It has come to my attention that some well meaning people are still confusing ketoacidosis and ketosis.

Ketoacidosis IS NOT KETOSIS! They are very different things. One is part of the standard fat mobilization metabolism and the other is a run-away syndrome experienced by some Type 1 Diabetics without insulin to regulate ketone production and in a state of hyperglycemia.

https://www.dietdoctor.com/low-carb/skeptical-doctors#ketosis

Ketoacidosis, however, is completely different from nutritional ketosis, where blood ketone levels usually range between 0.5-4 mmol/L and are accompanied by adequate insulin levels and normal blood glucose. Further, nutritional ketosis and ketoacidosis are physiologically very different, with the former having practically no health risk. The body is simply using mostly ketones for fuel, as opposed to mostly glucose. This basic physiological difference is important for every healthcare practitioner to understand.

Most doctors, and T1Ds, are only informed about ketoacidosis - because its an acute condition that must be treated immediately. In fact this is probably the only time a doctor will hear about “keto” in their entire medical training. It’s easy to see why people easily confuse the two states, but they are different and should not be confused.

Ketosis is the default state of the body, it is simply fat mobilization. When people sleep, when people skip a meal, when people are born, when people “Eat Less and Move More” - they are mobilizing fat for energy, and that is the metabolic state of ketosis.

From the paper above:

Ketosis is a fasting, metabolic-adapted state in mammals, which confers a species survival advantage during periods of adverse food challenge. Generally, the more advanced the brain and central nervous system, the greater their size in relation to total body size and therefore the greater their metabolic demands as a percentage of total metabolism and the greater their propensity for developing fasting ketosis.

The human neonate’s brain, for example, accounts for 60–70% of total energy consumption, with metabolism in the first two to three days following birth being largely via ketone bodies, rather than glucose;

Babies run on ketones, using ketosis, from the moment they are born.

On a carbohydrate-restricted regimen, there is a shift from glucose- to fat-based metabolism, whereby glucose is replaced by free fatty acids as the primary source for energy transduction

While free fatty acids can be readily utilised as fuel by many tissues, including the liver and muscles, the brain is a major exception, and instead must use water-soluble ketone bodies – b-hydroxybutyrate and acetoacetate – produced by the liver in direct response to changes in energy-substrate metabolism, as its primary substrate. In fasting individuals, ketone bodies will eventually meet around 70% of the brain’s energy demands (Voet et al. 2006)

The body requires constant energy, at all times, the liver can both produce glucose on demand, and ketones on demand. People who persist in a ketogenic metabolism power their brain primarily with ketones, which has many benefits, but the most significant one being that ketones pass into the brain even in individuals with high insulin resistance.

The utilisation of ketone bodies as brain energy substrate circumvents the requirement for gluconeo- genesis1 from protein, which would otherwise deplete muscle mass at an alarming rate to maintain glucose supplies to the brain.

This is very important - making ketones does not use protein. Muscles do not waste in ketosis. The body stores fat, and uses fat, normally without negative consequences.

In the absence of the ketogenic pathway, it has been suggested that in a totally fasting state, death would occur in around 10 days, rather than the 57–73 days a normal weight adult male can actually survive, because of the mobilisation of fat stores for energy (Veech 2004).

Producing glucose on demand uses protein, which is a limited and precious resource in humans.

Firstly, increased ketone concentration stimulates insulin secretion, which in turn hinders fatty acid mobilisation, independently inhibits ketogenesis and also enhances ketone utilisation, thereby reducing overall ketone-body concentration in the blood (Keller et al. 1989);

In non-T1D populations, ketones themselves are part of the self-regulation of ketone levels preventing ketoacidosis .

Levels of ketone bodies in the blood reach a maximum of 2–3 mM under physiological conditions, and within these levels, renal mechanisms for increasing ammonium (NH4+) excretion and reducing urea excretion spare electrolytes, maintain intra/extracellular fluid volume and result in no change in acid-base regulation (Cahill et al. 1973).

Under normal circumstances if ketones are too high they get peed away, to maintain blood acid balance.

The net effect is that life-threatening (keto)acidosis never occurs in an individual during fasting or periods of reduced carbohydrate intake where type 1 diabetes is absent (McGarry & Foster 2003).

Ketosis can therefore be seen as a regulated, controlled metabolic state, shifting primary cell metabolism from glucose to fat and freeing up what little glucose is available (obtained immediately from dietary intake or via synthesise from the glycerol product of triglyceride catabolism) for use by the brain and other obligate tissues.

Red blood cells, and 5-30% of brain cells, require glucose - the rest of the body can run on fat. This is why ketosis is not stressful on the body.

KETONES ARE NOT PATHOLOGICAL, KETONES ARE NOT DANGEROUS. In the same way that blood glucose is necessary and healthy in the proper ranges, the same is true for ketones.