What Causes Heart Attacks by Dr. Cowan

7/21/2019 What Causes Heart Attacks by Dr. Cowan

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What Causes Heart Attacksby Dr. Thomas Cowan

In this article, I lay out the case

that the spectrum of heart disease

that includes angina, unstable angina,

and myocardial infarction (heart

attack) is better understood from the

perspective of events happening in

the myocardium (heart) as opposed

to events in the coronary arteries (the

arteries that supply the heart). As we

ali know, the conventional view of

the cause of heart disease is that thecent ral events occur in the arteries.

In this article, I wili go into more

detail about why the conventional

theory is largely misleading, and then

I wili describe t he precise and weli

documented events that do lead to

heart attacks.

This new understanding is crucial

because, as the past 5 or so years

have shown, pursuing the coronary

artery theory has cost th is nation

biliions of doliars in surgical costs !

most of which are unnecessary ! andbiliions in medications that cause as

much harm as any benefits, and has

led many people to adopt a low!fat diet

and which only worsens the problem.

In contrast, by understanding the real

pathophysiological events behind

the evo lution of "ls, we wili be led

to a proper #$our ishing Traditions#

style diet, the use of the safe and

ine%pensive medicine g!strophanthin,

and most important,we wili be forced

to look at how heart disease is a true

manifestation of the cost of modernlife to human health. To overcome

the epidemic of heart disease, we

need a new medicai paradigm, a

new economic system, and a new

ecological consciousness& in short,

a new way of life. The coronary

theory misses ali of this, 'ust as it

misinterprets the actual pathological

even . .

In writing this article, Iam indebted

to the work of r. nut *roka and

his website www.heartattacknew.

com. +or ali who are interested in

this important sub'ect, it is advised

to read the entire webs ite and watch

the video on the website. +or health

professionals and researchers , your

understanding of this sub'ect is

incomplete without reading and

studying two items found in the

print version of the website The

Etiopathogenesis of Coronar y Heart

Oisease: A Heretica/ Theor y Based on

Morphology, by -. aroldi, and #/n

the -enesis of "yocardial lschemia,#

by *roka.

Rebuttal of the Conventional Theory

0ntil recently, it was thought that

most "ls were caused by progressive

blockage created by pla1ue buildup

in the ma'or arteries leading to the

heart (there are four ma'or coronary

arteries) . The pla1ue was thought

to be cho lesterol buildup in the

arterial lumen (inside of the vessel ),

which eventualiy cut off blood

supply to a certain area of the

heart, resulting in o%ygen deficiency

in that area, causing first pain

(angina), then progressing to ischemia

(heart attack). The simple solution was

to unblock the stenosis (blockage)

with either an angioplasty or stent, or,

if that was not possible, to bypass

the area with coronary bypass

grafting (2A-). *imple problem ,

simple solution.

3owever , problems became

apparent through a number of

avenues. +irst, a story related by a

cardiologist at a $orthern 2alifornia

heart symposium , at w hich I was

a speaker, points to the first

problem. 3e told us that during his

residency he was part of a trial

conducted in rural Alabama with

black men. In this trial, angiograms

(in'ections of dye into the coronary

arteries to detect blockages) wer e

dane on ali the men presenting with

chest pains. +or the ones who had a

single artery blocked, no treatment

was prescr ibed, and the researcherspredicted in their notes which part of

the heart would have a subse1uent

heart attack if one occurred. /f

course, they ali predicted that it

would be in the part of the heart

supplied by the blocked coronary

artery . Then they waited .

4ventualiy, many of the men did

return and did have "ls, but to the

researchers 5 surprise, less than 67

had a heart attack in the area of the

heart supplied by the original blocked

artery.

*econd, a large study conducted

in 89 by the "ayo 2linic on the

efficacy of bypasses, stents, and

angioplasty concluded that

a. bypass surgery relieves symptoms

(chest pain)&

b. bypass surgery does not prevent

further heart attacks&

c. only high!risk patients, those

whose lives are in acute danger ,

benefit from bypass surgery

with regard to a better chance of

survival.

