What is actually happening in there
Autophagy, mitophagy, mTOR, AMPK, ketogenesis, the growth hormone response. Each of these is real biology with named parts. Each is also routinely described online with more confidence than the measurements support. Every page here splits what has been seen in a living person from what has been seen in a mouse or a dish. It also tells you how it was measured, because in this field the way it was measured is usually the whole story.
12 body processes, 12 with a measurement in people cited.
Autophagy
Macroautophagy · Self-eating
The cell's recycling system. Worn-out parts get wrapped up, carried to the cell's digestion sac, and broken down into pieces the cell can use again.
6 studies in people of 6 cited
Mitophagy
Mitochondrial autophagy · PINK1/Parkin pathway
Recycling aimed at one target. Mitochondria that have stopped working well get tagged, wrapped and digested, so the cell keeps the ones that still make energy cleanly.
7 studies in people of 7 cited
Ketogenesis and beta-hydroxybutyrate
Ketosis · BHB · Ketone bodies
When food runs short, the liver breaks down fat faster than it can burn the pieces. It turns the extra into small molecules called ketones and sends them out as a fuel the brain can use when blood sugar is low.
7 studies in people of 13 cited
mTOR
mTORC1 · Mechanistic target of rapamycin
The switch that decides whether a cell should build or save. It is the reason protein, and not calories in general, is what ends the fasted state.
6 studies in people of 15 cited
AMPK
AMP-activated protein kinase
The cell's fuel gauge. It reads how much of the cell's energy has been spent, and when the reading drops, it switches on the jobs that make energy and switches off the jobs that use it.
2 studies in people of 8 cited
The growth hormone response
GH · Somatotropin · Counter-regulatory response
Growth hormone output rises several times over within two days of a fast. But IGF-1, the growth signal it normally works through, does not follow it, and that changes what the rise means.
7 studies in people of 7 cited
Insulin and insulin sensitivity during a fast
Selective insulin resistance
Insulin falls fast and early, and the body's tissues respond to it less, but only when it comes to sugar. That detail is what separates a normal fasting change from the insulin resistance of metabolic disease.
6 studies in people of 7 cited
Glycogen depletion and gluconeogenesis
Glycogenolysis · Making new glucose
The body does not burn through its stored sugar and then switch to making new sugar. It is already making most of its sugar from scratch within the first day. So the "metabolic switch" everyone talks about is not really a switch.
7 studies in people of 9 cited
FGF21
Fibroblast growth factor 21
A hormone from the liver. In mice, it is the signal of fasting. In people, it mostly responds to how little protein you ate, not how few calories, and a two-day fast does not move it at all.
6 studies in people of 8 cited
BDNF and the brain
Brain derived neurotrophic factor
The brain's switch to a new fuel during a fast is measured directly and solid in people. The claim that fasting raises BDNF was tested directly in people, and it did not happen.
7 studies in people of 10 cited
Sirtuins and NAD+
SIRT1 · SIRT3 · NAD+
A family of enzymes that can only work when the cell has NAD+ to spend, which ties them to how well fed the cell is. The two most quoted results backing this field did not hold up when others repeated them.
4 studies in people of 11 cited
Refeeding, the leucine threshold and refeeding syndrome
Breaking a fast · Hypophosphataemia
Coming out of a fast is its own event, with its own rules. In a truly malnourished person, it has its own danger. That danger is not that phosphate is lost. It is that insulin drives phosphate into cells all at once.
12 studies in people of 18 cited