- 95% Male sex Hormones
- 95% Female sex Hormones
- 95% of Adrenal Hormones
All are made from a master steroid in the body – Cholesterol
Your body only makes 10% of what it needs, the other 90% comes from dietary sources.
If adrenal glands are exhausted you are deficient in cholesterol.
Brain is 75% Mylan, this is made 100% from cholesterol
Elevated cholesterol is caused by:
- B3 (niacin) deficiency
- Omega 3 deficiency
- Chromium deficiency
- vanadium deficiency
- low thyroid
The causes that contribute to most cases of dyslipidemia in adults. The most important secondary cause in developed countries is a sedentary lifestyle with excessive dietary intake of saturated fat and trans fats. Trans fats are polyunsaturated or monounsaturated fatty acids to which hydrogen atoms have been added; they are commonly used in many processed foods and are as atherogenic as saturated fat. Other common secondary causes include diabetes mellitus, alcohol overuse, chronic kidney disease, hypothyroidism, primary biliary cirrhosis and other cholestatic liver diseases, and drugs, such as thiazides, β-blockers, retinoids, highly active antiretroviral agents, estrogen and progestins, and glucocorticoids.
Diabetes is an especially significant secondary cause because patients tend to have an atherogenic combination of high TGs; high small, dense LDL fractions; and low HDL (diabetic dyslipidemia, hypertriglyceridemic hyperapo B). Patients with type 2 diabetes are especially at risk. The combination may be a consequence of obesity, poor control of diabetes, or both, which may increase circulating FFAs, leading to increased hepatic VLDL production. TG-rich VLDL then transfers TG and cholesterol to LDL and HDL, promoting formation of TG-rich, small, dense LDL and clearance of TG-rich HDL. Diabetic dyslipidemia is often exacerbated by the increased caloric intake and physical inactivity that characterize the lifestyles of some patients with type 2 diabetes. Women with diabetes may be at special risk for cardiac disease from this form.
Patients with premature atherosclerotic cardiovascular disease, cardiovascular disease with normal or near-normal lipid levels, or high LDL levels refractory to drug therapy should probably have Lp(a) levels measured. Lp(a) levels may also be directly measured in patients with borderline high LDL-cholesterol levels to determine whether drug therapy is warranted. C-reactive protein and homocysteine measurement may be considered in the same populations.
Secondary causes: Tests for secondary causes of dyslipidemia—including measurements of fasting glucose, liver enzymes, creatinine, thyroid stimulating hormone (TSH), and urinary protein—should be done in most patients with newly diagnosed dyslipidemia and when a component of the lipid profile has inexplicably changed for the worse.