The Peskin Primer - Succesboeken

The Peskin Primer 

Understanding Professor* Peskin’s Approach 

The Perfect Ten — Ten Years in Ten Pages 

A decade of work by Prof. Brian Peskin 

Pages 1 - 10 

Relative Risk — Absolute Deception 

Why “Studies” are Misleading—Studies Aren’t Science 

Pages 11 - 25 

* Brian Peskin received an appointment as an Adjunct Professor at Texas Southern University in the 

Department of Pharmacy and Health Sciences (1998-1999).

The Perfect Ten — 10 Years in 10 Pages: 

A decade of work by Prof. Brian Peskin 

The world’s leading physiologic EFA expert — Prof. Brian Peskin 

Prof. Brian Peskin is a world-leading scientist 

specializing in parent EFAs — termed PEOs — and 

their direct relationship to both cancer and 

cardiovascular disease. While advancing the scientific 

understanding of the role of essential fatty acids in the 

body’s metabolic pathways, he has concurrently 

developed a means for alleviating cancer’s prime cause, 

as postulated by Nobel Prize-winner Otto Warburg, 

M.D., Ph.D., by increasing cellular oxygenation (The 

Hidden Story of Cancer, www.pinnacle-press. 

com). Amazingly, there is a fundamental cancer / 

heart disease connection, whereby the same physiologic solution solves 

both conditions. This information will lead to a new understanding of how 

to treat and prevent both cancer and heart disease. The basis for Peskin’s 

current work, grounded strictly in state-of-the-art science — in particular, 

physiology — can be found in his seminal work and peer-reviewed medical 

journal articles. Clinical physicians throughout the world have validated 

Prof. Peskin’s EFA recommendations. In the most exciting development to 

date, Brian’s theoretical conclusions were recently and completely validated 

in a physiological experiment by precise instrumentation capable of 

measuring arterial compliance. This experiment (IOWA experiment) 

provided the first conclusive clinical proof and validation of Prof. Peskin’s 

theory. Peskin Pharmaceuticals has a patent pending on the medicament 

that embodies this development. 

What is a Parent Essential Oil (PEO)? 

There are only two (2) essential fatty acids, LA (parent omega-6) and 

ALA (parent omega-3). They MUST come from food. To work properly, 

they MUST be NOT heated, chemically unprocessed, organically raised 

and processed to guarantee full physiologic functionality. Fast foods 

use adulterated, non-functional EFAs that can no longer be termed a fully 

functional parent essential oils. All other EFAs excluding ALA and LA 

are correctly termed EFA “derivatives.” This includes the most common 

derivatives such as AA, DHA, EPA, etc. What is not understood by most 

physicians is that derivatives are made in the body, from the parent EFAs, 

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on an “as needed” basis in extremely limited quantities. Consumption 

of derivatives from food is therefore not necessary, yet fish oil consists 

entirely of DHA and EPA in supra-pharmacological OVERDOSES, thereby 

overdosing the patient and causing damage instead of health. Few, if any, 

physicians ask to see the “normal standard” values of physiologic DHA/ 

EPA amounts in tissue and plasma compared to the parent PEO amounts 

in tissue and plasma. When they discover the truth of how little DHA and 

EPA there should be in relation to how much they’ve been administering, 

physicians are shocked and dismayed that they have been (unknowingly) 

harming their patients, and wish to correct their recommendation to Peskin 

Protocol PEOs (as per the above physician testimonials). Peskin Protocol 

PEOs are a (patent-pending) plant-based proprietary formulation unlike 

any in the world and can be obtained organically from precise mixtures 

of sunflower, safflower, pumpkin, and evening primrose seed oils and 

coconut oil. 

IOWA (Investigating Oils With respect to Arterial blockage) Experiment 

This is the first experiment using photoplethysmography to detail the 

differences in arterial flexibility between subjects taking PEOs and those 

taking fish oil. The results were staggering and shocking for those unfamiliar 

with Peskin’s work. IOWA is the first experiment conclusively proving the 

INFERIORITY of fish oil to PEOs as regards cardiovascular protection. 

The IOWA experiment (whose testing center is in Des Moines, Iowa) is run 

under the direction of Prof. Peskin (of Houston, Texas) in conjunction with 

renowned interventional cardiologist David Sim, M.D. (of Boise, Idaho). 

Long-term PEO supplementation in patients presenting with a broad 

spectrum of maladies resulted in: 35 subjects, 13 male and 22 female, aged 35- 

75. The median age was 62 years old. These volunteers were supplemented 

with plant-based essential fatty acids of the Peskin Protocol formulation for 

a period of 3 months to 48 months. 

