It safely shrinks tumors and breaks down cancer cells
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Why men want more ascorbyl palmitate and how to get it
There are tens of thousands of natural molecules produced by plants and animals…
…so it should come as no surprise when some of these natural molecules end up being potent antineoplastic agents — or anti-cancer treatments.
If any molecule can be thought to prevent cancer, it would be a statistical likelihood that it would be a natural compound.
Lapachol, baicalein, selenomethionine, and γ-tocopherol are all notable for their efficacy towards inhibiting cancer.
These natural molecules have been shown to prevent or inhibit thousands of cancers in lab animals, and clinical studies on humans strongly imply they can do so on us.
Ascorbyl palmitate is a surprisingly effective natural molecule, and it actually works in at least 2 distinct ways.
Ascorbyl palmitate is a simple palmitate ester of ascorbic acid, or vitamin C.
Ascorbyl palmitate has been demonstrated to inhibit lipid peroxidation even better than vitamin E.
Ascorbyl palmitate also potently suppresses the expression of the cancer enzyme ornithine decarboxylase.
Ornithine decarboxylase is perhaps the single most notorious cancer enzyme, often found upregulated approximately fourfold in rapidly-proliferating tumors.
Inhibiting this enzyme inhibits pathological cell proliferation because ornithine decarboxylase is rate-limiting during the synthesis of polyamines.
Polyamines are small molecules needed in the cell’s nucleus to unfurl DNA for replication.
Hyaluronidase is another enzyme strongly associated with cancer, and is also inhibited by ascorbyl palmitate at extremely low concentrations.
This enzyme is responsible for breaking-down hyaluronic acid polymers in the extracellular matrix, making room for newly dividing cells.
Cancer cells simply cannot arrogantly proliferate without first making room for their daughter cells.
Invasive yeast cells also excrete hyaluronidase for the same reason, and the invasiveness of Candida strains has been correlated with their expression of hyaluronidase.
Hyaluronidase activity found in the space around tumors is correlated with cancer proliferation and metastasis, and coincidentally none of it is found in the lysosomes where they belong.
It is apparent that during cancer, intracellular hyaluronidase is effluxed from the cell into the extracellular space.
Ascorbyl palmitate inhibits hyaluronidase from S. agalactiae by 50%, and at a low 4.2 μM concentration.
‘Thus, vitamin C palmitate is up to 1500 times more active than vitamin C and proved to be among the most potent inhibitors of bacterial and bovine hyaluronidases described to date.’ ―Botzki
Seeing as this prevents both the induction of ornithine decarboxylase and hyaluronidase, you’d theoretically have a very powerful antineoplastic agent.
An anti-cancer treatment that is also affordable, completely safe, and widely available.
Ascorbyl palmitate appears to prevent cancer replication at the cell level, and also invasiveness by preventing the breakdown of extracellular matrices.
Ascorbyl palmitate works in 2 distinct ways to achieve the same end, and for this reason it can be thought to work synergistically with itself.
Since ascorbyl palmitate has also been shown to prevent lipid peroxidation better than α-tocopherol, I cannot think of a reason not to consider using it — even for people not particularly worried about cancer.
Generalized lipid peroxidation increases the formation rate of lipofuscin, an intracellular inclusion body that accumulates in nondividing cells.
In centenarians, lipofuscin can be found occupying 75% of the interior volume of neurons.
Lipofuscin is nicknamed the “age pigment” for good reason.
Lipofuscin’s nickname serves as an effective warning against consuming excessive polyunsaturated fatty acids and free iron.
‘Ascorbyl palmitate was extremely effective at minimizing oxidation in all oils, and its effectiveness was concentration dependent. Ascorbyl palmitate showed significantly greater antioxidative activity than α-tocopherol for the reduction of oxidation in all oils.’ ―Lee
Ascorbyl palmitate is an under-researched molecule with not too much clinical data to go on, yet the studies that have been done show unbelievable results.
This study below demonstrates its ability to prevent cancer by inhibiting the notorious ornithine decarboxylase, one of the few cancer enzymes of primary importance.
These researchers even compared ascorbyl palmitate against free ascorbic and palmitic acids.
In this way, they could better infer its mechanism of action, and also give an intuitive way to comprehend its potency.
They used the classic tumor-promoter called tetradecanoylphorbol-13-acetate, a popular experimental treatment known to induce both prostaglandins and lipoxins — 2 classes of oxidized carcinogenic lipids.
Lipid products from lipoxygenase and cyclooxygenase are known to upregulate ornithine decarboxylase, initiating a DNA replication through the agency of polyamines.
Oxygenated lipids derived from omega-6 fatty acids are always the most potent ones, while saturated and monounsaturated fatty acids cannot even form carcinogenic oxidation products.
All of the eicosanoids derived from omega-3 eicosapentaenoic acid (EPA) and omega-9 mead acid have far less potency, as a general rule.
‘These results indicate that ascorbyl palmitate is at least 30-fold more effective than ascorbic acid as an inhibitor of some of the biochemical parameters associated with tumor promotion in mouse skin.’ ―Kaplan
This was essentially 2 simple experiments in 1, and both were done on shaved rats.
In the first experiment, the researchers applied tetradecanoylphorbol-13-acetate, followed by an assay for ornithine decarboxylase activity.
In the second they applied the carcinogen twice weekly for 20 sequential weeks.
In both trials: they gave the topical carcinogen mixed with either ascorbic acid, palmitic acid, ascorbyl palmitate, or sorbitan monopalmitate.
