Heart Disease Vitamin C PDF

Heart Disease Vitamin C and Linus Pauling by
Jeffrey Dach MD
Posted on June 26 2013
Heart Disease Vitamin C,

Ascorbate, Lysine and Linus Pauling
by Jeffrey Dach MD
This article is part one, for part two click here.
The Steam Roller is Not Joking – //////@\\\\\\\
I once had a conversation with a cardiologist friend of mine in which I casually mentioned the
Linus Pauling Theory of heart disease, and the subsequent idea that a non-toxic nutritional
supplement program with vitamin C and a few amino acids could prevent and reverse heart
disease. The response from my cardiologist friend was hearty laughter that anyone would even
suggest such a nonsensical idea, and surely you must be joking?
left image: courtesy wikimedia, roadroller

My cardiologist friend and the rest of the mainstream medical system has no clue about
the steamroller (above image) coming to health care aiming right at the huge profits
from diagnosis and treatment of heart disease, a multi billion dollar industry in the US.
The Cardiac Cath Lab and Cardiac Bypass Surgery Program will be flattened, the first
casualties of the internet medical information revolution providing information about a safe and
cheap supplement program to reverse heart disease called the Linus Pauling Protocol. Time has
come for the old dinosaurs to go. In the near future, thanks to Linus Pauling, heart disease will
become a curiosity of the past, like the disappearance of gastric ulcers after the invention of
antacids and antibiotics.
The Linus Pauling Protocol – Vitamin C

Vitamin C Deficiency Has Major Impact on Collagen
Production
Vitamin C is required to make a protein called collagen which is the major component of
connective tissues. The lack of Vitamin C is a deficiency disease called Scurvy.
Why is Collagen Important ?
Collagen is the most abundant protein in the body. It is the structural protein used to
make connective tissues, bones, teeth, hair, and arteries. Strong collagen is important for a
strong body.
Above Left image: “Unraveling Collagen“, Stainless Steel, height: 11 feet Julian Voss-Andreae, Orange Memorial Park Sculpture Garden, City of
South San Francisco, CA. 5/10/2006. Courtesy of Wikimedia Commons
Vitamin C Deficiency Results in Absent Lysine Crosslinking on Collagen
Vitamin C is required for strong collagen. How does this work? Vitamin C is required for lysyl
hydroxylase, an enzyme responsible for attaching the lysine residues together on adjacent
collagen strands. (see diagram below) Vitamin C deficiency results in weakened collagen
strands caused by disrupted lysine crosslinking. The resulting weakened collagen results in a
widespread problems in the connective tissues, bones, teeth, skin, hair, arteries, etc.
Steps in Collagen Synthesis (see diagram below Courtesy of Wikimedia)
How are the fibrils crosslinked? This is done with Lysine residues (see below diagram)
Fibril Cross Linking with Lysine and Lysyl Oxydase (see diagram below):
Left Above image courtesy of wikimedia commons lysyl oxidase.
Above image shows three steps in attachment of two fibrils (collagen strands) by
combining two lysine molecules with the help of an enzyme lysine hydroxylase which
requires vitamin C.
Full Blown Scurvy – Collagen Falls Apart
In the full blown Vitamin C deficiency disease called Scurvy, the structural elements of the
body literally fall apart. Collagen is broken down and not replaced. The joints wear out, the
small arteries begin to crack and degenerate, the skin shows easy bruising and bleeding as small
vessels rupture throughout the body, and the teeth may loosen and fall out.
Linus Pauling: Heart Disease is a Chronic Scurvy Condition
Linus Pauling was unquestionably the greatest scientist of the

twentieth century. All of modern biochemistry and molecular biology chemistry is based on
Linus Pauling’s work, especially his discovery and elucidation of the chemical bond. Pauling
is the only scientist to be awarded two unshared Nobel prizes.
Pauling’s later years were devoted to heart disease, and in 1989 he published “A Unified
Theory of Human Cardiovascular Disease,” in which he states that atherosclerotic plaques in
heart disease are actually part of a repair process, to repair the arterial damage caused by
chronic vitamin C deficiency.
Left Image: Linus Pauling Courtesy of Wikimedia
In essence, Pauling said that heart disease is a manifestation of chronic scurvy, and
atherosclerotic plaque is a mechanism evolved to repair or patch blood vessels and arteries
damaged by chronic vitamin C deficiency. Linus Pauling also said that atherosclerotic plaque
formation can be prevented or reversed with vitamin C, lysine and proline. These are
nutritional supplements available at any health food store for a few dollars.
Atherosclerotic Plaques Contain LipoProtein (a)
Plaque deposits found in human aortas are made up of a form of cholesterol called lipoprotein
(a) also called Lp(a).
Atherosclerotic Plaques Are Found at Maximal Mechanical Stress
Atherosclerotic plaques are not found randomly distributed throughout the arterial tree, rather
distribution is restricted to sites of high mechanical stress such as bifurcations, and areas of
motion such as the surface of the heart (coronary arteries). In the early 1950’s, a Canadian, G.
C. Willis, MD, made these same observations, and they have been confirmed by 60 years
of coronary and peripheral arteriography at major medical centers.
Exposed Lysine Crosslinks from Damaged Collagen is Site of LipoProtein (a) attachment
and Plaque Formation
Imagine stepping on your garden hose a thousand times a day. You

will soon notice cracks in the wall of the garden hose. This is the same process that happens in
the artery. As these cracks open up, the collagen strands in the wall of the artery are teased
apart. The triple helix collagen strands are normally bound together with lysine crosslinks
which are now teased apart and exposed to the circulating blood stream.
left Image: Lysine courtesy of WIkimedia
The Lysine residues look like little flags waving from the damaged collagen
strand. The exposed Lysine strands are available for binding to circulating Lipoprotein (a), a
special form of cholesterol that has lysine receptors, and is known to increase heart disease
risk. This attachment of lipoprotein(a) to the free lysine residues of damaged collagen initiates
the atherosclerotic process. Over time, this process builds larger plaque deposits which
eventually narrow the inner diameter of the artery causing a blockage, or leads to plaque
rupture and thrombosis, a catastrophic event which may cause heart attack or sudden death.
Animal experiments in genetically modified mice which have “knocked out” the lysine binding
sites on lipoprotein (a) show a fivefold reduction in atherosclerotic plaque formation.
Can You Make Vitamin C ? No You Can’t
We humans cannot make vitamin C in our liver as all other animals
do. We humans had a genetic mutation in our ancestry 50 million years ago which “knocked
out” the final enzyme in the hepatic synthesis of vitamin C. The missing enzyme is called GLO
(gulano lactone oxidase). Primates such as gorillas, chimpanzees and orangutans also share this
same GLO mutation and cannot make vitamin C. In adddition all primates share with humans
susceptibility to heart disease.
Above Image Vitamin C, a simple ring structure simikar to glucose, Ascorbate Courtesy of Wikimedia
All Animals Can Make Vitamin C, but the Guinea Pig Can’t
Except for humans and primates, all other animals have the three enzymes in the liver which
can synthesize vitamin C from glucose (a simple sugar). One major exception is the guinea pig,
which is really a rodent and not a pig, The guinea pig, for some unexplained reason, shares
with humans the identical GLO genetic mutation and also lacks the GLO enzyme just like we
do. This makes the guinea pig an ideal experimental model for human diseases. By the way,
although animals that make vitamin C never get heart disease, the guinea pig which lacks the
ability to synthesize vitamin C, also gets heart disease.
Animals That Make Vitamin C, Don’t Get Atherosclerotic Heart Disease
I though this was worth repeating.

(note: here I am referring to atherosclerotic vascular heart disease in animals. Dogs and Cats
DO succumb to other common types of heart disease such as cardiomyopathy and heart worm
etc.)
Animals That Don’t Make Vitamin C, Do Get Atherosclerotic Heart Disease
This should be starting to become clear now.

Animal Scientific Support for the Pauling Unified Theory
As mentioned above, guinea pigs are especially well suited

to study atherosclerosis because guinea pigs are unable to make their own vitamin C, and in
addition, they develop atherosclerotic plaques similar to those found in humans.
Left Image Guinea Pig Courtesy of Wikimedia
G. C. Willis, a Canadian doctor, conducted research with guinea pigs in the 1950’s showing
that guinea pigs deprived of dietary vitamin C developed atherosclerotic plaques, while guinea
pigs given plentiful vitamin C were protected. In addition,guinea pigs fed a vitamin C deficient
diet had elevated Lipoprotein (a) levels along with the increased atherosclerotic plaque
formation in the arteries.(link)(link)
Similar findings were demonstrated in genetically engineered mice lacking the GLO enzyme.
The GLO deficient mice fed a vitamin C deficient diet developed atherosclerotic plaques in the
aorta with characteristic deranged collagen crosslinking. GLO deficient mice fed vitamin C
were protected. (link)
Human Studies Suporting the Linus Pauling Theory
Optometrist, Dr. Sydney Bush’s retinal artery observations support the Pauling theory. Using
modern equipment to non-invasively photograph the retinal arteries of the eye before and after
Vitamin C supplementation in humans, Dr. Bush has documented reversal of atherosclerotic
plaque with Vitamin C supplementation.(link)
Coronary Calcium Score studies also support the Pauling Theory with favorable results after
treatment with Vitamin C and Lysine.
Anecdotal case evidence of reversal of heart disease can be found in the medical literature and
documented in Owen Fonorow’s book (see image below). In these cases, advanced heart
disease regresses after supplemention with the Linus Pauling Protocol. This is highly
significant because the natural course of heart disease is progression, and any intervetion that
alters the natural course of a diseae process is highly significant.
Message boards are a source of anecdotal cases reports supporting the Linus Pauling
Protocol. The Track Your Plaque Message Boards have documented many cases of regression
of atherosclerotic disease with protocols which include vitamin C as well as other nutritional
supplements. (There is a modest membership fee for TYP)
Why no drug company sponsored double blind placebo controlled studies? Since there are no
patents involved for natural supplements, and no drugs involved, no drug company would
ever invest the 250 million dollars to fund such a study with no potential for financial return.
The Physician’s Health Study – Don’t Waste Your Money On Vitamins !!

Using public funds, the NIH (National Institute of Health) funded a large study called The
Physicians’ Health Study II which evaluated Vitamins C and E in heart disease and
was published Nov. 9, 2008 in JAMA by Howard D. Sesso. The study found that Vitamin C
and E did not prevent mortality from heart disease, results which are completely opposite
to massive previously published research and anecdotal case reports.
A closer look shows a few glaring errors in study design. The Linus Pauliing Protocol was not
followed. The dosage of vitamin C was set too low, at one tenth the dosage recommended by
the Linus Pauling protocol, and lysine was not provided. While the Sesso study showed no
mortality benefit, many previous studies such as the Enstrom Study showed a striking 40%
reduction in all-cause mortality over 6 years from the same 500 mg daily vitamin C dosage.
The Paul Knecht study showed a 25% reduction in Heart Disease risk with daily 700 mg
Vitamin C. Two previous studies from Japan and Finland showed that Vitamin C reduces risk
for stroke, another atherosclerotic disease. There are many morelike these.
Since favorable results would be financially destructive to the drug and hospital industries, a
cynic might suggest that vested interests were at work in Sesso’s study intending to discredit
vitamin C . It is not difficult to design a medical study to fail. I regard this as merely another
example of the information war waged by corporate mainstream medicine against natural
medicine.
Enstrom Study, 500 mg Vitamin C Reduces Mortality 40% over 6 years

Enstrom showed that increasing vitamin C intake had a dramatic 40% reduction in mortality
benefit which exceeds any statin drug study ever conducted.
Linus Pauling Protocol For Prevention and Reversal of Plaque
If heart disease is chronic scurvy, caused by chronic vitamin C deficiency, then it makes sense
to supplement with vitamin C in the amounts needed to make strong collagen and prevent
arterial damage from mechanical stress.
In addition, Pauling devised a clever yet simple method to address the issue of Lipoprotein (a)
attaching to the lysine residues on the damaged collagen fibers in the arterial wall. He
recommended supplementing with 2-4 grams of lysine per day. The additional lysine in the
blood stream attaches to the receptor sites on the lipoprotein (a) molecules, inactivating the
lipoprotein(a) and preventing it from attaching to the arterial wall. This prevents the initiation
of the atherosclerotic process. In addition, Vitamin C and Lysine are both important precursors
for building strong collagen which makes strong arteries.
In addition to Lysine, some of the collagen crosslinking is done with another amino acid called
Proline, so proline was also added to the treatment protocol.
Where to Read About the Linus Pauling Protocol:
Above image, Cover of Linus Pauling Protocol Book courtesy of Owen Fonorow.
Read more about the Linus Pauling Protocol in this new book (above
image): Practicing Medicine Without a License by Owen Fonorow.
Owen Fonorow is perhaps the single most dedicated person devoted to the 1992 Linus Pauling
Protocol for prevention and reversal of heart disease.(link) A patent for the Linus
Pauling Protocol was issued in 1994.(link)
In 1996, a CAT scan coronary calcium score study validated the protocol
showing a 15% reversal of calcification indicating reversal of coronary
artery disease.
Another excellent book on the subject of Vitamin C and heart disease is,
Stop America’s #1 Killer by Thomas Levy MD, JD. 2006 (link). To read
more on the Linus Pauling Protocol, see this short four page booklet by
Owen Fonorow.(link) Or, read this excellent article by English and
Cass.(link)
What is the Linus Pauling Protocol?
L-ascorbate (Vitamin C) 5-6 grams a day in divided doses
L-Lysine 5 grams a day in divided doses
L-Proline 2-3 grams a day in divided doses
Tocotrienol Vitamin E
MK-7 Vitamin K2
These supplements can be obtained at any the health food store as tablets or capsules for 40 to
50 dollars a month.
Tower Labs Ascorcine 9

A convenient powder containing all the combined ingredients for the Linus Pauling Protocol is
called Ascorsine 9 and can be purchased at Tower Laboratories. This is a good choice
for anyone serious about preventing heart disease looking for an easy
product with everything in it.
Vitamin E, Good or Bad, Yes or No, Blessing or Curse?

