[Lotus]

Visceral Fat- 

So I'm reviewing scientific evidence about visceral fat and the high amount of associated systemic inflammation, (and in part by glucocorticoids storing fat in their receptors). A few other nasty things like IL-6 (interleukin-6) which is an inflammatory molecule, C-reactive protein (associated with type 2 diabetes, other bad diseases included too) are revealed . Anyways, back to glucocorticoids (which in high amounts can cause systemic inflammation too) so I think to myself what if you control inflammation you help turn off a certain pathway for DHT?, well....we know that DHT is very prevalent in visceral fat (indicated in post-menopause), I think it's entirely possible. 

It's not advisable simply to remove visceral fat through surgery (endangering surrounding internal organs). More to reduce the actual fat cell size (or in hopes I guess) to lower inflammation, in other words, lowering the bodies overall sysmtemic inflammatory response.

Here's one possibility (vitamin A).....a pro-aromatase and a possible anti-DHT weapon, btw carotenoids inhibit 5 alpha reductase....(say goodnight DHT). 

Vitamin A decreases pre-receptor amplification of glucocorticoids in obesity: Study on the effect of vitamin A on 11beta-hydroxysteroid dehydrogenase type 1 activity in liver and visceral fat of WNIN/Ob obese rats

11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) catalyzes the conversion of inactive glucocorticoids to active glucocorticoids and its inhibition ameliorates obesity and metabolic syndrome. So far, no studies have reported the effect of dietary vitamin A on 11β-HSD1 activity in visceral fat and liver under normal and obese conditions. Here, we studied the effect of chronic feeding of vitamin A-enriched diet (129 mg/kg diet) on 11β-HSD1 activity in liver and visceral fat of WNIN/Ob lean and obese rats. Male, 5-month-old, lean and obese rats of WNIN/Ob strain (n = 16 for each phenotype) were divided into two subgroups consisting of 8 rats of each phenotype. Control groups received stock diet containing 2.6 mg vitamin A/kg diet, where as experimental groups received diet containing 129 mg vitamin A/Kg diet for 20 weeks. Food and water were provided ad libitum. At the end of the experiment, tissues were collected and 11β-HSD1 activity was assayed in liver and visceral fat. Vitamin A supplementation significantly decreased body weight, visceral fat mass and 11β-HSD1 activity in visceral fat of WNIN/Ob obese rats. Hepatic 11β-HSD1 activity and gene expression were significantly reduced by vitamin A supplementation in both the phenotypes. CCAAT/enhancer binding protein α (C/EBPα), the main transcription factor essential for the expression of 11β-HSD1, decreased in liver of vitamin A fed-obese rats, but not in lean rats. Liver × receptor α (LXRα), a nuclear transcription factor which is known to downregulate 11β-HSD1 gene expression was significantly increased by vitamin A supplementation in both the phenotypes. This study suggests that chronic consumption of vitamin A-enriched diet decreases 11β-HSD1 activity in liver and visceral fat of WNIN/Ob obese rats. Decreased 11β-HSD1 activity by vitamin A may result in decreased levels of active glucocorticoids in adipose tissue and possibly contribute to visceral fat loss in these obese rats. Studying the role of various nutrients on the regulation of 11β-HSD1 activity and expression will help in the evolving of dietary approaches to treat obesity and insulin resistance.

http://nutritionj.biomedcentral.com/arti...2891-10-70

More to follow I hope.