It is our central immune hub beyond our spleen and lymph system, the thymus gland whose size vastly differs between age 20 and age 75. Perhaps the shrinking is a sort of evolutionary enhancement, allowing for the new to replace the old, except for one problem. If the only life span you can achieve is that of an insect, you cannot possibly achieve anything more than an insect. So, our designed immune spans also align with what we are capable of (or allowed to do) by evolution. Perhaps, if our efforts are not aligned with a universal design, our thymus will prevent us from building these warped designs, OR this is as good as it gets. Probably, it is a match between finding what the universe wants from us, and knowing how to get around artificial limitations. Potentially, thymic age is an artificial limitation imposed upon us. Do we just sit there and accept such sadism? Of course not.
Thymic involution
Apparently, thymic shrinkage is not a sealed fate. Loss of thymus is very much why the older succumb to evil viruses more often than their younger peers.
As no surprise goes, our human botched gene for the very last step of vitamin C synthesis is behind thymic shrinkage too. If whatever force that is alien to our advantage had not left us with a botched copy to remind us that we once had it, we may not have had to suffer the problem of thymic shrinkage with age and therefore shrugged off COVID-19 as just another cold.
High dietary intake of vitamin C suppresses age-related thymic atrophy and contributes to the maintenance of immune cells in vitamin C-deficient senescence marker protein-30 knockout mice.
Vitamin C is the gene rescue product you need to give humans, all of whom have a "nub," a reminder of what we all once had, a functional L-guluno-lactone-y-oxidase enzyme, which would have made us far more disease resistant, more resilient, and much higher functioning as the brain IS the greediest active sponge of vitamin C of all human organs. It probably makes you taller too, if you are interested in that in your kids - really I never worry about that.
Showing posts with label vitamin C. Show all posts
Showing posts with label vitamin C. Show all posts
Monday, April 27, 2020
Thursday, January 28, 2016
Seaweed is a replacement for vitamin C? I guess the space aliens have started pouring out of the hollow moon too.
No doubt seaweed is excellent food. Fucoidan is great for you. High dose oral vitamin C is an excellent preventive measure for degenerative diseases.
Seaweed contains: Fucoidan. Vitamin C. Fucoidan tightly binds vitamin c, dragging vitamin C around with it. Weight per weight, edible kelp has more vitamin C than oranges. Is an orange a substitute for vitamin C? Not yes and no. Just simply no. Oranges are a source of vitamin C. Seaweed is a source of vitamin C.
Is fucoidan a substitute for ascorbic acid (vitamin C)? Absolutely not. Not even a deranged third grader would be puzzled by the fact that vitamin C can only replace vitamin C. An alternate statement might be: "Fucoidan - A Substitute For Vitamin C." Nope. Not to mention the fact that the high molecular weight fucoidan doesn't enter the blood stream (or bind to arteries), that you have to inject intravenously an artificial preparation of low molecular weight fucoidan for any substantial tracing of thromboses, it is the vitamin C in seaweed doing vitamin C things, not seaweed. Anyone can wander into a normal grocery store and see (not vitamin C) for themselves. Pick up a pack of dried edible seaweed, look at the nutritional facts, and there it is - 20% of the USRDA of Vitamin C.
This is not Nobel Laureate science, which is why I have nothing whatsoever to do with this strange turn towards completely erroneous self-published, non-peer reviewed....artifacts of vitamin C being inside seaweed itself (and bound to fucoidan). You can only fathom what insanity is required for this sort of childish and infantile nonsense.
Only Vitamin C can serve where Vitamin C is needed. Even in 2016. It is best stated by Dr. Mark Levine of the US NIH:
Seaweed contains: Fucoidan. Vitamin C. Fucoidan tightly binds vitamin c, dragging vitamin C around with it. Weight per weight, edible kelp has more vitamin C than oranges. Is an orange a substitute for vitamin C? Not yes and no. Just simply no. Oranges are a source of vitamin C. Seaweed is a source of vitamin C.
Is fucoidan a substitute for ascorbic acid (vitamin C)? Absolutely not. Not even a deranged third grader would be puzzled by the fact that vitamin C can only replace vitamin C. An alternate statement might be: "Fucoidan - A Substitute For Vitamin C." Nope. Not to mention the fact that the high molecular weight fucoidan doesn't enter the blood stream (or bind to arteries), that you have to inject intravenously an artificial preparation of low molecular weight fucoidan for any substantial tracing of thromboses, it is the vitamin C in seaweed doing vitamin C things, not seaweed. Anyone can wander into a normal grocery store and see (not vitamin C) for themselves. Pick up a pack of dried edible seaweed, look at the nutritional facts, and there it is - 20% of the USRDA of Vitamin C.