In other words, the gold standard

for treating arterial blockages has,

at best, only minimal benefits.

lf you watch the video on the

heartattacknew.com website and

go to the +A: calied #The ;iddles

<

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TOWNSND !TTR" #A$ %&'(68

í

Heart Attacks "ls, which , as it turns out, is almost of "ls was done in 3eidelberg ine1ually invalid. the 6=>s. The conclusion was that

< thrombosis sufficient to cause the

*ol.ution,# it becomes clear why this #eet the )nstable *la+ue "l was found in only 87 of cases.

is so. ?arge, stable blockages ! those *o, we ali agree that the entir e aroldi, in the largest such study eve r

over =7 ! are in almost 67 of focus of cardiology ! the stable, done, found sufficient thro mbosis

the cases completely compensated by progressing, calcified pla1ue, the in @6 7 of cases.8 3e also found that

collateral blood vessels. In fact, the thing that we bypassed and stented the larger the area of the "l, the

view that the heart gets its blood only for years, the thing that we do 2T more often a stenosis was pr esent,

from the four ma'or vessels is itself scans of your arteries for, the thing and the longer the time between "l

false. *tarting soon after birth, the that we told you is from cholesterol and death , the higher the percentage

normal heart develops an e%tensive buildup in your arteries, the thing of stenosis. These two facts al low

network of small blood vessels called that #alternative cardiology,# such some researcher s to #cher ry!pick# the

collateral vessels , which eventually as the /rnish program, focused on number s and make the stenosis rate

compensate for the interruption of ! actually is not so important in the high, as they choose to study only

flow in any one (or more) of the ma'or etiology of heart attacks. on5t worry , those with lar ge "ls and who l ive the

vessels. though. e know that the focus of the longest after the "l event. ?ater in this

As *roka correctly points out problem must be the arteries , or so article, I will e% plain how the stenos is

in the video, coronary angiogram conventional thinking goes. Therefore , comes about as a conse1 uence of

the

! by failing to show the collateral enter the unstable, or f riable, pla1ue.

"l.

circulation, arid by creating spasms This insidious fellow doesn t actually Anothe r observation that

casts

in the coronary arteries through the create a large blockage& rather , its doubt on t he relevance of

the

in'ection of heavy dye under high a soft, #foamy# pla1ue that under coronar y artery theo ry of "l has to

do

pressure ! is notoriously inaccurate certain situations (we don t know with the proposed mechan ism of

how

at assessing the amount of stenosis in which situations) rapidly evolves thrombosed arteries cause ischemia,

the vessels as well as the true blood and abruptly doses off the involved whi ch is by cutting off t he blood

flow in the heart. To this day, most of arter y, c reating a downstream supply and t her eby t he o%ygen to the

the bypasses, stents, and angioplasties o%ygen deficit, followed by angina, tissues. The real ity is that when careful

are done on minimally symptomaticthen ischemia. These soft pla1ues measurements ar e done assessing the

patients who show a greater than are thought to be a combination of p8 (o%ygen leve i) of t he myoca

rdial

=7 blockage in one or more inflammatory #buildup# and ??, the cells during an "l, to the huge

coronary arteries. These arteries are e%act two things targeted by statin surprise of many, there is no o%ygen

almost always fully collateraliBed& the drugs . Therefore, the thinking goes, defic it ever s how n in an

evolving surgery does not restore blood flow because this type of pla1ue can

build "l.3 The p8 leveis do not change because the body had already doneup in anyones arteries, at any time, at ali th roughout the enti re event. I

its own bypass . Ask yourself lf it were everyone should be on statin drugs to wi ll come back to this later w hen

I true that an artery more than =7 prevent heart attacks. (*ome people describe what does change in every

blocked had no collateral circulation, even advocate putting therapeuti c evolving "l ever studied. A gain, the

how would that person still be aliveC doses of statins in municipal water 1uestion must be asked, if th is

theory And does it really make sense that

supplies .) Angiogram studies

have is predicated on the loweri ng of the

the eventual "l is caused when the been presented to show the evolution p8 in the myocardi al ce l ls, and in

stenosis goes from =9 7 to =D 7C of these unstable pla1ues as proof that fact the p8 doesnt change, then

This is an insignificant difference they are the true cause of the ma'ority e%actly what did happenC

and is completely nonsensical. Eet of "ls. The conclusion is that throm bosis

this is what most of the procedures As I will show in the ne%t section, associated with "l is a real

are meant to accomplish, to unblock acute thrombosis does happen phenomenon , but in no pathological

the stenosis, which, as the video in patients having "ls, but it is a study has it been found in more

shows actuall has no blood!flow consequ ence, not the cause, of the than 57 of deaths, w hich



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G s why emergency procedures

ember , the only patients who

5!!!# from by pass and stents

are ost criticai, acute patients) can

el pful immediately post!"I

to e flow in those patients

who ot have

ade1uate collateral

ation to that part of their heart.

