Tag Archives: ketosis

Ketoacidosis

Nutritional ketosis is a normal, physiological response to carbohydrate and energy restriction.  A ketogenic diet is an effective weight loss strategy for many.  Ketoacidosis, on the other hand, is a pathological condition caused by insulin deficiency.  The common theme is low insulin; however, in ketoacidosis, blood glucose levels are very high.  Ketone levels are elevated in both states, although are 10-20x higher in ketoacidosis (~0.5-2 vs. > 20 mM).  Nutritional ketosis and ketoacidosis should not be confused with one another, and a ketogenic diet doesn’t cause ketoacidosis.

In ketoacidosis, gluconeogenesis occurs at a very high rate and the lack of insulin prevents glucose disposal in peripheral tissues.  Skeletal muscle protein breakdown contributes gluconeogenic substrates, exacerbating the problem.  This can cause blood glucose to reach pathological levels, exceeding 250 mg/dL.

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On resistant starch and blood glucose control

For overall health and well-being, fermented foods like sauerkraut and kefir are great.  Especially when following a low carbohydrate diet which is generally low in the types of foods which feed the gut microbiome.

For those with gastrointestinal problems, the gut microbiota is probably involved.  Whether it is bacterial overgrowth or dysbiosis, gut bugs are usually the culprit.  Treatment options vary widely, ranging from global extermination with vinegar & a low fibre diet (as per Jane Plain), or remodeling the microbiome with a prebiotic like galactooligosaccharides.   Probiotics like bifidobacteria can help, too, if they’re administered with either prebiotics or fermented foods (they need something to nourish them in transit).  Dark chocolate is also an excellent vessel.  Resistant starch is another option, although the question remains as to whether or not this is compatible with a low carbohydrate diet.

Resistant starch has been around for a while, and when I was in school it received about 10 minutes of attention during the fibre lecture.  But Jimmy Moore and Richard Nikolay have been talking about it a lot lately so I decided to freshen up on the topic.  In brief, it can be therapeutic for GI issues, but some studies have shown mixed effects on glucose & insulin metabolism.  The former is virtually unarguable, but I found the latter interesting.  And the impact of resistant starch on ketosis is included as well.

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Impact of a low-carbohydrate, high-fat diet on gut microbiota.

NPR recently reported on a study where the participants ate either a meat-based, fiber-free ketogenic diet or a vegetarian diet and had their gut microflora analyzed.  The low carb diet was much higher in fat, and as such, increased the prevalence of a microbe involved in fat digestion.  “Bilophila.”  The article focused on this one and cited a 2012 study where Bilophila was associated with intestinal inflammation… however, the ketogenic diet increased the levels of Bacteroides and decreased Firmicutes.  These are the two that brought the whole gut microbe-obesity connection into the spotlight.  The microbiome in obese mice is characterized by low Bacteriodetes and high Firmicutes. Fecal transplants from obese mice to lean mice causes them to gain weight.  Little is known about Bilophila relative to Bacteriodetes & Firmicutes, and I suspect the focus was on Bilophila because the authors wanted something negative to say about a meat-based, fiber-free ketogenic diet, and that 2012 mouse study suggested Bilophila could be their answer.

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Dietary protein, ketosis, and appetite control.

Dietary protein has a purpose, and that purpose is not carbs.”  Nor is it to break ketosis or stall weight loss.  

Drastically increasing protein intake may reduce the degree of ketosis in the context of a large energy surplus, but this is likely due more specifically to the large energy surplus than the protein.  This would explain why Warrior dieters (1 meal meal per day) often report reduced ketones if they eat too much protein.  It’s more likely that the 2000 kcal bolus is exerting it’s anti-ketotic effect by being a large energy surplus, such that anything other than 90% fat would blunt ketosis.  It’s not the proteins… Want proof?  Here’s an n=1 to try: give up Warrior dieting for a few days and try 3 squares.  My bet is that you’ll be able to increase protein intake and still register ketones as high or higher than before.  There are data to support this and reasons why it may not matter (below).

disclaimer: I don’t think “deep ketosis” is necessary to reap the benefits of carbohydrate-restriction.  But if you love high ketone meter readings, then this might be a better strategy to maintain deep ketosis while getting adequate protein. win-win.

if I hear: “oh no, I was kicked out of ketosis!” one more time… 

All of the studies below are confounded one way or another, but so are we humans.