This is not Nobel Laureate science, which is why I have nothing whatsoever to do with this strange turn towards completely erroneous self-published, non-peer reviewed....artifacts of vitamin C being inside seaweed itself (and bound to fucoidan). You can only fathom what insanity is required for this sort of childish and infantile nonsense.
Only Vitamin C can serve where Vitamin C is needed. Even in 2016. It is best stated by Dr. Mark Levine of the US NIH:
Vitamin C: the known, the unknown, and Goldilocks.
Sunday, January 25, 2015
Partial and Total Loss of Arterial Collagen XVIII Causes Atherosclerosis
Loss of Collagen XVIII Enhances Neovascularization and Vascular Permeability in Atherosclerosis
Some factions claim that loss of arterial collagen is causal to atherosclerosis without being very specific about the mechanism (where? the adventitia? the endothelial basement? The media? how? immune side? smc autophagic? oxidative? proteolytic? autolysis?) and refer to studies done before regarding deranged hepatic metabolism of cholesterol during scurvy which causes a certain hyperlipidemia by bile metabolism deficiency and consequent lack of fecosteroid excretion. Others will look at ratios of Collagens I, III, IV, and even V in the atherosclerotic plaque and their ratios during atherosclerosis. However, the specific mechanism of collagen loss and atherosclerosis has never been scientifically described in a definitive study until this one. Through simple logic, (common sense), it follows that singular or combinatory losses of the other arterial collagen subtypes would provide the same result experimentally, either in vitro or in vivo.
The Maeda paper showing that scurvy causes Evans Blue extravasation and gross damage to the arterial wall did not describe any atheromas, hyperplasias, or plaques because the mice die from scurvy before they can incur cumulative atherosclerosis. They did prove that scurvy causes arterial degradation to the extent that lipoproteins and anything else can enter the artery that can't transgress a healthy, vitamin C (ascorbate) replete artery wall.
The implied connection between atherosclerosis and scurvy is collagen. While ascorbate isn't the only vitamin involved in collagen synthesis, it is the only one that when absent will prevent proper polymerization of hydroxyl residues. There is nothing to debate in this regard. No ascorbate = no assembled collagen. There may be pro-collagen formation and its strands, but they will never be assembled correctly into their "stronger than steel" fibers without vitamin C, but remain a useless stockpile of components.
It is important to note that the correct ratios of the various collagens is exceedingly important. While much focus has been made on COL4 basement membranes in conferring tensile strength and resistance to metastasis, too much of COL4 without the other collagens in balance can cause mitochondrial death by integrin signaling abnormalities, as well as aberrant vitamin A processing. It is not as simple as to say "the more collagen the better." Not whatsoever is it that simple, and such a conclusion could be disastrous in clinic. Fibrosis is a disorder of too much of the wrong collagen in the wrong place at the wrong time and is a devastating disorder.
However, if the intrinsic collagens in the artery, such as COLXVIII, vanish, arteries become much more prone to lipid intrusion and the chain of events that occur after that. As such, the normal constituency of arterial collagens, many of them not even recognized by conventional histopathology stains and immunohistochemistry, prevent large particle lipoprotein intrusion. Collagen XVIII is a subtype that is virtually ignored in cardiology, yet possibly one of the most important subtypes. It logically follows that deficiencies in the most commonly acknowledged collagens of the arterial media and basement membrane, COLI, COLIII, and COLIV, would cause similar problems of pathological permeability to both the clotting cascade biomolecules as well as the whole gamut of lipoproteins. This deposition of foreign matter is understood for over five decades as being the causal moment of atherosclerosis, but it is still not widely accepted in 2015 that the collagenous and protein barrier of the artery built by vitamin C dependent enzymes is important to prevent this permeability event.
