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Documentation

• The Lecture at Stanford Medical School

• The Scurvy-Heart Disease Connection

• “Health for All by the Year 2020”

• “The Hague Constitution”

• Petition for Vitamin Freedom

• About the Author

• Clinical Study: Natural Reversal of Heart Disease

• References

WHY ANIMALS DON’T GET HEART ATTACKS – BUT PEOPLE DO!

12 DOCUMENTATION

The Lecture at Stanford Medical School

The Scurvy-Heart Disease Connection:

Solution to the Puzzle of Cardiovascular Disease

On May 4, 2002, I was privileged to give the following lecture

at a symposium on nutrition at Stanford Medical School in

Palo Alto, California.

“I would like to congratulate Stanford University for addressing

the need for preventive and natural answers to the number one

cause of death in the industrialized world. I will present to you

the facts that atherosclerosis, heart attacks and strokes are not

diseases, but the direct result of long-term vitamin deficiency.

And, therefore, they can be prevented by natural means, with-

out pharmaceutical drugs or surgical intervention.

For more than a century,

this medical institution

has gracefully served the

interests of the pharma-

ceutical cartel by pro-

moting its multi-billion

dollar business with

heart disease.

Current Hypotheses for Atherosclerosis

Can Explain Peripheral Vascular Disease

But Not Coronary Artery Disease

For more than a decade, the pharmaceutical cartel has vigorously

fought my discovery of the scurvy-heart disease connection,

realizing that it threatens the very basis of this business. In that

fight, they have also abused many medical opinion leaders.

Researchers:

Hypothesis:

Goldstein & Brown

Hypercholesterolemia

Steinberg

Oxidized LDL

Ross

Response to Injury

Libby

Inflammation

Now, the growing acceptance of the scurvy-heart disease

connection can no longer be ignored. My lecture at Stanford

University was a historic event because it broke the strangle-

hold of the pharmaceutical cartel on established medical insti-

tutions. The doctors who organized the event deserve some

credit for opening these closely guarded gates of medicine.

Heart disease is an early form of the sailor's disease scurvy. In

my presentation, I can only focus on the most compelling evi-

dence. For more details, I encourage you to visit our research

website www.dr-rath-research.org.

Twenty minutes of my lecture

felt like an earthquake to

the house of cards that is

pharmaceutical cardiology.

Cellular Medicine has now

opened the doors for new

generations of doctors and

cardiologists, enabling them

to save millions of lives.

All existing hypotheses of atherogenesis have one problem in

common — they defy human logic. If high cholesterol levels,

oxidized LDL or bacteria damage the vascular wall, athero-

sclerotic plaques would occur along the entire vascular

pipeline. Inevitably, peripheral vascular disease would be the

primary manifestation of cardiovascular disease. This is clearly

not the case.

It doesn't require a degree from Stanford or any other medical

school — any layperson can solve the ‘Football Field Riddle.’

Delivering my lecture at

Stanford University

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WHY ANIMALS DON’T GET HEART ATTACKS – BUT PEOPLE DO!

12 DOCUMENTATION

The “Football Field Riddle”

The “Scurvy-Heart Disease Connection”

Scurvy

Heart

Disease

Cardiovascular disease is an early form of the

sailor s disease scurvy. In both cases, lack of vitamin

C in the vascular cells is the underlying problem.

The total surface area of the

blood vessel system in a per-

son is comparable to the size of

a football field.

In scurvy, a complete depletion of ascorbate in the

body dissolves the structure of the blood vessel wall

causing leaks, blood loss, and eventually death.

But in 90% of the cases, it clogs

in the same small spot the

size of the marker for the extra

point kick.

In cardiovascular disease, ascorbate deficiency

gradually develops over decades, allowing time for

vascular repair mechanisms (plaque formation).

The arteries, veins and capillaries in our bodies compose a

pipeline that is 60,000 miles long and covers the area of a foot-

ball field. But this pipeline fails in 90% of the cases at one spe-

cific spot: the coronary arteries, which are the length of only

one billionth of the total vascular pipeline. If high cholesterol

— or any other risk factor circulating in the bloodstream —

could cause damage to this pipeline, it would clog every-

where, not just at one spot. Obviously, elevated cholesterol

cannot be the primary cause of coronary artery disease.

The sailors of earlier centuries died within a few months from

hemorrhagic blood loss due to a lack of endogenous ascorbate

synthesis combined with a vitamin-deficient diet. When the

Indians gave those sailors tea from tree barks and other vita-

min-rich nutrition, blood loss was stopped and the vascular

wall healed naturally. Thus, the damage was repaired!

