Wilmorej -- The omega-3 fatty acids are in the brain and nerves, the omega-6 fatty acids are in organs like the heart and kidneys, the muscles are almost entirely saturated & monounsaturated fats in a 50-50 ratio, and those fats appear in all tissues abundantly.

People have worried about eating brains due to prions / mad cow disease. Cold water fish may be a less risky method, though brains were eaten by our hunter-gatherer ancestors.

If the meat is lean, just add oil. Olive oil works great.

With all due respect, Dr. De Vany, I must disagree with some of the conclusions you draw from those figures.

First, the fact that the LH and FSH drop in testosterone groups merely shows that the body perceives high levels of testosterone and therefore is lowering is own production. The HTPA works on a negative feedback loop by which higher levels of T result in a corresponding decease in the body's urgency to make it. We would also expect to see lower LH and FSH values in males with naturally high T (e.g., 1000 ng/dl). This does not mean that these men have no sex drive. High LH and FSH values are not necessarily a good thing. Often it can be quite the opposite, in fact. Moreover, a drop in LH and FSH can be mitigated by combining hCG with exogenous testosterone use.

Second, the men are not being emasculated in the sense that they look and feel feminine. They are in the sense that their testicles are shrinking and less effective. But I'm sure these men are more muscular and have higher sex drives than the non-testosterone groups.

Third, as you note, the SHBG dropped in both testosterone groups. This is a good thing. Although you disagree, it is clear that the less SHBG circulating, the less T that is tightly bound. The result is that more T is free to bind to tissue receptor sites. As you point out, the relationship between SHBG and T is not linear, but is definitely present. Thus, having high T and low SHBG is an ideal androgenic situation.

Finally, you made some reference to breast pain. I'm confident that this stems from gynocomastia or a disorder related to high estrogen. Without question, when testosterone is elevated to such extreme degrees, the body will convert some to estrogen. When T is that high, even a small amount being converted to E will result in abnormally high levels of E in men. Hence the gyno. The question is what would have happened if these men were using substances to prevent the T from being converted to E through aromatase activity.

In sum, this is not a fair comparison. When administered by a knowledgeable professional, testosterone combined with estrogen lowering substances and hCG will result in very high levels of androgenic hormones with a corresponding increase in sex drive, muscle mass, and a sense of well being. I dare say nothing natural can match that.

I am struggling with a "healthy fats" issue: here in the Midwest, there are very few types of high omega-3 fatty fish available, so I am looking at an alternative source, namely grass-fed (or naturally raised) beef, chicken, turkey, pork, lamb and goat. One of local farmers appears to be willing to grind up all of the edible parts of the animal(s) to make patties. This would seem to provide a food source that would closely approximate the food available to our ancestors. I assume the omega 3/omega 6 ratios would be good for this type of meat, but haven't been able to find a good analysis of it on the web. I also would worry about excess protein, since these are pretty lean animals. Any thoughts out there?

I just read the following text in Runners's World; it boils down to that you don't need to take anti oxidants to increase your lifespan if you're eating low carb:
"Treatment of nematodes with different antioxidants and vitamins prevents extension of life span"
Glucose Restriction Extends Caenorhabditis elegans Life Span by Inducing Mitochondrial Respiration and Increasing Oxidative Stress
Summary
Increasing cellular glucose uptake is a fundamental concept in treatment of type 2 diabetes, whereas nutritive calorie restriction increases life expectancy. We show here that increased glucose availability decreases Caenorhabditis elegans life span, while impaired glucose metabolism extends life expectancy by inducing mitochondrial respiration. The histone deacetylase Sir2.1 is found here to be dispensable for this phenotype, whereas disruption of aak-2, a homolog of AMP-dependent kinase (AMPK), abolishes extension of life span due to impaired glycolysis. Reduced glucose availability promotes formation of reactive oxygen species (ROS), induces catalase activity, and increases oxidative stress resistance and survival rates, altogether providing direct evidence for a hitherto hypothetical concept named mitochondrial hormesis or “mitohormesis.” Accordingly, treatment of nematodes with different antioxidants and vitamins prevents extension of life span. In summary, these data indicate that glucose restriction promotes mitochondrial metabolism, causing increased ROS formation and cumulating in hormetic extension of life span, questioning current treatments of type 2 diabetes as well as the widespread use of antioxidant supplements."

surf to and I am interested what you think: http://www.cellmetabolism.org/content/article/abstract?uid=PIIS1550413107002562

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