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I was reading in the university health news daily website that a study performed by researchers at the University of Texas . Anderson Cancer Center found that men with prostate cancer who ate 3 tablespoons of milled or ground flax seeds each day had decreased prostate cancer cell proliferation compared to similar men who did not eat flax seeds. According to the American Cancer Society, men who supplement their diets with flax seed have lower PSA levels and slower growth of benign as well as cancerous prostate cells.
Perhaps the effect of phytoestrogenic in humans it’s not fully understood as yet.
Cheers

Jackson et al. (2001) reported a significantly reduced frequency of HLA class II type DQ7 allele in patients with variant CJD (vCJD; see 123400 ), but not in those with classical CJD. In a sample of 50 British Caucasians with variant CJD compared with 26 patients with sporadic CJD and 197 cadaveric controls, the frequency of the DQ7 allele was far reduced, being present in 12% of variant CJD patients versus 46% of sporadic CJD patients and % of the cadaveric controls (P = ). Individuals not carrying the DQ7 allele have a -fold relative risk of contracting variant CJD versus others who do carry the DQ7 allele. The DQ7 allele is also known as DQB1*0301/4/9.

The fetal adrenal cortex lacks expression of the enzyme early on, thus mineralocorticoids (. aldosterone ) and glucocorticoids (. cortisol ) cannot be synthesized. This is significant because cortisol induces type II pneumocytes of the lungs to synthesize and secrete pulmonary surfactant ; without pulmonary surfactant to reduce the alveolar surface tension , premature neonates may die of neonatal respiratory distress syndrome . If delivery is unavoidable (. because of placental abruption , or pre-eclampsia / HELLP syndrome ), then glucocorticoids (. cortisol) can be administered.

Hypercortisolism can occur in several disorders other than Cushing's syndrome [ 1,2 ]. When such patients present with clinical features consistent with Cushing's syndrome, they may also be referred to as having physiologic hypercortisolism or pseudo-Cushing's syndrome. Clinically, patients with these physiologic forms of hypercortisolism seldom have the cutaneous (ie, easy bruising, thinning, and friability) or muscle (ie, proximal muscle atrophy and weakness) signs of Cushing's syndrome [ 3 ]. However, these conditions/disorders should be excluded when evaluating patients for Cushing's syndrome. (See "Establishing the diagnosis of Cushing's syndrome", section on 'Exclude physiologic hypercortisolism' .)

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Hypercortisolism can occur in several disorders other than Cushing's syndrome [ 1,2 ]. When such patients present with clinical features consistent with Cushing's syndrome, they may also be referred to as having physiologic hypercortisolism or pseudo-Cushing's syndrome. Clinically, patients with these physiologic forms of hypercortisolism seldom have the cutaneous (ie, easy bruising, thinning, and friability) or muscle (ie, proximal muscle atrophy and weakness) signs of Cushing's syndrome [ 3 ]. However, these conditions/disorders should be excluded when evaluating patients for Cushing's syndrome. (See "Establishing the diagnosis of Cushing's syndrome", section on 'Exclude physiologic hypercortisolism' .)

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