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tjohnson_nb wrote: I would still like to see how high plasma levels can be pushed to with lipo C - like taking 1 gram per 1/2 hr all through the day.
Saw wrote:
Since hydrogen peroxide can only be produced in the extracellular space (not blood vessels)
It sounds like you could never duplicate the IV C effect using any amount of lipo c, since lipo c is intracellular,
so the vitamin c is only released when the liposome enters the cell.
tjohnson_nb wrote:Saw wrote:
Since hydrogen peroxide can only be produced in the extracellular space (not blood vessels)
It sounds like you could never duplicate the IV C effect using any amount of lipo c, since lipo c is intracellular,
so the vitamin c is only released when the liposome enters the cell.
I thought I read that the liposomes are transported to the liver, where the ascorbate is released into the bloodstream.
The similarity in the plasma response curves for liposomal vitamin C and the standard
commercial formulation, shown in Figure 1 (5 g doses), is interesting. There is a hint that
the liposomal form has a slower onset to peak level and a broader profile. Liposomes are
absorbed from the gut and into the liver, before being released into the blood stream. This
response can be seen more clearly in the 20 g dose, in Figure 2. It is apparent that sustained
levels of plasma ascorbate, above the previously assumed maximum of 220 mM L21, are
possible with oral intakes of liposomal vitamin C.
The lymphatic system that extends throughout the whole body is one of useful targets for efficient drug delivery. The intestinal lymphatic drug delivery has been actively studied to date because administered drugs can avoid the first-pass metabolism in the liver, resulting in improvement of oral bioavailability. Drugs must be hydrophobic in order to be transported into the intestinal lymphatics because the lipid absorption mechanism in the intestine is involved in the lymphatic delivery. Therefore, various lipid-based drug carrier systems have been recently utilized to increase the transport of drug into the intestinal lymphatics. Lipidic molecules of the lipid-based drug delivery systems stimulate production of chylomicrons in the enterocytes, resulting in an increase in drug transport into lymphatic in the enterocytes. This review summarizes recently reported information on development of liposomal carriers for the intestinal lymphatic delivery and covers important determinants for successful lymphatic delivery.
tjohnson_nb wrote:From Hickey et al. Emphasis mine.The similarity in the plasma response curves for liposomal vitamin C and the standard
commercial formulation, shown in Figure 1 (5 g doses), is interesting. There is a hint that
the liposomal form has a slower onset to peak level and a broader profile. Liposomes are
absorbed from the gut and into the liver, before being released into the blood stream. This
response can be seen more clearly in the 20 g dose, in Figure 2. It is apparent that sustained
levels of plasma ascorbate, above the previously assumed maximum of 220 mM L21, are
possible with oral intakes of liposomal vitamin C.
I don't know if this means that the ascorbate is 'un-encapsulated' in the liver or what?
However, in this document http://www.sciencedirect.com/science/article/pii/S1818087613000135, it says;The lymphatic system that extends throughout the whole body is one of useful targets for efficient drug delivery. The intestinal lymphatic drug delivery has been actively studied to date because administered drugs can avoid the first-pass metabolism in the liver, resulting in improvement of oral bioavailability. Drugs must be hydrophobic in order to be transported into the intestinal lymphatics because the lipid absorption mechanism in the intestine is involved in the lymphatic delivery. Therefore, various lipid-based drug carrier systems have been recently utilized to increase the transport of drug into the intestinal lymphatics. Lipidic molecules of the lipid-based drug delivery systems stimulate production of chylomicrons in the enterocytes, resulting in an increase in drug transport into lymphatic in the enterocytes. This review summarizes recently reported information on development of liposomal carriers for the intestinal lymphatic delivery and covers important determinants for successful lymphatic delivery.
So, I am a bit confused.
exitium wrote:
By default anything thats "digested" goes through the liver before it hits the bloodstream. This has caused problems for the delivery of many drugs over the years because the liver as part of its job destroys these chemicals. To get around this many drugs have to be altered to survive this first liver pass, however the chemical alteration is often times very hard on the liver and is still only marginally effective at getting the drug into the blood stream. Lipid based drugs (ie liposomes) allow the drug to be delivered right through the lining of the stomach/intestines and by and large bypass the first liver pass.
tjohnson_nb wrote:exitium wrote:
By default anything thats "digested" goes through the liver before it hits the bloodstream. This has caused problems for the delivery of many drugs over the years because the liver as part of its job destroys these chemicals. To get around this many drugs have to be altered to survive this first liver pass, however the chemical alteration is often times very hard on the liver and is still only marginally effective at getting the drug into the blood stream. Lipid based drugs (ie liposomes) allow the drug to be delivered right through the lining of the stomach/intestines and by and large bypass the first liver pass.
Then I find it odd that Hickey et al said what they did - it seems to imply the opposite.
tjohnson_nb wrote:Please see this again, I think you misunderstand.
http://www.vitamincfoundation.org/forum/viewtopic.php?p=34955#p34955
The first paragragh is from Hickey et al, the 2nd is from the sciencedirect site.
exitium wrote:
My apologies, I did misunderstand and you do bring up a good point. I think the key is to better understand the measurement technique to see if applies equally to raw ascorbate as well as liposomal. If both forms have the same effect on the test medium then at least we would know that the liver didnt necessarily unencapsulate the ascorbate.
"The technique depends on reduction of ferric to ferrous ions by ascorbate, which is simultaneously converted to dehydroascorbate"
I was under the impression the benefit of liposomal was that the encapsulated ascobate was much more readily taken up by the cells in the body so if the liver removed the encapsulation then it would seem to defeat that purpose and the encapsulation was only beneficial to get the ascorbate past the liver.
tjohnson_nb wrote:exitium wrote:
My apologies, I did misunderstand and you do bring up a good point. I think the key is to better understand the measurement technique to see if applies equally to raw ascorbate as well as liposomal. If both forms have the same effect on the test medium then at least we would know that the liver didnt necessarily unencapsulate the ascorbate.
"The technique depends on reduction of ferric to ferrous ions by ascorbate, which is simultaneously converted to dehydroascorbate"
I was under the impression the benefit of liposomal was that the encapsulated ascobate was much more readily taken up by the cells in the body so if the liver removed the encapsulation then it would seem to defeat that purpose and the encapsulation was only beneficial to get the ascorbate past the liver.
Yes I was also wondering how they measure ascorbate if it is still in a liposome in the bloodstream. Maybe someone who knows more physiology here can tell us.
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