Cardiology
Statins and cancer
– the hidden story
Both the West and the Middle East share rising heart disease and
cancer incidence rates. Brian Peskin, with David Sim, MD and Amid Habib,
MD, review current research literature and suggest a causal link between
increased widespread statin use for battling heart disease (by lowering
LDL cholesterol) and the concurrent increase in cancer.
As early as the late 1990s,
almost half of all Americans
and Europeans died of heart
disease.1 By 2010, virtually
all Americans are predicted
to die either of heart disease
or cancer.
Atherosclerotic
coronary artery disease
(CAD), a “clogging” of the
arteries, became the number
one killer of Americans in
2006, with cancer a close
second. Now, in spite of
widespread use of cholesterol-
lowering drugs, heart
disease remains the top
killer in Western countries
as well as in the Middle
East.2
In addition to the
rising incidence rate of heart
disease we also see a concurrent
rise in cancer rates
throughout the industrialised
West and the Middle
East. For example, we see a
very troubling trend in
cancer rates in the Gulf state
of Oman. Oman, with a
population of over two
million citizens, established
a countrywide cancer
registry in 1994. Since
undertaking this project
they have recorded cancer
rates comparable to Western
countries. The cancer rate
revealed during a five-year
study (1993-1997), although
less than in America and
Europe is significant because
it is rising.3
Egypt also has developed a
significant cancer problem,
prompting their National
Cancer Institute (NCI), the
largest comprehensive
cancer center in Egypt, to
state: “The present [cancer]
hospital with its 550 beds is
overloaded by patients
referred from all over the
country.”4
Egyptian women
lead breast cancer contraction
rates in the Arab world
and, along with men, share
the greatest percentage of
lymphoma in that region of
the world as well.
Lebanese men have the
highest rates of both
prostate and bladder cancer
in the Arab world and
Lebanese women have the
greatest percentage of
uterine cancer,5 while breast
cancer is the number one
killer of women in the
United Arab Emirates.6
Could the medical establishment
inadvertently be
exacerbating the rising incidence
of both cancer and
heart disease in both the
West and the Middle East
through widespread use of statins, their preferred
cholesterol-lowering drug?
The Statin-Cancer Connection
An explosive article
published in the 2007 issue
of Journal of the American
College of Cardiology7
revealed that statins, previously
reported to have relatively
few serious side
effects, can significantly
increase the risk of cancer.
Specifically, the increased
risk of cancer has been
significantly correlated with
the lowering of LDL (low
density lipoprotein) cholesterol
– an unforeseen negative
outcome. With statin
use, the increase in cancer deaths counteracts the
supposed lower cardiac
mortality associated with
lower cholesterol, resulting
in a neutral effect or
increased overall mortality.
TRANSLATION: With statin use, even if you don’t
die of a heart attack – you
will likely die of cancer.
Wouldn’t it be more desirable
to lead a full life while
also avoiding both cancer
and heart disease?
Statins’ effectiveness called
into question
Prepare to be shocked. Statins, which represent
huge profits to the pharmaceutical
industry, have been
the preferred drug of most
cardiologists. However,
statins are now being shown
to not prevent or reduce
heart disease. The inability
of statins to have a positive
impact on heart disease was
predicted in the Journal of
the American Medical
Association (JAMA) over 10
years ago when they
concluded that low cholesterol,
by itself, did not
significantly prevent heart
disease8: “Our findings do
not support the hypothesis
that hypercholesterolemia
[high LDL cholesterol levels]
or low HDL-C [high density
lipoprotein cholesterol – aka
“good” cholesterol] are
important risk factors for
all-cause mortality, coronary
heart disease mortality, or
hospitalization for myocardial
infarction or unstable
angina in this cohort of
persons older than 70
years.”
These (and other) poor
outcomes prompted the
recent medical journal
article entitled “LDL
Cholesterol: “Bad Cholesterol
or Bad Science,” published
in the Journal of American
Physicians and Surgeons9: “No
tightly controlled clinical
trial has ever conclusively
demonstrated that LDL
cholesterol reductions can
prevent cardiovascular
disease or increase
longevity.
“The concept that LDL is
bad cholesterol is a
simplistic and scientifically
untenable hypothesis.”
