ONE
PHARMACIST’S VIEW OF CORONARY HEART DISEASE:
COMPARING THE “LIPID THEORY” WITH THE
“UNIFIED THEORY”
By Mike Ciell, R.Ph.
EXECUTIVE
SUMMARY
Conventional
wisdom argues that cholesterol, an oily substance produced in the body, is the
enemy and must be managed to prevent coronary heart disease. Fighting
cholesterol is inherent in the “Lipid Theory” of heart disease.
Alternatively, Linus Pauling, two-time Nobel laureate and Ph.D. and Matthias Rath,
M.D., created the “Unified Theory” of heart disease, identifying vitamin C,
L-lysine, and L-proline as critical nutritional agents that could both improve
blood vessel function (flow) and reduce cholesterol plaques (blockages).
Some researchers have said that vitamin C is the equivalent of “nature’s
perfect statin.”
Most
animals produce vitamin C endogenously (within their bodies) and never
demonstrate signs of cardiovascular disease. Humans, alternatively, must
rely on dietary ascorbate to maintain health, and when insufficient supplies of
ascorbate are present, humans suffer from a variety of chronic diseases,
including coronary heart disease.
Pauling’s
and Rath’s research provides evidence that cholesterol plaques are actually the
body’s back-up mechanism for repairing damaged blood vessels, and that if you
provide the body with enough free-circulating vitamin C, along with L-lysine
and L-proline, the body’s primary mechanism for making vascular repairs can be
employed and cholesterol numbers can ultimately fix themselves.
CORONARY
HEART DISEASE – THE LEADING CAUSE OF DEATH IN AMERICA TODAY
Coronary
heart disease (CHD), the most
common form of cardiovascular disease, is the leading cause of death in America.
Over 13 million Americans suffer from CHD,
which results in more than one million heart attacks per year, of which more
than one half will be fatal. These statistics are in sharp contrast with
the cardiac health of Americans at the beginning of the 20th
century.
HEART
DISEASE USED TO BE RELATIVELY RARE
In 1900
heart attacks were almost nonexistent, and most cases of heart disease that did
occur were usually the result of an infectious disease (rheumatic fever for
example) or congenital heart defects. In the ensuing decades, this once
rare condition steadily rose in frequency to become the leading cause of
death in America.
The big
question: “What has caused this problem?” Social changes since 1900 are
certainly in play, including:
§ Widespread use of cigarettes after
WWI,
§ A huge increase in refined sugar
use,
§ Sedentary suburban lifestyles, and
§ Packaged, chemical-laden food
replacing fresh, raw choices
Ask any
reasonably-educated person with heart disease what the problem is and you’re
likely to hear things like, “I have to watch my diet, get more exercise, stop
smoking” and so forth. Good starting points, but, as I cover in this
article, there’s more.
KOREAN
WAR AUTOPSY CONNECTION
It was
during the Korean War that doctors thought they had discovered the “real” cause
of heart disease. Autopsies on young soldiers killed in action showed
well-developed atheromas (arteriosclerotic plaques) in their coronary and
carotid arteries. Additionally, fatty streaks of the intima of their
arteries, arterioles, and heart muscle existed.
While
similar fatty streaks were observed in dead Korean and Chinese soldiers, the
well-developed atheromas found in American soldiers were conspicuously absent.
Analysis of the plaques found showed it was a saturated fat (palmitic
acid). The atheromas also contained quite a lot of a familiar waxy
substance—better known as cholesterol.
THE
“LIPID THEORY OF CARDIOVASCULAR DISEASE”
Thus, out
of the battlefields of Korea
was born “The Lipid Theory of Cardiovascular Disease.” For almost 60 years,
this “lipid theory” has been central to medical explanations of and treatment
for cardiovascular disease.
Simply
put, the Lipid Theory posits that a diet high in cholesterol and saturated fat
will cause “gooey” substances (cholesterols) to be deposited in the blood
vessels, clogging them up. Clogged blood vessels clearly restrict blood
flow to the heart, ultimately causing angina. Eventually a piece or
“clot” will break loose, causing a TIA (angina or a mini stroke), a stroke or a
full-blown heart attack.
