On May 17, 4:15 pm, "Andrew B. Chung, MD/PhD" <
lov...@thetruth.com>
wrote:
> Kumar wrote:
> > Andrew, in the Holy Spirit, boldly wrote:
>
> > > "Compared with the hyperglycemic condition, the patients (with type-2
> > > diabetes) ingested on average 25 ± 10% more energy during euglycemia
> > > (645 ± 75 vs. 483 ± 37 kcal; P = 0.029)."
>
> > > Source:
http://care.diabetesjournals.org/content/28/12/2884.full
>
> > > Yes, being able to ingest more means the type-2 diabetics were
> > > hungrier and euglycemia for type-2 diabetics is wonderfully healthier
> > > than hyperglycemia.
>
> > > Be hungrier, which really is wonderfully healthier, especially for
> > > type-2 diabetics ...
>
> > >
http://WDJW.net/BeSmart
>
> > > ... because we care about type-2 diabetics,
>
> > > HeartDoc Andrew <><
>
> > Hello,
> > Best Greetings.
>
> Hello Kumar, hope you're wonderfully hungry too :-)
>
>
http://WDJW.net/WonderfullyHungry
Thanks. Yes.
>
> > To me following research article look to hold quite logical validity
> > in better understanding of diabetes type2:-
>
> > Diabetic may start in intestines;
> >
https://news.wustl.edu/news/Pages/23409.aspx
>
> > How do you assess it?
>
> Thehttp://WDJW.net/VATstarts accumulating around the intestines when
> there is overeating (i.e. eating more than the right amount, which is
> 32 oz of daily food).
>
> > Since inflamation is linked to insulin resistance and thinness of
> > mucus/mucus membrane can hold validity to inflammation and altred
> > absorption, it appears that this research should hold validity??
>
> Yes.
This is important snip from this link:
"Instead, Wei says, the mice got sick because of a defect in fatty
acid synthase. The mice without fatty acid synthase had lost the
protective lining of mucus in the intestines that separates the
microbes from direct exposure to cells. This allowed bacteria to
penetrate otherwise healthy cells in the gut, making the mice sick.
Fatty acid synthase is required to keep that mucosal layer intact,”
Wei says. “Without it, bad bacteria invade cells in the colon and the
small intestine, creating inflammation, and that, in turn, contributes
to insulin resistance and diabetes...”
Inflammation and insulin resistance reinforce each other. Inflammatory
substances can cause insulin resistance and inhibit the production of
insulin, both of which interfere with the regulation of blood sugar.
In turn, insulin resistance is known to promote inflammation.
Further study showed that the ability to build the thin, but
important, layer of mucosal cells was hindered by faulty FAS."
Does it suggest VAT accumulation or fat/lipoprotien deficiency? I
think this link suggest lower lipids(so lower lipoprotiens in cell
membranes) causing comparatively thin or senstive cell membrane.
It may be important to understand; 1. how faulty FAS taken place? 2.
Does it make call membrane thin & senstive? 3. How it alter mucus
layer?
Probably this theory may also suggest altered senstivity due to
thining of cell membranesw at other parts?
Btw, whether bile secration is altered due to prolonged Dibetic
type2---either due to low lipid levels(esp. cholestreols) in blood(as
bile is made from Cholestreols) or otherwise?
>
> > Best regards.
>
> To you as well :-)
>
> Be hungrier, which really is wonderfully healthier especially for
> diabetics and other heart disease patients:
>
>
http://groups.google.com/group/sci.med.cardiology/msg/9642aafa0aad16eb?
>
> ...because we mindfully choose to openly care with our heart,
>
> Andrew <><
> --
> Andrew B. Chung, MD/PhD
> EmoryIMVC.org Cardiologist
> and Author of the 2PD-OMER Approach:
http://groups.google.com/group/sci.med.cardiology/msg/9ad0c19df5ffc2f7?- Hide quoted text -
>
> - Show quoted text -