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Dietary protein does not negatively impact blood glucose control.

“Dietary protein-derived amino acids have a purpose, and that purpose is not carbs.”

At a reasonable level of dietary intake, protein is used for the maintenance of organs & tissues.  Lean body mass.  It’s functional.  Protein isn’t stored in any appreciable capacity, and most excess is either oxidized or stored as glycogen.  Theoretically, about 50-60% of protein-derived amino acids can be converted into glucose, mathematically, but it’s not what you think…

“At a reasonable level of dietary intake.”  A recent publication took a look at this (Fromentin et al., 2013).   They set out to determine how much protein is converted to glucose under “optimal gluconeogenic conditions.”  That is, the subjects were 12 hours fasted, which is a physiologically relevant, optimal gluconeogenic condition.  They were then given 4 eggs (~23 g protein) that were labeled with two stable isotopes (15N & 13C, derived from hens fed isotope-enriched diets!).  Throughout the entire study duration, the subjects were infused with a third isotope, 2H-glucose.  By collecting and analyzing the enrichment of isotopically-labeled metabolites like expired CO2, urea, and glucose, the researchers were able to determine the fate of those 23 grams of protein.

Some of the dietary protein-derived amino acids were used for protein synthesis, others were oxidized.  But blood glucose levels did not change.  Nor did the rate of gluconeogenesis.

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Implications of the circadian nature of ketones.

Ketosis.  Happens during starvation and also by restricting carbohydrates (and protein, to a lesser degree)… might be important for epilepsy and bipolar disorder, too.

ketogenesis

Ketostix measure urinary acetoacetate (AcAc) and reflect the degree of ketosis in the blood probably about 2-4 hours ago.  Blood ketone meters measure beta-hydroxybutyrate (bHB) right now.  bHB fluctuates to a greater degree, eg, it plummets after a meal whereas AcAc takes longer to decline.  AcAc/bHB is usually around 1, but increases after a meal (Mori et al., 1990):Ketone body ratio

Conversely, when glucose levels decline and fatty acid oxidation increases, liver redox potential drops which reduces AcAc/bHB.

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The curiosities of nicotin..ic acid

Niacin vs. ketosis

Part I.  Rodents

It is thought: niacin causes red itchy face (> 100 mg/d) and acutely lowers FFAs; chronically, it raises some questionable fraction of HDL (> 1000 mg/d) and probably causes diabetes.

It is speculated: niacin binds a particular “ketone” receptor (GPR109?) (physiological relevance?).

It is known: niacin is ketogenic in rats.  Repeat: niacin is ketogenic in rats.

Niacin aka nicotinic acid and nicotamide aka niacinamide both fulfill the requirement for Vitamin B3 (ie, prevent pellagra).  But only the former causes flushing… and only the former is ketogenic (two apparently unrelated phenomena).

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40 years ago a group of researchers turned ketosis into poetry.

But first, a brief primer.  In red.

“The glucose muscle-sparing effect of fat-derived fuels” 

or, the Randle Cycle 2.0.  it’s like a course in life enhancement.

Part I.  Intermediary metabolism

The glucose-fatty acid cycle
The Randle Cycle, as originally proposed, states that fatty acid oxidation inhibits glucose oxidation.  This is good because during starvation, every tissue than can survive on fatty acids instead of glucose should do so, sparing as much precious glucose as possible for the brain.

The glucose-sparing effect of fat-derived fuels
A critical vital horcrux to this is in the oh-so-humbly-disguised phrase “fat-derived fuels.”  The fat-derived fuels are ketones, and they are rescuing the brain from starvation (ie, neuroglycopenia); they do so by supplementing glucose as a fuel source.  Ketones are good at this; many tissues are happy to oxidize ketones when they are available.

The glucose muscle-sparing effect of fat-derived fuels
Ketones are derived from fat.  During prolonged starvation, glucose comes from skeletal muscle amino acids (eg, alanine).  Ketones spare glucose.  Thus, ketones spare muscle.  QED.

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