Biologist Ray Peat has written about this.  Go to his site at www.raypeat.com and look for the essay on this subject.  Basically, stress will cause this, such as too much estrogenic exposure.  After menopause, for example, estrogen gets retained in tissues and causes these kinds of problems.  Again, Ray Peat has some essays directly related to this phenomenon.

Peat's interest is at the tissue/organ level, whereas I've been investigating on the molecular level.  Studies I cite in this context are those such as the following:

 

QUOTE:  The extremely high sensitivity of polyunsaturated fatty acids (PUFAs) to oxygen is apparently used by nature to induce stepwise appropriate cell responses. It is hypothesized that any alteration in the cell membrane structure induces influx of Ca2+ ions. Ca2+ ions are required to activate degrading enzymes, such as phospholipases and lipoxygenases (LOX) that transform PUFAs bound to membrane phospholipids to lipidhydroperoxides (LOOHs). Enzymatic reduction products of LOOHs seem to serve as ligands of proteins, which induce gene activation to initiate a physiological response. Increasing external impact on cells is connected with deactivation of LOX, liberation of the iron ion in its active center followed by cleavage of LOOH molecules to LO * radicals. LO * radicals induce a second set of responses leading to generation of unsaturated aldehydic phospholipids and unsaturated epoxyhydroxy acids that contribute to induction of apoptosis. Finally peroxyl radicals are generated by attack of LO * radicals on phospholipids. The latter attack nearly all types of cell constituents: Amino- and hydroxyl groups are oxidized to carbonyl functions, sugars and proteins are cleaved, molecules containing double bonds such as unsaturated fatty acids or cholesterol suffer epoxidation. LOOH molecules and iron ions at the cell wall of an injured cell are in tight contact with phospholipids of neighboring cells and transfer to these reactive radicals. Thus, the damaging processes proceed and cause finally necrosis except the chain reaction is stopped by scavengers, such as glutathione. Consequently, PUFAs incorporated into phospholipids of the cell wall are apparently equally important for the fate of a single organism as the DNA in the nucleus for conservation of the species. This review intends to demonstrate the connection of cell alteration reactions with induction of lipid peroxidation (LPO) processes and their relation to inflammatory diseases, especially atherosclerosis and a possible involvement of food. Previously it was deduced that food rich in cholesterol and saturated fatty acids is atherogenic, while food rich in n-3 PUFAs was recognized to be protective against vascular diseases. These deductions are in contradiction to the fact that saturated fatty acids withstand oxidation while n-3 PUFAs are subjected to LPO like all other PUFAs...  UNQUOTE.

 

Source:  Mol Nutr Food Res. 2005 Nov;49(11):999-1013.

 

On the internet:  http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=16270286&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus