Zinc is an essential nutrient for mammals. Zinc has only one oxidation state Zn 2+ but it has many coordination states, which can alter without demanding energy. Coordination states depend on prevailing pH. In soils the coordination state changes from octahedral (nonphysiologic) form to tetrahedral (physiologic) form when pH rises to about 6.5. Weathering processes of common soil mineral mica are also pH dependent. Large scale argricultural field liming began from 1950's onward in the Western Countries and since that time the incidence of Type 1 diabetes (T1D) began to increase in the Western Countries. Liming elevates soil pH often near 6.5 and favours mosaic mica-vermiculite nanoparticle formation in which vermiculite corner binds zinc in tetrahedral (physiological) coordination state. In this pH mica corner remains in native form and offers the plane for soluble pMHC molecule (binded with antigenic beta-cell specific self peptide) to adhere on mica and as a consequence to trigger the activation of autoreactive CD4 and/or CD8 T cells. Beta-cell specific autoantigens are released because abundant zinc derived from endocytosed zinc-mica-vermiculite particles in lysosomes leads to incresed beta-cell apoptosis, also the physiological neonatal beta-cell mass remodeling enhance beta-cell specific auto-antigen release. Furthermore enterovirusinfections during first years of life are common and can release beta-cell specific auto-antigens. The probable disease mechanism is dealt with this review article.

The incidence and prevalence of multiple sclerosis (MS) have increased much since 1950s. Environmental factors must play a decisive role because the heredity can not be mutated so fast. No one has proposed the mechanical pathway between MS and environmental factors. The aim of this study is to reveal what environmental factors induce multiple sclerosis. From animal models it is known that aggresive T cells (able to cross bloob-brain barrier) are induced in lung. Soil dust containing both weathered mica particles and vitamin B12 containing clay particles ("transformation smectite" particles) can activate myelin specific CD4+ T cells in lung. CD4+ central memory type T cell (resting phenotype) receptor is activated by soluble MHC II when it is anchored on mica particle surface and T cell adheres also on the same mica surface. Further prerequisite is that at the same time smectite clay particle intercalated with vitamin B 12 is endocytosed into the same T cell. T cell activation requires 1) T cell receptor activation and 2) T cell metabolic changes from oxidative phosphorylation to aerobic glycolysis. In classical activation model co-receptor B 28 activation changes T cell metabolism to oxidative glycolysis. In this case at the wrong time dosed vitamin B 12 changes T cell metabolism to oxidative glycolysis using anaplerotic feeding of TCA-cycle, permitting T cell activation to effector phenotype aggressive T cell. The hypothesis is based on new findings in immunobiology and on epidemiological observations.