Conventional
thinking has centered on removing “causative” agents – cholesterol and bad fats
-- to stop coronary heart disease.
For
decades we have used diet and drugs to attempt to reach ever-lowering
“cholesterol levels” recommended by the American Heart Association.
Tragically,
statistics show that heart disease continues to be on the rise, claiming ever
more lives.
A
PLUMBER’S TAKE ON “PLUGS” IN THE SYSTEM
So what’s
wrong with the Lipid Theory? Any plumber looking at the Lipid Theory model
would say, “It simply doesn’t make sense.”
Let’s
start by thinking about “sludge” in a plumbing system. Sludge tends to
plug up the smallest pipes in the system first—not the largest.
Likewise,
if the system is cardiovascular, you would expect sludge (plaques) to build up
first in the capillaries and arterioles, long before appearing in
the carotid and coronary arteries. The first blockages, similarly, you
would expect to occur way downstream of the pump, not in close proximity to the
heart, where the pressure is the greatest.
Yet, this
is not the way cholesterol plugs up arteries. It’s the exact
reverse. So a plumber’s take would be that something else is happening.
THE
MYTH ABOUT “GOOD” & “EVIL” (FATS)
When
autopsied plaques have been analyzed, they are found to contain cholesterol,
but of a very particular type. The offending cholesterol is a
highly-oxidized variety of LDL
cholesterol attached to a specific protein (Apo
A). The whole complex is called Lipoprotein A or Lp(a) – more on Lp(a)
further in this article.
The fats
found inside these plaques, as it turned out, were unsaturated
fats (not the supposedly “evil” saturated fats). Fatty streaks in the
intima of the arteries are saturated fat, but this appears to be quite
normal, since it is the same in many animals.
Avoiding
saturated fat, using “healthy” polyunsaturated oils, and building a diet on a
base of carbohydrates (grains, breads, and starchy veggies) has been drummed
into us by well-meaning authorities, including luminaries such as: the USDA,
the American Heart Association, and the American Diabetes Association
Yet, it
is a basic physiological fact that all carbohydrates are metabolized to
glucose. If glucose is not used for fuel, it is automatically converted
to and stored as saturated fat (only a small part-about 100 grams - will
actually ever be stored as glycogen).
Telling
people to avoid eating saturated fat – while simultaneously telling them
to eat food that will be converted into saturated fat -- fails a basic
logic test. Fat, I will argue, is not the real problem.
ANIMAL
MODELS, A GENETIC MUTATION, & MODERN DIETS
It helps
at this point to explain some genetic history. Only a few animals (the
higher apes, the guinea pig, and a species of fruit bat) ever show coronary
heart disease. Heart disease, however, appears only when these
animals are fed a diet that is lacking in adequate amounts of vitamin C.
Zookeepers
learned the connection between vitamin C and heart health a long time ago. When
their gorillas were fed a diet of early versions of processed “gorilla-chow,”
instead of a diet rich in vitamin C from fresh fruits and vegetables, they got
sick and developed heart disease.
In
contrast, bears -- whose cholesterol levels can be three times as high as man’s
and whose heart rates slow way down during hibernation – remarkably never show
any atherosclerosis.
So what’s
going on in bears and other animals that is missing in humans, apes, guinea
pigs and some fruit bats?
Endogenous
Production of Ascorbate and a Genetic Mutation
Other
animals produce vitamin C endogenously (which means most animals manufacture
ascorbate inside their bodies), and this production of vitamin C is
essential to maintaining health, including maintaining healthy arteries.
For example,
a 150-pound goat has a typical blood concentration of ascorbate equivalent to
taking 13,000 mg (13 grams) of vitamin C per day. And, ascorbate
concentrations rise much higher in times of stress. Compare this
abundance of vitamin C in a goat with the paltry 60mg recommended daily
allowance for humans. Consider further the percentage of people who do
not get enough vitamin C from their diets, and it’s no wonder that heart
disease is so prevalent.
