Uterine Fibroids

Uterine fibroids are benign tumors of the uterine smooth muscle whose growth is fundamentally driven by a hormonal environment of estrogen dominance secondary to low thyroid function. 2 Peat argued that normalizing thyroid is the single most effective intervention, as adequate thyroid hormone lowers estrogen while simultaneously increasing the activity of enzymes that break down fibrotic tissue. 2 He documented a case in which a woman with a tennis-ball-sized fibroid blocking her fallopian tubes achieved complete resolution and became pregnant within months by taking enough thyroid to maintain a resting pulse of 110 beats per minute, which suppressed her estrogen and visibly shrank the tumor on monthly ultrasounds. 3

The pathophysiology of fibroids is a specific instance of a generalized fibrotic process driven by excitotoxicity and energy failure. Peat described fibrosis as an abnormal progression of extracellular matrix formation involving increased collagen volume, density, and pathological cross-linking, analogous to the stiffening of aging tissues. 2 Estrogen is a powerful promoter of this process; chronic estrogen treatment produces fibrosis of practically all tissues, and the fibrotic tissue later becomes a site for cancer development. 9 The condition is inseparable from hypothyroidism, which creates a leaky, edematous cellular state and shifts the ratio of estrogen to progesterone and androgens unfavorably high. 2 This same mechanism underlies related conditions including endometriosis and breast fibrocystic disease. 6

Several nutritional and hormonal factors directly oppose the fibrotic process. Vitamin D and calcium are recognized as important anti-fibroid factors, and Dinkov has highlighted evidence that maintaining vitamin D blood levels above 30 ng/mL may shrink or remove fibroids, with synergism between vitamin D and bioidentical progesterone allowing for lower effective doses of each. 2 Progesterone itself has the strongest antifibromatogenic action among the steroids, working partly through its effects on collagenase and fibroblasts and partly by displacing estrogen from tissues. 9 Peat noted that progesterone was tested and does work for shrinking fibroids, though it functions partly through supporting thyroid activity. 5 Magnesium, taurine, and niacinamide also have protective functions that can help reduce or reverse inflammatory and fibrogenic processes. 8

Dietary strategies center on minimizing substances that promote the nitric oxide pathway and maximizing protective nutrients. Avoiding polyunsaturated fats helps maintain proper urea formation rather than shifting arginine metabolism toward nitric oxide, which is involved in fibrotic processes. 2 Protein deficiency is thrombogenic and likely excitotoxic, while excess tryptophan increases serotonin production and excess arginine increases nitric oxide formation. 8 The amino acid glycine, which constitutes a very high percentage of collagen, serves as an inhibitory transmitter and has remarkable protective activities against toxins. 8 Peat recommended blood testing to check thyroid, estrogen, and vitamin D status as a starting point for addressing fibroids, and emphasized that keeping carbon dioxide production high by optimizing thyroid function is protective against the serotonin and nitric oxide pathways that drive fibrosis. 2