Steve Hickey and Hilary Roberts come right out on page 167 of their book, and make the
statement, “Vitamin C and Tocotrienols can reverse coronary artery disease”. They would add
the Tocotrienol form of Vitamin E to the Linus Pauling Protocol. Regarding heart disease, and
atherosclerotic vascular disease, the authors state that “on the available evidence, the
combination of Vitamin C and Tocotrienols could be curative with no known harmful
effects.” For a more complete discussion of Vitamin E, see my article, Vitamin E, Curse or
Blessing? by Jeffrey Dach MD.
Opposition to the Linus Pauling Protocol by Mainstream Medicine
If you are facing the prospects of coronary artery bypass surgery (left image), you might ask the
obvious question: Why hasn’t my cardiologist told me about this information and started me on
the Linus Pauling Protocol?
Most cardiologists either don’t know about it or ignore it because of the information war going
on between mainstream medicine and natural medicine. Cardiologists read medical journals
which regularly run incorrect and biased articles saying Vitamin C is useless for prevention and
reversal of heart disease, such as the Nov 9 2008 Sesso study. (link).
Above image: coronary artery bypass operation courtesy wikimedia.
Diagnosing and treating heart disease with expensive tests and procedures such as coronary
angiography, angioplasty, stenting and bypass operations is the most profitable part of hospital
big business. That’s why hospitals compete and fight with each other over the rights to expand
and build larger cardiac cath labs and cardiac bypass operation programs. These programs are
huge money makers for the national hospital system.
What would happen if there was a cheap and effective way to reverse and prevent heart disease,
(ie. the Linus Pauling Protocol)? Heart disease would become an uncommon illness. With
fewer heart patients to treat, the multi-million dollar cath labs and cardiac bypass programs at
your local hospital would become obsolete and disappear. This would be a financial
catastrophe for mainstream medicine.
No More Construction Cranes?

With so much money and vested interest at stake, you can imagine why it is not prudent for a
cardiologist to bring up the benefits of the Linus Pauling Protocol in friendly
conversation while lunching in the Doctor’s Dining Hall. That would be an instant ticket off
the medical staff roster and out the hospital door, and the end of a lucrative cardiology
practice. What cardiologist in their right mind would do that? It is easier for the mainstream
cardiologists to simply laugh it off as a joke and go back to the cath lab, do more procedures
and make some money to pay their bills. Above left image: Hospital expansion project for new cardiac cath lab and cardiac
surgery theater. Courtesy wikimedia.
This article is part one, for part two click here.
Update 2015: Cha, John, Aleksandra Niedzwiecki, and Matthias Rath. “Hypoascorbemia
induces atherosclerosis and vascular deposition of lipoprotein (a) in transgenic mice.”
American journal of cardiovascular disease 5.1 (2015)
Related articles:
Preventing Heart Attacks with Ouabain
Reversing Heart Disease With Calcium Score by Jeffrey Dach MD (Part One)
Linus Pauling Protocol for prevention of Heart Diease Part Two by Jeffrey Dach MD
Cholesterol Lowering Statin Drugs for Women, Just Say No by Jeffrey Dach MD
Lipitor and The Dracula of Modern Technology by Jeffrey Dach MD
Financial Disclosure: I have no financial interest in Vitamin C Foundation, Tower
Labororatories or LivOn Labs, Track Your Plaque, nor do I receive income from the sale of any
books mentioned here.
Link to this article:http://wp.me/P3gFbV-qL
Jeffrey Dach MD
References and Links
Willis Studies on Vitamin C Guinea Pig Model and Atherosclerosis

http://www.vitamincfoundation.org/pdfs/WillisGround.pdf
AN EXPERIMENTAL STUDY OF THE INTIMAL GROUND SUBSTANCE IN
ATHEROSCLEROSIS, G.C. Willis, Canad. M. A. J. Vol 69, 1953, p. 17-22
http://www.vitamincfoundation.org/pdfs/WillisSerial.pdf
SERIAL ARTERIOGRAPHY IN ATHEROSCLEROSIS, G. C. Willis, A. W. Light, W.S.
Cow, Canad. M. A. J. Dec 1954, Vol 71, 1954, p. 562-568
http://www.vitamincfoundation.org/pdfs/WillisTissue.pdf
ASCORBIC ACID CONTENT OF HUMAN ARTERIAL TISSUE, G. C. Willis, S. Fishman,
Canad. M. A. J., April 1, 1955, Vol 72, Pg 500-503
http://www.vitamincfoundation.org/pdfs/WillisAthero.pdf
THE REVERSIBILITY OF ATHEROSCLEROSIS, G. C. Willis, Canad. M. A. J., July 15,
1957, Voll 77., Pg 106-109
http://www.vitamincfoundation.org/pdfs/
CAPILLARY RUPTURE WITH INTIMAL HEMORRHAGE IN THE CAUSATION OF
CEREBRAL VASCULAR LESIONS, J. C. Paterson, Arch Path, Vol 29, 1940, Pg 345-354
http://www.vitamincfoundation.org/pdfs/
SOME FACTORS IN THE CAUSATION OF INTIMAL HEMORRHAGES AND IN THE
PRECIPITATION OF CORONARY THROMBI, J. C. Paterson, Canad. M. A. J., Feb 1941, Pg
114-120
Guinea Pigs are excellent model for atherosclerosis
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1435897
Nutr Metab (Lond). 2006; 3: 17.
Guinea pigs: A suitable animal model to study lipoprotein metabolism, atherosclerosis and
inflammation by Maria Luz Fernandez1 and Jeff S Volek2
http://jn.nutrition.org/cgi/content/full/131/1/10
Journal of Nutrition. 2001;131:10-20.
Guinea Pigs as Models for Cholesterol and Lipoprotein Metabolism Maria Luz
http://ci.nii.ac.jp/naid/110002603577/
Japanese circulation journal Vol.35, No.12(19711200) pp. 1559-1565
EXPERIMENTAL ATHEROSCLEROSIS WITH ASCORBIC ACID DEFICIENCY by
FUJITANI TAKAO et al.
Influence of ascorbic acid deficiency on serum and hepatic lipid and on the aorta were studied.
Two groups of ascorbic acid deficient guinea pigs were made by feeding with scorbutic diet
with or without 5% coconut oil for two weeks (group 3 and 1).
Control animals of the experimental groups were fed with the same diet of previous two groups
and received 25 mg of ascorbic acid subcutaneously for the same period (group 2 and 4).
Moderate increase of triglyceride and cholesterol ester and beta-lipoprotein in the serum of
ascorbic acid deficiency (group 1), and markedly to approximately twice of normal in the
ascorbic acid deficiency with coconut oil feeding (group 3).
Increase of serum lipids and depression of plasma lipoprotein lipase activity by ascorbic acid
deficiency was prevented by ascorbic acid administration as observed in the control
groups. Histological examination of the aorta revealed edematous swelling of the ground
substance in the intima and media in the scorbutic, and early atheromatous lesions of
accumulated foam cells in the intima of the ascorbic acid deficiency with coconut oil
feeding. These findings suggest that any factors disturbing ascorbic acid metabolism induce an
increase of serum lipids and altered vascular wall metabolism, and consequently follows
atherosclerosis.
Landmark Linus Pauling Articles

http://www.pnas.org/content/87/23/9388.full.pdf
Immunological evidence for the accumulation of lipoprotein(a) in the atherosclerotic lesion of
the hypoascorbemic guinea pig. M Rath, L Pauling – Proceedings of the National Academy of
Sciences, 1990 – National Acad Sciences. Vol. 87, pp. 9388-9390, December 1990
http://www.pnas.org/content/87/16/6204.full.pdf
Hypothesis: lipoprotein (a) is a surrogate for ascorbate.
M Rath, L Pauling – Proceedings of the National Academy of Sciences 1990
Another link to same article:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=2143582
Proc Natl Acad Sci U S A. 1990 August; 87(16): 6204–6207. Hypothesis: lipoprotein(a) is a
surrogate for ascorbate. M Rath and L Pauling
Journal of Orthomolecular Medicine, 6(3-4): 144-46, 1991.Case Report: Lysine/Ascorbate-
Related Amelioration of Angina Pectoris by Linus Pauling Lysine Ascorbate Related
Amelioration of Angina Pectoris by Linus Pauling Journal of Orthomolecular Medicine 1991
http://orthomolecular.org/library/jom/1992/pdf/1992-v07n01-p005.pdf
A Unified Theory of Human Cardiovascular Disease Leading the Way to the Abolition of This
Disease as a Cause for Human Mortality M Rath, L Pauling – J Ortho Med, 1992 –
http://www.americanhearthealthservices.com/images/Cellular_Essentials.pdf
JOURNAL OF APPLIED NUTRITION, VOLUME 48, NUMBER 3, 1996 ORIGINAL
REPORT Copyright – International Academy of Nutrition and Preventive Medicine
NUTRITIONAL SUPPLEMENT PROGRAM HALTS PROGRESSION OF EARLY
CORONARY ATHEROSCLEROSIS DOCUMENTED BY ULTRAFAST COMPUTED
TOMOGRAPHY Matthias Rath, M.D. and Aleksandra Niedzwiecki, Ph.D.
Other supportive articles
http://www.ncbi.nlm.nih.gov/pubmed/1588941
Mol Cell Biochem. 1992 Apr;111(1-2):41-7.
Protective role of ascorbic acid against lipid peroxidation and myocardial injury.
Chakrabarty S, Nandi A, Mukhopadhyay CK, Chatterjee IB. Department of Biochemistry,
University College of Science, Calcutta, India.
Ascorbic acid (AH2) is a potential scavenger of superoxide radical and singlet oxygen. In
the guinea pig, marginal AH2 deficiency results in intracellular oxidative damage in the
cardiac tissue as evidenced by lipid peroxidation, formation of fluorescent pigment and loss of
structural integrity of the microsomal membranes. The oxidative damage does not occur due to
lack of enzymatic scavengers of reactive oxygen species such as superoxide dismutase, catalase
and glutathione peroxidase. Also, glutathione transferase activity is not decreased in AH2
deficiency. Lipid peroxidation, fluorescent pigment formation and protein modification
disappear after AH2 therapy. These results, if extra-polated to human beings, would indicate
that chronic subclinical AH2 (ascorbate) deficiency may result in progressive oxidative
damage which in the long run may lead to permanent degenerative diseases in the heart.
High Blood sugar worsens effect of vitamin C Deficiency
Atherosclerosis. 2001 Sep;158(1):1-12.
Hyperglycemia-induced ascorbic acid deficiency promotes endothelial dysfunction and the
development of atherosclerosis.Price KD, Price CS, Reynolds RD.
Dehydroascorbic acid, the oxidized form of vitamin C, is transported into mammalian cells via
facilitative glucose transporters and hyperglycemia inhibits this process by competitive
inhibition. This inhibited transport may promote oxidative stress and contribute to the increase
in atherosclerotic cardiovascular disease observed in patients with diabetes mellitus.
http://www.ajcn.org/cgi/reprint/23/1/27.pdf
Am J Clin Nutr. 1970 Jan;23(1):27-30.
Ascorbic acid and atherosclerosis.Shaffer CF.
Anti-Vitamin C Articles, Failure of Vitamin C
http://jama.ama-assn.org/cgi/content/full/2008.600
Vitamins E and C in the Prevention of Cardiovascular Disease in Men
The Physicians’ Health Study II Randomized Controlled Trial – JAMA-EXPRESS Howard
D. Sesso, ScD, MPH; Julie E. Buring, ScD; William G. Christen, ScD; Tobias Kurth, MD,
ScD; Charlene Belanger, MA; Jean MacFadyen, BA; Vadim Bubes, PhD; JoAnn E. Manson,
MD, DrPH; Robert J. Glynn, ScD; J. Michael Gaziano, MD, MPH JAMA. 2008;300(18):2123-
2133. Published online November 9, 2008
Basic research and observational studies suggest vitamin E or vitamin C may reduce the risk of
cardiovascular disease. However, few long-term trials have evaluated men at initially low risk
of cardiovascular disease, and no previous trial in men has examined vitamin C alone in the
prevention of cardiovascular disease.
Objective To evaluate whether long-term vitamin E or vitamin C supplementation decreases