Some
millions of years ago, a genetic mutation occurred, causing humans to rely on
their diets for vitamin C. This mutation was not life-threatening, however,
because our early ancestors thrived in the tropics, where vitamin C was in
ready supply in fresh fruits and vegetables.
Scurvy
(and heart disease) became a real problem for ancestors who settled in other
regions of the world, areas with less readily-available dietary
ascorbate.
During
the Ice Ages, however, many of our ancestors did indeed succumb to scurvy and
heart disease, when plant-foods were not as plentiful.
Ancestors
who were able to survive possessed a valuable genetic mutation, whereby damaged
(leaky) blood vessels could be patched by a “back-up mechanism,” an animal food
component called cholesterol. Modern humans inherited this ability to use
cholesterol to make repairs, which, in other animals, are made through an
abundance of freely-circulating vitamin C.
CHOLESTEROL
CARRIERS & MECHANISMS OF MOVING CHOLESTEROL IN THE BODY
Now let’s
talk about cholesterols. LDL
has been called the bad or “lethal” cholesterol, while HDL
is considered the “healthy” cholesterol. I’m afraid this is nothing but
nonsense. There is no “good” or “bad” cholesterol. LDL and HDL
are just two different types of cholesterol “carriers.”
When it
comes to how cholesterol moves in the body, I believe it was Dr. Andrew Saul
who used the analogy of a bus line, which is an apt one. Since
cholesterol is an oily substance that travels through a watery
bloodstream, it must be carried (similar to passengers and cargo on a
bus) to various destinations in the body.
The
HDL “Bus Line”
The HDL cholesterol molecule has a higher protein-to-lipid
ratio (contains more protein than lipid material). Protein is denser than
lipid, hence the name “high density lipoprotein”.
The HDL “bus line” thus carries a single “bag” of this
dense cholesterol as cargo in each of its buses. In this way, the HDL cholesterol gets a ride straight to the liver
and is eliminated as bile acids via the gall bladder and intestines.
The
LDL “Bus Line”
The LDL cholesterol molecule, in contrast, has more
lipid or “oil” content, thus a lower protein-to-lipid ratio, and hence the name
“low-density lipoprotein.” The LDL
“bus line,” in contrast, carries two “bags” of cholesterol as cargo.
The LDL bus line transports cholesterol to a variety of
sites in the body, where it is used to repair and/or protect tissues or to be
used in the synthesis of many vital compounds.
LDL cholesterol’s role is so important that nature lets the LDL bus line transport twice the number of
cholesterol “passengers” as the HDL
bus line does. LDL
cholesterol is thus taken to important destinations in the body such as:
- Skin, where cholesterol
reacts with sunlight to produce the “best kind” of Vitamin D (think
healthy bones),
- Sex hormones (the estrogens,
testosterone, and progesterone) and their “precursor” molecules (DHEA,
DHEA-S and pregnenolone, as well as adrenal stress hormones like
cortisol),
- Nerve cells so they are
well-insulated and don’t short circuit,
- Scar tissue to repair tissue
injuries,
- Cell walls to “waterproof” us
so we don’t melt in the rain or when we take a bath, and
- Blood vessels for vital
cardiovascular repairs, as well!
The body
was designed pretty exquisitely, and clearly cholesterol’s real mission to save
our lives, not to kill us.
CHOLESTEROL
READINGS & HEALTH – THE HIGHS & LOWS
Now,
without looking at specific numbers (like we medical professionals love to do),
let’s consider three cases and determine what a person’s cholesterol readings
suggest about health:
- High
LDL - A relatively high LDL reading may indicate that the body needs
to repair a lot of things and transport cholesterol to areas of stress or
disrepair.
- Low
HDL - A low HDL
reading may mean the body needs to hold on to cholesterol to both make
repairs and to synthesize molecules that are scarce.
- Lower
LDL & High HDL -- A lower LDL
and high HDL reading is
likely to indicate the body’s systems are pretty well maintained.