As this article was going to
press, the Journal of American
College of Cardiology
published “Beyond Low-
Density Lipoprotein
Cholesterol – Defining the
Role of Low-Density
Lipoprotein Heterogeneity
in Coronary Artery Disease,”
reporting more discouraging
findings (Mudd et al, 2007;
50:1735-1741): “…despite
more aggressive interventions
by lowering LDL-C
levels, the majority of CAD
(coronary artery disease)
events go undeterred [not
prevented]…
“Measurement of apolipoprotein (apo)B has
been shown in nearly all
studies to outperform LDLC
and non-HDL-C as a
predictor of CAD events and
as an index of residual CAD
risk.”
This recent finding and its
implications will be the key
to explaining the statincancer
connection.
Cholesterol-lowering drugs
were known to cause cancer
a decade ago
A dire warning about statin
use was published by two
physicians, Thomas B.
Newman and Stephen B.
Hulley,10 at the University of
California in San Francisco in
1996. This same warning was
published in the cancer journals
over a decade ago. One
example appeared in Cancer
Research11:
“Several trials of cholesterol
lowering with drugs to
prevent cardiovascular
disease events have demonstrated
an increase in cancer
incidents in the subjects
treated with lipid-altering
drugs. The trials were randomised, doubleblinded,
and lasted an
average of 5 years…. A
statistically significant
excess of malignancy was
seen in elderly subjects and
women randomized to the
drug groups.”
None of these studies or
their conclusions has ever
been refuted, yet we continue
to prescribe more and more
cholesterol-lowering drugs.
Are physicians missing something?
Yes.
Arterial plaques
– it’s not the saturated fat
For decades, saturated fat
was blamed for the buildup
of arterial plaque, the
material that can significantly
narrow the diameter
of arteries. However, a
landmark article published
in the Lancet in 1994 shattered
that myth.12 The
investigators analysed
plaque and found it
contained more than 10
different compounds, none
of which consisted of saturated
fat. There are also
other independent analyses
confirming the lack of saturated
fat in any arterial
plaque.13,14
Arterial plaque—normally, a
harmless natural repair
mechanism
As the vasculature ages, it is
constantly repaired with
new collagen. A number of
other repair mechanisms are
concurrently working, with
cholesterol and Lp(a)
lipoprotein acting as “sticky
patches” to seal cracks when
injury or damage to an arterial
wall occurs.
In healthy individuals,
arterial plaques form as a
result of these patching
activities, but without
serious consequences.
However, in many individuals,
the plaques do not
disappear, but build up over
time. To explain these
perplexing observations, we
need to explore cholesterol’s
makeup.
Importance of cholesterol— “Good” or “Bad” terms are misleading
Cholesterol itself can’t be
“bad” because it is critical in
the production of the
hormones estrogen, progesterone,
and testosterone,15
keeping our skin water- and
chemical-resistant, manufacturing
bile salts for digestion
of fats, forming our
bones, and delivering
precious PEOs (Parent
Essential Oils) to all the cells
of our body. Without plenty
of cholesterol, we would all
be dead.16
While free cholesterol
does exist in the body, 80-
90% is esterified, meaning it
is chemically bound to a
fatty acid, with a strong
preference given to parent
omega-6, as shown in Figure 1
(in which R represents the
hydrocarbon portion of the
fatty acid).
The structure of cholesterol
itself never changes
That’s right; the esterified
component changes. It is
only the hydrocarbon
[alkyl] portion of the ester
group that changes. If you
term something as “bad,”
presumably you want to get
rid of it, or at least get it as
low as possible.
This is what
the pharmaceutical industry
is saying. However, if you
got rid of all the LDL-C you
would be wiping out valuable
fatty acids, as well as a
mechanism for removing
oxidised fatty acids that
should be removed from the
body. It would be like stopping
“garbage collection”.
These cholesteryl esters
are transported throughout
the body in lipoprotein
particles (Figure 2) that are
classified according to the
ratio of protein to fat, or
more simply, the density of
the particle, in the
following increasing order:
chylomicrons, very low
density lipoprotein, intermediate
density lipoprotein,
low density lipoprotein
(LDL), and high density
lipoprotein (HDL).17
Importance of esterified
cholesterol
Esterified cholesterol
comprises the majority of
LDL. LDL is much more
than just “cholesterol,”
although few people,
including nutritionists and
physicians, understand this.
