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There are numerous benefits to being in a fasted state from a the perspective of mitochondrial health and exercise has similar benefits. Having healthy mitochondria is absolutely essential to good health and impaired mitochondrial function is linked to many chronic diseases. Neurons are particularly susepticible to dyfunctional mitochondria. The process by which the body determines whether it is a fasted or fed state is the Randle Cycle. The fasted state is characterized by low insulin and the presence of ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone), which are a produced by the liver from triglycerides.  Most cells with mitochondria readily use ketones for fuel.  The presence of ketones will cause uncoupling of adipose mitochondria so that they generate heat in addition to producing ATP, which increases the body's metabolic rate.  Ketones help the muscle mitochondria become more coupled so that they are more energy efficient in producing ATP. Benefits of being in the fasted state are:

  • Increased mitochondrial biogenenis (more mitochondria)
  • Increased mitochondrial fusion (enhanced ATP production)
  • Favourable mitochondrial function (less oxidative stress, enhanced ATP production, umcoupling of adipose tissue while maintaining coupling of muscle tissue)

It appears that metabolizing longer-chain saturated fats promotes mitochondrial biogenesis though reverse electron transport via Reactive Oxygen Species (signaling molecules) in the mitochondria's electron transport chain. Increased low-level ROS synthesis (see Mitohormesis) causes localized insulin resistance at the cellular level, which prevents the uptake of glucose. Basically, the higher the ratio of FADH2 to NADH (F/N ratio), the greater the amount of reverse electron transport (RET), which in turn encourages the mitochondrial biosynthesis. Reverse electron transport occurs marginally with F/N=0.46 and not at all with F/N<0.46. Fat oxidation generates greater amounts of FADH2 than glucose oxiation and fat metabolism generates ketones. Because ketones deactive the cell's insulin receptor, they also help prevent the glucose uptake in adipose tissue. Since Linoleic Acid has no RET effect, it acts like a supercharged carbohydrate because it contains 9 calories/gram vs 4 for glucose and it is likely a significant contributor to the obesity epidemic. Industrial seed oils (eg, canola/rapeseed, corn, cotton, peanut, safflower, soybean, sunflower) are a key component of processed foods.

Fatty Acid
(found in)
Carbon
Chain
Length
Carbon
Double
Bonds
(Saturation)
F/N
Ratio
Drives
RET?
Lignoceric acid
(peanut oils and most natural fats)
C24 0 0.489 ↑ ↑ ↑ ↑
Behenic acid
(ben tree seed oil)
C22 0 0.488 ↑ ↑ ↑ ↑
Arachidic acid
(durian fruit, cupuaçu butter, corn oil, peanut oil, cocoa butter)
C20 0 0.487 ↑ ↑ ↑ ↑
Stearic acid
(beef tallow & other animal fats, cocoa & shea butter)
C18 0 0.486 ↑ ↑ ↑ ↑
Palmitic acid
(palm oil, butter, cheese, milk, meat, cocoa butter, soybean oil, sunflower oil)
C16 0 0.484 ↑ ↑ ↑
Myristic acid
(nutmeg, palm kernel oil, coconut oil, butterfat, bovine milk, breast milk)
C14 0 0.481 ↑ ↑ ↑
Lauric acid
(goats milk, coconut & palm oil)
C12 0 0.478 ↑ ↑ ↑
Capric acid
(goats milk, coconut & palm oil)
C10 0 0.474 ↑ ↑
Caprylic acid
(goats milk, coconut & palm oil)
C8 0 0.467 ↑ ↑
Erucic acid
(wallflower seed, high erucic acid rapeseed, & mustard oil)
C22 1 0.465
Paullinic acid
(guarana seed oil)
Gadoleic acid
(cod liver oil)
Gondoic acid
(jojoba oil)
C20 1 0.462
Oleic acid
(olive & sunflower oil, poultry fat & lard)
C18 1 0.457
Caproic acid
(goats milk, coconut & palm oil)
C6 0 0.455
Palmitoleic acid
(macadamia oil)
C16 1 0.452
Butyric acid
(butter & other dairy products, human breast milk, sauerkraut & other fermented foods)
C4 0 0.429
Linoleic Acid
(safflower, sunflower, corn, soybean oils, sesame, & almonds )
C18 2 0.429
Alpha-linolenic acid (ALA)
(flaxseed, walnuts, chia, hemp, and many common vegetable oils. )
C18 3 0.400
Glucose C6 (ring) N/A 0.20