The median duration of use was 24 months. Half of the subjects used the 

PEO formulation for less than 24 months and half used it for more than 

24 months. Twenty-five of the subjects improved their arterial flexibility. 

That’s a stunning 73% effectiveness (absolute — not relative). The average 

improvement was a 9 year decrease in biological arterial age, making 

their effective age younger than their physical age. 

What is outstanding is the NNT (number needed to treat to see an effect 

in just one person) was 1.4. Pharma considers an NNT of less than 50 a 

good result for the effectiveness of their drugs. For example, for statins, the 

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NNT to “prevent” one cardiovascular event is >80. That means more than 

80 people would need to take a statin to see a single positive outcome. In 

contrast, just 1.4 people taking parent essential oils are required to see a 

positive outcome in 1 person. The statistical significance of the experiment, 

according to Alex Kiss, PhD, a statistician who has worked as consultant to 

the National Institute of Health (NIH) and is co-author of numerous peerreviewed 

medical journal papers, including New England Journal of Medicine 

and Cancer, is extremely high (99.85%), compared to most studies, which 

come in at only 95%. This experiment is 30 times more accurate than the 

average clinical study. That means the results can’t be due to chance or 

error. The mean (average) arterial (biological) age of the subjects dropped 

over 8.8 years — making each of them in effect a younger patient! 

Predictable failure of fish oil 

In a completely different group of subjects, fifteen (15) subjects (7 males and 

8 females aged 46-74, average age was 60 years old) were consuming fish 

oil supplements for at least 6 months prior to switching to PEOs. Baseline 

analysis was performed prior to switching to PEOs. After an average time 

duration of PEO use of only 3.5 months, another scan was performed. 

Thirteen (13) of the 15 patients improved. That’s an 87% effectiveness 

rate, a NNT of only 1.2, and a reduction in biological arterial age of 11.1 

years, measured by standard population samples. One subject remained 

unchanged, and one subject worsened (by a mere 1 year, which is statistically 

irrelevant). The statistical significance was 99.99%. CONCLUSION: you 

can take this result “to the bank.” 

It gets even more exciting. In subjects with high cholesterol, simply 

replacing their fish oil with PEOs improved 6 of the patients. Here the 

NNT to improve the vascular system in those with high cholesterol was 

an incredible 1.2. One subject with both diabetes and high cholesterol 

improved. Again, statins would need more than 80 people treated to effect 

one less cardiovascular event, an NNT of 80 (at best, as some studies show 

statins have an NNT of 300+). In two patients on statins, both improved 

their arterial flexibility by 20 years with the PEO formulation. Here, we 

have a group of people across all walks of life – no special groups were used 

and no particular groups were excluded. Using fish oil, the biological mean 

(arithmetic average) arterial biological age was 49. After using PEO, it fell 

to 38 — 11 years YOUNGER. CONCLUSION: compared to PEOs, fish oil 

worsens the cardiovascular system. 

3

Fish oil (and krill oil) don’t work in clinical practice 

(despite most everyone saying they do) 

Sometimes, ingrained beliefs, even those without scientific foundation, are 

hard to change. As has occurred with many other nutritional supplements 

once in the limelight, there is little, if any, scientific validity to fish oil 

and krill oil’s miraculous claims. It is simply another case of “finance 

masquerading as science”— in this case, developing new markets for fish 

— and of medicine’s long history of mistakes and wrong recommendations. 

Making money is fine when you truly help people, but not when you harm 

them, even unknowingly. Results consisting of mere “associations,” and 

“studies“ conducted without valid experiments in which only one variable 

is changed at a time are meaningless. That’s why the recommendations 

from most “studies” are later reversed and withdrawn, which leaves the 

lay public confused. 

In sharp contrast, the IOWA experiment is definitive and remarkable in 

proving PEOs increase arterial compliance (flexibility). When physicians 

hear of IOWA, they realize this information is irrefutable because these 

results, unlike those of other “studies,” are not open to interpretation; the 

machine output of photoplethysmography is akin to measuring one’s weight 

with a scale. IOWA’s landmark results afford a unique and significant 

opportunity. Melatonin was hailed decades ago as a “wonder supplement,” 

then faded into obscurity because its benefits were never based on science. 

IOWA’s results are based solely on science and the positive results are 

predicted theoretically. These results, like gravity, are here to stay. 

