Vitamin B5 (Pantothenic Acid)

Turns food into fuel

Pantothenic acid is turned into coenzyme A (CoA) in five steps. The first step, done by the enzyme pantothenate kinase, controls the overall rate. CoA's working end is a sulfur group (from cysteine) that forms a high-energy bond with carbon fragments, called a thioester. That bond makes the attached fragment reactive enough to be passed on, burned or built into something larger. Biochemists sometimes describe CoA as a "carrier handle" for carbon.¹

Almost every fuel passes through it:

• Carbohydrate: pyruvate dehydrogenase attaches the two-carbon piece of pyruvate to CoA, making acetyl-CoA, the molecule that feeds the TCA cycle.
• Fat: every fatty acid is first attached to CoA before it can enter the mitochondria and be broken down two carbons at a time, with each piece leaving as acetyl-CoA.
• Protein: leucine, isoleucine, lysine and other amino acids end up as acetyl-CoA, succinyl-CoA or similar CoA compounds.
• Inside the TCA cycle: succinyl-CoA is one of its intermediates. It is also the starting point for making heme.

Acetyl-CoA is where all the fuels meet. From there, carbon is either burned for energy or built into fat, cholesterol and ketones. Cells adjust how much CoA they make to their energy state, and pantothenate kinase is shut down by its own end products.¹

Burns and builds fat

B5 is needed for fat in both directions, because it supplies two different "handles":

• Breaking fat down uses CoA itself. Fatty acids are activated as fatty acyl-CoA, moved into mitochondria (via carnitine) and broken down into acetyl-CoA.
• Building fat uses 4′-phosphopantetheine, the pantothenate-containing arm of CoA. It is attached to the acyl carrier protein inside fatty acid synthase. That flexible arm holds the growing fatty-acid chain and swings it between the enzyme's active sites as two carbons are added each round, until it reaches palmitate (C16).¹
• Cholesterol and ketones are both built from acetyl-CoA via HMG-CoA, the compound statins block on its way to cholesterol. Ketones form when the liver has more acetyl-CoA than its TCA cycle can handle. See Statins & LDL.

Whether fat is burned or built depends on hormones and energy state, not on how much B5 is around. B5 is needed for both directions, but it doesn't steer either one. Claims that high-dose B5 helps with weight loss or acne aren't supported by solid trials.

Makes acetylcholine

Acetylcholine is the neurotransmitter for memory and attention, for the parasympathetic "rest and digest" system, and at every nerve–muscle junction. It is made in one step. The enzyme choline acetyltransferase moves the acetyl group from acetyl-CoA onto choline. So B5 (as acetyl-CoA) and choline (from eggs, liver and phospholipids) are the two raw materials. Cholinergic neurons draw on the same acetyl-CoA they burn for energy, so their energy metabolism and neurotransmitter supply are tied together.

The clearest proof that the brain needs CoA comes from genetics. Mutations in PANK2, the brain's main mitochondrial pantothenate kinase, cause pantothenate kinase-associated neurodegeneration (PKAN). It is a progressive movement disorder with iron buildup in the basal ganglia, which appears on MRI as an "eye of the tiger" sign.² PKAN is a defect in making CoA, not a shortage of dietary B5, so ordinary B5 supplements don't fix it. But it shows that neurons can't tolerate a local CoA shortfall.

Intake

The adequate intake is about 5 mg/day. The name comes from Greek pantothen, "from everywhere", and it is in almost every food, so deficiency from diet alone is essentially unknown. Gut bacteria also make some. Food CoA is broken down to free pantothenate in the gut before absorption, and absorption saturates at high doses.

Top foods

• Beef liver: about 6–7 mg in 3 oz, more than a day's worth
• Shiitake mushrooms, cooked: about 2.6 mg per ½ cup
• Sunflower seeds: about 2 mg in 1 oz
• Avocado: about 2 mg per fruit
• Chicken: about 1 mg in 3 oz
• Milk: about 0.9 mg per cup

Deficiency

Deficiency has only been produced on purpose. In 1950s experiments, volunteers ate a pantothenate-free diet, some also with a blocking compound, and developed fatigue, irritability, sleep problems, stomach upset, numbness and painful "burning feet." The symptoms went away with pantothenate. Burning-feet syndrome was also reported in malnourished prisoners of war in World War II. Outside starvation, deficiency doesn't occur.