iodine and gut problems +humic acids and zeolites

[Guest guest]

I

posted this to another list looking at zeolites and iodine. Want to put

it here also because of the comment on reduced iodine

availability in the gut. I'm guessing that compromised guts

make getting the iodine in all the harder. I might be why some

people need much higher levels to load. I would love to see a

celiac study and iodine loading.

(zeolites,

humic acids and fulvic acids all seem ot have the mechanism of being

highly reactive and carrying things places...they are in the clay

groups)

Lynn

http://www.pjbs.orgpjnonline/fin295.pdf

Mineral transfer: Humic acids act as dilator

increasing cell wall permeability. This increased permeability allows easier

transfer of minerals from the blood to the bone and cells. Calcification of a

bovine improved by 16% (Kreutz and Schlikekewey, 1992). There are also

changes in intracellular divalent calcium 500 to 2000 mg kg-1 bw for the treatment of

diarrhoea, levels (Yang et al., 1996).

However, literature also reports binding of iodine

from foods

(Summers et al.,1989) so that antithyroideal effects could be supposed.

But reverse concluded by (Huang below. et al., 1994) that the humic

acids do not induce goiter, but they may enhance the goitrogenic effect of

low iodine.

From a recent study by the author at the

Institute of Animal Nutrition, Nutrition Diseases and Diatetics, University of

Leipzig, Germany indicated the absence of goiter genic effect in broiler

showing lack of dose related effects on visceral organs and histomorphometric

parameters of thyroid gland (Table 3 and 4).

Just as fulvic acid carries

ife-sustaining minerals to the body they also captures and removes toxic metals from

the body.

Fuchs et al.,1982, indicated that the HA had differentiated effects upon

trace elements in laboratory rat. Plasma iron levels were hardly affected,

while copper and zinc levels suppressed with a tendency for recovery after 60

days. Seffner et al., 1995, could show that small amounts of

concentration in blood result in histological signs of goitre and trace it back

to a reduced iodine availability in the

intestine.

So, it is contradictory of the recent findings

of the author because (Table 3 and 4)

Seffner et al.,

1995, applied to drinking water, were comparable to our 2.4 g kg-1 feed. The rat diet

contained 0.9 mg I kg-1. Authors experimental diet contained 2.5 mg added I kg-1 feed.

Both dosages were quite

above the requirement or the allowance data. Probably, (i) high iodine of diet

inhibited peritoneum the potential occurrence of goitre, (ii) the method was

too rough to detect the initial stage of iodine deficiency, and (iii) length of

the feeding trial was to short.