Myelination

Myelination is the process by which oligodendrocytes—glial cells with sheet-like processes—wrap themselves in thin layers around the conductive axons of nerve cells, forming a multilayered enclosure called myelin composed of proteins and complex lipids, including cholesterol. 2 This process is fundamentally dependent on thyroid hormone; oligodendrocytes absorb T3 under the influence of thyroid, and their absorption is promoted by butyrate, an anti-stress substance found in butter and coconut oil. 2 Peat argued that thyroid is responsible for both myelination and hormone formation, and that in conditions like multiple sclerosis, the problem is specifically with myelination rather than with the nerve cells themselves. 5

Peat rejected the standard textbook view that myelin functions primarily as an electrical insulator enabling saltatory conduction, calling this idea a "fetish" that obstructed progress in biology. 4 Instead, he emphasized that oligodendrocytes are steroid-synthesizing cells that produce pregnenolone when activated, and he considered it obvious to ask whether their local production of pregnenolone in response to stress or fatigue is relevant to the conduction processes of the nerves they surround. 2 The brain's white matter is extremely rich in cholesterol, and maintaining sufficient energy—through sugar, thyroid, and progesterone—is necessary to synthesize cholesterol and myelin fast enough. 7 Stress activates enzymes that attach fatty acids to cholesterol, forming esterified cholesterol, a process promoted by estrogen and associated with tissue deterioration. 7

The breakdown of myelin, according to Peat, is driven by a chronic, slight energy deprivation that causes tissue edema. 6 When energy is low—for example, when thyroid is deficient—cells take up water and swell, and while myelin is being taken down in the normal turnover process, it cannot be resynthesized efficiently because the organism cannot make sufficient pregnenolone and progesterone. 6 Thyroid, progesterone, and pregnenolone are all involved in the formation of new myelin and in the prevention of the edema that damages it, while saturated fatty acids also support myelin reformation. 2 The methylation pathway is additionally involved in making the myelin coating of nerves, with a substantial portion of the body's methylation capacity directed toward synthesizing creatine for cellular energy. 9

Peat connected myelination to broader developmental and degenerative processes. He noted the historical, erroneous belief that babies do not experience pain before myelination is complete around 18 months, a view he considered a form of "mind blindness" or autism-like lack of empathy. 3 In old age, brain steroids fall to about 5% of their youthful levels, yet glial cells become more numerous and myelin formation typically continues without problem, unlike in multiple sclerosis where myelination specifically fails. 5 This suggested to Peat that Alzheimer's disease might involve a specific premature loss of brain pregnenolone production, while MS involves a deficiency of thyroid or of T3 within the oligodendrocytes, leaving those cells deficient in their ability to produce pregnenolone locally for the nerve fibers they surround. 5