With no need for a lot of cholesterol, excess cholesterol is regularly
eliminated.
As a
goal, we want to strive for the third case, with a high percentage of the total
cholesterol being of the HDL
variety. In mathematical terms, total cholesterol over HDL should be less than 3.5 or:
TC/HDL
< 3.5
However,
when we “artificially” lower our cholesterol through pharmacological inhibitors
(like “statin” drugs), we really cannot infer anything about our state of
health with regards to cholesterol levels.
With
drugs, we can make less cholesterol available to block our blood vessels, but
at the same time, we will make less cholesterol available to perform vital
functions (like converting sunlight to vitamin D, insulating nerve cells,
healing scars, etc.).
Total
cholesterol, as it turns out, has never been an indicator of who is more
likely to suffer a heart attack. In fact, Dr. William Castelli, director
of the prestigious Framingham Study, said:
“The more saturated fat one ate, the more cholesterol one
ate, the more calories one ate, the lower peoples’ serum cholesterol…we found
that the people who ate the most cholesterol, ate the most saturated fat, ate
the most calories, weighed the least and were the most physically active.”
The ongoing
Framingham population study also found that there was virtually no difference
in coronary heart disease events for individuals with cholesterol levels
between 205 mg/dl and 294 mg/dl – where the vast majority of the U.S.
population lands.
Even for
those with extremely high cholesterol levels, up to almost 1200 mg/dl, the
difference in CHD events compared
to those in the normal range was trivial. Now that being said, please do not
take this as carte blanche to consume as much saturated fat and calories as you
want.
Castelli’s
comments were made decades ago, when much of our livestock was still grass-fed
and the adding of hormones and growth enhancers (both of which become
concentrated in animal fat) was just beginning.
Diets
high in domestic animal fat and partially hydrogenated
poly-unsaturates (metabolic poisons) have their own set of health risks. As
an aside, this is my main concern with Dr. Atkins’ dietary guidelines. Without
emphasis on the quality of fats and proteins and balancing complex
carbohydrates into the equation, we may be trading short-term health benefits
for long term health risks.
Anyway,
because cholesterol supports so many essential physiological processes, it
doesn’t make a lot of sense to pharmacologically inhibit cholesterol production
to “get our numbers right.” In fact, in study after study, the group with
the lowest cholesterol levels had the highest mortality (death due to
all causes).
I find
the mortality rates for those with the lowest cholesterol readings particularly
troubling. I believe it’s far better to help our bodies make necessary
repairs and let the numbers “fix” themselves. Nature ultimately does not
waste energy, so when less cholesterol is needed, less cholesterol will be
produced.
LINUS
PAULING’S UNIFIED THEORY OF CARDIOVASCULAR DISEASE -- MAKING REPAIRS NATURALLY
A lot of
people have heard that Linus Pauling had some theory about vitamin C and heart
disease treatment. It’s true and it’s called the “unified theory of human
cardiovascular disease,” which posits that ascorbate deficiency is one of the
primary causes of cardiovascular disease.
Using
data gleaned from literally hundreds of published research papers by
world-class scientists (MDs and PhDs), Pauling and his research partner, Matthias Rath, MD,
described the link between cardiovascular disease and vitamin C.
In their
“Unified Theory of Human Cardiovascular Disease,” genetic differences, in
species which are susceptible to CVD,
are taken into account. The Unified Theory explains how the human body
precisely regulates blood concentrations of cholesterol and provides compelling
evidence that, with proper nutrition (and not drugs) cardiovascular disease can
be prevented and even reversed.
THE COMMON GROUND AND
DIFFERENCES OF THE TWO THEORIES
Both the Lipid Theory and the Unified Theory agree that
atherosclerotic plaques are deposited in response to injury of the blood vessel
wall. Drs. Brown and Goldstein were awarded the Nobel Prize in Medicine in 1985
for this discovery.
Pauling and Rath, however, had a different concept of
cause and effect, proposing that the genetic weakness of certain species (that do
not produce ascorbate endogenously) must be addressed nutritionally, to
promote healthy blood vessels.
