clarke et al., 2013):

 

ketone ester

 

They did this thrice daily, so some people were getting up to 170 grams.

ONE HUNDRED SEVENTY GRAMS

 

[keep that number in mind]

 

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Tissue-specific fatty acid oxidation

Does it matter where fatty acids are oxidized, liver or skeletal muscle?  Of course, they’re oxidized in both tissues (quantitatively much more in the latter), but relative increases in one or the other show interesting effects on appetite and the regulation of fat mass [in rodents].

Warning: a lot of speculation in this post.

A LOT.

It’s known that LC diets induce a spontaneous decline in appetite in obese insulin resistant patients.  Precisely HOW this happens isn’t exactly known:  the Taubes model?  improved leptin signaling?  probably a little bit of both, other mechanisms, and possibly this one:

 

Exhibit A. Oxfenicine

 

oxfenicine

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Saturated fat, cholesterol, and carbohydrates

“You catch more flies with honey…”

^^^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.

 

 

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Vegetable oil fatty acids are not essential. 

They are conditionally essential at best, only if docosahexaenoic acid (DHA) is lacking.  We can’t synthesize omega 3 fatty acids, and indeed they do prevent/cure certain manifestations of “essential fatty acid (EFA) deficiency” (Weise et al., 1958), but DHA can do all that and more.  Not that I recommend this, but a diet completely devoid of 18-carbon vege oil fatty acids will not produce EFA deficiency in the presence of DHA. (“vege,” rhymes with “wedge”)

Essential fatty acid metabolism

 

The “parent essential oils” are linoleic acid (LA) and alpha-linolenic acid (ALA).  The others, which I think are more important and the truly “essential” ones are eicosapentaenoic acid (EPA), arachidonic acid (AA), but mostly just DHA.

The first manifestation of EFA deficiency is dermatitis (Prottey et al., 1975).  Some people say LA is necessary to prevent this, but it would be better phrased as “LA prevents dermatitis;” not “LA is necessary to prevent dermatitis.”  All of the evidence suggesting LA is essential is in the context of DHA deficiency.

Technically, we can convert a bit of ALA to DHA, estrogen helps, testosterone doesn’t (women have better conversion rates)… and I’d speculate that the reverse is probably easier (DHA –> ALA).

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Insulin, dietary fat, and calories: context matters!

Jane Plain recently wrote a great article about the relationship between insulin, dietary fat, and calories.  There are a lot of data on this topic, which collectively suggest: context matters! 

For example,

Insulin and ketone responses to ingestion of MCTs and LCTs in man. (Pi-Sunyer et al., 1969)

14 healthy subjects, overnight fasted; dose: 1g/kg.

In brief, MCTs are more insulinogenic than corn oil.  But it’s not a lot of insulin.  Really.  Enough to inhibit lipolysis, perhaps, but that’s not saying much… & certainly not enough to induce hypoglycemia.

Pi-Sunyer MCT Corn oil

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