Indeed, estrogen is a major cause of suppression, probably one of the biggest. Like you mentioned, aromatase, because of excess fat tissue, is a much greater cause of elevated estrogen and suppressed T than endotoxins.
https://www.physiology.org/doi/full/10.1152/ajpendo.00279.2017
"We recognize that the impact of chronic-low level inflammation on testosterone levels seen in our observational study was relatively minor, thereby suggesting that other mechanisms such the conversion of testosterone to estrogen by adipose tissue aromatase probably play a more dominant role in obesity related hypogonadism (9)."
I was just adding that endotoxins and PUFAs and other inflammatory promoting substances/compounds also increase the aromatase and promote estrogen and they also inhibit normal testicular function. But the increased estrogen is the greatest cause yes. Aspirin is a great example of something that inhibits the aromatase and lowers inflammation and can significantly increase T.
Incidentally, COX inhibitors seem to have anabolic effects in the elderly most likely due to that decreased inflammatory budren. Also, COX itself seems to have an inhibitory effect on steroidogenesis and inhibiting it with say aspirin may work similar to a SERM. This would explain why NSAID have anabolic effects in older men.
Inhibition of cyclooxygenase-2 activity enhances steroidogenesis and steroidogenic acute regulatory gene expression in MA-10 mouse Leydig cells. - PubMed - NCBI
Cyclooxygenase-2 regulation of the age-related decline in testosterone biosynthesis. - PubMed - NCBI
COX2-Regulated Testosterone Biosynthesis in Male Aging
https://watermark.silverchair.com/e...uQayLZwc4_PzigE9p8MA2iFPl4Yib1moWF0hZ7Dr6mMfQ
Effect of ibuprofen and acetaminophen on postexercise muscle protein synthesis. - PubMed - NCBI