*o again, ali the e%isting theories asto the relevance of the coronary

arteries in thH evolution of the "l are

fraught with inconsistencies .

lf this is so, what then does cause

"lsC

The tiolo,y of #yocar-ial lschemia

Any accurate theory of the cause

of myocardial ischemia must account

for the risk factors most associated

with heart disease. These are being

male, having diabetes, smoking

cigarettes, and e%periencing chronic

nervous system is divided into two

branches, which in health are always

in a balanced but ready state. The

sympathetic, or fight!or!fl ight, system

is centered in our adrenal medulia

and uses the chemical adr enaline

to tell our bodies that danger is

afoot, its time to run. lt does so by

activating a series of biochemical

responses , the center of which are

the glycolytic pathways that

accelerate the breakdown of glucose

to be used as 1uick energy so that

we can make our escape.

In contrast, the parasympathetic

branch, centered in the adrenal

corte%, 6s the rest!and!digest

arm of the autonomi c nervous

system . The particular nerve of the

parasympatheti c chain that innervates

the heart is calied the vagus nerve. lt

slows and rela%es the heart whereas

Heart Attacks

life. hat s dangerous to our health

is the ongoing, persistent decrease

in our parasympathetic , or life

restoring, activity. Ths decrease in

parasympathetic activity is mediated

by the t hr ee chemical transmitters of

the par asy mpathetic ner vous system

acety lcholine, $/, and c-"J. This

is where it becomes fascinating,

for it has been shown that wome n

have stronger vagai act ivity than

men, probab ly accounting for the

se% difference in the incidence of

"l.8 3yperte ns ion causes a decrease

in vaga i activity, s moki ng causes a

decrease in vagai activity, diabetes

causes a decrease in vaga i activ ity,

and physical and emotional stress also

causes a dec rease in parasympathetic12

psychologicalKemotionalstress.

thesympatheticbranchaccelerates

activ ity .9

-

*o alithe

significant

lnterestin

gly, nane

of these

riskfactors

directly

link to

pathology

of the

coronary

arteries.

iabetes

and

cigarette

use cause

disease in

thecapillaries,

not the

large

vessels,

and stress

has no

direct

effect on

coronary

arteries

that we

know of.

In

addition,during

the past

f ive

decades

or so,

the four

main

medicine

s of

modern

cardiolog

y !

!

blockers,

nitrates,

aspirin,

and

statin

drugs !

ali have

some

benefits

for heart

patients

(albeit ali

withserious

drawbacks

as weli),

which

must be

addressed

in any

comprehe

nsive

theory of

myocardial

ischemia,which I wili

attempt to

do here.

The

real

revolution

to come

in the



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preventio

n and

treatmen

t of

heart

disease

has

been

inaugurat

ed

through

our

under sta

nding of

the role

of the

autonomi

c

nervous

system in

the

genesis

of

ischemia

and its

measure

ment

through

the tool

of heart!

rate

variability

. +irst,

some

brief

backgrou

nd. e

have

two

distinct

nervous

systems.

The first,

the

central

nervous

system,

contrais

conscious

functions

such as

muscle

and

nerve

f unction.

The

second

nervous

system

is calied

the

autonom

ic (or

unconsci

ous)

nervous

system

(A$*),

which

contrais

the

function

of our

internai

organs.

The

autonom

ic

and

constricts

the heart.

lt is the

imbalance

of these

two

branches

that is

responsibl

e for the

vast

ma'or ity

of heart

disease.

0sing

heart!r ate

variability

monitoring,

which

gives a

real time,

accurate

depiction

of

the

status of

these two

branches

of the A$*, it has

been s

hown in

four

studies

that

patients

with

ischemic

heart

disease

have, on

average, areduction

of

parasympa

thetic act

iv ity of

mor e than

a third.

Typicaliy,

the worse

the

ischemia,

the lower

the

parasymp

athetic

activity

(5K69@) .

+urthermo

re, about

D7 of

ischem ic

events

have

been

shown

to be

pr eceded

by

significant

, often

drastic,

reductions

in

parasymp

athetic

activity

related to

physical

activity,

emotional

upset, or

other

causes.6

This

finding

contrasts

with

others

that show

that

people

who

have

normal

parasymp

athet ic

activity,

then

have an

abrupt

increase

in

sympathet

ic activity

(physica l

act iv ity,

or often

an

emotional

shock),

never s

uff er from

ischemia.

