GSE
CVD - Weak vessel walls due to chronic scurvy
CVD - Weak Walls due to chronic scurvy
Atherosclerotic plaques are not the cause of CVD.
Instead they are a means by which the body repairs damaged arterial
walls, weakened
by a lack of collagen resulting from a long-term, low-level
Vitamin C deficiency
The answer
to what is really going on in CVD was discovered over a decade ago by two men:
- The brilliant, biochemist,
physicist, molecular biologist Dr. Linus Pauling. Tthe world's onl y recipient of two unshared Nobel prizes,awarded nearly 40 honorary degrees, PHDs and DScs;
- The renowned Dr. Matthias
Rath, a research physician
from Germany.
Dr.
Pauling, who died in 1994 at the age of 93, devoted his last years working with
Rath to discover the root causes of cardiovascular disease.
In 1985, Brown and Goldstein were awarded a Nobel Prize in medicine for their
major finding that atherosclerotic
plaque deposits formed in the coronary and brain arterial walls as a response to
injury (lesions) to the arterial walls, by attaching to lysine and proline
binding sites exposed in the walls by the injury.
Rath and his
colleagues at Hamburg University found that the main constituent of plaques was
not in fact LDL cholesterol (as formally believed),
but a similar
cholesterol-based protein called lipoprotein(a) or Lp(a)
Rath and Pauling met, and then decided to
work together to answer the following questions:
(1) Why did the lesions form in the first place?
(2) Why did the Lp(a) plaques form on the lesions?
(3) Why do heart patients and others at risk of cardiovascular disease and
stroke have more LDL and Lp(a) cholesterol in their bloodstream?
Rath and Pauling discovered that CVD is primarily a consequence of
Vitamin C deficiency
To properly REPAIR and
RENEW constantly decaying arterial walls
(and also every other
tissue in the body),
your body must produce a binding
protein called COLLAGEN, which requires ample quantities of
Vitamin C (aka ascorbate
or
ascorbic acid) - if you don't have enough
Vitamin C to make collagen, then artery wall
lesions will not repair properly; if you took no
Vitamin C at all, you would experience scurvy, the lesions would rupture
and you would die of internal bleeding. This is how British sailors died in the
1500-1800's on long voyages without access to
Vitamin C .
COLLAGEN
The
most abundant protein in your body; the "cement"that holds together
arteries, skin, cartilage, ligaments, and tendons; decreases
significantly with age, and its deficiency is the source of several
serious degenerative diseases (e.g. rheumatoid arthritis)
If you don't have enough Vitamin C, then LDL and Lp(a)
cholesterol will accumulate in your bloodstream. The liver intentionally
manufactures Lp(a) and LDL cholesterol ascomponents of repair material for a C-deficient
damaged artery (lesions are usually formed in the highest-stress areas, such as
at the entrance to the coronary arteries); additionally
ascorbate is used to convert cholesterol to
bile for excretion through the intestines.
Your body compensates with a temporary "fix" to at least try to keep you
alive long enough to reproduce and so keep the human race going.
In a healing response to a breakdown of collagen,
Lp(a) - "The Repair Man" is attracted to the lesions, forming repair
patches, called arterial plaques.
Combining with other repair substances (E.g. fibrin),
the plaques grow in
size until the blood flow is partially / completely cut off (usually due to blockage by a blood clot that forms when the plaque ruptures)
or an artery bursts. Eventually, possible consequences include:
•
Angina;
• Arrhythmia;
• Heart attack. Usually arterial plaque ruptures and forms a blood clot
(thrombus) which travels (embolus) until it blocks the coronary artery providing
blood to the heart; other consequences related to ischemia (low blood supply)
include, high blood pressure, angina, arrhythmia or death;
• Stroke. By blocking / bursting
(hemorrhage) the small arteries in the brain; this can lead to limb paralysis on
one side of the body, and/or an inability to understand or formulate speech, or
to see one side of the visual field in both eyes;
•
Death.
Most mammals produce their own
Vitamin C
and do not have CVD (exceptions include humans,
non-human primates (apes, monkeys, lemurs), guinea pigs, the European hedgehog
and the fruit bat)- most animals
convert glucose to
Vitamin C in their kidneys or liver.
A nimals that produce their own ascorbate
generally do not have CVD and do not have significant Lp(a) in their bloodstream . Humans are no longer able to produce
Vitamin C , because some time
long ago there was a mutation of the gene which encodes for the enzyme
L-Gulono-g-Lactone, necessary to convert
glucose
to Vitamin C . As such, cardiovascular disease is not really a disease, but rather
the consequence of a missing enzyme!
Some things don't change!
In 1593, Admiral Hawkins
informed the British Admiralty that a daily ration of citrus fruits
prevented the Dainty's crew from getting scurvy during a voyage to
the South Pacific. This was later confirmed by Commodore James
Lancaster in 1601, and in a book published by famous medical doctor
John Woodall in 1636, and by a controlled study published in a book
by Dr. James Lind in 1753, and by Captain James Cooke, who kept his
ships stocked with fresh fruits and vegetables on his famous
round-the-world trip and lost only one of his 118-man crew (but not
to scurvy).
Finally in 1804,
211 years after Admiral
Hawkins first enlightened the British Admiralty to the solution to
scurvy , regulations were enacted requiring sailors to
consume a daily ration of lime juice, which totally eliminated
scurvy for the British sailor, who was thereafter nicknamed "Limey".
An estimated 2 million
sailors died of scurvy during this period of time.
How much Vitamin C do we need ?
In his previous research
on Vitamin C,
Pauling discovered that the 60mg amount of daily
Vitamin C
recommended by the FDA is 30 to 300 times smaller than the concentration found
in other mammals.
i.e.
Humans, whose entire
C intake must come from their diet, need to
eat about 3-12 grams of Vitamin C
/day to have as much ascorbate as other
animals (adjusting for body
weight).
In 1991 Rath and Pauling published their groundbreaking paper explaining the
cause of CVD:
"Solution to the Puzzle of Human
Cardiovascular Disease: Its Primary Cause is Ascorbate Deficiency Leading to the
Deposition of Lipoprotein(a) and Fibrinogen/Fibrin in the Vascular Wall."
Later, in 1994, Rath and Pauling obtained a patent on a cure for atherosclerosis
that comprises Vitamin C and Lysine. Later,
proline was added to improve the cure:
CVD -A Simple Cure