the risk of major cardiovascular events among men.
Design, Setting, and Participants The Physicians’ Health Study II was a randomized, double-
blind, placebo-controlled factorial trial of vitamin E and vitamin C that began in 1997 and
continued until its scheduled completion on August 31, 2007. There were 14 641 US male
physicians enrolled, who were initially aged 50 years or older, including 754 men (5.1%) with
prevalent cardiovascular disease at randomization.
Intervention Individual supplements of 400 IU of vitamin E every other day and 500 mg of
vitamin C daily.
Main Outcome Measures A composite end point of major cardiovascular events (nonfatal
myocardial infarction, nonfatal stroke, and cardiovascular disease death).
Results During a mean follow-up of 8 years, there were 1245 confirmed major cardiovascular
events. Compared with placebo, vitamin E had no effect on the incidence of major
cardiovascular events (both active and placebo vitamin E groups, 10.9 events per 1000 person-
years; hazard ratio [HR], 1.01 [95% confidence interval {CI}, 0.90-1.13]; P = .86), as well as
total myocardial infarction (HR, 0.90 [95% CI, 0.75-1.07]; P = .22), total stroke (HR, 1.07
[95% CI, 0.89-1.29]; P = .45), and cardiovascular mortality (HR, 1.07 [95% CI, 0.90-1.28]; P =
.43). There also was no significant effect of vitamin C on major cardiovascular events (active
and placebo vitamin E groups, 10.8 and 10.9 events per 1000 person-years, respectively; HR,
0.99 [95% CI, 0.89-1.11]; P = .91), as well as total myocardial infarction (HR, 1.04 [95% CI,
0.87-1.24]; P = .65), total stroke (HR, 0.89 [95% CI, 0.74-1.07]; P = .21), and cardiovascular
mortality (HR, 1.02 [95% CI, 0.85-1.21]; P = .86). Neither vitamin E (HR, 1.07 [95% CI, 0.97-
1.18]; P = .15) nor vitamin C (HR, 1.07 [95% CI, 0.97-1.18]; P = .16) had a significant effect
on total mortality but vitamin E was associated with an increased risk of hemorrhagic stroke
(HR, 1.74 [95% CI, 1.04-2.91]; P = .04).
Conclusions In this large, long-term trial of male physicians, neither vitamin E nor
vitamin C supplementation reduced the risk of major cardiovascular events. These data
provide no support for the use of these supplements for the prevention of cardiovascular disease
in middle-aged and older men.
Trial Registration clinicaltrials.gov Identifier: NCT00270647
http://circ.ahajournals.org/cgi/content/full/105/12/1396
Vitamin C, Collagen, and Cracks in the Plaque, by Peter Libby, MD; Masanori Aikawa, MD
PhD
Most fatal acute myocardial infarctions result from a fracture of the plaque’s fibrous cap. We
proposed the hypothesis some years ago that the level of collagen in the fibrous cap depends on
a dynamic balance of synthesis and degradation.1 We further showed that inflammatory
cytokines can regulate both the expression of genes that direct interstitial collagen synthesis in
vascular smooth muscle cells and the interstitial collagenases (matrix metalloproteinases 1, 8,
and 13) required to initiate the breakdown of collagen fibrils.2–5 Given the capital importance
of collagen in protecting the plaque from rupture and hence thrombosis, the metabolism of this
complex molecule merits consideration in depth. See p 1485
The formation of mature fibrillar collagen involves many steps beyond gene transcription
(Figure). The initial translation product, the procollagen peptide chain, undergoes extensive
posttranslational modification: an especially noteworthy point during this period of exploration
of the proteome. Collagen contains unusual amino acids, hydroxyproline and hydroxylysine,
formed by a vitamin C–dependent process that entails enzymatic transfer of hydroxyl groups to
selected proline and lysine residues in the nascent procollagen chains. Glycosyl transferases
then add sugar moieties to the procollagen chains. The hydroxylated and glycosylated
monomers then self-assemble into helical trimers as they traverse several intracellular
compartments. Trimming the nonhelical tails (the telopeptides) from both ends of the
procollagen molecule by proteinases yields the mature interstitial collagen triple helix secreted
by smooth muscle cells in arteries. These building blocks then further self-aggregate into
multimers and form interstitial collagen fibrils, linear structures as strong as steel wires.
The ascorbate-dependent addition of polar hydroxyl groups to the side chains of proline and
lysine may aid the self-assembly and stability of the collagen fibril by forming interchain
hydrogen bonds. The absence of sufficient ascorbic acid (vitamin C), a required cofactor for
prolylhydroxylase, thus impairs the formation of stable collagen. The human phenotype of
vitamin C deficiency, scurvy, classically involves fragility of blood vessels. In 1753, James
Lind described the skin of scorbutics as “…covered with several reddish, bluish… spots…
resembling an effusion of blood.”6 Lind’s discovery that food rich in vitamin C provided a cure
for scurvy spurred England’s subsequent naval supremacy and putatively changed the course of
history. Of course, chemical characterization of vitamin C as the antiscorbutic factor did not
occur until the 1930s. (Interested readers may find Albert Szent-Györgi’s dispute with the
editor of the Biochemical Journal regarding publication of the structure of vitamin C amusing.7
Cardiologists know Szent-Györgi better for his later discovery of the biochemical basis of
muscle contraction).
Study of vitamin C’s role in vivo has proven challenging. Unlike humans, usual experimental
animals can synthesize vitamin C and thus cannot be made scorbutic. Maeda’s group has
recently introduced a targeted mutation that makes mice dependent on dietary vitamin C,
allowing manipulation of ascorbate levels. In this issue of Circulation, Nakata et al8 studied
atheroma in hypercholesterolemic and scorbutic mice. They find no change in lesion size, but
they observe decreased collagen content in the lesions. Such changes should impair the
biomechanical strength of the plaque and make it more prone to rupture. This finding extends
the burgeoning evidence that changes in collagen metabolism can influence crucial
characteristics of the atherosclerotic plaque. Our recent in vivo studies also showed that
alterations in collagen synthesis and catabolism induced by lipid lowering or statin treatment
influence the collagenous structure of atheroma in rabbits.9–11 It would have been of interest
to evaluate overall protein content in these lesions, as we showed almost 2 decades ago that
ascorbate can augment noncollagen protein synthesis by cultured arterial smooth muscle
cells.12
We do not know whether scorbutic humans with atherosclerosis would experience increased
plaque rupture, a curious but currently clinically irrelevant question. In addition to its
antiscorbutic action, vitamin C has potent antioxidant properties. Physiological concentrations
of ascorbic acid can inhibit in vitro oxidative modification of LDL, a critical event during
atherogenesis.13 For this reason, many individuals take this and other antioxidant vitamins in
hope that combating oxidative stress can forestall atherosclerosis and its complications.
Vitamin C has other antiinflammatory effects as well, including decreased leukocyte adhesion
to the endothelium and increased bioavailability of atheroprotective nitric oxide (NO).
Administration of vitamin C for 10 days (2 g/d) reduces adhesion of monocytes obtained from
cigarette smokers to cultured endothelial cells.14 Vitamin C’s potency generally exceeds that of
vitamin E as an antiinflammatory and antiatherogenic agent. For example, intake of vitamin C,
but not vitamin E, inhibits oxidized LDL-induced leukocyte adhesion to endothelium in
hamsters.15 Physiological concentrations of ascorbic acid also increase synthesis and activity
of NO in vitro.16 Vitamin C also inhibits activation of nuclear factor-B (NF-B), a key regulator
of inflammatory gene expression.(17 ) Administration of vitamin C can improve endothelial
dysfunction in hypercholesterolemic patients.18 Ascorbate’s effect on plaque collagen content
adds another theoretical rationale for using vitamin C in patients at risk for atherosclerotic
events.
Unfortunately, we lack clinical evidence that would permit us to translate this basic
science into practice. The recently reported (but as yet unpublished) Heart Protection Study
(HPS) administered a cocktail of antioxidant vitamins (vitamin C 250 mg, vitamin E 600 mg,
beta-carotene 20 mg/d) to a large group of individuals at high risk for atherosclerotic events for
a period of 5 years. The vitamins had absolutely no effect on a variety of end points,
including coronary events 19 (see also The Heart Protection Study Investigators
at http://www.hpsinfo.org/). Brown and colleagues recently reported acceleration of coronary
atherosclerosis in patients treated with a combination of statins and a cocktail of antioxidant
vitamins (vitamin C 1000 mg, vitamin E 800 IU, beta-carotene 25 mg/d) in the HDL-
Atherosclerosis Treatment Study (HATS).20
To what may we attribute this apparent failure of a plausible and widely used therapeutic
approach? First, these studies may have employed suboptimal doses of the vitamins used, or
interactions among them may have mitigated a beneficial effect of one or the other
supplements. In this regard, vitamin E monotherapy showed no benefit on atherosclerotic
events in both the Heart Outcomes Prevention Evaluation (HOPE) and GISSI studies.21,22 In
these various studies, the degree of preexisting disease or inadequate duration of treatment
might have limited the benefit of the antioxidants. Yet, the striking beneficial effects observed
in the statin treatment arms of both the HPS and HATS20 and of the angiotensin converting
enzyme inhibitor in the HOPE study21 establish the mutability of outcomes measured in these
patient populations in the same trials. Partition of fat-soluble vitamin E into the lipid phase of
plaque or lipoproteins might shield it from the cooperative antioxidant effect of water-soluble
ascorbate, excluded from these lipid milieux. Thus, more potent or amphipathic antioxidants
might interrupt oxidative stress during atherogenesis more effectively than the vitamins.
Although vitamin deficiencies lead to disease, consumption of pharmacological amounts of
these substances in individuals who maintain vitamin-sufficient diets may not prevent disease.
Indeed, malnutrition hardly applies to our patients with atherosclerosis. Contemporary
developed societies seem at much higher risk of dietary surfeit than lack.
It is curious indeed that many remain suspicious of pharmacological lipid-lowering, a strategy
now proven unequivocally to prevent myocardial infarction and stroke and to prolong life as
well. Yet, many individuals readily consume costly vitamin supplements devoid of benefit in
clinical trials. This situation may reflect in part a failure of the medical community to
communicate effectively with the public regarding evidence-based medicine and the life-saving
benefits of preventive strategies. The present results of Nakata et al8 reinforce the importance
of collagen metabolism in determining the structure of atherosclerotic plaques. However,
current clinical and experimental evidence suggests that the best way to influence favorably the
balance of collagen synthesis and degradation in atheroma at hand today remains lipid-
lowering, not vitamin C.
Enstrom Study 500 mg Vitamin C Reduces Mortality 40% over 6 years

Epidemiology. 1992 May;3(3):194-202
Vitamin C intake and mortality among a sample of the United States population.Enstrom JE,
Kanim LE, Klein MA.School of Public Health, University of California, Los Angeles 90024.
We examined the relation between vitamin C intake and mortality in the First National Health
and Nutrition Examination Survey (NHANES I) Epidemiologic Follow-up Study cohort. This
cohort is based on a representative sample of 11,348 noninstitutionalized U.S. adults age 25-74
years who were nutritionally examined during 1971-1974 and followed up for mortality (1,809
deaths) through 1984, a median of 10 years. An index of vitamin C intake has been formed
from detailed dietary measurements and use of vitamin supplements. The relation of the
standardized mortality ratio (SMR) for all causes of death to increasing vitamin C intake is
strongly inverse for males and weakly inverse for females.
Among those with the highest vitamin C intake, males have an SMR (95% confidence interval)
of 0.65 (0.52-0.80) for all causes, 0.78 (0.50-1.17) for all cancers, and 0.58 (0.41-0.78) for all
cardiovascular diseases; females have an SMR of 0.90 (0.74-1.09) for all causes, 0.86 (0.55-
1.27) for all cancers, and 0.75 (0.55-0.99) for all cardiovascular diseases.
Comparisons are made relative to all U.S. whites, for whom the SMR is defined to be 1.00.
There is no clear relation for individual cancer sites, except possibly an inverse relation for
esophagus and stomach cancer among males. The relation with all causes of death among males
remains after adjustment for age, sex, and 10 potentially confounding variables (including
cigarette smoking, education, race, and disease history).
25% reduction in Heart Disease Risk with 700 mg Vit C

http://www.ajcn.org/cgi/content/full/80/6/1508
American Journal of Clinical Nutrition, Vol. 80, No. 6, 1508-1520, December 2004
Antioxidant vitamins and coronary heart disease risk: a pooled analysis of 9 cohorts Paul
Knekt et al.
Epidemiologic studies have suggested a lower risk of coronary heart disease (CHD) at higher
intakes of fruit, vegetables, and whole grain. Whether this association is due to antioxidant
vitamins or some other factors remains unclear.
Objective:We studied the relation between the intake of antioxidant vitamins and CHD
risk.Design:A cohort study pooling 9 prospective studies that included information on intakes
of vitamin E, carotenoids, and vitamin C and that met specific criteria was carried out. During a
10-y follow-up, 4647 major incident CHD events occurred in 293 172 subjects who were free
of CHD at baseline.
Results: Dietary intake of antioxidant vitamins was only weakly related to a reduced CHD risk
after adjustment for potential nondietary and dietary confounding factors. Compared with
subjects in the lowest dietary intake quintiles for vitamins E and C, those in the highest intake
quintiles had relative risks of CHD incidence of 0.84 (95% CI: 0.71, 1.00; P = 0.17) and 1.23
(1.04, 1.45; P = 0.07), respectively, and the relative risks for subjects in the highest intake
quintiles for the various carotenoids varied from 0.90 to 0.99. Subjects with higher
supplemental vitamin C intake had a lower CHD incidence. Compared with subjects who did
not take supplemental vitamin C, those who took >700 mg supplemental vitamin C/d had a
relative risk of CHD incidence of 0.75 (0.60, 0.93; P for trend < 0.001). Conclusions:The
results suggest a reduced incidence of major CHD events at high supplemental vitamin C
intakes.
Vitamin C Deficiency In the US
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=15117714
Am J Public Health. 2004 May; 94(5): 870–875. PMCID: PMC1448351
Vitamin C Deficiency and Depletion in the United States: The Third National Health and
Nutrition Examination Survey, 1988 to 1994 Jeffrey S Hampl, et al. In conclusion, our data
indicate that a considerable number of children and adults in the United States are
vitamin C deficient or depleted.
Owen Fonorow Articles on Vitamin C
http://www.internetwks.com/owen/TheoryPaper.htm
The Unified Theory, The Long Neglected Theory of Cardiovascular and Heart Disease By
Owen Richard Fonorow 2002
1) CV Mortality declines after Vitamin C Consumption increases after publication of Linus