Fish oil supplements were an initial attempt at correcting EFA deficiencies 

due to the widespread consumption of processed foods, but its constituents 

are far from being correct physiologically for most tissue. In fact, contrary to 

helping patients, fish oil is harmful for most patients. With today’s stateof-the-art 

science spearheaded by Prof. Peskin, we can move far beyond fish 

oil and significantly improve patient outcomes. PEOs’ significant positive 

effects in increasing cardiovascular compliance (increased arterial 

flexibility) compared to fish oil — IOWA experiment — resulted in an 

11.1-year biological age improvement (a younger patient). The following is 

a representative sampling of international physicians using Peskin Protocol 

PEOs instead of fish oil: 

“Having implemented EFA supplementation for over 25 years, 

clinical results were mediocre until I began using the Peskin 

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Protocol. Dr. Rudin’s work with flax oil was important but 

lacked clinical effectiveness; likewise with Horrobin regarding 

GLA from Borage, Black Currant, and Evening Primrose oils. 

Unlike the studies suggested, fish oil, too, was disappointing. 

Finally, I read The Hidden Story of Cancer, which introduces 

the Peskin Protocol. Once implemented, I experienced clinical 

success. Although Brian’s book deals extensively, but not 

exclusively, with cancer prevention, utilizing his protocol I 

have seen positive results (dermatological, cardiovascular, 

pediatric, and neurological) in over 100 of my patients.” 

Abram Ber, M.D., Homeopathy 

(Phoenix Scottsdale, AZ) 

“As a practicing cardiologist, I have a strong interest in both 

the treatment and prevention of cardiovascular disease. As 

Brian details, the paramount discovery by Otto Warburg 

regarding oxygenation must also be considered the most 

important physiologic discovery in the cardiovascular disease 

arena. Brian has advanced the basic science principles 

of Warburg into a practical, cost-effective formula – the 

Peskin Protocol – for patient care utilizing an increased 

scientific understanding of Omega-6 and Omega-3 essential 

fatty acid ratios. For those patients in my practice, and 

others I am aware of (hundreds) willing to embrace 

these basic principles, I have seen clinical improvement 

and success without adverse effects. Brian Peskin, in my 

opinion, has diligently and carefully “teased out” from the 

available, published scientific data base the links necessary 

to explain, understand, and help combat the most prominent 

cardiovascular state faced by patients.” 

David Sim, M.D., Interventional Cardiologist (Boise, ID) 

“I have been using the Peskin Protocol EFAs for the last 

five months. I have had excellent reports from patients. 

Previously, I was recommending fish oil to almost all my 

patients. Some improved, specifically those with joint pains 

and heart disease. However, I did not see any improvement 

in my diabetic / HTN patients or those w/dermatologic 

problems. In fact, the latter group actually got worse. These 

patients had eczematous type rashes and psoriasis. After 

reviewing Brian’s data regarding the concentration ratios of 

parent Omega-6 to parent Omega-3 in various tissues, it all 

made sense – five out of six (83%) of my worst dermatologic 

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cases showed good to very good improvement in as little 

as three months with Peskin Protocol. Just taking Omega-3 

alone (flax or fish oil) without regard to the appropriate 

balance can adversely affect diabetic patients. This was 

proven in two of my patients. These patients kept meticulous 

effect of diet on their glucose levels. Without changing their 

diets, they noticed significant elevations in the glucose 

levels after Omega-3 fatty acids for three to four months; 

one patient had an increase of 40 points. After starting the 

proper balanced blend of parent Omega-6 and -3, not only 

did their BS normalize to more normal values, but they felt 

better overall and both commented that their energy level 

improved. Use of the Peskin Protocol in clinical practice 

has made a strong believer out of me, and I will continue to 

recommend this product to ALL my patients and refer them 

to Peskin’s research for more information.” 

Angelo A. Della Pietra, M.D., D.O., Family and Integrative Medicine 

(Poughkeepsie, New York) 

“I had been taking high-dose fish oil for many years in an 

attempt to prevent C-V disease and retard inflammation. 

However, I noticed that my fasting blood sugars were always 

in the high range (100-115) and measurements of oxidative 

stress also reflected high levels. No one could explain it since 

my hemoglobin a1c always stayed low. Since switching to 

the parent EFAs (PEOs), as recommended in The Hidden 

Story of Cancer, my FBS came down to 84. My lipids also 

looked better than ever. I think many of our colleagues do 

not appreciate the dangers of high dose fish oil. Derivative 

EFAs like fish oil easily oxidize, and although some surrogate 

markers may improve, the final cost is still unknown. Thanks 

so very much for your book.” 

A4M Fellowship physician Ira L Goodman, M.D. 

Ophthalmic Surgeon (retired), Holistic Medicine 

“Impeccable research and novel insights of sheer genius. 

Brian’s accomplishment is singular - no groups, no public 

money, only elegant science showing how proper use of EFAs 

is the missing link for practical application of Otto Warburg’s 

discovery. This knowledge is priceless for your future 

health.” 