While Pauling and Rath saw cholesterol as clearly correlated
with cardiovascular disease, they did not consider cholesterol as the
enemy.
The Lipid
Theory, on the other hand, argues that cholesterol is the enemy.
Consequently, those who embrace the Lipid Theory emphasize:
- Decreasing the amount of
cholesterol and lipids (“patch material”) in the body through diet and
drugs
- Making the blood itself less
sticky (by means of blood thinners such as Coumadin, Plavix, aspirin,
etc.), to ensure adequate blood flow and prevent heart attacks.
To help
put these theories into context better, let’s turn to one of my favorite
topics: biochemistry.
THE BIOCHEMISTRY OF IT ALL
Biochemistry
is literally the “chemistry of life,” and, as a pharmacist, this is one of my
specialties. Biochemistry helps us understand the structure and function
of cellular components, including proteins,
carbohydrates,
lipids,
nucleic acids,
and other biomolecules,
as well as enzyme-mediated
reactions.
When I’m
researching something new, I like to understand what is going on at a molecular
level. To make the case for the Unified Theory, it’s valuable first to
understand the roles of lipoprotein A, collagen, and vitamin C.
Lipoprotein
A or Lp(a)
Lipoprotein
A, otherwise known as Lp(a), is another special cholesterol carrier (bus
line) found only in species that do not produce their own ascorbate
(Vitamin C).
Like LDL, the Lp(a) bus carries two “bags” of
cholesterol, which are covered with a protein coat called apo(a). This coat
allows cholesterol to move through the watery bloodstream. However, unlike LDL, Lp(a)'s protein coat is very sticky --
think of the “a” as meaning “adhesive.”
In a
non-ascorbate producing animal, the amount of Lp(a) is inversely
proportional to the amount of circulating ascorbate. That means that
higher vitamin C concentrations lead to less production of the sticky Lp(a)
particles.
Under
stress and when insufficient vitamin C is in circulation, the ability to
produce Lp(a) allows the body to patch damaged blood vessels and prevent death
by hemorrhage.
Thus, the
“sticky” Lp(a) particle circulates through the vessels and adheres to spots
where a blood vessel wall is damaged. Due to the Velcro-like surface of
Lp(a), circulating LDL particles
also will adhere where Lp(a) is busy patching damaged blood vessels, escalating
the process of atherosclerosis formation.
Interesting
Facts About Lp(a)
· Lp(a) levels are influenced
by genetics (inheritance)
· Diet does not influence
Lp(a) levels
· Cholesterol-lowering drugs have
not been shown to lower Lp(a) levels
· Both ascorbate (vitamin C) and
niacin (vitamin B-3) have been shown to lower Lp(a) levels
·
Natural amino acids,
L-lysine and L-proline, prevent the outer coat (apo-a) of a Lipoprotein A
carrier from being sticky. These amino acids convert apo-a from a
“Velcro” to a “Teflon” quality. L-lysine and L-proline also help remove
plaque that is already present in blood vessels (by preferentially binding with
receptors on Lp(a) and, thus, displacing Lp(a) cholesterol from artery walls).
· Lp(a) is the single greatest
risk factor predicting restenosis of blood vessels (the narrowing of blood
vessels after widening in bypass surgery)
Collagen
Collagen
is by far the most abundant protein in the body. While literally a fiber,
collagen acts like a “glue,” which holds our cells together. Collagen is
actually the body’s preferred repair substance, whether for closing
wounds, healing blood vessels, or helping the skin remain wrinkle-free.
The
collagen fiber looks like a 3-strand rope. The “rope” consists of a strand of
L-glycine molecules, a strand of L-proline molecules, and a strand of L-lysine
molecules. These strands of amino acid chains are twisted around each other in
a helical fashion and, in fact, do look like a rope.
When an
injury occurs and the collagen fiber breaks, the frayed ends dangle just
as if a rope were cut.