PAuling Book published 1970. US is only industrialized country to experience a 40% drop in
CV disease.
2) Most high order mammals make their own vitamin C (3-11 g daily) do not have CV
(cardiovascular) disease as seen in humans.
3) Animals such as the Guinea pig which cannot make their own vitamin C, also have
cardiovascular disease, same as humans if they are fed a Vitamin C deficient diet.
4) The Willis Guinea Pig Experiments in the 1950’s show that depriving the animal of vitamin
C causes atherosclerosis which is quite similar to the human lesion. No plaque forms in the
control group getting “adequate” vitamin C. (Source: The Reversibility of Atherosclerosis, G.
C. Willis, Canad M. A. J, July 15, 1957, Vol 77)
5) Pauling and Rath showed the apo(a)/Lp(a) increased in the animals deprived of vitamin C,
but not in the controls. (Source: Immunological evidence for the accumulation of Lp(a) in the
atherosclerotic lesion of the hypoascorbemic guinea pig, Pauling/Rath, Pro. Nat. Acad. Sci
USA, Vol 87, pp 9388-9390, Dec 1990, Biochem)
6) The heart disease process begins with a lesion in the artery. (Source: Brown-Goldstein
Scientific American 1982, and Linus Pauling Heart Disease Video)
7) Veins, in general, do not suffer plaque deposits. (Source: Common knowledge from the
medical Literature)
8) Plaques are often localized to areas of mechanical stress, at bifurcations, and the surface of
the heart (coronary arteries or carotid arteries). (Source: An Experimental Study of the Intimal
Ground Substance in Atherosclerosis, G. C. Willis, Canad M. A. J., July 1953, Vol 69, pg 17)
9) Vitamin C is required (and used up) making collagen – the most abundant protein in the
human body. (Source: Roger J. Williams, Nutrition Against Disease, 1971, Linus Pauling
HOW TO LIVE LONGER AND FEEL BETTER, 1986)
10) Scurvy is caused by a deficiency in making collagen which is in turn caused by a lack of
vitamin C. (Source: James Lind, 1753, Linus Pauling HOW TO LIVE LONGER AND FEEL
BETTER 1986)
11) The Beisiegel studies in Germany of post-mortem human aortas in 1989 determined that
plaque consists of Lp(a) and only Lp(a) – no ordinary LDL. (Source: Morphological detection
and quantification of lipoprotein(a) deposition in atheromatous lesions of human aorta and
coronary arteries in Virchows Arch A Pathol Anat Histopathol 1990;417(2):105-11, Niendorf
A; Dietel M; Beisiegel U; Arps H; Peters S , Wolf K; Rath M and Lipoprotein(a) in the arterial
wall. Beisiegel U; Rath M; Reblin T; Wolf K; Niendorf A, Eur Heart J 1990 Aug;11 Suppl
E:174-83)
12) Elevated cholesterol has been correlated with CVD, but many studies were conducted
before Lp(a) was known, Lp(a) was lumped in with LDL. In September, 2000, an Oxford meta-
analysis of 27 large studies showed that people with elevated Lp(a) are 70% more like to suffer
a heart attack or stroke. (Source: Circulation Sep 2000)
Radio Interviews
mms://rense.gsradio.net/rense/windows_media/
WMHigh/May2008/kx2u91/rense_052208_hr2.wma
Owen Fonorow First Interview MAy 2008 on Jeff Rense
1/2 to 1 million cardiovascular deaths per year can be prevented with vitamin C. There are
about a million cardiac procedures (angioplasty, stent, bypass) per year. We have a genetic
defect in the inability to make vitamin C. We have a defect in GLO enzyme which happened
50 million years ago. High level primates, guineas pig and fruit bat cannot make vitamin
C. People with angina and chest pain usually get better in 10 days on Vitamin C and
Lysine. WHen they stop the supplements, they may have a recurrence of pain. Case report of a
patient: Unique E and High Vitamin C (6 grams), Lysine (6 grams) reverts EKG back to
normal. About 6 months after stopping, heart problems recurr. 50 million years ago,
Lipoprotein (a) evolved with Lysine binding site to allow us to evolve. Lipoportein (a) forms
cholesterol plaque in absence of Vitamin C. Medical Study: Examination of aortas, lipoprotein
(a) found in plaque. Most people live with chronic low levels of vitamin C. Cardio-C drink mix
with Pauling recommendation. Contains 2-3 grams of Lysine, 3 grams of Vitamin C. After 12
years of experience: it does reverse atherosclerosis which is a symptom of chronic
scurvy which builds plaque in the arteries.
(Bush) White atheromas can be seen in retinal arteries. In the Vitamin C group, these plaques
reverse, This work was published. With 10 grams of Vitamin C a day, and it takes a month to
reverse soft atheromas. Calcified atheromas takes longer. Once case took 2 years to
reverse.Cardio-Retinometry: We see amazing reversals in a very short time. Not noticed by
cardiologists.Vitamin C is safe with no adverse effects. Therapeutic Dosage: take 500 mg-
1000mg Vitamin C every 4 hours. Non-Chinese Vitamin C made in Europe Vitamin C
Foundation.
Cost is : 24 dollars a month auto-ship Cardio C. Liposomal Vitamin C is available for people
with gas and diarrhea. More expensive.
Second Radio Interview

mms://rense.gsradio.net/rense/windows_media/WMHigh/Aug2008/r8r10x/
rense_081408_hr2.wma
Radio Interview on Vitamin C and Heart Disease with Owen Fonorow Aug 2008
Heart Disease and Vitamin C, Linus Pauling Genius discovered a way to stop and reverse heart
disease in humans. Owen Fonorow, Vitmain C Foundation. So simple, yet so
crucial. Remarkable breakthrough in human health and well ness. Book: Practicing Medicine
Without A License, the story of Linus Pauling and Heart Disease by Owen Fonorow. Carol
Smith experience relase and recovery on three ocassions. Basic theory is that most of animal
species produce own bitamin C in the liver. Humans cannot make vitamin C, and we suffer
cardiovascular disease.
The species that make vitamin C can make collagen which keeps artieries strong. In the
absence of vitamin C production we have evolved cholesterol plaques to repair the
arteries causing occluded arteries and heart attacks. We can no longer produce vitamin C due
to a genetic defect. Lysine binding site. Lysine is the second component. High dose, needs
powser and avoid pills. Collagen is the major protein of connective tissue and arteries. Lack of
vitamin C causes weak collagen.
http://www.internetwks.com/owen/
Health Articles by Owen Fonorow, Orthomolecular Naturopath (Orthomopath)
(c) 1996-2008 Owen Fonorow.
http://practicingmedicinewithoutalicense.com/protocol/excerpt_chp7.pdf
Chapter 7 Practicing Medicine WIthout a License summary of Pauling therapy to reverse heart
disease
http://www.vitamincfoundation.org/ Vitamin C Foundation, Owen Fonorow
Article Summarizing Linus Pauling Theory of Heart DIsease
http://www.nutritionreview.org/library/collagen.connection.html
Linus Pauling’s Unified Theory of Human Cardiovascular Disease
The Collagen Connection Jim English and Hyla Cass, MD
Pauling Therapy for the Reversal of Heart Disease
1. Vitamin C: to bowel tolerance – as much as you can take without diarrhea. For most people
this will be in the range of five to ten grams (5,000-10,000 mg.) each day. Spread this amount
into two equal doses 12 hours apart. (Vitamin C prevents further cracking of the blood vessel
wall – the beginning of the disease.)
2. L-Proline: 3 grams twice per day (acts to release lipoprotein(a) from plaque formation and
prevent further deposition of same).
3. L-Lysine: 3 grams twice each day (acts to release lipoprotein(a) from plaque formation and
prevent further deposition of same).
4. Co-enzyme Q10: 90-180 mg. twice per day (strengthens the heart muscle).
5. L-Carnitine: 3 grams twice per day (also strengthens the heart muscle).
6. Niacin: Decreases production of lipoprotein(a) in the liver. Inositol hexanicotinate is a form

of niacin which gives less of a problem with flushing and therefore allows for larger therapeutic
doses. Begin with 250 mg. at lunch, 500 mg. at dinner and 500 mg. at bedtime the first day;
then increase gradually over a few days until you reach four grams per day, or the highest dose
under four grams you can tolerate. Be sure to ask your doctor for liver enzyme level tests every
two months or less to be sure your liver is able to handle the dose you are taking.
7. Vitamin E: 800-2400 IU per day. (Inhibits proliferation of smooth muscle cells in the walls
of arteries undergoing the atherosclerotic changes.)
References for Cass article:
1. Marcoux C; Lussier-Cacan S; Davignon J; Cohn JS.

Association of Lp(a) rather than integrally-bound apo(a) with triglyceride-rich lipoproteins of
human subjects.
Biochim Biophys Acta 1997 Jun 23;1346(3):261-74.
2. Ensenat D, Hassan S, Reyna SV, Schafer AI, Durante W.

Transforming growth factor-b1 stimulates vascular smooth muscle cell L-proline transport by
inducing system A amino acid transporter 2 (SAT2) gene expression. Biochem. J. (2001) 360,
(507-512)
3. White AL; Lanford RE. Cell surface assembly of lipoprotein(a) in primary cultures of
baboon hepatocytes.
J Biol Chem 1994 Nov 18;269(46):28716-23.
4. Klezovitch O; Edelstein C; Scanu AM. Evidence that the fibrinogen binding domain of
Apo(a) is outside the lysine binding site of kringle IV-10:
a study involving naturally occurring lysine binding defective lipoprotein(a) phenotypes.
J Clin Invest 1996 Jul 1;98(1):185-91.
5. Boonmark NW; Lou XJ; Yang ZJ; Schwartz K; Zhang JL; Rubin EM; Lawn RM.
Modification of apolipoprotein(a) lysine binding site reduces atherosclerosis in transgenic mice.
J Clin Invest 1997 Aug 1;100(3):558-64.
6. Phillips J; Roberts G; Bolger C; el Baghdady A; Bouchier-Hayes D; Farrell M; Collins P.

Lipoprotein (a): a potential biological marker for unruptured intracranial aneurysms.
Neurosurgery 1997 May;40(5):1112-5; discussion 1115-7.
7. Stubbs P; Seed M; Moseley D; O’Connor B; Collinson P; Noble M.
A prospective study of the role of lipoprotein(a) in the pathogenesis of unstable angina.
Eur Heart J 1997 Apr;18(4):603-7.
8. Shinozaki K; Kambayashi J; Kawasaki T; Uemura Y; Sakon M; Shiba E; Shibuya T;

Nakamura T; Mori T.
The long-term effect of eicosapentaenoic acid on serum levels of lipoprotein (a) and lipids in
patients with vascular disease. J Atheroscler Thromb 1996;2(2):107-9.
9. McCully KS, Homocysteine metabolism in scurvy, growth and arteriosclerosis. Nature

1971;231:391-392.
10. Pauling L, Rath M. Pro. Nat. Acad. Sci USA, Vol 87, pp 9388-9390, Dec 1990.
11. Carr AC, Frei B. Toward a new recommended dietary allowance for vitamin C based on
antioxidant and health effects in humans. American Journal of Clinical Nutrition
1999;69(6):1086-1107.
12. Simon JA, Hudes ES. Serum ascorbic acid and gallbladder disease prevalence among US
adults: the Third National Health and Nutrition Examination Survey (NHANES III). Arch
Intern Med. 2000;160(7):931-936.
13. Stephen R, Utecht T. Scurvy identified in the emergency department: a case report. Journal
of Emerg Med. 2001;21(3):235-237.
14. Cameron E, Pauling L. Supplemental ascorbate in the supportive treatment of cancer:

Prolongation of survival times in terminal human cancer. Proc Natl Acad Sci U S A.
1976;73(10):3685-3689.
http://www.orthomolecular.org/library/jom/1992/pdf/1992-v07n03-p153.pdf
[PDF] Reducing the Risk for Cardiovascular Disease with Nutritional Supplements M
Rath. Niacin and ascorbate have been reported to lower plasma lipoprotein-a levels. … with the
binding of lipoprotein-a to collagen and other matrix components. …
LipoProtein (a) is independent marker of atherosclerosis
Chest. 2002;121:1589-1594. Elevated Serum Lipoprotein(a) Level Is an Independent Marker of
Severity of Thoracic Aortic Atherosclerosis Marcel Peltier, MD et al.
Conclusion: This prospective study indicates that serum Lp(a) level is an independent marker
of severity of thoracic aortic atherosclerosis detected by multiplane TEE. These findings
emphasize the role of Lp(a) as a marker of atherosclerotic lesions in the major arterial
locations.
Lipoprtein (a) detected in arterial wall contributing to plaque formation

