However, intracellular esterases are also capable of cleaving the methyl group of methylmalonic acid and generating the parent molecule malonic acid.Bacterial fermentation in the gut is a quantitatively significant source of propionate, which is a precursor for methylmalonic acid. Alongside this, propionic acid is also absorbed through the diet, as it is naturally present in certain foods or is added as a preservative by the food industry, especially in baked goods and dairy products. In addition, methylmalonate is formed during catabolism of thymine.In a study with fibroblasts, increased accumulations of triglycerides, an altered profile of fatty acid chain length and the presence of odd chain fatty acids were detected. A partial degradation due to accumulated methylmalonic acid and the use of propionyl-CoA as a starter unit for fatty acid synthesis is suggested as a possible cause, supported by the observation of a higher expression of CD36, which imports fatty acids into the cell.In vitro, a connection between free methylmalonic acid and malonic acid to neurotoxicity could be established. Malonyl-CoA decarboxylase deficiency
Malonyl-CoA decarboxylase acts as a catalyst in the conversion of malonyl-CoA to acetyl-CoA and CO2. It is speculated that in MCD deficiency, the excess of mitochondrial malonyl-CoA increases methylmalonic acid levels, as a result of an inhibitory effect on methylmalonyl-CoA mutase. In the cytoplasm, malonyl-CoA acts as an inhibitor of the mitochondrial outer membrane enzyme carnitine palmitoyltransferase I (CPT1), which consequently inhibits fatty acid oxidation.
Recommendations for the use of the lowest effective dose for the shortest duration  help to prevent adverse endometrial effects.Some treatments have been developed more recently. These include selective estrogen receptor modulators, vaginal dehydroepiandrosterone, and laser therapy. Other treatments are available without a prescription such as vaginal lubricants and moisturizers. Vaginal dilators may be helpful. Since GSM may also cause urinary problems related to pelvic floor dysfunction, a woman may benefit from pelvic floor strengthening exercises. Women and their partners have reported that estrogen therapy resulted in less painful sex, more satisfaction with sex, and an improvement in their sex life. Epidemiology
Up to 50% of postmenopausal women have at least some degree of vaginal atrophy. It is likely to be underdiagnosed and undertreated. Terminology
Vulvovaginal atrophy, and atrophic vaginitis have been the preferred terms for this condition and cluster of symptoms until recently. These terms are now regarded as inaccurate in describing changes to the entire genitourinary system occurring after menopause. The term atrophic vaginitis suggests that the vagina is inflamed or infected. Though this may be true, inflammation and infection are not the major components of postmenopausal changes to the vagina. The former terms do not describe the negative effects on the lower urinary tract which can be the most troubling symptoms of menopause for women. Genitourinary syndrome of menopause (GSM) was determined to be more accurate than vulvovaginal atrophy by two professional societies. The term atrophic vaginitis does not reflect the related changes of the labia, clitoris, vestibule, urethra and bladder.