If
adequate ascorbate is present, the amino acids at the broken ends are
hydroxylated. That means the “end” molecules of L-glycine, lysine and proline
are chemically changed to L-hydroxyglycine, L-hydroxylysine and
L-hydroxyproline. This allows them to be spliced back together (much
like a sailor splicing a rope together). This simple chemical change also
explains why vitamin C has the ability, not only to repair the damage, but also
to start breaking up existing plaques, as will soon become apparent.
Of all
the amino acids, L-glycine is the simplest one chemically and, in general, is
always in ample supply in the body. L-proline and L-lysine, the other two
amino acids in the collagen fiber, however, are not always in ample supply, and
the body benefits from supplementation to ensure good collagen synthesis.
Vitamin
C -- Ascorbate or Ascorbic Acid
By now,
you may have surmised that vitamin C is the lynchpin of the Unified
Theory. Vitamin C, or rather the lack of sufficient ascorbate, has
implications in practically every chronic disease -- osteoporosis,
diabetes, arthritis, cancer, macular degeneration, allergies, and chronic or
re-occurring infections are just a few examples.
Unfortunately,
most people, including doctors, think of vitamin C as the substance that
prevents scurvy. A small daily dose of 60 mg is sufficient to prevent
scurvy, and conventional wisdom has been that additional vitamin C will just
create expensive urine.
Pauling
and Rath, however, hypothesized that most humans suffer from chronic,
sub-acute scurvy and CVD is merely
one of the symptoms of the underlying disease. Have your gums ever bled
when you flossed your teeth? Have you ever had a nosebleed for no apparent
reason? Have you ever had a wound that was slow to heal? If so, you may
have (had) a deficiency in ascorbate in your system.
When a
person develops a chronic condition (which adds stress to the body and further
depletes already inadequate ascorbate stores), many tell-tale symptoms scurvy
often appear. The correct diagnosis is typically missed and scurvy sequelae are
instead called symptoms of some chronic disease (i.e., poor wound healing in
diabetics, hemorrhages in diseases like Crohn’s and ulcerative colitis, etc.).
Some salient facts about vitamin C
and cardiovascular disease
· During the 1950’s, a brilliant
Canadian physician, Dr. G. C. Willis, demonstrated that vitamin C was indeed
related to cholesterol metabolism. A deficiency in ascorbate caused
increased cholesterol synthesis (production). Feeding animals increased
amounts of cholesterol reduced their vitamin C levels, and, conversely, vitamin
C supplementation decreased cholesterol levels. Dr. Willis also showed that
vitamin C could reverse atherosclerosis in guinea pigs, a species that does not
produce ascorbate endogenously.
· In 1971, British physician, Dr.
Constance Spittle, demonstrated that patients with existing CVD exhibited a transitory rise in blood
cholesterol when given vitamin C therapy, while patients with no CVD showed the reverse, namely, lower blood
cholesterol levels. Spittle’s explanation: the vitamin C therapy was actually
healing the vessel walls, thus releasing the cholesterol from the existing
plaques. By the way, this research was published in the prestigious British
medical journal, The Lancet.
·
Finally,
in 1985, when Mevacor (the first statin drug) was the hot new pharmaceutical,
Dr. H. J. Harwood, Jr. showed that vitamin C was in fact “nature’s perfect
statin.” Low vitamin C levels trigger the enzyme HMG-CoA Reductase to increase its activity and
catalyze the synthesis of more cholesterol to ensure an adequate supply of
“patch material.” Alternatively, high vitamin C levels were shown to inhibit
the enzyme activity and cause cholesterol levels to fall. Dr. Harwood’s research shows a fundamental difference
between drugs and nutrients: drugs can only inhibit or accelerate a biochemical
process whereas nutriceuticals allow the body to modulate (i.e.
up regulate or down regulate) enzymatic activity based on the body’s current
physiological needs.
