At 10.22pm I took as follows all spaced apart by 7 minutes each...
65mg of ester C
1/4 of a Solgar 2.5mg chelated copper
65mg of ester c
1/3 of VRP methylselenocysteine, 1/3 of Selenium L-selenomethionine with 70 mg of Trimedica MSM
1/10 of a Solaray manganese capsule
1 whole capsule of Houston No-fenol
1 Nutracology germanium
5 drops Ethical nutrients Mycellized vit A
1/4 Source naturals 5mg Melatonin with B6
1 hour later I was wide awake and really cheerful,
It was well worth staying up that extra hour to ingest all the above as
I'd been ready to crash before taking them all and quite astonished
at the resulting change that ensued.
written by Eileen Prunster
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i post i wrote on who_knows titled 'vitamin e anti viral' on the 25th/06/06
took 100 iu of blackmores alpha d tocopherol this morning and i feel
it was protective on going to town late this afternoon
100iu is to much too take daily but is another anti viral supplement modulation
the things which are postively pro viral are iron and vit d i think
vit d is anti-yeast and anti-bacteria however, turning on pathways that make peptides against them
for migriane vit e reduces blood platlet adhesion, but you will get rebound of course once vit e levels drop?
i am an old mouse (hence the old cats after me)
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Vitamin E-enhanced IL-2 production in old mice: naive but not memory
T cells show increased cell division cycling and IL-2-producing capacity.
Adolfsson O, Huber BT, Meydani SN.
Nutritional Immunology Laboratory, Jean Mayer U.S. Department of
Agriculture Human Nutrition Research Center on Aging, Tufts
University, 711 Washington Street, Boston, MA 02111, USA.
Aging is associated with reduced T cell function, as demonstrated by
decreased T cell proliferation and IL-2 production. These changes
respond to supplemental vitamin E both in animals and humans, in part
by the reduction of T cell suppressive PGE(2), the production of
which by macrophages is increased with age. To evaluate whether
vitamin E has a direct PGE(2)-independent effect on T cell responses,
T cells purified from the spleens of young and old mice were
preincubated with vitamin E or vehicle control. Activation-induced
cell division of T cells from old mice was lower than that by young,
and the production of IL-2 following 48-h activation was less by T
cells from old mice. There was an age-related decline in both the
number of IL-2+ T cells and the amount of IL-2 produced per cell.
Despite decreased IL-2 protein at 48 h, the expression of IL-2 mRNA
at 6 h and IL-2 protein production at 6 and 16 h was greater by T
cells from old mice compared with that of young. Age-related decline
in cell division and IL-2 production at 48 h was only observed within
the naive T cell subpopulation. Vitamin E increased both cell-
dividing and IL-2-producing capacity of naive T cells from old mice,
with no effect on memory T cells. These data indicate that naive T
cells exhibit the greatest age-related defect and show for the first
time that supplemental vitamin E has direct immunoenhancing effect on
naive T cells from old mice.