Maximal Ascorbate Cmax in Humans with Oral Dosing and Its Efficacy Threshold:

Taking 3 grams/4 hours can achieve 220uM Vitamin C in blood.

What type of cancer might respond to this oral dosing?  Lymphoma.

Proc Natl Acad Sci U S A. 2008 August 12; 105(32): 11105–11109.

What needs to be clarified is what direct cytotoxic effect additional ascorbate has and what immune cell augmenting effects that ascorbate has as an immune system side therapy.  The direct cytotoxic effect is one important mechanism, but it could not be the only one in the immunosurveillance against aberrant cells that happens routinely before solid tumor carcinogenesis.  It must be remembered that cells accumulate ascorbate against a gradient, often to 100 times higher concentration than what is in the serum environment.  1mM-4mM concentrations in lymphocytes is an unremarkable baseline concentration.  Given the stoichiometric depletion of ascorbate in an active immune response, it is not surprising that bowel tolerence in humans increases greatly in times of immune system challenge by any of the assorted antigens that it would face in fungal, bacterial, or viral infection as ascorbate is literally burned up like fuel.

Dynamic immune system cells operate in very extreme environments and burn through a lot of ascorbate.

Ascorbate burn rate by macrophages

Well known ascorbate burn by IL- therapy activating immune "killer cells" resulting in severe vitamin C depletion.

Neutrophils, our first line defense microbe eaters, use oxidative burst and may soak up an additional 8,000 umoles/L in times of attack.

So then, flux of reduced ascorbate through the physiology much like the running of water through a washing vessel of fixed volume may be more important than Cmax.  If the same dose of oxidized ascorbate remained stagnant through the vessel of the same size as a vessel through which reduced ascorbate were constantly running through, there would be less redox activity and more redox activity, respectively.  So the focus upon Cmax without examining immune cell function may be misguided especially in terms of daily immunosurveillance and prevention of cancer or immune system remission and/or mitochondrial reversion of early cancer.

The field of Vitamin C science has been partially demystified in the last 3 decades, but there is still much to be elucidated.

Vitamin C Reduces Field Rodent Lifespan Paper

A desperate absurdist attempt to "pull the wool over the sheep's eyes" was just made by picking up a field rodent that makes its own vitamin C and giving it two doses - a little bit more, and a lot more.  Typical for the people who want to make money off sick people, they touted this as new evidence that you shouldn't take extra vitamin C.  They measured the lifespan of these two groups and found that the group given a lot more died sooner than the group given a little more.

Here is the Achilles' Heel of the study.  There was no Zero Vitamin C group.  Why?  Because unlike humans and primates that do not make their own vitamin C, the field rodent would happily live its full life with zero dietary vitamin C.  So in effect, the little bit of vitamin C group is not zero + a little more, but what the rodent made in its own liver + a little more.  This is more than slightly misleading.  By not divulging the endogenous status of the field rodent's vitamin C synthesis, they are implying that the field rodent does not make vitamin C and that additional vitamin C kills the rodent.  Disingenuous yet with the cool dissimulation of people with an agenda to accept bribes from large corporations, it seems like a logical argument.  Except it isn't.

A person, any person anywhere on Planet Earth will die within a year without vitamin C in their diet.  The group omitted the zero vitamin C group, because the field rodent does not need it thanks to its own vitamin C generation in its own liver.  People do not possess this ability.  To properly match the studies, we would have demanded a zero vitamin C group for the field rodents and observed the life shortening qualities of vitamin C.  Then we would try this on humans and compare.

The results, which would be illegal and inhumane, would be the following:

Field rodents (n=100) + no vitamin C = full life span.
Humans (n =100) + no vitamin C = 100% mortality

The conclusion would then not be that supplemental vitamin C shortens human life, but extends it by 1,000,000%.  This absurd numerical conclusion of +1,000,000% is just as absurd as comparing the performance of a submarine on land versus in the ocean, or the effects of vitamin C on life extension in an animal that already makes its own to one that doesn't.

The last several decades of independent academic research have definitively and conclusively shown that Vitamin C and other antioxidants help to extend life span, not shorten it in humans.  A singular mass hypnosis piece in the pop media pimped by corporate funding contradicts thousands of scientists' findings across the globe.

What happens when a person doesn't take enough vitamin C, but just a tiny fraction of what you need?  This is still what will happen to you in 2013:

If some corporate shills had their way, we'd all just reverse centuries of scientific progress and go back to being scurvy pirates.  They should probably refresh themselves on medical documentation of scurvy.
 

OTC Saw Palmetto's Benefits against 5-alpha reductase II

Several unpatentable, human food plants can provide the same 5-alpha-reductase inhibitory effects as finasteride.  One is Saw Palmetto.

Potency of a novel saw palmetto ethanol extract, SPET-085, for inhibition of 5alpha-reductase II.

Vitamin C Prevents Formation of "Millions of Cracks" in Arterial Lining:

The endogenous NOS system is augmented by ascorbate, sparing nitric oxide and also activating eNOS.  Without it, stress fiber contraction occurs of the endothelial cells, detaching cells from one another and creating the leaky junctions described by Tarbell.  When this occurs, the size exclusion barrier function to LDL, Lp(a), and other macromolecules that otherwise could not cross the lining under convective flow easily permeate into the subendothelial basement membrane collagen fibers, proteoglycans, and any medial smooth muscle layers that are then accessible. 

Nitric oxide mediates tightening of the endothelial barrier by ascorbic acid.

Ascorbate stimulates endothelial nitric oxide synthase enzyme activity by rapid modulation of its phosphorylation status.

Through active modulation of a paracrine/autocrine small molecule factor, nitric oxide, ascorbic acid rapidly and potently inhibits endothelial permeability at physiologically achievable sub-millimolar concentrations, with the effect asymptotically increasing with diminishing returns up to 4mM ascorbate.