it's hard to test for zinc deficiency. [2010 update: not hard. optimal serum value average 18.2 - 18.4 umol/L] you would have to look at your dietary sources, if you get enough, if you do things that are known to strip zinc from your system, that kind of thing.
diabetes may not cause amenorrhea, but so far i have read that diabetics are typically low on zinc - zinc helps with the regulation of blood sugar -and also zinc deficiency can cause sexual dysfunction including amenorrhea. and zinc deficiency can screw up your immune system.
here's a blurb i found:
Zinc deficiency usually results from inadequate intake of foods high in zinc, such as seafood, oatmeal, bran, meat, eggs, and nuts, or from impaired absorption caused by short bowel syndrome, Crohn's disease, or pancreatic insufficiency. It may also be due to excessive intake of foods containing iron, calcium, vitamin D, and the fiber and phytates in cereals, that bind zinc to form insoluble chelates that prevent its absorption. It occasionally can results from blood loss caused by parasitism. Alcohol, cirrhosis, dialysis, burns, draining wounds, and corticosteroids increase renal excretion of zinc. (http://www.med-help.net/ZincDeficiency.html
and here's a study:
Saudi Med J. 2006 Mar;27(3):344-50.
Serum zinc levels in diabetic patients and effect of zinc supplementation on glycemic control of type 2 diabetics.
Al-Maroof RA, Al-Sharbatti SS.
Ministry of Health, Baghdad, Iraq.
OBJECTIVE: The present study is an attempt to assess serum zinc level in a sample of diabetic patients (both type 1 and type 2 diabetics) in comparison with those of apparently healthy controls, and to ascertain the relationship between the levels of serum zinc with some epidemiological variables. Furthermore, a trial of zinc supplementation for 3 months conducted to assess the effect of zinc supplementation on glycemic control of the studied type 2 diabetic patients, and the factors that affect the response to this supplementation. METHODS: Collection of data was carried out during the period between November 2002 to February 2003 at the Diabetic Center of Merjan Teaching Hospital in Babil Governorate, Iraq. In the first part of the study (a case-control study), the diabetic group included 133 diabetic patients (type 1 and 2) who were chosen from patients attending the Diabetic Center during the period of the study. The control group included 133 apparently healthy subjects who were selected from the workers of the same hospital. Selection of cases and controls was carried out by using systematic random sampling procedure. In the second part of the study (single blind were intervention study), type 2 diabetic patients (101 patients) divided into 2 groups; the first group included 50 patients supplemented with oral zinc sulfate (30 mg of elemental zinc/cap/day) for 3 months and second group included 51 patients given placebo and designed as control group. RESULTS: The first part of the study shows that the mean value for serum zinc level was significantly lower in diabetic patients than healthy controls (64.2 +/- 12.6 microg/dl for type 1 diabetics, and 68.9 +/- 11.9 microg/dl for type 2 diabetics versus 83.4 +/- 12.5 microg/dl for healthy controls). Using simple linear regression, significant positive correlation was found between serum zinc level and years of education and significant negative correlation was found between serum zinc level and baseline HbA1c% value, in the diabetic group. While significant positive correlation found between serum zinc level and estimated zinc intake in the control group. Using multiple regression analysis, serum zinc level showed significant positive correlation with gender (being a male compared with female), and estimated zinc intake and significant negative correlation with diabetes state (diabetic compared with non-diabetic), residence (urban compared with rural residents), and plant protein intake. The second part of the study shows that the mean value for HbA1c% concentration of the supplemented group decreased significantly at the end of the 3 months of follow up, while no significant changes were found in the mean value for HbA1c% of the control group. The present study showed that the change in HbA1c% after supplementation had significant negative correlation with baseline HbA1c% value. CONCLUSION: Diabetic patients have significantly lower mean serum zinc levels compared with healthy controls. Zinc supplementation for type-2 diabetics has beneficial effects in elevating their serum zinc level, and in improving their glycemic control that is shown by decreasing their HbA1c% concentration.
and another interesting autoimmune tidbit (don't know how much you've read about ms yet but this article is just screaming that zinc is important for the kinds of cell functions that are screwed up in ms):
Zinc and immune function: the biological basis of altered resistance to infection
AH Shankar and AS Prasad
Department of International Health, The Johns Hopkins University School of Public Health, Baltimore, MD 21205, USA. firstname.lastname@example.org
Zinc is known to play a central role in the immune system, and zinc- deficient persons experience increased susceptibility to a variety of pathogens. The immunologic mechanisms whereby zinc modulates increased susceptibility to infection have been studied for several decades. It is clear that zinc affects multiple aspects of the immune system, from the barrier of the skin to gene regulation within lymphocytes. Zinc is crucial for normal development and function of cells mediating nonspecific immunity such as neutrophils and natural killer cells. Zinc deficiency also affects development of acquired immunity by preventing both the outgrowth and certain functions of T lymphocytes such as activation, Th1 cytokine production, and B lymphocyte help. Likewise, B lymphocyte development and antibody production, particularly immunoglobulin G, is compromised. The macrophage, a pivotal cell in many immunologic functions, is adversely affected by zinc deficiency, which can dysregulate intracellular killing, cytokine production, and phagocytosis. The effects of zinc on these key immunologic mediators is rooted in the myriad roles for zinc in basic cellular functions such as DNA replication, RNA transcription, cell division, and cell activation. Apoptosis is potentiated by zinc deficiency. Zinc also functions as an antioxidant and can stabilize membranes. This review explores these aspects of zinc biology of the immune system and attempts to provide a biological basis for the altered host resistance to infections observed during zinc deficiency and supplementation.