Today, we all get some vitamin C in the diet, and open scurvy is

rare. But it is not enough, and almost everyone suffers from

chronic vitamin deficiency. Over decades, microscopic lesions

develop along the vascular wall, especially in areas of high

mechanical stress, such as the coronary arteries (pumping heart).

The solution to the puzzle of cardiovascular disease, therefore,

must lie in the explanation of coronary artery plaques as the

predominant manifestation of cardiovascular disease. To solve

this puzzle, we need to refocus our attention away from the

bloodstream and its constituents to the one and only relevant

target: the stability of the vascular wall.

Just as in the sailor's disease scurvy, vitamin C induces the nat-

ural repair of the blood vessel wall in cardiovascular disease,

leading to a halt in the progression and even to the natural

regression of vascular lesions.

The following picture shows the connection between cardio-

vascular disease and the sailor's disease scurvy. Unlike ani-

mals, the human body cannot synthesize vitamin C. Ascorbate

deficiency results in two distinct morphological changes in the

vascular wall: impaired vascular stability due to decreased col-

lagen synthesis and loss of the endothelial barrier function.

In contrast to current models of atherogenesis, the ‘Scurvy-Heart

Disease Connection’ answers all the key questions in cardiology

today.

1. Why do we get infarctions of the heart and not of the nose or ears?

The answer can be reduced to two factors: structural impair-

ment of the vascular wall due to vitamin deficiency combined

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WHY ANIMALS DON’T GET HEART ATTACKS – BUT PEOPLE DO!

12 DOCUMENTATION

Why People Get Heart Attacks,

But Not “Nose Attacks”

Why Animals Don’t Get Heart Attacks

Diastole

(Relaxing Phase)

Systole

(Contracting Phase)

The underlying weakness of

the blood vessel wall due to

vitamin deficiency is primarily

exposed at sites of extreme

mechanical stress.

With the rarest of exceptions, animals

don t develop arteriosclerosis.

Prominent examples are bears. They

have average blood cholesterol levels

of about 600 mg/dl. They don t get

heart attacks because they produce

their own vitamin C, which stabilizes

their artery walls.

Due to the continuous heart

pumping, the coronary arter-

ies are the most stressed

areas and the primary sites of

vascular damage and repair

(plaque formation).

With every heartbeat,

the coronary arteries are squeezed flat.

with the mechanical stress from pulsatile blood flow in the

coronary arteries. It is at this unique spot where the underlying

structural impairment is exposed first.

3. Why don’t animals get heart attacks, but people do?

Why are bears and other hibernators with cholesterol levels of

600 mg/dl not extinct from an epidemic of heart attacks? The

answer: Animals produce their own vitamin C in amounts

between one gram and 20 grams (six teaspoons) each day,

compared to the human body weight. These amounts of ascor-

bate are obviously sufficient to optimize the stability of their

vascular walls — without any necessity for statins and other

cholesterol lowering drugs.

2. Why do we get arteriosclerosis, but not venosclerosis?

The hypothesis that cholesterol, bacterial infections, chlamy-

dia and other blood risk factors cause plaques would

inevitably also lead to clogging of veins and lead to veno scle-

rosis. This is clearly not the case. The scurvy-heart disease

connection provides the only logical answer to this question.

4. Why are all important risk factors for cardiovascular

disease closely connected to ascorbate deficiency?

Why People Get Arterio sclerosis,

But Not Veno sclerosis

All risk factors for cardiovascular disease known today, including:

Arteriosclerosis

Main Cause of Death

Venosclerosis

Essentially unknown

Arteriosclerosis is the cause

of every second death.

• carbohydrate metabolism — such as diabetes

• lipid metabolism — high cholesterol and other hyperlipidemias

• amino acid metabolism — such as homocysteinuria

Venosclerosis is unknown

unless a vein is implanted as

an artery such as in coro-

nary bypass surgery. Then,

veins, too, develop plaques.

are closely connected to deficiencies in vitamin C and other

micronutrients essential for vascular cell metabolism. The

common denominator of these metabolic disorders is to pro-

vide compensatory stability for the vitamin-deficient vascular

wall. This is also the reason why ascorbate deficiency

increases fibrinogen and thromboxane levels while decreasing

endothelial-derived relaxing factors (NO) and prostacyclin.

This is logical proof that not

cholesterol, but vascular wall

weakness exposed by mechan-

ical stress causes infarctions.

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277

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