Arteriosclerosis. 1989 Sep-Oct;9(5):579-92.Links
Detection and quantification of lipoprotein(a) in the arterial wall of 107 coronary bypass
patients. Rath M, Niendorf A, Reblin T, Dietel M, Krebber HJ, Beisiegel U.Medizinische Kern
und Poliklinik, Universitäts-Krankenhaus Eppendorf, Hamburg, FRG.
The aim of this study was to determine the extent of accumulation of lipoprotein(a) [Lp(a)] in
human arterial wall and to define its potential role in atherogenesis. Biopsies routinely taken
from the ascending aorta of 107 patients undergoing aortocoronary bypass surgery were
analyzed for lipid and lipoprotein parameters, which were then correlated to serum values. A
significant positive correlation was established between serum Lp(a) and arterial wall
apolipoprotein (apo)(a) by enzyme-linked immunosorbent assay. High serum Lp(a) also led to a
significant increase of apo B in the arterial wall. No significant correlation was found between
apo B in serum and aortic tissue. Apo B was found to be partially linked to apo(a) in the aortic
extract. Furthermore, apo(a) was found to be intact, as determined by its molecular weight in
sodium dodecyl sulfate electrophoresis. This technique also revealed that the apo(a) isoform
pattern of aortic homogenate was comparable to the individual serum pattern.
Immunohistochemical methods demonstrated a striking colocalization of apo(a) and apo B in
the arterial wall, predominantly located extracellularly. Both proteins were increased in
atherosclerotic plaques. With density gradient ultracentrifugation, Lp(a)-like particles could be
isolated from plaque tissue. This initial study showed that Lp(a) accumulates in the arterial
wall, partly in the form of lipoprotein-like particles, therefore contributing to plaque formation
and coronary heart disease.
Atherosclerosis. 1995 Mar;113(2):179-88.
Extraction of lipoprotein(a), apo B, and apo E from fresh human arterial wall and
atherosclerotic plaques.Reblin T, Meyer N, Labeur C, Henne-Bruns D, Beisiegel
U. Medizinische Kernklinik und Poliklinik, Universitätskrankenhaus Eppendorf (UKE),
Hamburg, Germany.
Several studies have analysed apo(a) quantitatively in arterial wall tissue derived from post
mortem samples. The purpose of this study was a qualitative analysis of Lp(a) in fresh human
arterial wall tissue. It was evaluated whether Lp(a) exists as an intact lipoprotein or whether it
is degraded. Additionally it was analysed whether there are differences in the apolipoprotein
composition between lesion-free and diseased human arterial wall tissue. Serum and intimal
tissue samples taken from the abdominal aorta and the inferior caval vein of 18 organ donors
were analysed for lipids, Lp(a), and apolipoproteins apo B and apo E. Serum and tissue
parameters were correlated. In the aortic tissue, higher Lp(a) and apolipoprotein levels were
observed in the diseased samples. The total amount of Lp(a) recovered during three different
extraction procedures was 5 micrograms/g wet weight in tissue free of plaque and 11.8
micrograms/g wet weight in atherosclerotic tissue. The corresponding values for apo B and apo
E were 4.3 and 6.1 micrograms/g wet weight vs. 5.0 and 9.1 micrograms/g wet weight. After
density gradient centrifugation of the aortic tissue extracts, it was shown that the major parts of
apo(a) and apo B detected in the lesion-free vessel wall were present as Lp(a)-like particles. In
the diseased tissue Lp(a) was partly dissociated into LDL-like particles and free apo(a). With
this study we confirm that Lp(a) accumulates in the arterial wall, preferentially in
diseased tissue, and that Lp(a) particles, deposited in atherosclerotic plaques, are partly
degraded to LDL-like particles and free apo(a) in atherosclerotic plaques.
http://www.jlr.org/cgi/reprint/32/2/317
Journal of Lipid Research Volume 32, 1991 317
Quantification of apo[a] and apoB in human atherosclerotic lesions by Judith M. Pepin et al.
ndation, Cleveland, OH 44195
Lysine Binding Site in Lipoprotein (a) – LBS knockout study
http://www.pubmedcentral.nih.gov/articlerender.fcgi?rendertype=abstract&artid=508329
J Clin Invest. 1997 September 15; 100(6): 1493–1500.
Lipoprotein(a) vascular accumulation in mice. In vivo analysis of the role of lysine binding
sites using recombinant adenovirus by S D Hughes et al.
Although the mechanism by which lipoprotein(a) [Lp(a)] contributes to vascular disease

remains unclear, consequences of its binding to the vessel surface are commonly cited in
postulated atherogenic pathways. Because of the presence of plasminogen-like lysine binding
sites (LBS) in apo(a), fibrin binding has been proposed to play an important role in Lp(a)’s
vascular accumulation. Indeed, LBS are known to facilitate Lp(a) fibrin binding in vitro. To
examine the importance of apo(a) LBS in Lp(a) vascular accumulation in vivo, we generated
three different apo(a) cDNAs: (a) mini apo(a), based on wild-type human apo(a); (b) mini
apo(a) containing a naturally occurring LBS defect associated with a point mutation in kringle
4-10; and (c) human- rhesus monkey chimeric mini apo(a), which contains the same LBS
defect in the context of several additional changes. Recombinant adenovirus vectors were
constructed with the various apo(a) cDNAs and injected into human apoB transgenic mice. At
the viral dosage used in these experiments, all three forms of apo(a) were found exclusively
within the lipoprotein fractions, and peak Lp(a) plasma levels were nearly identical
(approximately 45 mg/dl). In vitro analysis of Lp(a) isolated from the various groups of mice
confirmed that putative LBS defective apo(a) yielded Lp(a) unable to bind lysine-
Sepharose. Quantitation of in vivo Lp(a) vascular accumulation in mice treated with the
various adenovirus vectors revealed significantly less accumulation of both types of LBS
defective Lp(a), relative to wild-type Lp(a). These results indicate a correlation between
lysine binding properties of Lp(a) and vascular accumulation, supporting the postulated
role of apo(a) LBS in this potentially atherogenic characteristic of Lp(a).
GLO Gulano Lactone Oxidase Genetic Defect
Biochim Biophys Acta. 1999 Oct 18;1472(1-2):408-11.
Random nucleotide substitutions in primate nonfunctional gene for L-gulono-gamma-lactone
oxidase, the missing enzyme in L-ascorbic acid biosynthesis. Ohta Y, Nishikimi M.
Humans and other primates have no functional gene for L-gulono-gamma-lactone oxidase
that catalyzes the last step of L-ascorbic acid biosynthesis. The 164-nucleotide sequence of
exon X of the gene was compared among human, chimpanzee, orangutan, and macaque, and it
was found that nucleotide substitutions had occurred at random throughout the sequence with a
single nucleotide deletion, indicating that the primate L-gulono-gamma-lactone oxidase genes
are a typical example of pseudogene.
http://www.jbc.org/cgi/content/abstract/269/18/13685
J. Biol. Chem., Vol. 269, Issue 18, 13685-13688, 05, 1994
Cloning and chromosomal mapping of the human nonfunctional gene for L- gulono-gamma-
lactone oxidase, the enzyme for L-ascorbic acid biosynthesis missing in man. by M Nishikimi
et al.
Man is among the exceptional higher animals that are unable to synthesize L-ascorbic acid
because of their deficiency in L-gulono- gamma-lactone oxidase, the enzyme catalyzing the
terminal step in L- ascorbic acid biosynthesis.
Genetically Engineered Vitamin C Deficient Mouse Model shows disruption of Collagen

Fibers in Aorta and Carotid Bifurcation.
http://www.pnas.org/content/97/2/841.full
PNAS January 18, 2000 vol. 97 no. 2 841-846
Aortic wall damage in mice unable to synthesize ascorbic acid by Nobuyo Maeda et al.
By inactivating the gene for l-gulono-γ-lactone oxidase, a key enzyme in ascorbic acid
synthesis, we have generated mice that, like humans, depend on dietary vitamin C. Regular
chow, containing about 110 mg/kg of vitamin C, is unable to support the growth of the mutant
mice, which require l-ascorbic acid supplemented in their drinking water (330 mg/liter). Upon
withdrawal of supplementation, plasma and tissue ascorbic acid levels decreased to 10–15% of
normal within 2 weeks, and after 5 weeks the mutants became anemic, began to lose weight,
and die. Plasma total antioxidative capacities were approximately 37% normal in homozygotes
after feeding the unsupplemented diet for 3–5 weeks. As plasma ascorbic acid decreased, small,
but significant, increases in total cholesterol and decreases in high density lipoprotein
cholesterol were observed.
The most striking effects of the marginal dietary vitamin C were alterations in the wall of
aorta, evidenced by the disruption of elastic laminae, smooth muscle cell proliferation,
and focal endothelial desquamation of the luminal surface. Thus, marginal vitamin C
deficiency affects the vascular integrity of mice unable to synthesize ascorbic acid, with
potentially profound effects on the pathogenesis of vascular diseases. Breeding the vitamin C-
dependent mice with mice carrying defined genetic mutations will provide numerous
opportunities for systematic studies of the role of antioxidants in health and disease.
Rupture of Elastic Lamina, Smooth Muscle Cell Proliferation, and Injury of the Luminal
Surface in the Thoracic Aorta.
Ascorbic acid is an important cofactor for the hydroxylation of proline and lysine necessary for
the crosslinking of collagen and elastin, important structural components of vessel wall (18,
19). Inspection under both light microscopy and TEM of cross sections of the thoracic aorta
from animals with low levels of plasma and tissue ascorbic acid revealed marked alterations
in the pattern and integrity of the elastic laminae. Prominent breaks and fragmentation of
the elastica were located in both the superficial and deep media (Fig. 5 . The endothelial cells
overlying the areas of internal elastic lamia disruption were attenuated as a result of the
accumulation of basement membrane material, collagen/elastic tissue, and aggregates of
smooth muscle cells. Some smooth muscle cells had an altered morphology, were devoid of
cytoplasmic filaments, and contained myelin figures indicative of cellular degeneration (not
shown). Small clusters of smooth muscle cells, ranging from a few to a diffuse collections of
several cells, were present within the subintima below the basement membrane and above the
superficial elastic lamina (Fig. 5 C). Most of the smooth muscle cells present within the intima
were mildly activated as judged by a slight increase in their rough endoplasmic reticulum.
Small collections of elastic fibers were located between smooth muscle cells both in the intima
and in the deep media, suggesting that reorganization of the elastic lamina is a dynamic process
in these mice.
The most striking pathological finding in our current study is the presence of abnormalities in
the aortic walls of the vitamin C-deficient mice. The simplest explanation of this pathology is
that the fragmentation of elastic lamina is caused by defects in the crosslinking of collagen
and elastin because of the need for vitamin C to generate hydroxylysine and
hydroxyproline.
Support for this explanation is provided by the observations of similar fragmentation of elastic
fibers in mice with the Blotchy allele at the X-linked Mottled locus (33). The Mottled locus
codes for a copper-transporting ATPase, which is necessary for lysyl oxidase activity to
crosslink collagen and elastin (34).
Similar aortic wall changes also have been seen in young rats treated with β-aminopropionitrile,
an inhibitor of lysyl oxidase (35, 36). However, although the aortic wall abnormalities in
Blotchy mice progress to gross dilatation, aneurysm, and aortic rupture, the abnormalities seen
in our vitamin C-deficient mice appear to be more subtle.
The lesions in the aortic arch of vitamin C-deficient mice are longitudinal and most frequently
are seen near the takeoff of the carotid where the blood flow related shear-stress is high.
We did not find platelets, fibrin, or other blood cells in the areas with endothelial alteration. But
there is a marked increase in the extravasation of macromolecules into the aortic wall in these
areas as evidenced by the distribution of Evans blue in the vitamin C-deficient mice.
In conclusion, we have generated mice lacking l-gulono-γ-lactone oxidase, a key enzyme for
ascorbic acid synthesis. The mutant mice, like humans, entirely depend on dietary vitamin C,
and they show changes indicating that the integrity of their vasculature is compromised. When
combined with the batteries of mutant mice generated in recent years, the Gulo −/− mutant
mouse should provide unique opportunities for exploring the interactions between genetic
determination and environmental factors, such as oxidative stress, and the effects on these
interactions of different levels of vitamin C in the diet.
Collagen and Ascorbate a Review