In

other

words ,

withouta

preceding

decrease

in

par asymp

athetic

act iv ity,

activation

of the

sy

mpathetic

nervous

system

does not

lead to

"l.7

Jresuma

bly, we

are

meant to

have

times of

e%cess

sympathe

tic activ

ity& that

is

normal

riskfactorshavebeenshownto

downre

gula te

the

act

ivity of

theregene

rative

nervou

s

system

in the

heart.

/n theother hand,

themain

drugsused

in

cardiol

ogy !

nitrates

stimula

te

$/

(nitrou

s

o% ide)

product

ion,

which

upregul

ates

the

parasy

mpathe

tic

nervou

s

system.

Asp irin

and

statin

drugs

also

st imula

te the

product

ion of

A23

and

/,

two of

the

princip

al

mediat

ors of

the

parasy

mpathet

ic

nervous

system

(until

they

cause

a

reboun

d

decrea

se in

these

substa

nces, w

hich

then

makes

the

parasy

mpathe

tic

activi ty

even

worse).

+inaliy,

blocker

s are

calied

!

blocker

s

because they

block

the

activity

of the

sympat

heti c

nervou

s

system

.

To

summ

ar iBe,

the

risk

factors

and

interve

ntions

that

have

actuali

y been

borne

out

throug

h time

a li he

lp

balanc

e the

A$*.

hateve

r their

effect

on

pla1ue

and

stenosi

s

development isof minar

relevance.

*o, whatis the

se1uenceof events

that lead

s to an "lC

+irst,

and in

the vast

ma'orityof cases

the

patholog

y wili

not

proceed

unless t

his

conditio

n is

met,

there is

adecreas

ed ton ic

act ivity

of the

parasym

pathetic

nervo us

system.

Then

comes

an

increase

in thesympath

etic

)<



70 TOWNSND !TTR" #A$ %&'(

Heart Attacks the hemodynamics of the arteries

embedded in that section of the

nervous system is a medicine f rom the

strophanthus plant called ouabain,

> heart, causing the sheer pressure that

nervous system act6v6ty , usually aruptures the unstable pla1ues, which

physical or emotional stressor , whichfurther blocks the artery and worsens

raises adrenaline production , whichthe hemodynamics in that area of the

directs the myocardial cells to breakheart. /nly this e% planation tells us

downglucose using aerobic glycolysis

why pla1ues rupture,what thei r role in

(remember, no change in blood flowthe "l process is, and when and how

as

measured by the p8 in the cells

they should be addressed & that is, only

hasoccurred). This development in the most criticai, acute situations . redirectsthe metabolism of the

/nly this e%planation accounts for ali

Gheart away from its preferred and

the observable phenomena associated

most efficient fuel source, whichwith heart disease. The true origin of

is ketones and fatty acids . Thisheart disease could not be more clear.

e%plains why heart patients often feelThe final 1uestion is, why is

tir ed before their events. This alsothis understanding of heart disease

e%plains why a high!fat, low!glucoserelevant, besides being of academic

diet is crucial for heart health. As ainterestC The first and obvious answer

result of the sympathetic increaseis that if you dont know the cause, you

and resulting glycolysis, a dramaticcant find the solution. The solution

increase in lactic acid productionis to protect our parasympathetic

occurs in the myocardial cells. Thisactivity, use medic ines that support

happens in virtually 67 of "ls,it, and nourish the heart with

with no coronary artery mechanismwhat it needs. $ourishing our

re1uired.13 14 As a resultof the increaseparasympatheti c nervous system is

in lactic acid in the myocardialbasically the same as dismantling a

cells, a local iBed acidosis occurs.way of life for which humans are ill

This acidosis causes the calcium tosuited. This way of life, in my view ,

be unable to enter the cells, makingis otherwise known as industrial

the cells less able to contract. 15 ThisciviliBation . The known things that

inability to contract causes localiBednourish the parasympath etic nervous

edema, dysfunction of the walls of system are contact with nature, loving

the heart (called hypokinesis , therelations, trust, economic security (a

on stress echoes and nuclear thalliumworld over), and se% ! in a sense, a

stress tests), and eventually necrosiswhole new world.