Some factions claim that loss of arterial collagen is causal to atherosclerosis without being very specific about the mechanism (where? the adventitia? the endothelial basement? The media? how? immune side? smc autophagic? oxidative? proteolytic? autolysis?) and refer to studies done before regarding deranged hepatic metabolism of cholesterol during scurvy which causes a certain hyperlipidemia by bile metabolism deficiency and consequent lack of fecosteroid excretion. Others will look at ratios of Collagens I, III, IV, and even V in the atherosclerotic plaque and their ratios during atherosclerosis. However, the specific mechanism of collagen loss and atherosclerosis has never been scientifically described in a definitive study until this one. Through simple logic, (common sense), it follows that singular or combinatory losses of the other arterial collagen subtypes would provide the same result experimentally, either in vitro or in vivo.
The Maeda paper showing that scurvy causes Evans Blue extravasation and gross damage to the arterial wall did not describe any atheromas, hyperplasias, or plaques because the mice die from scurvy before they can incur cumulative atherosclerosis. They did prove that scurvy causes arterial degradation to the extent that lipoproteins and anything else can enter the artery that can't transgress a healthy, vitamin C (ascorbate) replete artery wall.
The implied connection between atherosclerosis and scurvy is collagen. While ascorbate isn't the only vitamin involved in collagen synthesis, it is the only one that when absent will prevent proper polymerization of hydroxyl residues. There is nothing to debate in this regard. No ascorbate = no assembled collagen. There may be pro-collagen formation and its strands, but they will never be assembled correctly into their "stronger than steel" fibers without vitamin C, but remain a useless stockpile of components.
It is important to note that the correct ratios of the various collagens is exceedingly important. While much focus has been made on COL4 basement membranes in conferring tensile strength and resistance to metastasis, too much of COL4 without the other collagens in balance can cause mitochondrial death by integrin signaling abnormalities, as well as aberrant vitamin A processing. It is not as simple as to say "the more collagen the better." Not whatsoever is it that simple, and such a conclusion could be disastrous in clinic. Fibrosis is a disorder of too much of the wrong collagen in the wrong place at the wrong time and is a devastating disorder.
However, if the intrinsic collagens in the artery, such as COLXVIII, vanish, arteries become much more prone to lipid intrusion and the chain of events that occur after that. As such, the normal constituency of arterial collagens, many of them not even recognized by conventional histopathology stains and immunohistochemistry, prevent large particle lipoprotein intrusion. Collagen XVIII is a subtype that is virtually ignored in cardiology, yet possibly one of the most important subtypes. It logically follows that deficiencies in the most commonly acknowledged collagens of the arterial media and basement membrane, COLI, COLIII, and COLIV, would cause similar problems of pathological permeability to both the clotting cascade biomolecules as well as the whole gamut of lipoproteins. This deposition of foreign matter is understood for over five decades as being the causal moment of atherosclerosis, but it is still not widely accepted in 2015 that the collagenous and protein barrier of the artery built by vitamin C dependent enzymes is important to prevent this permeability event.
Tuesday, December 2, 2014
Dr. Robert F. Cathcart III, M.D. was right...in 1975
While combinations upon the base of high dose Vitamin C are fairly new, the application of high dose Vitamin C against viral ailments is a very old idea that was actually put into practice by Dr. Cathcart. As with most things in medicine, things that are both cheap and effective tend to get buried by the new widget or pill for sale. Cathcart was no crank, or belligerent lecturer, but a practicing physician with very strong credentials.
His experience as an actual practicing doctor in the USA, employing Vitamin C as a medicine, clearly shows that a little sprinkle (91 mgs) is quite far away from what you need as a therapeutic dose.
He explains this clearly, unambiguously, in 1981 in the Orthmolecular Psychiatry, one of the few non-corporate aligned outlets that would display an efficacious medicine for humanity that would not bankrupt it. Yes, we should constantly remember that while people are well-meaning, well-meaning people working for a business are lead by business interests not human interests. So then the chicken chase goes on for the patent drug, the newest widget and pill to be able to sell at the same time a widely available and safe cure might exist.
The Method of Determining Proper Doses of Vitamin C for the Treatment of Disease by Titrating to Bowel Tolerance
Anyone who tries to revert back to little sprinkles of Vitamin C does not understand the topic and worse will not achieve a cure or effect. Might as well do nothing then...
Here is the PubMed entry which documents his experience in healing patients with Vitamin C:
Vitamin C in the treatment of acquired immune deficiency syndrome (AIDS).