Yale J Biol Med. 1985 Nov-Dec;58(6):553-9.Related Articles, Links
Regulation of collagen biosynthesis by ascorbic acid: a review. by Pinnell SR.
L-ascorbic acid is an essential cofactor for lysyl hydroxylase and prolyl hydroxylase, enzymes
essential for collagen biosynthesis. In addition, L-ascorbic acid preferentially stimulates
collagen synthesis in a manner which appears unrelated to the effect of L-ascorbic acid on
hydroxylation reactions. This reaction is stereospecific and unrelated to intracellular
degradation of collagen. The effect apparently occurs at a transcriptional or translational level,
since L-ascorbic acid preferentially stimulates collagen-specific mRNA. In addition, it
stimulates lysyl hydroxylase activity but inhibits prolyl hydroxylase activity in human skin
fibroblasts in culture.
Lysine Binding Sites on Liporotein (a) – Fivefold reduction in atherosclerosis when Lysine
Binding Sites Eliminated with Mutation.
http://www.jci.org/articles/view/119565
Published in Volume 100, Issue 3 J. Clin. Invest. 100(3): 558-564 (1997).
Modification of apolipoprotein(a) lysine binding site reduces atherosclerosis in transgenic mice.
N W Boonmark et al.modification-of-apolipoprotein-a-lysine-binding-site-reduces-
atherosclerosis-in-transgenic-mice-boonmark-1997
Lipoprotein(a) contributes to the development of atherosclerosis through the binding of its
plasminogen-like apolipoprotein(a) component to fibrin and other plasminogen substrates.
Apolipoprotein(a) contains a major lysine binding site in one of its kringle domains.
Destruction of this site by mutagenesis greatly reduces the binding of apolipoprotein(a) to
lysine and fibrin. Transgenic mice expressing this mutant form of apolipoprotein(a) as well as
mice expressing wild-type apolipoprotein(a) have been created in an inbred mouse strain. The
wild-type apolipoprotein(a) transgenic mice have a fivefold increase in the development of
lipid lesions, as well as a large increase in the focal deposition of apolipoprotein(a) in the
aorta, compared with the lysine binding site mutant strain and to nontransgenic
littermates. The results demonstrate the key role of this lysine binding site in the pathogenic
activity of apolipoprotein(a) in a murine model system.
J Clin Invest (1997) 100: 558-64. Modification of apolipoprotein(a) lysine binding site reduces
atherosclerosis in transgenic mice by NW Boonmark et al. modification-of-apolipoprotein-a-
lysine-binding-site-reduces-atherosclerosis-in-transgenic-mice-boonmark-1997
Collagen Triple Helix
http://www.ohiolink.edu/etd/send-
pdf.cgi/Person%20Margaret%20M.pdf?acc_num=ysu1196173663
Collagen consists of three polypeptide chains, termed alpha chains, which are arranged in a
parallel triple helix. There are two α1 chains and one α2 chain (Goodsell, 2003). Although each
chain has a helical arrangement, they only have this conformation when associated with the two
other alpha chains and is then referred to as possessing a superhelical configuration (Goodsell,
2003). This superhelical arrangement, consisting of primarily Collagen I and III fibers form an
elaborate network between nearly all cells and constitutes the major structural element in bone,
tendon, cartilage and teeth.
http://www.cqs.com/cvd.htm
A Simple Preventive and Therapy for Cardiovascular Disease (CVD) Jonathan Campbell,
Health Consultant Natural Therapies for Chronic Illness & Health Maintenance
RETINAL PHOTOS CONFIRM VITAMIN C PILLS CAN REVERSE ARTERY
DISEASE
http://www.hullcontactlensclinic.co.uk/cardior.htm
CardioRetinometry Dr. Sydney J Bush. PhD. DOpt. (IOSc. London) Optic nerve heads (Disc)
Before Vitamin C 2002, After Vitamin C 2004, Un-retouched images showing retinal arteries
opening and veins carrying more blood.. The white line down the arteries is lighter and thinner
showing less cholesterol in the 2004 image. which also shows ‘lost’ vessels reappearing. This is
what is now said to happen in heart muscle as new anastomoses open when arteries become
blocked.
http://www.bmj.com/cgi/eletters/329/7457/79#68348
CardioRetinometry 23 July 2004 Sydney J Bush, Optometrist. CardioRetinometrist 20-22
Brook St. HULL HU2 8LA
Wong TY et al. Prospective cohort study of retinal vessel diameters and risk of hypertension.
BMJ 2004 329:79 (10th July)pub 2nd Jne.
Bush SJ. Cardioretinometry Rapid Response BMJ 23rd July
Bush SJ. “Emperor’s New Clothes?” Rapid Response 25th Nov. 2004
Bush SJ. ‘Optician’ Letters 9th May 2003 and later in 2004.
Guinea Pig and GLO defect

http://en.wikipedia.org/wiki/Guinea_pig
Like humans, but unlike most other mammals, guinea pigs cannot synthesize their own vitamin
C and must obtain this vital nutrient from food. If guinea pigs do not ingest enough vitamin C,
they can suffer from potentially fatal scurvy.
Inai Y et al. (2003), “The Whole Structure of the Human Non-Functional L-Guluno-gamma-
Lactone Oxidase Gene – the Gene Responsible for Scurvy – and the Evolution of Repetitive
Sequences Thereon,” J Nutr Sci Vitaminology 49:315-319.
The whole structure of the human nonfunctional L-gulono-gamma-lactone oxidase gene–the
gene responsible for scurvy–and the evolution of repetitive sequences thereon. Inai Y, Ohta Y,
Nishikimi M.
L-Gulono-gamma-lactone oxidase (GULO), which catalyzes the last step of ascorbic acid
biosynthesis, is missing in humans. The whole structure of the human gene homologue for this
enzyme was disclosed by a computer-assisted search. Only five exons, as compared to 12 exons
constituting the functional rat GULO gene, remain in the human genome. A comparison of
these exons with those of their functional counterparts in rat showed that there are two single
nucleotide deletions, one triple nucleotide deletion, and one single nucleotide insertion in the
human sequence. When compared in terms of codons, the human sequence has a deletion of a
single amino acid, two stop codons, and two aberrant codons missing one nucleotide besides
many amino acid substitutions. A comparison of the remaining human exon sequences with the
corresponding sequences of the guinea pig nonfunctional GULO gene revealed that the same
substitutions from rats to both species occurred at a large number of nucleotide positions. From
analyses of the molecular evolution of Alu sequences in the human GULO gene homologue, it
is thought that two Alu sequences were inserted in the vicinity of a presumed position of lost
exon 11 during the same period as GULO lost its function. It is predicted that six LINE-1
sequences located in and near the gene homologue were inserted not during that period.
http://www.jbc.org/cgi/content/abstract/267/30/21967
J. Biol. Chem., Vol. 267, Issue 30, 21967-21972, Oct, 1992
Guinea pigs possess a highly mutated gene for L-gulono-gamma-lactone oxidase, the key
enzyme for L-ascorbic acid biosynthesis missing in this species
M Nishikimi, T Kawai and K Yagi
Heart Disease in US declined after 1970 publication of Linus Pauling Book on Vitamin C, Vitamin C
and the Common Cold.
http://www.cdc.gov/mmwr/preview/mmwrhtml/mm4830a1.htm
MMWR Weekly – Decline in CVD Death Rates, Achievements in Public Health, 1900-1999:
Decline in Deaths from Heart Disease and Stroke — United States, 1900-1999
http://www.vitamincfoundation.org/forum/index.php
Vitmain C Foundation Message Board
Link to this article: http://wp.me/P3gFbV-qL
Jeffrey Dach MD
www.jeffreydachmd.com
www.drdach.com
www.naturalmedicine101.com
www.truemedmd.com
Disclaimer
http://www.drdach.com/wst_page20.html www.drdach.com disclaimer
The reader is advised to discuss the comments on these pages with his/her personal physicians
and to only act upon the advice of his/her personal physician Also note that concerning an
answer which appears as an electronically posted question, I am NOT creating a physician —
patient relationship. Although identities will remain confidential as much as possible, as I can
not control the media, I can not take responsibility for any breaches of confidentiality that may
occur .
(c) 2008-2013 Jeffrey Dach MD All Rights Reserved This article may be reproduced on the
internet without permiss
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About Jeffrey Dach MD
Medical Director of TrueMedMD, a Clinic in Davie Florida specializing in Bioidentical Hormones and Natural thyroid.
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Coronary Calcium Score Benefits of Aged Garlic

Posted on June 12, 2015

How to Reduce Calcium Scores ?
Jim has an elevated coronary calcium score in the 95% percentile indicating high risk for future
heart attack. He is being treated by his cardiologist with daily aspirin and atorvastatin (lipitor),
a statin drug to reduce cholesterol.
Currently we are following a number of similar patients with elevated coronary calcium score
treated with statin drugs by their cardiologist. The elevated calcium score indicates higher risk
for future coronary event such as chest pain, angina, heart attack etc. Current cardiology
dogma dictates treatment with statin drugs to lower cholesterol, thus preventing heart disease.
Cholesterol Theory has Been Falsified

The problem with this cardiology dogma is the cholesterol theory of atherosclerotic disease has
been falsified by many studies which are summarized nicely by Dr. William R Ware from the
University of Ontario. Dr Ware’s fine article in Medical Hypotheses 2009, reveals there is no
correlation between serum cholesterol and the amount of atherosclerotic plaque when
reviewing either autopsy studies or coronary calcium score studies.(9) Thus, the theory that
elevated cholesterol causes atherosclerotic plaque is essentially falsified.
Statin Drugs Disappointing for Calcium
Score
Two randomized trials using statin drugs to reduce calcium scores showed disappointing
results.(10,11) Left Image CAT scan showing calcified coronary artery (yellow arrow).
In Dr. Houslay’s trial published in Heart 2006, 102 patients were randomized and treated for
two years with either 80 mg/d atorvastatin (lipitor) or placebo.(10) As expected, the statin
treated group had a 53% reduction in LDL cholesterol, while the placebo group had no change
in theirs. The researchers were expecting benefit from the statin treatment. They found the
opposite. Paradoxically, the statin group had greater increase in calcium score (26%) than the
placebo group (only 18%). The authors concluded:“statin treatment does not have a major
effect on the rate of progression of coronary artery calcification.”(10)
The second trial by Dr Schmermund in Circulation 2006 randomized 471 patients with no pre-
existing coronary artery disease, treated for one year with either low dose (10mg/d) or high
dose (80 mg/d) atorvastatin therapy. In the high dose group (80 mg/d) the LDL cholsterol was
reduced from 106 to 87 mg/dL (approximately 20% reduction). However, the low dose
statin group had no change in LDL cholesterol from baseline (108 vs 109 mg/dL). The
authors were expecting reduction in progression of calcium score in the high dose statin group
with a 20% reduction in LDL cholesterol. They were surprised to find no difference in calcium
scores between the two groups. The high dose atorvastatin group actually had slightly greater
progression of calcium score (27%) vs (25%) for the low dose group. The authors
concluded,”Coronary artery calcification (CAC) progression showed no relationship with on-
treatment LDL cholesterol levels.” (11)
According to Dr. Gill in a 2010 report: as of the year 2010 there had been five randomized
controlled studies showing that statin drug treatment does not reduce coronary calcium
score. Worse, the statin treatment showed progression of coronary calcium score
indistinguishable from the non-treated placebo group.
What Interventions Have Been Successful in Reduced
Calcium Score ?
As we can see from the above studies, statin drugs are quite effective for lowering cholesterol,
yet fail to reduce or slow progression of calcium score. Again, this provides even more
evidence falsifying the cholesterol theory of atherosclerotic heart disease. Perhaps we should
look elsewhere for a treatment modality in the patient with elevated calcium score. Left image
courtesy of Matthew J Budoff MD and OCWeekly Magazine.
Dr. Matthew J Budoff did just this, exploring the use of Aged Garlic in retarding progression of
calcium score in three studies. (1-3)
In the first study published in 2006 Journal of Nutrition, twenty three “high risk” patients
maintained on a stable dose of statin drug and aspirin were randomized to either placebo or 4
mL of Aged Garlic (1200 mg KYOLIC Aged Garlic Liquid) After one year of treatment, the
Aged Garlic group showed a 7.5 %progression of calcium score, considerably lower than
the 22.2% progression in the placebo group. (1) Remember that both groups were maintained
on statin drugs during the one year study.
In the second study by Dr Budoff published in Preventive Medicine 2009, sixty five
“intermediate risk” patients, all maintained on statins, were randomized and treated for one
year with either placebo or Aged Garlic Extract (250 mg). (2) In addition, the garlic group was
vitamins: Vitamin B12 (100 microg), folic acid (300 microg),Vitamin B6 (12.5 mg) and l-
arginine (100 mg) . (The product used was: Kyolic 108 Aged Garlic by Wakunaga) After one
year of treatment, the Aged Garlic Group had significantly less Coronary Artery Calcification
progression (6.8%) compared to the placebo group (26.5%). (see Table 2, Budoff Preventive
Medicine 2009). In addition the Garlic Group had “favorable improvement in oxidative
biomarkers and vascular function”(1)
Left Image: Fig 2 showing Aged Garlic Group left
and placebo right. Aged Garlic Group(left bars) shows lower progression of calcium score
(blue bar), reduction in IgG IgM MDA LDL, IC/apoB oxidative bio-markers and reduction in
Homocysteine (red bar) compared to placebo (right). Courtesy of Aged garlic extract retards
progression of atherosclerosis Budoff Preventive medicine 2009 .
A third study by Dr Matt Budoff in the 2012 Journal of Cardiovascular Research randomized
65 firefighters to one year treatment with either Aged Garlic plus Co-Q-10 (Kyolic Aged
Garlic-Co-Q10 Formula 110, Wakunaga ) or to placebo. (3) Some were taking statin drugs.
About 25% of the Aged Garlic+CoQ10 were on statins, compared to 31% of placebo group
were on statins.
After one year of treatment the aged Garlic

group showed less progression of calcium score (32 vs. 58 absolute) and (18.9% vs
27.4%). CRP was also lower in the Garlic group. See Left Image :Table One courtesy Budoff
2012 (3).
Definitive Garlic/Calcium Score Study By Dr Matt Budoff Published 2015 (Effects of Aged
Garlic on Coronary Artery Calcification Budoff Matt Hom C J Nutr Food Sci 2015)
Four placebo-controlled, double-blind, randomized studies were pooled with 210 patients (182
completed the study). All had (Calcium Score) CAC at baseline and at 12 months. At 1 year,
median CAC progression was significantly lower in the AGE (Aged Garlic Extract)
group,10.8 than the placebo group 18.3. There were no differences in serum cholesterol or CRP
(C-reactive protein) levels between the groups.
Additional Benefits of Garlic
In a 2013 study by Dr. Kumar, Garlic was found beneficial as an adjunct to Metformin 500 mg
twice a day (BID) in obese diabetics.(12) Garlic lowers blood pressure has been found useful
in hypertensive patients.(13) In addition, Garlic has anti-microbial properties and has uses as an
anti-microbail agent (4-8).
Garlic Reduces Calcium Score Progression, Mechanism of Action