Since they used ascorbyl palmitate’s 2 breakdown products, and also a very similar compound, they could eliminate the chance of inhibition coming from its hydrolysis products and/or other nonspecific interactions.
Ascorbyl palmitate was the clear winner, by far: it inhibited rat tumors by 91%.
Although the author explains this effect through the pathway he apparently specializes in, protein kinase C, there is also reason to suppose this effect is mediated through lipid peroxidation.
For instance: They noted a 45 to 50% decrease in ascorbic acid content of the cell upon application of the carcinogen, implying that free radical lipid peroxidation had taken place.
It has been demonstrated by other researchers that the inhibition of lipoxygenase and cyclooxygenase together will prevent all carcinogenic changes following tetradecanoylphorbol-13-acetate.
Since prostaglandin E2 reverses the inhibition, a person can rightly assume that oxygenated lipids are highly involved in cancer induced in this manner.
Tumors always are accompanied by an upregulation of ornithine decarboxylase and elevated polyamines whenever they are looked for.
Ornithine decarboxylase can be upregulated by simply adding prostaglandin E2 to the cell media.
‘At this time, ascorbyl palmitate treatment had decreased the average number of tumors per mouse by greater than 90%.’ ―Kaplan
And just as you might expect, the molecules that inhibited the tumors the most also prevented ornithine decarboxylase activity the most — ascorbyl palmitate being the most effective in both cases.
This could imply that the downstream effectors are polyamines: small molecules that’ve been shown to reliably bind DNA and enhance its transcription since the ’60s.
In fact, ornithine decarboxylase activity is an obligatory event for skin cancer following tetradecanoylphorbol-13-acetate.
Since polyamines are needed to replicate the ‘housekeeping genes’ that control cell metabolism, a high rate of cell proliferation simply cannot be supported without them.
This is also why avoiding ω-6 fatty acids is effective, because the less linoleic acid a person consumes, the fewer carcinogenic arachidonic acid, 2-series prostaglandins, and 4-series leukotrienes are formed.
You simply cannot form these carcinogenic lipids without arachidonic acid and/or its ω-6 precursors.
Selenomethionine has been shown to inhibit ornithine decarboxylase by competing for the enzyme directly.
It should then be no surprise that selenomethionine reduces prostate cancer incidence by 63% in humans.
Baicalein also powerfully suppresses cancer, yet does so more indirectly: Baicalein is the most well-known inhibitor of 15-lipoxygenase, yet this has eluded explanation because it doesn’t actually bind the enzyme.
Yet after noting that baicalein also inhibits glyoxalase, and thus increases cellular methylglyoxal, the mechanism of baicalein’s action suggests itself:
There’s a key arginine residue necessary for 15-lipoxygenase activity called “the Hornung Determinant,” an amino acid needed to attract the lipid and position it within the enzyme. Methylglyoxal reacts with accessible arginine residues such as these, thereafter transforming the guanidino sidechains into hydroimidazolone rings — permanently disabling 15-lipoxygenase in this case.
‘The topical application of 4 μmol of ascorbyl palmitate inhibited by 60 to 76% the induction of epidermal ornithine decarboxylase activity and DNA synthesis that occurred after a single topical application of 2 μmol of TPA whereas similar doses of ascorbic acid had no inhibitory effect. The topical application of 4 μmol of ascorbyl palmitate together with 5 μmol of TPA twice weekly for 20 weeks to previously initialed mice inhibited by 91% the number of tumors per mouse.’ ―Kaplan
Coincidentally, the dose of ascorbyl palmitate that had lowered ornithine decarboxylase activity 76% and rat tumors by 91% (4 μmol) is comparable to its IC50 on hyaluronidase (4.2 μM).
This double-inhibitory effect at very low concentrations places ascorbyl palmitate in a class of its own for cancer inhibition, and its complete lack of toxicity at any reasonable dose level and low price makes it all the better.
Ascorbyl palmitate is absorbed intact and has been found in cortical tissues at 776 μM, in cats, and with no toxicity. These concentrations are considerably higher than those needed to inhibit the 2 procancer enzymes it’s been shown to interfere with: ornithine decarboxylase and hyaluronidase.
Hyaluronidase promotes tumor malignancy by liquifying the extracellular space surrounding the cells.
Hyaluronidase does this so reliably that it’s expression is perfectly correlated against prostate cancer grade.
Ascorbyl palmitate also has vitamin C-like activity, perhaps even before being hydrolyzed into free palmitic and ascorbic acids.
Of course, both these molecules are perfectly safe at any reasonable dose, and vitamin C also also appears to inhibit cancer by synthesizing collagen.
Slower growing tumors are often found encapsulated within a collagenous barrier, and collagen prevents rapid cell division by fortifying the extracellular matrix.
Because all cells will multiply when unrestrained by their surroundings, especially cancer cells, proper collagen turnover also acts to inhibit.
This effect of “contact inhibition” was rigorously demonstrated in the 1970s by NASA researcher Clarence Cone, who showed that cell membrane potential drops and cells divide when they lose contact with their surroundings.
‘Contact inhibition’ can be overcome by the presence of hyaluronidase, an enzyme that hydrolyzes the extracellular matrix along with chondroitin sulfatase. Ascorbyl palmitate inhibits this enzyme in concentrations easy-to-achieve orally.
Ascorbyl palmitate is safe, affordable, widely available, and because it has 2 unique mechanisms of action…
…it should synergize with other effective natural treatments like baicalein, γ-tocopherol, and selenomethionine.
—-Important Message for Men Who Want More Vitamin C—-
Why my Super C is better than any other type of vitamin C
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