If someone thinks a viral disease which can be spread through needle sticks somehow has something to do with morality, they should discuss this idea with their medical doctor or nurse and listen to what they have to say about plagues that arise by "immorality." Better yet, find one of the many children born with the disease and tell them how they are immoral before they know the meaning of it. Now that the inane and tedious medieval fingerpointers have been given their aggrandizements, the science can be returned to:
Here is the body of the text in regular html on Vitamincfoundation.org:
VITAMIN C IN THE TREATMENT OF ACQUIRED IMMUNE DEFICIENCY SYNDROME (AIDS)
"Why eradicate a disease when you can profit by selling non-working pills for it and weaponize its stigma as a sociopolitical gambit" - The body of fiscal corporate thought.
His experience as an actual practicing doctor in the USA, employing Vitamin C as a medicine, clearly shows that a little sprinkle (91 mgs) is quite far away from what you need as a therapeutic dose.
He explains this clearly, unambiguously, in 1981 in the Orthmolecular Psychiatry, one of the few non-corporate aligned outlets that would display an efficacious medicine for humanity that would not bankrupt it. Yes, we should constantly remember that while people are well-meaning, well-meaning people working for a business are lead by business interests not human interests. So then the chicken chase goes on for the patent drug, the newest widget and pill to be able to sell at the same time a widely available and safe cure might exist.
The Method of Determining Proper Doses of Vitamin C for the Treatment of Disease by Titrating to Bowel Tolerance
Anyone who tries to revert back to little sprinkles of Vitamin C does not understand the topic and worse will not achieve a cure or effect. Might as well do nothing then...
Here is the PubMed entry which documents his experience in healing patients with Vitamin C:
Vitamin C in the treatment of acquired immune deficiency syndrome (AIDS).
If someone thinks a viral disease which can be spread through needle sticks somehow has something to do with morality, they should discuss this idea with their medical doctor or nurse and listen to what they have to say about plagues that arise by "immorality." Better yet, find one of the many children born with the disease and tell them how they are immoral before they know the meaning of it. Now that the inane and tedious medieval fingerpointers have been given their aggrandizements, the science can be returned to:
Here is the body of the text in regular html on Vitamincfoundation.org:
VITAMIN C IN THE TREATMENT OF ACQUIRED IMMUNE DEFICIENCY SYNDROME (AIDS)
"Why eradicate a disease when you can profit by selling non-working pills for it and weaponize its stigma as a sociopolitical gambit" - The body of fiscal corporate thought.
Monday, July 7, 2014
1957: The Scurvy-Atherosclerosis Connection is Observed in Guinea Pigs
Dr. G.C. Willis made some of the first observations of this phenomenon in 1957.
The Reversibility of Atherosclerosis (In Guinea Pigs)
Below is a picture of intimal hemorrhage induced by scurvy.
Below on the left is lipid accumulation (red) in a scurvy guinea pig liver,
and a normally supplemented liver on the right for comparison.
Dr. G.C. Willis' catalog of Vitamin C-Atherosclerosis work spanning back to 1957 is free for review here:
The Free Site for Dr. G.C. Willis' Work
Sunday, December 27, 2009
Well if it isn't Vitamin C again. Inducible Pluripotent Stem Cells Need It.
The race towards rejuvenating the body by literally rebuilding it continues on in the milieu of stem cells. There is still quite a large misunderstanding of what one is, and actually there isn't one, there are many from many sources. Right now, your body is churning out cells from your own stem cells in your bone marrow, muscles, organs, everywhere. The problem is to keep this process going in an organized way well into old age. Too little, and you get the familiar loss of function of old age. Too much, and you get things like cancer.
Another promising new field of work is taking any cell from the adult body which contains the chromosomal makeup of the entire body except in rare chimeric cases, and taking it back to a primordial source cell. This inducible pluripotent stem cell (IPSC) can be tweaked to become an entirely different cell, offering hope for organ and tissue regeneration and repair or even rebuilding entire systems in the future.
Some grouchy old persons will be annoyed to read that you can't do it efficiently without Vitamin C.
Another promising new field of work is taking any cell from the adult body which contains the chromosomal makeup of the entire body except in rare chimeric cases, and taking it back to a primordial source cell. This inducible pluripotent stem cell (IPSC) can be tweaked to become an entirely different cell, offering hope for organ and tissue regeneration and repair or even rebuilding entire systems in the future.
Some grouchy old persons will be annoyed to read that you can't do it efficiently without Vitamin C.
Sunday, September 6, 2009
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