My previous article discussed the failure of the cholesterol hypothesis, and recent revelations
about atherosclerotic plaque as infected biofilm, and the association with increased gut
permeability, also called “Leaky Gut”. This would certainly explain our somewhat
paradoxical findings in the three studies by Dr Matthew Budoff showing Garlic more effective
than statin drugs. A natural antimicrobial agent, the lowly Garlic bulb, shows ability to retard
progression of calcium score while the high and mighty statin drug fails, even though
cholesterol is reduced.
Garlic as Anti-Microbial
Although various mechanisms have been proposed to explain the benefits of Garlic in
cardiovascular disease, I would like to concentrate on Garlic as an anti-microbial agent.(4-
8) Unlike conventional antibiotics which may disrupt the normal intestinal flora, Garlic’s
antimicrobial properties act against pathogenic gut bacteria with relative sparing of the
beneficial, “friendly” gut bacteria.(4) Dr Bayan in 2014 says: “garlic exerts a differential
inhibition between beneficial intestinal microflora and potentially harmful
enterobacteria”(4) Dr Rees studied Garlic’s antimicrobial activity finding broad spectrum
activity against “many bacteria, yeasts, fungi and virus. All microorganisms tested were
susceptible to garlic.”(5) Dr Filocamo in 2012 studied Garlic in a bacterial population
representative of the colonic microbiota. Lacto-baccillus was more resistant to Garlic
compared to the Clostridial which was was more susceptible. The author suggested
the “consumption (of garlic) may favor the growth of these beneficial bacterial species in the
gut. Garlic intake has the potential to temporarily modulate the gut microbiota.”(6) A full
discussion of the antimicrobial spectrum of Garlic can be found in an excellent article in 2015
by Dr Packia Lekshmi (7) Mark Slevin’s 2012 article reported on natural products with
vascular protective properties and significant anti-atherogenic potential. Dr Slevin mentions
Aged Garlic, Resveratrol and Green Tea extract (ECGC ) as the most promising (8)
Pseudomonas BioFilm in Atherosclerotic Plaque Material
Dr Bernard Lanter studied athersclerotic plaque specimens, identifying Pseudomonas 16S
rRNA genes in 6 of 15 cases, indicating colonization by Pseudomonas biofims. (14) The
virulence of Pseudomonas is attributed to Quorum Sensing, the ability of the bacterial cells to
communicate with one another to form Bio-Films. (16) Dr. Bjarnsholt considers disruption of
this Quorum Sensing to be the key to controlling Psudomonas Biofilm infections. That is
exactly what Garlic does. In Vitro and In Vivo animal studies show Garlic inhibits quorum
sensing and virulence of Pseudomonas. (15) An excellent way to study the effect of Allicin,
the active ingredient in Garlic, on the PSeudomonas organism is to tag the bacteria with the
Green Flourscent Protein (GFP). This was done published in the 2013 with an elegant series of
in-vitro experiments using Allicin treated GFP-modified Pseudomonas organisms.(17) Dr.
Lihua’s group showed that:
“Allicin treatment not only reduced the adhesion ratio of P. aeruginosa, but also inhibited EPS
(extracellular polysaccharide) secretion and down-regulates production of some Quorum
Sensing -controlled virulence factors. These results imply that allicin can disturb the formation
and
maturation of P. aeruginosa biofilm, and suggest that allicin may represent a promising
therapeutic candidate for the management of P. aeruginosa biofilms.”(17)
Poly-Microbial Colonization
Others have found diverse colonies of bacterial, fungal and protozoal life-forms colonizing
biofilms in atherosclerotic plaque specimens (18-20), In view of this, investigating other
botanical agents with known antimicrobial activity might also be useful, such as Olive Leaf
extract, Oregano Oil, Berberine,etc. Perhaps a combination of such natural products would
have a more powerful synergistic effect. Other natural anti-microbials such as colloidal silver,
and Iodine should be considered as well. This would be a fertile area for future research.
Garlic Reduces Plaque in Genetically Modified Mice
One might say the benefits of Garlic on slowing calcium

score progression are nice, but what about preventing plaque formation itself? This question
was studied in atherosclerotic mice by Ayelet Gonen’s group at the Institute of Lipid and
Atherosclerosis Research, Sheba Medical Center, Tel Hashomer Israel. Dr. Gonen studied the
effect of daily Allicin treatment (the active ingredient in Garlic) in mice genetically modified
to form atherosclerotic plaque in the aortic sinus. These were Apo-E knockout mice, and LDL
receptor knockout mice. Daily allicin (9 mg/kg) reduced the atherosclerotic plaque area
by 70% in apoE-deficient mice and by 60% in LDL receptor knockout mice.(21) This is rather
impressive. They went further, showing allicin binds directly to the LDL particle preventing
LDL oxidation, and inhibits macrophage uptake and degradation of the LDL particles. This,
they speculated , was the mechanism for atherosclerosis prevention. Left Image courtesy
of Ayelet Gonen
Garlic and Atherosclerotic Plaque Regression – Ayelet Gonen
Above image
Fig. 1. Daily treatment with allicin reduced the atherosclerotic lesion area in apoE mice. (A =
placebo treated , B) Allicin treated. Courtesy of Antiatherogenic effect of allicin Pathobiology
2005 Gonen.
Future Research
As mentioned above, independent researchers have found polymicrobial organisms colonizing
biofilms in atherosclerotic plaque.
One question I have is this: Why not conduct a series of experiments using these
same techniques to look for infected biofilms in the atherosclerotic plaque material in animal
models of atherosclerosis ? Perhaps the Institute of Lipid and Atherosclerosis Research might
collaborate and share mouse plaque specimens with Drs. Fry, Lanter and Ott. This would
answer an important question. What is the timing of the infection in the plaque? Is infection a
prerequisite for plaque formation. or, does infection seed the plaque afterwards? Exactly when
in the life cycle of the atherosclerotic plaque does the infection occur? Is Garlic’s preventive
mechanism solely a result of preventing LDL oxidation and inhibiting macrophage uptake as
Dr Gonen speculates ? Or does infection also play a role in these supposedly “pristine” animal
models of knockout mice genetically bred to form atherosclerosis ? These and other question
could be answered by studying plaque from animal models using the 16s RNA cloning and
flourescent imaging techniques used in Dr Lanter, Ott and Fry’s labs.
Eliminate Wheat – Benefits of Gluten Free Diet
Dr William Davis, cardiologist from Wisconsin, brought attention to the adverse effects of
wheat consumption in his book, Wheat Belly. Dr Davis strongly recommends a wheat free diet
for those patients with elevated calcium score. This is the cornerstone of treatment to reduce
calcium score progression.(24-26)
Our program for Elevated Calcium Score:
Aged Garlic
MK-7 version of Vitamin K2
Berberine
Co-Q-10,
L-Arginine
Reveratrol, Pterostilbene
Homocysteine reducing program (B6, B12, Methylfolate)
LinusPauling Protocol (Lysine, Proline, Vitamin C, Tocotrienols, MK-7 Vit K2)
William Davis Track Your Plaque Protocol (Niacin, Omega-3 Fish Oil, Vitamin D3, Vitamin
K2, Eliminate Wheat products)
Weight Reduction,
Hormone Optimization (optimize thyroid, testosterone, estrogen progesterone)
Heal the Leaky Gut (Probiotics, Glutamine, Colostrum)
Eliminate NSAIDS, PPI’s which cause dysbiosis and leaky gut.
Eliminate Pesticides, Glyphosate and GMO food, eat Organic.
Update 2016: Benefits of Di-Allyl-Sulfate from garlic review article. See:Rao, P. S. S., et al.
“Diallyl sulfide: potential use in novel therapeutic interventions in alcohol, drugs, and disease
mediated cellular toxicity by targeting cytochrome P450 2E1.” Current drug metabolism 16.6
(2015): 486.
Update 2016: Matsumoto, Suguru, et al. “Aged Garlic Extract Reduces Low Attenuation
Plaque in Coronary Arteries of Patients with Metabolic Syndrome in a Prospective Randomized
Double-Blind Study–3.” The Journal of nutrition 146.2 (2016): 427S-432S. 27 patients with
Metabolic Syndrome consumed 2400 mg Aged Garlic Extract (AGE) per day and another 28
patients took placebo. The per cent change in low attenuation plaque was significantly reduced
in the AGE group (-1.5% ) compared with the placebo group (+0.2% ).
ticles With related Interest:
LDL Cholesterol, Versus the Calcium Score, What Gives?
Coronary Calcium Score Paradigm Shift in Cardiology
Vitamin K is there Anything It Cant Do- Benefits for calcium Score
Atherosclerotic Plaque as Infected Biofilm
Preventing Heart Attacks with Ouabain
Thyroid Pills Prevent Heart Attacks
How to Reverse Heart Disease with the Coronary Calcium Score
Heart Disease Vitamin C and Linus Pauling
Jeffrey Dach MD
7450 Griffin Road Suite 180
Davie FL 33314
954-792-4663
Links and References
1) http://jn.nutrition.org/content/136/3/741S.full
Budoff, Matthew. “Aged garlic extract retards progression of coronary artery calcification.”
The Journal of nutrition 136.3 (2006): 741S-744S. Aged garlic extract retards progression of
atherosclerosis Budoff Preventive medicine 2009
2) http://www.ncbi.nlm.nih.gov/pubmed/19573556
Budoff, M. J., et al. “Aged garlic extract supplemented with B vitamins, folic acid and L-
arginine retards the progression of subclinical atherosclerosis: a randomized clinical trial.”
Preventive medicine 49.2-3 (2009): 101.
Previous studies demonstrated that aged garlic extract reduces multiple cardiovascular risk
factors. This study was designed to assess whether aged garlic extract therapy with supplements
(AGE+S) favorably affects inflammatory and oxidation biomarkers, vascular function and
progression of atherosclerosis as compared to placebo.
METHODS: In this placebo-controlled, double-blind, randomized trial (conducted 2005-2007),
65 intermediate risk patients (age 60+/-9 years, 79% male) were treated with a placebo capsule
or a capsule containing aged garlic extract (250 mg) plus Vitamin B12 (100 microg), folic acid
(300 microg), Vitamin B6 (12.5 mg) and l-arginine (100 mg) given daily for a 1 year. All
patients underwent coronary artery calcium scanning (CAC), temperature rebound (TR) as an
index of vascular reactivity using Digital Thermal Monitoring (DTM), and measurement of
lipid profile, autoantibodies to malondialdehyde (MDA)-LDL, apoB-immune complexes,
oxidized phospholipids (OxPL) on apolipoprotein B-100 (OxPL/apoB), lipoprotein (a) [Lp (a)],
C-reactive protein (CRP), homocysteine were measured at baseline and 12 months. CAC
progression was defined as an increase in CAC>15% per year and an increase in TR above
baseline was considered a favorable response.
RESULTS: At 1 year, CAC progression was significantly lower and TR significantly higher in
the AGE+S compared to the placebo group after adjustment of cardiovascular risk factors
(p<0.05). Total cholesterol, LDL-C, homocysteine, IgG and IgM autoantibodies to MDA-LDL
and apoB-immune complexes were decreased, whereas HDL, OxPL/apoB, and Lp (a) were
significantly increased in AGE+S to placebo.
CONCLUSION: AGE+S is associated with a favorable improvement in oxidative biomarkers,
vascular function, and reduced progression of atherosclerosis.
3) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3425023/
Zeb, Irfan, Budoff M et al. “Aged Garlic Extract and Coenzyme Q10 Have Favorable Effect on
Inflammatory Markers and Coronary Atherosclerosis Progression: A Randomized Clinical
Trial.” Journal of Cardiovascular Disease Research 3.3 (2012): 185–190. PMC. Web. 11 June
2015.
Aged garlic extract (AGE) and coenzyme Q10 (CoQ10) have been shown to affect multiple
cardiovascular risk factors. The current study evaluates the effect of AGE combined with
CoQ10 on inflammatory markers and progression of coronary atherosclerosis compared with
placebo.
Methods and Results: In this placebo-controlled, double-blind, randomized trial, 65
intermediate risk firefighters (age 55 ± 6 years) were treated with a placebo capsule or a capsule
containing AGE and CoQ10 (AGE+CoQ10, 1200 and 120 mg, respectively) daily for 1 year.
All participants underwent coronary artery calcium (CAC) scanning and C-reactive protein
(CRP) at baseline and at 12 months. At 1 year, mean CAC progression was significantly lower
in AGE+CoQ10 (32 ± 6 vs. 58 ± 8, P = 0.01) than placebo. Similarly, CRP were significantly
decreased in AGE+CoQ10 compared with placebo (-0.12 ± 0.24 vs. 0.91 ± 0.56 mg/L, P <
0.05). After adjustment for age, gender, conventional cardiac risk factors, and statin therapy,
AGE+CoQ10 was associated with 3.99 fold (95% 1.3–12.2, P = 0.01) lack of CAC progression
compared with the placebo.
4) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4103721/
Bayan, Leyla, Peir Hossain Koulivand, and Ali Gorji. “Garlic: A Review of Potential
Therapeutic Effects.” Avicenna Journal of Phytomedicine 4.1 (2014): 1–14. Print.
It has been documented that garlic exerts a differential inhibition between beneficial intestinal
microflora and potentially harmful enterobacteria
5) http://www.ncbi.nlm.nih.gov/pubmed/24420031/
World J Microbiol Biotechnol. 1993 May;9(3):303-7. doi: 10.1007/BF00383068.
A quantitative assessment of the antimicrobial activity of garlic (Allium sativum).
Rees LP1, Minney SF, Plummer NT, Slater JH, Skyrme DA.
An aqueous extract of freeze-dried garlic (Allium sativum), when incorporated into growth
media, inhibited many representative bacteria, yeasts, fungi and a virus. All microorganisms
tested were susceptible to garlic. Quantitative assessment of the minimum inhibitory
concentrations for bacteria and yeasts showed values ranging from 0.8 to 40.0 mg garlic ml(-1).
Fungal radial colony growth was inhibited by at least 25% at concentrations as low as 2.0 mg
garlic ml(-1). The 50% endpoint neutralization titre for rotavirus was 2.4 to 2.8 μg ml(-1).
Lactic acid bacteria were the least sensitive microorganisms to the inhibitory effects of garlic.
In mixed culture studies of Lactobacillus acidophilus and Escherichia coli, garlic prevented the
establishment of E. coli, although the final outcome of competition was not affected.
6) http://www.ncbi.nlm.nih.gov/pubmed/22480662
Filocamo, Angela, et al. “Effect of garlic powder on the growth of commensal bacteria from the
gastrointestinal tract.” Phytomedicine 19.8 (2012): 707-711.
Garlic (Allium sativum) is considered one of the best disease-preventive foods. We evaluated
in vitro the effect of a commercial garlic powder (GP), at concentrations of 0.1% and 1% (w/v),
upon the viability of representative gut bacteria. In pure culture studies, Lactobacillus casei
DSMZ 20011 was essentially found to be resistant to GP whereas a rapid killing effect of
between 1 and 3 log CFU/ml reduction in cell numbers was observed with Bacteroides ovatus,
Bifidobacterium longum DSMZ 20090 and Clostridium nexile A2-232. After 6h incubation,
bacterial numbers increased steadily and once the strains became resistant they retained their
resistant phenotype upon sub-culturing. A colonic model was also used to evaluate the effect of
GP on a mixed bacterial population representing the microbiota of the distal colon. Lactic acid
bacteria were found to be more resistant to GP compared to the clostridial members of the gut
microbiota. While for most bacteria the antimicrobial effect was transient, the lactobacilli
showed a degree of resistance to garlic, indicating that its consumption may favour the growth
of these beneficial bacterial species in the gut. Garlic intake has the potential to temporarily
modulate the gut microbiota.
7) Antimicrobial Spectrum Allium Garlic Packia Lekshmi 2015
Packia Lekshmi, N. C. J., et al. “Antimicrobial Spectrum of Allium Species–A Review.”
History 15.44 (2015): 1-5.
8) pdf vascular protective supplements anti_atherosclerotic Slevin Mark Vasc Cell
2012 . Slevin, Mark, et al. “Unique vascular protective properties of natural products:
supplements or future main-line drugs with significant anti-atherosclerotic potential.” Vasc Cell
4.1 (2012): 9.
9) cholesterol atherosclerosis falsified coronary artery plaque Ware Medical Hypotheses
2009 Ware, William R. “The mainstream hypothesis that LDL cholesterol drives
atherosclerosis may have been falsified by non-invasive imaging of coronary artery plaque
burden and progression.” Medical hypotheses 73.4 (2009): 596-600.
10) Houslay, E S et al. “Progressive Coronary Calcification despite Intensive Lipid‐lowering
Treatment:A Randomised Controlled Trial.” Heart 92.9 (2006): 1207–1212. PMC. Web. 11
June 2015.
To evaluate the effect of intensive lipid‐lowering treatment on coronary artery calcification in a
substudy of a trial recruiting patients with calcific aortic stenosis.
Methods In a double blind randomised controlled trial, 102 patients with calcific aortic stenosis
and coronary artery calcification were randomly assigned by the minimisation technique to
atorvastatin 80 mg daily or matched placebo. Coronary artery calcification was assessed
annually by helical computed tomography.
Results 48 patients were randomly assigned to atorvastatin and 54 to placebo with a median
follow up of 24 months (interquartile range 24–30). Baseline characteristics and coronary artery
calcium scores were similar in both groups. Atorvastatin reduced serum low density lipoprotein
cholesterol (−53%, p < 0.001) and C reactive protein (−49%, p < 0.001) concentrations whereas
there was no change with placebo (−7% and 17%, p > 0.95 for both). The rate of change in
coronary artery calcification was 26%/year (0.234 (SE 0.037) log arbitrary units (AU)/year; n =
39) in the atorvastatin group and 18%/year (0.167 (SE 0.034) log AU/year; n = 49) in the
placebo group, with a geometric mean difference of 7%/year (95% confidence interval −3% to
18%, p = 0.18). Serum low density lipoprotein concentrations were not correlated with the rate
of progression of coronary calcification (r = 0.05, p = 0.62).
Conclusion In contrast to previous observational studies, this randomised controlled trial has
shown that, despite reducing systemic inflammation and halving serum low density lipoprotein
cholesterol concentrations, statin treatment does not have a major effect on the rate of
progression of coronary artery calcification.
11) Schmermund, Axel, et al. “Effect of Intensive Versus Standard Lipid-Lowering Treatment
With Atorvastatin on the Progression of Calcified Coronary Atherosclerosis Over 12 Months A
Multicenter, Randomized, Double-Blind Trial.” Circulation 113.3 (2006): 427-437.
Background— Recent clinical trials have suggested that intensive versus standard lipid-
lowering therapy provides for additional benefit. Electron-beam computed tomography
provides the opportunity to quantify the progression of coronary artery calcification (CAC) in
serial measurements.
Methods and Results— In a multicenter, randomized, double-blind trial, 471 patients (age 61±8
years) who had no history of coronary artery disease and no evidence of high-grade coronary
stenoses (>50% diameter reduction) were randomized if they had ≥2 cardiovascular risk factors
and moderate calcified coronary atherosclerosis as evidenced by a CAC score ≥30. Patients
were assigned to receive 80 mg or 10 mg of atorvastatin per day over 12 months. Progression
of CAC volume scores could be analyzed in 366 patients. After pretreatment with 10 mg of
atorvastatin for 4 weeks, 12 months of study medication reduced LDL cholesterol from 106±22
to 87±33 mg/dL in the group randomized to receive 80 mg of atorvastatin (P<0.001), whereas
levels remained stable in the group randomized to receive 10 mg (108±23 at baseline, 109±28
mg/dL at the end of the study, P=NS). The mean progression of CAC volume scores, corrected
for the baseline CAC volume score, was 27% (95% CI 20.8% to 33.1%) in the 80-mg
atorvastatin group and 25% (95% CI 19.1% to 30.8%) in the 10-mg atorvastatin group
(P=0.65). CAC progression showed no relationship with on-treatment LDL cholesterol levels.
12) Kumar, Rahat et al. “Antihyperglycemic, Antihyperlipidemic, Anti-Inflammatory and

