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Thanks for the bump :) ...

Re: zinc - I found it made me feel not so good when I tried supplementing, so cut it out fairly quickly.

2009 Jun;9(2):132-44.

T-lymphocytes: a target for stimulatory and inhibitory effects of zinc ions.
Hönscheid A, Rink L, Haase H.

Institute of Immunology, Medical Faculty, RWTH Aachen University, 52074 Aachen, Germany.

Abstract
The trace element zinc is a crucial cofactor for many proteins involved in cellular processes like differentiation, proliferation and apoptosis. Zinc homeostasis is tightly regulated and disturbance of this homeostasis due to genetic defects, zinc deficiency, or supplementation influences the development and the progression of various infectious and autoimmune diseases. The immune system is strongly impaired during zinc deficiency, predominantly the cell-mediated response by T-lymphocytes. During zinc deprivation T-lymphocyte development, polarization into effector cells, and function are impaired. This leads to reduced T-cell numbers, a decreased ratio of type 1 to type 2 T-helper cells with reduced production of T-helper type 1 cytokines like interferon-gamma, and compromised T-cell mediated immune defense. Accordingly, disturbed zinc homeostasis increases the risk for infections, and zinc supplementation restores normal immune function. Furthermore, several disorders, like mycobacterial infections, asthma, diabetes, and rheumatoid arthritis are accompanied by decreased zinc levels and in some cases disease progression can be affected by zinc supplementation. On the molecular level, apoptosis of T-cell precursors is influenced by zinc via the Bcl-2/Bax ratio, and zinc ions inhibit caspases-3, -6, -7, and -8. In mature T-cells, zinc interacts with kinases involved in T-cell activation, like protein kinase C and the lymphocyte protein tyrosine kinase (Lck), while higher zinc concentrations are inhibitory, reducing the activities of the interleukin-1 receptor-associated kinase (IRAK) and calcineurin. Taken together, zinc homeostasis influences T-lymphocytes via several molecular targets, leading to a modulation of T-cell-dependent immune responses.

Results: The patient noticed the discharge blue sweat for a period of 2 months before
he came to seek treatment. The patient’s medical and medication history is
noncontributory except that the patient was taking hypertensive drugs. The
conditions were ultimately treated with prescription antiperspirant Xerac-AC and
Drysol; they completely eliminated both the smell of bromhidrosis and the discharge
of chromhidrosis. This is the first time an antiperspirant deodorant was reported to
have significantly diminished both the smell and discharge of bromhidrosis and
chromhidrosis, respectively. The patient’s undergarments revealed excessive copper
and zinc levels, which may be the cause for the blue color of the sweat. However,
the etiology is still unknown, and further research in patients with similar conditions
should be investigated.