In this series, we will look at the basics of metabolism and discuss the very well-known science around obesity. Many of the diseases that bedevil humanity flow from obesity, including cancer and Type 2 diabetes, and so understanding metabolism and the causes of obesity is ground zero in the fight for a long life and good health.

Diet, eating, and the scientific version of eating, called metabolism, has been subjected to various frameworks over the years. As Michael Pollen has pointed out in his excellent books, food used to be what your mother gave you to eat, and you shared it with your extended family. The food framework was culture; Greeks ate olives, Germans drank beer, Japanese ate sushi, and so forth. It has only recently been the case that people considered food from a ‘macro’ basis, concerning themselves with proteins, fats, and carbohydrates. Ironically, about the same time people took a scientific view of food, poor eating habits became the norm.

In considering this scientific framework, food writers and theorist have thought about the evolutionally path of human metabolism. In this ‘evolutionary framework,’ food was viewed from the unreliable and varied inputs of the past. Early humans were not even agriculturists; they were hunter-gatherers, and food was sometimes scarce. In the summer, there was different food than in the winter. The hunters hunted game, which meant there would be fat and protein, and the gatherers gathered grains and fruits, which meant there would carbohydrates. And so, the human body developed ways to turn both potential food sources into energy that would power the brain, heart, muscles, and other vital tissues.

When the gatherers provided the food, the body used the insulin pathway to maintain energy. The gatherers would gather up the berries and fruits, the tribe would eat, the food would be converted to glucose, their pancreas would secrete insulin, the insulin would escort the glucose into the cells of their rugged bodies, and this would provide needed energy. The excess would be stored as fat in the adipose tissue for the coming winter.

What happened with the hunters provided the food? When they killed an elk in winter, what pathway did the metabolism take? This brings us to ketosis.

As noted, when insulin falls, and the glucagon reserve is depleted, the liver releases ‘ketone bodies’ which begins the process of releasing energy from the previously stored fat reserves.

Going to the wiki definition, we find this:

Ketone bodies are water-soluble molecules that contain the ketone groups produced from fatty acids by the liver (ketogenesis). They are readily transported into tissues outside the liver, where they are converted into acetyl-CoA (acetyl-Coenzyme A)—which then enters the citric acid cycle (Krebs cycle) and are oxidized for energy.

So, ‘ketone bodies’ are ways to produce energy outside of the glucose/insulin/glucagon pathway.

What is the Krebs cycle?

The citric acid cycle (CAC) – or the Krebs cycle, is a series of chemical reactions to release stored energy through the oxidation of acetyl-CoA derived from carbohydrates, fats, and proteins.

The Krebs Cycle is the way food is turned into energy so that the mitochondria in the body can burn it, and ‘ketone bodies’ are molecules that allow fat energy to enter the Krebs cycle and power the body. This alternative method of metabolism allows the hunters to feed the tribe. The term ‘ketones’ refers to a much larger set of chemical compounds but the ‘ketone bodies’ released by the liver are only three: hydroxybutyrate (3-OHB), acetoacetate, and acetone.

So, what is ketosis? Again, to the wiki:

When the rate of synthesis of ketone bodies exceeds the rate of utilization, their concentration in blood increases; this is known as ketonemia. This is followed by ketonuria – excretion of ketone bodies in urine. The overall picture of ketonemia and ketonuria is commonly referred to as ketosis. The smell of acetoacetate and/or acetone in breath is a common feature in ketosis.

Ketosis is when the body has fully converted out of the insulin cycle, there is no more glucose to burn, and fat metabolism has begun. When the tribe member gets hungry, and the hunters offer a big slab of fatty meat, the tribesman eats it it, and their body, instead of releasing insulin in response to the gatherer carbohydrate offering, releases more ‘ketone bodies’ and the state of ketosis begins or continues. The body burns the incoming fat or the stored fat, and the insulin fat storing pathway is never triggered.

One often hears about a metabolic state called ketoacidosis which is when elevated ketone bodies are driving the pH/acid levels in the body out of balance. In a person with diabetes, as level of glucose in the blood rises, the body still doesn’t produce insulin in the response. However, the body perceives the lack of insulin and begins to release ketones, thinking that fat metabolism is what is required even though the blood is laden with unused glucose. This toxic situation is sometimes called ‘diabetic ketoacidosis,’ or DKA for short. High glucose, no insulin, and ketone bodies define DKA, and it is deadly. People with diabetes have provided a control group for the study of metabolism, but thousands upon thousands of these involuntary pioneers have died of DKA. The sad path of Type 1 and Type 2 diabetes is something that should be noted and eliminating it should be a national priority, but it isn’t.

Type 1 diabetes used to be called ‘juvenile diabetes’ because it typically began in childhood and it was the result of a rogue immune response which killed the cells in the pancreas that makes insulin. Before the discovery of insulin, these poor kids didn’t live long. Type 2 diabetes was referred to as ‘adult onset’ diabetes because it was the result of ‘insulin resistance’ which meant the pancreas still made insulin, but there wasn’t enough insulin to clear the blood of all the stacked up glucose. Researchers now talk of ‘Type 3’ diabetes which is dementia, or Alzheimer’s. This comes about later in life, because high blood sugar clearly has a detrimental effect on the brain.

There is no corresponding Type 1, 2 or 3 pathway in ketone and fat metabolism.

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