·
There is
another very important difference in the mechanism of action of the statins
compared with that of vitamin C. The statins, by their mechanism of inhibition
of HMG-CoA reductase, also inhibit
the production of enzyme CoQ-10. Vitamin C on the other hand actually increases
the production of this important enzyme. CoQ-10, which incidentally is
transported in the bloodstream by lipoproteins also, is thought to be the first
antioxidant depleted when LDL is
subjected to oxidation thus furthering the plaque forming process. The
importance of this is illustrated by the fact that in 1989 the pharmaceutical
giant,Merck, received a US
patent permitting them to add CoQ-10 to their “statins” Mevacor and Zocor.
However, to date, they have seen no financial need to do so.
Pauling’s Final PieceS of the Puzzle –
L-LYSINE & L-PROLINE
Pauling repeated many of the experiments previously cited, and he
found that vitamin C did in fact help reverse some of the plaque in heart
disease (remember, vitamin C chemically changes the end amino acid residues).
However, there were still blockages in the blood vessels of the experimental
animals.
Remembering that plaques formed only in the damaged areas of
the vessels -- and that damaged collagen “looked like a frayed 3 strand
rope” -- he theorized there would be bonding sites (receptors) on the Lp(a)
that would be specific to the amino acid fragments of collagen (glycine,
lysine, and proline).
Being ubiquitous in the body, Pauling ruled L-glycine out,
reasoning that Lp(a) would not stick anywhere there is a glycine moiety
(glycine particle).
L-Lysine Binds with Lp(a) Receptors
Pauling then turned his attention to L-lysine, hypothesizing that
lysine receptors on the Lp(a) may account for why Lp(a) sticks exclusively to
the damaged collagen fibers.
To understand what Pauling was up to with lysine, it’s useful to
imagine the way the body uses antihistamines. An antihistamine binds to
histamine receptors (steals their parking places if you will) and thus
preventing allergens from attaching and causing an allergic response.
Similarly, Pauling added L-lysine to the vitamin C he gave his
test animals. Sure enough, the Lp(a) became way less sticky and more of
the plaques were removed. The L-lysine essentially acts as a “male” end
of a plug to the “female” receptors in Lp(a). This is how Lp(a) attaches to the
broken strands -- just like a plug in a wall socket. When there is extra
L-lysine circulating in the bloodstream, the L-lysine “plugs in” to and seals
Lp(a)’s “sockets”, thus creating a smooth, inert Lp(a) particle, which can no
longer adhere to the body. It is exactly like a parent putting a childproof
plug into an empty outlet -- no other plugs or little fingers are able
to attach.
While the extra lysine is “sealing the sockets” on L(p)a, remember
that vitamin C has changed the “plug” itself. By converting the end amino
acids to “hydroxyaminos”, it essentially replaced the “standard plug” with a
“European” type plug. Now there is no way at all for the L(p)a to “make the connection.”
In chemistry we say different reactants (here vitamin C and L(p)a)
have different affinities to the same substrate (the dangling
amino acids of the broken collagen fiber). The reactant with the greatest affinity
will preferentially bind to the substrate and displace reactants already
bound but having a weaker affinity to the substrate (in this case, the “good
guys” have the greatest affinity and the “bad guys” fall off). For all of these
reasons, one can readily see that the combination of L-lysine and vitamin C is
indeed a very powerful “plaque-buster”. The combination is, in fact, so
powerful that Pauling and Rath were awarded a U.S. patent for a solution
containing ascorbate and L-lysine to remove plaques from donor organs prior to
transplant surgery.
You see, once a transplanted organ is in place, blood must quickly
perfuse through the new organ or areas of tissue will necrose (die). Bathing
transplanted organs in their vitamin C-lysine solution prior to implantation
quickly removed any plaques in the major vessels and greatly enhanced
transplantation outcomes. Pretty impressive for vitamin C and a lowly
amino acid, don’t you think?
L-Proline binds with Additional Lp(a) Receptors
Encouraged by their results with L-lysine, Pauling and Rath began
to look at L-proline. L-proline is a unique amino acid, with a five-member ring
structure, which contains the amine portion of the molecule (it’s the only imino
amino acid).
<
The biochemical significance of this is that L-proline prefers
to be in oil rather than water. L-proline is thus lipophilic
as opposed to the hydrophilic L-lysine.