It is essential to understand
the term cholesterol “esters”
if you hope to understand
the vital role of LDL in your
body. Medical journals
confirm this important
fact18: “LDL contains up to
80% lipid, including
polyunsaturated fatty acids
and cholesterol, mainly
esters. Linoleic acid, [is] one
of the most abundant fatty
acids in LDL…”
Furthermore, HM Sinclair,
a top EFA researcher and
famous English nutritional
biochemist;
(www.britathsoc.org/bas_hugh_
sinclair.html), made clear in
1984 that about 20% of the
free fatty acids of the phospholipids
in both LDL and
HDL are composed of parent
omega-6, too.19 America’s top
cardiology publication, the
Journal of American College of
Cardiology (2007;50(18):1735-
1741), published that it is the
esterified cholesterol that is
the problem in heart disease,
but didn’t address the reason why or how to solve it.
Esterification of omega-6
with cholesterol was known
as early as 1941,20 and is one
of the keys to understanding
the statin-cancer connection.
However, due to widespread
inaccurate terminology,
we first need to
discuss PEOs, EFAs, and EFA
derivatives.
Parent Essential Oils (PEOs):
An essential difference
The term “Essential Fatty
Acids” is so frequently
misused that I was
compelled to coin a new
phrase, Parent Essential Oils
(PEOs).
“PEOs” refer to the only
two true essential fatty acids:
parent omega-6 (LA) and
parent omega-3 (ALA). The
term “parent” is used because
these are the whole, unadulterated
form of the only two
essential fats your body
demands, as they occur in
nature. Once PEOs are
consumed, your body
changes only 5-10% of them
to “derivatives.”21-23 That
means 90-95% stay in the
parent form in the cell and
mitochondrial
membranes.24,25 There are a
host of omega-6 and omega-
3 derivative-based oils being
marketed to physicians as
EFAs that are in fact nonessential
derivatives such as
EPA (eicosapentaenoic acid),
DHA (docosahexaenoic acid),
and GLA (gamma-linolenic
acid). Fish oils are made up
almost exclusively of omega-
3 derivatives. Scientifically
and biochemically, calling
these derivatives “EFAs” is
wrong. Derivatives are not
EFAs because they are not
essential – your body has the
ability to make them as
needed from the PEOs.
Taking fish oil and other
health-food-store “EFAs”
often leads to pharmacological
overdoses, which can be
very harmful.
Food processing adulterates
most parent pmega-6
In the past several decades,
processed foods – in particular,
frozen foods and restaurant cooking oils –
have increasingly incorporated
trans fats (hydrogenated)
and other
unhealthy fats and oils
resulting in less parent
omega-6 for incorporation
into cell membranes, and
conversion into arachidonic
acid, which is a source of
many prostanoids and
leukotrienes used in inflammatory,
immune, and
signaling functions.26,27
One of the important
features of cell membranes is
their fluidity, which results
from local disordering of the bilayer induced by the cis
double bonds of unadulterated
unsaturated fatty
acids.28 Membrane fluidity
increases when more PEOs
(functional parent EFAs, in
particular, parent omega-6)
are available to incorporate
in the membrane lipid bilayer.
When natural PEOs
are replaced by trans fats
(hydrogenated), the fluidity
changes, and that can cause
significant reduction in critical
cellular O2 transfer.
A category of synthetic fat
that is increasingly used as a
substitute for trans fats is interesterified fats termed IE
fat. Consequently, IE has its
own set of health problems
such as abnormally raised
resting blood glucose
levels.29,30
Commentary
It is important to understand
that cooking oil
manufacturers avoid omega-
3 oils because they are much
more unstable than the
parent omega-6 series oils.
Therefore, most omega-3 in
the diet is unadulterated
and of no concern in our
analysis of adulterated PEOs.
Many seeds, nuts,
grains, eggs, etc. contain
omega-3 and omega-6
unsaturated fatty acids, but
typically the amount of
omega-6 far outweighs the
amount of omega-3; flax
seeds are an exception.
Even when margarine and
other hydrogenated products
contain relatively few
trans fats – as little as 1-2% –
this translates to an enormous
number of defective
trans fat molecules. In
absolute numbers there are
an enormous 1x1021 molecules
in each tablespoon of
oil.
Therefore, the potential
to cause great damage,
either integrally in the
cellular structure, or in
biochemical reactions, is
highly significant since
many of us consume much
more than a single tablespoon
of processed oil each
day. Add to this number of
defective oil molecules the
huge number of defective
fat molecules from other
processed sources and you
should be terrified at what
you, your family, and your
patients have been
consuming for decades.
