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.

Macrophages and T-Lymphocytes Secrete Collagen

There are several potential sources of origin for the capsule collagen that surrounds a dormant or benign tumor that is not a pseudo-capsule generated from compression of the stromal tissues.  One overlooked source of the capsule demonstrated by Vaage in 1991 is the immune system itself, with lymphocytes and macrophages surrounding aberrant, immunogenic cells with a collagen capsule.  Research regarding the involvement of macrophages and lymphocytes in useful and pathological collagenous fibrosis is an important facet of fibrosis mechanisms that is still highly relevant today, in 2012.  Of course, any collagen synthesis requires Vitamin C/ascorbic acid/ascorbate.  Innate defense and cytotoxic immune cells in particular use vastly large quantities of it, accumulating it against an osmotic gradient to 100-fold more than the surrounding serum or plasma.

Collagen production by macrophages in tumour encapsulation and dormancy.

Fibrous Capsule of a dormant (not growing) tumor (Vaage 1991)

T-Lymphocyte Secreted Collagen Fibers, Vaage 1991

 

 

"Millions of Cracks" in Artery Wall = Leaky Junctions

In Tarbell's research, 90% of LDL, the delivery particle that solubilizes otherwise insoluble cholesterol gets through the first layer of an artery through a "leaky junction."  The normal pores in the first layer of an artery are just too small for anything other than albumin and micromolecules in water to get through.  Nothing gets through a tight junction.  Large gaps, leaky junctions, occur only when the layer of cells divides or is injured, pulling away from each other and revealing the subintimal layer.  Only 10% of LDL gets through by active vesicular consumption. 

Stretch and Shear Interactions Affect Intercellular Junction Protein Expression and Turnover in Endothelial Cells.

Shear stress and the endothelial transport barrier

"Million of Cracks in Artery Wall" = Leaky Junction

Headline: "Deficient Cholesterol: A Common New Factor in Autism"

The importance of cholesterol to the central nervous system cannot be underestimated, as is demonstrated by this group with the improvement of symptoms with parenteral supplementation in patients:

http://www.greatplainslaboratory.com/home/eng/cholesterol.asp

Their PDF File

Hydraulic stress in thrust fittings and accelerating curves of arterial system generate inflammatory gene expression

Normal mice just don't get atherosclerosis.  Just never.  In every lab on Planet Earth, these hardy beasts must be genetically handicapped in ways that humans never are, and then poisoned with massive doses of lard or high blood pressure hormone to induce a similar pathology to that which develops in humans over decades (not overnight).  When the LDL cholesterol receptor is ablated, and then these mice insulted with the lard or AngII, they exhibit a pattern of inflammation in their arteries at the high pressure regions, the branches or "thrust fitting" joints as a master plumber would call them or in high acceleration curves.  At these points, white blood cells stick to the intimal surface, forming the first lesions of atherosclerosis called foam cell lesions that look like butter from afar, but under the microscope are distinctly living white blood cells.  As things progress further, these cells may die leaving a trash dump of necrotic debris including the accumulated cholesterol delivered via lipoproteins.

The NF-κB signal transduction pathway in aortic endothelial cells is primed for activation in regions predisposed to atherosclerotic lesion formation

The lesions don't happen haphazardly and randomly, but predictably in mechanical stress sites where inflammatory gene expression is activated, consequently drawing the ire of our own immune system cells and acute phase reactants.

The first barrier to the living wall of muscle cells of the artery are the endothelial cells that sit happily on top of their collagen basement membrane, in tight formation with not much that can slip through their cell junctions bigger than small organic molecules.  When there is damage, either directly to an endothelial cell, causing endothelial denudation, or by well meaning white blood cells causing collateral damage, the collagen membrane floor is revealed, which is sticky to many problematic things including the infamous Lp(a) which sticks to exposed lysyl residues of collagen strands.  The wall is then vulnerable to insudation by clotting systems as they should or activated platelets that stick to collagen.

To prevent all this from occurring, the thing to do would be to dial down the inflammatory signals that turn on NF-Kappa Beta, a ubiquitous nexus and hub for many inflammatory processes both useful and malignant.

As you might have guessed, there are nutritional means to do this without relying on hazardous, poisonous, expensive, and annoying prescription drugs, none of which are designated as specific NF-kappa B inhibitors anyways.

For example,
Antioxidants like Vitamin C can turn this switch off
Molecules from herb extracts can turn this switch off.
simple amino acids can halt this stress signal.
Resveratrol can turn this switch off.

and many other functional foods...