Since Lp(a) is a combination of a water-loving protein (apo a) and
the oily cholesterol, Pauling and Rath hypothesized that lipophilic proline
would block any receptors that might exist on the oily portion of Lp(a). When
they added L-proline to their vitamin C-lysine solution, the effects were
astonishing. Blockages completely cleared.
By having extra L-proline in the bloodstream (in addition to the
supplemented L-lysine and vitamin C) all of the receptor sites on the L(p)a are
“sealed” and the molecule does ,in essence, become “Teflon coated”.
With sufficient supply, vitamin C preferentially binds to
and hydroxylates (chemically alters) dangling lysine and proline ends
(in areas where the artery was damaged). After hydroxylation, the lysine and
proline strands in vessel walls no longer “fit” the Lp(a)’s receptor sites, and
some of the Lp(a) particles (or plaque patches) start to strip away from the
vessel walls. The experiments of Willis and Spittle previously cited confirm
this process.
SOME FINAL THOUGHTS
The conundrum of “causation” versus “correlation” – it’s an
age-old question and is an important question when it comes to cardiovascular
disease.
Think about a child who has seen a number of house fires. He
correctly observes that firemen are always present at house fires and
concludes, erroneously, that firemen must cause these fires. The
child does not yet understand that the firemen are actually there to save the
day.
It’s the same thing with the Lipid Theory, where cholesterol is
seen as an evil cause of cardiovascular disease, simply because it is highly
correlated with the disease.
With the Unified Theory, we instead view cholesterol,
homocysteine, C-reactive protein, and Lp(a) for what they really are: the
body’s dire attempt to save itself. These so-called “bad guys” are really just
markers of malnutrition and proliferate when the body is under stress.
Treating the symptoms of nutritional deficiency with drugs becomes
nothing more than an experiment, where we get to observe the toxic effects on a
malnourished body. Unfortunately, it has now become standard to treat
side effects with other drugs. And, in my profession, this is called polypharmacy.
As a first-year pharmacy student, I was told over and over again:
“Never practice polypharmacy!” Instead, we were taught to replace
the offending therapy to get rid of unwelcome or dangerous side effects.
Not so today, where prescriptions are layered on top of one another.
As a cautionary note, while polypharmacy is generally
considered a bad professional practice, I am not advocating that anyone reading
this article drop their prescriptions (there may be some extenuatuing
circumstances - i.e., an allergy or intolerance to an alternative
therapy). I am advocating for informed discussions with medical
practitioners, as well as the addition of a nutritional approach to supplement
conventional approaches.
Meanwhile, I often have wondered what it would be like if
first-year medical, nursing, and pharmacy students were introduced to the
Unified Theory? I’m not naïve enough to expect this any time soon, but
part of writing this paper was about documenting good science that merits more
attention by mainstream medicine.
I find it practically criminal that, despite overwhelming
scientific evidence, the Center for the Study of Alternative and Complementary
Medicine of the NIH has not done one clinical trial to test
Pauling’s and Rath’s work. The Center is funded by tax dollars, so you would
think that an incredibly affordable solution to the number one cause of death
in this country would get some attention, but, alas, not so far.
Meanwhile, I feel privileged to get information on the Unified
Theory in front of so many people through Our Health Co-op. May my
article be read widely and contribute not only to better awareness, but also to
making the case for formal clinical trial research -- someday!
Until then, here’s to your health and to our community!
Mike Ciell, Registered Pharmacist
Member, Our Health Co-op
Tampa, Florida
August 24, 2004
Medical Disclaimer: Information provided in this article is for
educational purposes only. Our Health Co-op makes no claims or
representation regarding treatment, cure, or mitigation of any specific disease
or condition. Please consult your own doctor, healthcare practitioner,
and/or pharmacist for any health problem (before deciding to self-treat or
making any changes to your prescribed medications). If you are ill, we
recommend you see a qualified health professional.
Copyright
© 2004. Our Health Co-op. All rights reserved
Source: http://www.ourhealthcoop.com/pauling.htm