Avoiding fat isn’t a CAD solution
– PEOs are
As the New England Journal
of Medicine makes clear:
“Diets high in polyunsaturated
fat (PEOs) have been
more effective than low-fat,
high-carbohydrate diets in
lowering cholesterol as well
as the incidence of heart
disease.”31 The key is making
sure the PEOs are unadulterated.
Otto Warburg, MD, PhD:
“Lowered cellular oxygen
equals cancer!”
Just as oxygen deprivation
causes heart disease,
sustained oxygen deprivation
causes cancer, too. Over
70 years ago, the Nobel
prize-winning physician
and master chemist Otto
Warburg, MD, PhD, demonstrated
that a sustained
reduction of 35% in the
level of cellular oxygen
causes cancer, and does so
each and every time the
deficiency occurs for an
extended period.
Oxygen
deprivation is cancer’s
prime cause and the high
ratio of fermentation to
respiration is cancer’s prime
characteristic.32,33 (In the
August 2007 Townsend Letter
for Physicians at
(www.brianpeskin.com/townse
nd.html) Cancer’s prime
cause, cellular hypooxygenation
(hypoxia), was
directly proved by
American research scientists
in the 1950s.34,35 Back
then they didn’t know how
to increase cellular oxygenation;
whereas today we do,
and this is the key in
answering why the “statincancer”
connection occurs
and how to prevent its
tragic consequences.
Commentary
1.
Warburg proved
depressed cellular respiration
and phosphorylation
are the cancercausing
effects of
decreased cellular
oxygen.36
2. Physico-chemical experiments
(Campbell, et
al.37) show that parent
omega-6 (LA) can bind
twice as much oxygen
and disassociates
(releases its oxygen) at a
much higher pressure
(physiologically useful),
much closer to haemoglobin,
than non-essential
oleic acid does.37
Therefore, the 35%
cancer-causing hypooxygenation
(deprivation)
threshold is
breached with insufficient
or adulterated
parent omega-6.
3. Oxygen disassociation
curves for oleic acid
compared with omega-6,
prove a 50% reduction
in oxygen transfer is
possible.
4. Decreased cellular
oxygenation can therefore
systemically occur
in any membrane – any
tissue in the body can
become a potential
cancer site.37
5. Campbell et al.’s seminal
experiment37 conclusively
showed a 50%
reduction in oxygenation
when a PEO deficiency
occurred. Now
imagine this effect
coupled with already
lowered parent omega-6
esterified cholesterol
from statins. The chain
of events is: Lowered
Cholesterol = Fewer
PEOs = Less Cellular O2
= Cancer.
In summary
We have explained in detail
that the common link
between LDL cholesterol
and decreased oxygenation
occurs because cholesterol is
esterified with large
amounts of parent omega-6
before it is combined with
lipoprotein as LDL particles
for transportation within
the body.20,38 Even though
statins increase the uptake
of LDL cholesterol from the
blood, they decrease
overall cellular LA because
absolute levels of cholesterol
are decreased. This
affects oxygen transmission
across the cell membranes
since the structure of the
phospholipids that form a
major portion of the cell
membrane are a reflection
of the composition of
unsaturated fatty acids and bioavailability in the
blood.28
Defective LDL cholesterol
becomes a “Defective
Delivery System”
With the consumption of
organic, unprocessed, PEOs
from natural sources such as
walnuts, almonds, Brazil nuts,
sunflower seeds or their
(unprocessed) cooking oils
rather than adulterated oils
and trans fats, LDL cholesterol
should be made up of
significant amounts of properly
functioning LA. However,
since LDL cholesterol is the
transport vehicle for PEO
delivery into your cells, it
does not care about the state
of the essential fatty acids it is
carrying. LDL cholesterol will
transport adulterated essential
fats already damaged by food
processors into the cell. It is
primarily the adulterated
(defective) parent omega-6
that causes plaque, not saturated
fat. So, while statins
reduce LDL cholesterol by
reducing the defective parent
omega-6 from processed food
it is carrying, and therefore
reducing plaque, at the same
time the statins are lowering
the transport of vital
oxygenating unadulterated
PEOs into the cells. This is the
reason why patient cholesterol
numbers steadily
decrease, yet patient heart
attacks continue to increase.
The popular belief, even
among physicians, is that
the evidence like the
METEOR (2007) trial, for
example, shows there is a
decrease in heart attacks in
patients taking statins. The
facts are that although
cholesterol was lowered and
halted progression of atherosclerosis,
in the placebo
group no patient suffered a
serious cardiovascular event
whereas in the treatment
group (rosuvastatin) there
were eight serious cardiovascular
events including heart
attack and angina, a bad
outcome.