Adenosine Deaminase– Lowering Effects of Garlic in Patients with Type 2 Diabetes Mellitus
with Obesity.” Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy 6 (2013): 49–
56. PMC. Web. 12 June 2015.
13) Xiong, X. J., et al. “Garlic for hypertension: A systematic review and meta-analysis of
randomized controlled trials.” Phytomedicine 22.3 (2015): 352-361.
14) Lanter, Bernard B., Karin Sauer, and David G. Davies. “Bacteria present in carotid arterial
plaques are found as biofilm deposits which may contribute to enhanced risk of plaque
rupture.” MBio 5.3 (2014): e01206-14.
15) Harjai, K., R. Kumar, and S. Singh. “Garlic blocks quorum sensing and attenuates the
virulence of Pseudomonas aeruginosa.” FEMS immunology and medical microbiology 58.2
(2010): 161.
16) Bjarnsholt, Thomas, and Michael Givskov. “The role of quorum sensing in the
pathogenicity of the cunning aggressor Pseudomonas aeruginosa.” Analytical and bioanalytical
chemistry 387.2 (2007): 409-414.
17) Allicin_Pseudomonas_BioFilm_Quorum-Sensing Microbiology Lihua 2013
Lihua, Lin, et al. “Effects of allicin on the formation of Pseudomonas aeruginosabiofinm and
the production of quorum-sensing controlled virulence factors.” Pol J Microbiol 62 (2013):
243-51.
18) Ott, Stephan J., et al. “Detection of diverse bacterial signatures in atherosclerotic
lesions of patients with coronary heart disease.” Circulation 113.7 (2006): 929-937.
19) Ott, S. J., et al. “Fungal rDNA signatures in coronary
atherosclerotic_Ott_2007_Athrosclerosis Fungal rDNA signatures in coronary
atherosclerotic plaques.” Environmental microbiology 9.12 (2007): 3035-3045.
20) Putative biofilm-forming organisms in the human vasculature: expanded case reports and
review of the literature. Stephen Eugene Fry, Jeremy Eugene Ellis, Matthew Andrew Shabilla,
Delyn Lorene Martinez, Renatta Schwarz, Richard Heuser, Constantine Moschonas .
Phlebological Review 2014; 22, 1: 24–37 Biofilm_forming organisms human vasculature
Stephen Eugene Fry Phlebological Review 2014
21) Gonen, Ayelet, et al. “The antiatherogenic effect of allicin: possible mode of
action.” Pathobiology72.6 (2005): 325-334. Antiatherogenic effect of allicin Pathobiology
2005 Gonen
22) ANTI ATHEROGENIC EFFECT OF ALLICIN MODE OF ACTION Ayelet Gonen , Aviv
Shaish, and Dror Harats, Institute of Lipid and Atherosclerosis. Research, Sheba Medical
Center, Tel Hashomer and Sackler Faculty of Medicine, Tel Aviv University, Israel
24) Statin scare By Dr. Davis | May 23, 2016
25) The Wheat Belly lifestyle BEGAN with heart health
By Dr. Davis | September 15, 2015
26) My Wheat Belly turning point By Dr. Davis | June 11, 2015
27) The Effects of Aged Garlic Extract on Coronary Artery Calcification
Progression Christopher Hom, Yanting Luo and Matthew Jay Budoff*
Los Angeles Biomedical Research Institute, Torrance, California, USA
Hom C, Luo Y, Budoff MJ (2015) The Effects of Aged Garlic Extract on Coronary Artery
Calcification Progression. J Nutr Food Sci S5:005. Effects of Aged Garlic on Coronary Artery
Calcification Budoff Matt Hom C J Nutr Food Sci 2015
Background: Aged Garlic Extract (AGE) has been shown to lower LDL, reduce the progression
of coronary atherosclerosis, improve vascular function, and have a favorable effect on oxidative
biomarkers. Since AGE has been shown to have several potential anti-atherosclerotic
properties, including stimulation of microcirculation in peripheral arteries, it was chosen as the
agent of study to evaluate its ability to inhibit progression of coronary atherosclerosis.
Objective: No study of sufficient power to date has evaluated the ability of AGE to inhibit
vascular calcification, a marker of plaque formation in human coronary arteries. We sought to
evaluate the ability of AGE to inhibit coronary artery calcium (CAC).
Methods: Four placebo-controlled, double-blind, randomized studies were pooled to determine
whether the atherosclerotic plaque burden detected by CAC will change at a different rate
under the influence of AGE as compared to placebo. 210 patients were enrolled, and 182
completed the study protocol. All participants underwent CAC scanning at baseline and at 12
months. A two-sample median test was used to compare medians of CAC progression between
the garlic- and placebo-treated groups. CAC progression was also categorized into three groups
(<15%, 15-20%, and >20%) prior to adjustment for age and gender.
Results: At 1 year, median CAC progression was significantly lower in the pooled AGE group
(10.8, 95% Confidence Interval (CI) 0.0-30.7, n=106) than the placebo group (18.3, 95% CI
3.1-34.0, n=103; P=0.0385). There were no significant differences in individual serum
cholesterol parameters or serum C-reactive protein levels between the groups. Further, after
adjustment for age and gender, AGE was associated with a 1.78 fold (95% CI 0.320-0.990,
P=0.046) reduction in CAC progression compared with placebo.
Conclusions: This pooled study indicates the ability of AGE to inhibit the rate of progression of
coronary calcification, as compared to placebo, over 1 year independent of statin therapy or
gender.
Jeffrey Dach MD
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Garlic is more effective than statin drugs for slowing calcium score progression.
Author
Jeffrey Dach MD

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left image: courtesy wikimedia, roadroller

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References for Cass article:

1. Marcoux C; Lussier-Cacan S; Davignon J; Cohn JS.

2. Ensenat D, Hassan S, Reyna SV, Schafer AI, Durante W.

6. Phillips J; Roberts G; Bolger C; el Baghdady A; Bouchier-Hayes D; Farrell M; Collins P.

8. Shinozaki K; Kambayashi J; Kawasaki T; Uemura Y; Sakon M; Shiba E; Shibuya T;

9. McCully KS, Homocysteine metabolism in scurvy, growth and arteriosclerosis. Nature

14. Cameron E, Pauling L. Supplemental ascorbate in the supportive treatment of cancer:

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