Brown et al. found a "marked accumulation" of retinal exudate in patients with high triglyceride levels (Brown et al. 1984). Dodson and Gibson in a study on patients with type 2 diabetes found that hypercholesterolemia was a risk factor in the development of diabetic maculopathy (Dodson and Gibson 1991). In epidemiological studies Chew et al., and Klein et al. found that increased blood lipid levels are associated with diabetic retinopathy in that subjects with elevated lipids had a greater risk of developing high-risk PDR and a greater risk of vision loss from DME (Chew et al. 1996; Klein et al. 1991). Chowdhury et al. conclude that a toxic effect of LDL on pericytes could be enhanced by LDL glycation or oxidation (Chowdhury et al. 2002).

Although there has been some variation in study conclusions, epidemiological and observational studies have generally concluded that low endogenous testosterone levels in men are associated with lipid profiles consisting of decreased high-density lipoprotein (HDL) cholesterol levels and increased total cholesterol, triglycerides and LDL levels compared to normal or higher levels. This is referred to as Hypoandrogen Metabolic Syndrome (HAM) and often accompanies the metabolic syndrome of central obesity and insulin resistance (Kaushik et al. 2010). Multiple studies have reached a similar conclusion and found that men with higher levels of testosterone generally have better lipid profiles including high HDLs and lower triglycerides (Kaushik et al. 2010). Supplementation of testosterone in hypoandrogenesis is generally considered to decrease HDLs and only modestly affect LDLs (Mendelsohn and Karas 2005). Lower testosterone levels in men have also been linked to central adiposity, insulin resistance, hyperinsulinemia and type 2 diabetes (Webb and Collins 2010). Testosterone, acting through the adipocyte androgen receptors, increases expression of P-adrenergic receptor, protein kinase A, and lipase (Wu and von Eckardstein 2003).

The actions of estrogens on the blood lipid levels of women have been studied for many years. Lipid levels are affected by the action of endogenous sex steroid hormones and hormone replacement therapy (HRT) on liver lipoprotein metabolism. In an analysis of several studies Mumford et al. found that total cholesterol and LDL levels were highest during the follicular phase of the menstrual cycle and were lower during the luteal phase. They found HDLs to be higher during the follicular and peri-ovulatory phases. In a meta-analysis of sex steroid use by transsexual individuals, Elamin et al. found a reduction in HDL in female to male patients receiving androgens and an increase in HDLs in male to female patients receiving estrogens. They found triglyceride levels increased in both female to male patients receiving androgens and male to female patients receiving estrogens (Elamin et al. 2010).

After menopause it has been found that LDLs and triglyceride levels rise and HDL levels decrease. HRT appears to positively affect lipid levels by lowering total cholesterol, LDLs and raising HDLs, but negatively affects lipid levels by raising triglycerides (Mendelsohn and Karas 2005). Some controversy has arisen over the delivery method of HRT. Nanda et al. found that HRT transdermal therapy (estrogen 50 ^g/ day) had the advantage of lowering triglyceride levels as opposed to oral (conjugated equine estrogens 0.625mg/ day) (Nanda et al. 2003). The Women's Health Initiative (WHI) trial and the Heart and Estrogen/Progestin Replacement Study (HERS) found that a favorable lipid profile developed using exogenous estrogens, but also found using estrogen with progestin was associated with elevated levels of CVD. Progesterone is believed to either have a neutral effect on lipids or to negatively affect estrogen's positive effects (Hulley et al. 1998; Mumford et al. 2011; Rossouw et al. 2002).



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