(www.drbriffa.com/blog/2007/03/30/hailed-meteortrial-results-not-as-stellar-as-weare-
led-to-believe/). In addition,
this randomised controlled
trial had a number of serious
flaws that were pointed out
in an editorial in JAMA,
which accompanied the
article (Lauer MS, JAMA,
2007;297:1376-8).
Stop blaming cholesterol
LDL cholesterol continues to
be improperly blamed for a
myriad of health problems
while the real culprit is defective
PEOs. LDL cholesterol has
no alternative but to transport
these killers throughout our
body since, due to food
processors’ requirement for
extended shelf-life in the oils
they sell, we have insufficient
properly functioning LA in
our diets.
The nutritionists
never make this critical
connection and incorrectly
identify the “problem” as LDL
cholesterol.
To repeat: the reason for
the ineffectiveness of statins
to stop heart disease is they
simply can’t eliminate
enough of the defective
PEOs being transported in
LDL esterified cholesterol.
In addition, they simultaneously
remove correctly
functioning PEOs, because
they reduce its cholesterol
carrier – a doubly bad
effect. This is why the
absolute LDL number is
irrelevant if the diet
contains sufficient unadulterated
PEOs. Statins don’t
discriminate between eliminating
functional, unadulterated
PEOs and nonfunctional,
adulterated PEOs.
Reducing LDL cholesterol
increases blood clots and facilitates
metastasis of cancer
Defective parent omega-6 is
also the root cause of thrombosis
(blood clots forming in
the arteries) and then being
unable to dissolve away
naturally, as they do with
external cuts. As referenced
earlier, blood clots are a
tremendous problem with
cancer cases, responsible for
over 80% of the cancer
mortality rate because they
facilitate cancer transport
throughout the body when it
would not have spread
otherwise. This fact was
known in 1958.39,40
Experiments from Florida
Hospital Institute of
Translational Research shows
that blood clots are often
caused by biochemical
factors contained in small
cancerous tumours, like TF
(Tissue Factor), that is otherwise
found only in normal
tissue − not in the blood −
that normally causes clotting
only from vascular injury.
When cancer cells carrying
TF enter the blood, small
clots are formed on the
cancer cell’s surfaces. The
blood platelets, which are
small cells that stick to
injured blood vessels to help
prevent blood loss, then stick
to the clot-covered cancer
cell. This sticky 'sandwich' of
cancer cell, blood clot and
platelets is able to stick to the
inside of the blood vessel
wall. A clot provides a “safe
haven” for the cancer cell,
giving it the time it needs to
squeeze between the cells
that line the blood vessel and
escape into the tissues, where
it can multiply into a
secondary tumour.
AA is important to counteract
cancerous clotting and CAD
Humans obtain arachidonic
acid (AA) either ready-made
in food or from the parent
omega-6, if it is unadulterated.
AA is not harmful: it is the precursor to prostacyclin
– the most potent antiaggretory
agent (natural
“blood thinner”) and
inhibitor of platelet adhesion.
41 Lowering esterified
LA through the lowering of
LDL cholesterol automatically
decreases the body’s
natural anti-aggretory AA.41
In view of the above, this is
a very bad effect as it will
directly lead to increased
risk of a blood clot and ultimately
contracting cancer
(and CAD).
Atherogenesis, adulterated
PUFAs, and LDL cholesterol:
More connections
The eminent researcher HM
Sinclair published his
finding that PEO deficiency
causes an enormous permeability
increase in skin
along with increased capillary
fragility.42 We will use
this information and
connect it to the vascular
system in an unexpected
way.
Intima is 100% parent omega-6
We need to know the innermost
arterial layer, the intima, is epithelial tissue
which is 100% parent omega-
6; there is no omega-3 in
skin.43,44 The delicate intima
requires unadulterated
parent omega-6 and doesn’t
get enough because of
surplus adulterated fats or
because statins decrease LDL
cholesterol, which transports
the parent omega-6 and
lowers the associated LA to
hypo-oxygenating, cancercausing
levels.
The authors of the
following journal article
understood the Parent
Essential Oil connection in
1982, but few of us heard
the news reported in British
Medical Journal45 in 1982
that LA and most polyunsaturated
fatty acids,
including AA and EPA,
were found to be lower
(depleted) in heart attack
victims. Their conclusion
was that the fatty acid
patterns of the phospholipids
[PEOs] constitute an
independent risk factor for
heart disease.
