Schaff et al. reported that,
"In conclusion, we showed for the first time for TSH that the two
dominant intracellular signal transduction systems (cAMP formation and IPs
release) are activated to different degrees by hTSH glycosylation variants."
They showed that non-fucosylated TSH did not activate the IP (inositol phosphate)
pathway, although non-fucosylated TSH could still activate the cAMP (cyclic AMP).
Mannose enriched TSH could activate either IP or cAMP.
Also, to the type O's, the experimental method for binding fucose was to use lentil lectin.
From this, I inferred that I did not want to be fucose deficient, unless I wanted an inactive
inositol phosphate pathway for signal transduction in my nervous system.
IP pathway is closely linked to calcium neurochemistry.
Please don't ask me to delve too much deeper; that's a doctoral topic and a half.
Could you e-mail me some refs on some of your discussion points?
Your inferences are intriguing and you extrapolate farther out than I usually go without at least a study or two.