of the tissue, which we call an "l.The medicine that supports ali

The localiBed tissue edema also altersaspects of the parasympathetic

r. Tom 2owan discove r ed the work of the two men w ho wo uld have the most

influence on his career w hile teaching gar dening as a Jeace 2or ps

volunteer in *waB iland, *outh Af rica. 3e r ead N utri tion and hys i cal

!egener ation, by eston Jrice, and a fellow volunteer e%pla ined the

ar cane principies of ;udolf *teiner s biodynamic agriculture. These events

inspir ed him to pursue a med icai degr ee. Tom gr aduated fro m "ichigan *tate

0nivers ity 2ollege of 3uman "edicine in 1984. After his r esidency in fam ily

pr act6ce at L ohnson 2ity 3ospital in 'ohnso n 2ity, $ew Eo r k, he set up an

anthr oposo phical medicai practice in Jeterborough, $ew 3ampshi r e. r .

. 2owan relocated to *an +r ancisco in 2003.

r. 2owan has served as v ice pr esident of the Jhysicians Association for

A nthr oposop hical "edicine and is a founding boar d member of the eston

A. Jr ice +oundation. ur ing his car eer he has studied and wr itten about

many sub'ects in medicine. These include nutrition, homeopathy , anthr oposo

phical medicine,and her bal medicine. 3e is the principal author of t he book

T he " ourfol d ath to Hea /ín g, w hich was published in 2004 by $ew Trends

. . . Jublishing, and is the coauthor of The Nour ishi ng Trad i tions Boo# of Ba$y and

C hlfd 2ar e, publMshed m 201 3. 3e wr ites the N As k the octor # column in % i se Tr ad iti ons in "ood "ar & i ng and

the H ea /ín g Arts, the foundation 5s 1uarterly magaB ine, and has lectured throughout the 0* and (&nada. 3e has

thr ee gr own childr en and currently pr actices medicine in *an +rancisco, w her e he r es ides w ith his w if e, ?y nda

*m6th 2owan. r. 2owan sees patients at his office in *an +rancisco,does long!distance consults by telephone, and

N s acceptmg new pat6ents. 3e also gives lectur es and pr esentations.

or g!strophanth in. -!strophanthin

is an endogenous hormone

made in the adrenal corte% from

cholestero l, w hose production is

inhibited by statin dr ugs, that does

two things that are cr ucial for heart

health and are done by no other medicine. +irst, it stimulates the

production and liberation of A 23,

the main neur otransm itter of the

parasympathetic nervous system.

*econd, and cruc ially, it conve rts

lactic ac id ! the main metabo lic

poison in this process! into pyr uvate,

one of the main and preferred fue ls of

the myocard ial cells. In other wo

rds, it converts a #poison # into a

nutrient.

Jerhaps this #magic# is w hy

2hinese medicine practit ioner s saythat the kidneys (i.e., adrenals,

wher e ouaba in is made) nourish

the heart. In my years of using

ouabain in my practice, I have not

had a single patient who had an "l

wh ile taking it. lt is tr uly the gift to the

heart.

+inally, this understa nding of

heart disease leads us to the cor r ect

diet, one that is loaded with healthful

fats and f at!so l uble nutr ients, and

is low in the pr ocessed

carbohydrates and sugar s that are

the hallmar k of industrial, civ iIiBed

lif e.

Notes1. Doerr W et ai. Berlin-He id elberg- ew Yor! "#ringer $

2. Baro ldi % & "il'er (. The Etiopathogenesis o)

Coronary

Heart Di sease: * Heretical Theory Based on Morpho/ogy.

3. He l )ant& + H & ,orreter "& Ha/#ton + & Hat l& e/#

H% & %orlin +. oronar3 eart dieae. Di))erent ia lhemo-ynamic metabolic an- electroca r-io,ra/hic effects

in sub0e-s with an- without an,ina -urin, atrial /acin,.

Circulation. 1970$42!60 1-615.

4. "r oa . n te genei o) /oardial ie/ ia .

Cardio/. 2004$93!768-783. doi!10.100700392-004-

1. Takase 2 et ai. Heart rate variability in /atients with

-iabetes mellitus ischemic heart -isease an-

con,estive eart )a ilre f Electrocard io /. 1992$25!79-88.

6. "roa. # it.

3. Sroka 4 et ai. Hea rt rate variability in myocar- ial ischemia

dr i ng dail li)e. : Electrocardiol. 1997$30!45-56

8. "roa. # it

9. "roa. lbid.

1. "roa. lbid.

1 ; "roa. lbid.



70 TOWNSND !TTR" #A$ %&'(

What Causes Heart Attacks by Dr. Cowan

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