Commentary
This BMJ article “hits the
nail on the head”.
Deficiency of PEOs is associated
with increased heart
attack risk. Don’t think that
the solution is to minimise
parent omega-6 (along with
parent omega-3), because of
“oxidation” concerns. It is
true that, in part, fats and
oils oxidise for energy.
Normal oxidation of fatty
acids (for energy production)
proceeds in the mitochondria
via beta oxidation
after activation by acyl-CoA
synthetase.
Adulterated parent
omega-6 deposits in cell
membranes lead to
abnormal oxidation –
oxidation from adulterated
oils at the site of vascular
injury causing injurious
inflammation. Abnormal
oxidation involves formation
of hydroperoxides from
the double bonds of the
PEOs. This harmful partial
oxidation involves no energy
(ATP) production.
All cells oxidise fuels for
energy and this is a normal
process. However, food
processing oxidises PEOs
prematurely forming
nonfunctional foods which
cause vascular injury and
destroy the body’s inherent
repair mechanism.
The solution
Ensure that patient’s diet
contains generous amounts
of unadulterated PEOs with
a ratio of LA:ALA greater
than 1:1 and less than 2.5:1
by eating unadulterated,
unprocessed foods. To make
simpler and easier with
noncompliant patients,
patients should consider
supplements.46
Have patients minimise
foods containing significant
amounts of trans fats
(hydrogenated), interesterified
fats, and other adulterated
hypo-oxygenating fats.
My research strongly
supports the (prophylactic)
use of an unprocessed
organic supplement with a
ratio of parent omega-6 to
parent omega-3 of between
1:1 and 2.5:1. With this
ratio, suggested use is 725
mg per 18 kg of body weight
(e.g. 3 grammes for a 72.5-
kg. person on a daily basis).
I term this the “Peskin
Protocol.” For an in-depth
analysis of how this specific
ratio is determined see “The
Scientific Calculation of the
Optimum Omega-6/3 Ratio,” at
www.CambridgeMedScience.org.
(“Optimum PEO Ratio”) or
www.BrianPeskin.com (“EFA
Report”).
The Author
■ Brian Peskin is the
primary contributing
medical researcher at the
Cambridge International
Institute for Medical Science
(www.CambridgeMedScience.org).
He has exclusively devoted
the past five years to the
cause and solution of
cancer. This article is based
on information in The
Hidden Story of Cancer,
written by Brian Peskin with
clinical researcher Amid
Habib, MD, FAAP, FACE.
This book is available from
Pinnacle Press, P.O. Box 56507,
Houston, Texas 77256, USA, or
by phoning +1-713-979-0065
internationally.
Brian Peskin earned his
Bachelor of Science degree in
Electrical Engineering from
Massachusetts Institute of
Technology (MIT) in 1979.
He founded the field of Life-
Systems Engineering Science
in 1995. Peskin was
appointed adjunct professor
at Texas Southern University
in the Department of
Pharmacy and Health
Science from 1998-1999.
Peskin combines theory
with practicality in a very
unique way. He is the first to
acknowledge he is often
the messenger of the information
already published
in leading medical textbooks
and medical journals.
His unique insights
have on occasion led a few
malcontents to label him a
“quack”.
● For more information visit
www.BrianPeskin.com and
www.CambridgeMedScience.org.
■ David Sim, MD is a
leading cardiologist practicing
in Boise, Idaho, USA.
■ Amid Habib, MD is a
leading endocrinologist practicing
in Orlando, Florida, USA.
■ Special thanks to Debra Peskin, Pharm. D., Marissa
Carter, PhD, and Daveda
Lamont for their assistance
in this article.
BusinessWeek published
this article – 17 January 2008 –
“Do Cholesterol Drugs Do Any Good” suggesting that the benefits of
statins are overstated.
Brian Peskin had this article published in Medical Hypothesis in
2007.
Chronic cellular hypoxia as the prime cause of cancer: What is the
de-oxygenating role of adulterated and improper ratios of
polyunsaturated fatty acids when incorporated into cell membranes?
Read it here…
http://cambridgemedscience.org/articles/medhyp-08.pdf
References
1. Guyton A, Hall J. Textbook of
Medical Physiology. 9th ed. Philadelphia, PA: W.B. Saunders; 1996:873.
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Date
of upload: 22nd Jan 2008