Brian N. Vonk, M.D., Board certified: Internist, Cardiologist 

and Radiologist (Norfolk, Nebraska) 

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“This information could prove to be one of the most significant health 

discoveries of the 21st century. It is extraordinary. Finally, an effective and 

practical program of cancer prevention. Brian Peskin has put together a 

program that must be called ‘brilliant.’ It is a must... for all.” 

Stephen Cavallino, M.D., Emergency Physician, Prototherapy Specialist, 

(Reggio Emilia, Italy) 

How and why PEOs work when omega-3 derivative fish oil 

doesn’t work? 

Physiology is the prime science utilized to determine the correct tissue amounts of parent 

omega-6, parent omega-3, and their derivatives. Once these values are known, biochemistry 

may then be utilized. Fortunately, these physiologic values have already been determined, 

making it immediately obvious why fish oil can’t possibly work as claimed because, aside 

from the brain and nervous system, the body has little use for DHA/EPA. The prime 

issue that everyone overlooks is that the body can easily supply the brain and nervous 

system with adequate parent PEOs without the risk of overdosing on EPA/DHA. There is 

a maximum of

Amounts of EPA/DHA in fish oil 

It is common amongst fish oil capsule manufacturers to have in excess of 300 mg of EPA 

and over 200 mg of DHA, with insignificant amounts of other omega-3 derivatives. They 

typically recommend 2 capsules each day for a total of over 600 mg EPA and 400 mg 

DHA daily. Three grams of PEOs per day is the general prophylactic dosage. Therefore 

the amount of parent omega-3 (ALA) is approximately 1,000 mg. Given that 2% maximum 

of this would be converted into the omega-3 derivative DHA, that would mean the body 

would naturally convert only 20 mg to DHA. Contrast this with the fish oil dosage of more 

than 400 mg, i.e., a DHA pharmacological overdose by a factor of 20! EPA overdose is 

even worse, as only 0.26% of ALA is normally converted. Of the 1,000 mg of ALA in Peskin 

Protocol PEOs, just 2.6 mg is converted, whereas the fish oil supplement provides over 

600 mg or a 250-fold pharmacological overdose of EPA. This is analogous to giving the 

patient 250 aspirin tablets — you would kill him! Krill oil has less of the overdose amounts 

(approximately 130 mg EPA and 70 mg DHA per capsule) but it is still quite harmful. 

Given these facts, is it any wonder that fish oil categorically fails in experimental tests? No, 

of course not. Recommending these pharmacological overloads without compensating 

PEOs or omega-6 based derivatives is even worse, because of the gross disparity between 

the omega-6 and omega-3 series derivatives. Fish oil is harmful to most patients and the 

IOWA experiment proves its enormous NEGATIVE effect in the cardiovascular area. 

Photoplethysmography (PTG) / Digital Pulse Analysis (DPA) and 

why I trust it 

Photoplethysmography (PTG) is a noninvasive method to measure arterial 

compliance (flexibility). Processing of this waveform by digital pulse 

analysis (DPA) affords clinicians a superb diagnostic tool. “Hardening 

of the arteries” is a prime cause of heart disease. Therefore, reversing or 

eliminating hardening of the arteries leads to significantly less patient heart 

disease. A digital pulse analyzer (DPA) can measure arterial flexibility. This 

device is simple. You put your finger in a plastic clip. It emits a soft laser 

light into your fingernail, much like an oxygen analysis with the common 

pulse oximeter. The waveform it reads is an incredibly accurate measure 

of the elasticity (or stiffness) of both your large (aorta) and small arteries of 

8

the cardiovascular system. Arterial rigidity is a direct reflection of arterial 

damage and arteriosclerosis. Computer software analysis allows simple 

and precise computation of the speed and volumes of the blood along with 

the associated waveforms over time. Mathematically, second derivatives (a 

tool of calculus) of the PTG waveforms are then taken to produce another 

waveform termed an accelerated plethysmograph (APG). This output is 

compared with outputs of known population values so it is easy to provide 

a “biological age” of the arteries based on already scanned populations. 

Supplementation with PEOs resulted in substantial improvement in arterial 

flexibility — i.e., a younger patient. 

Flax, krill, and coconut oils ... Aren’t they good? 

Flax oil contains much more parent omega-3 than omega-6 — a backwardsphysiologic 

ratio. Krill oil is in the same category as fish oil. Furthermore, 

no human would ever naturally eat krill, as it is a food for whales, seals, 

penguins, squid, various fish, and sea birds, not humans — as they are simply 

9

too small to bother with. Most of the krill catch is used for aquaculture and 

aquarium feeds, as bait in sport fishing, or in the pharmaceutical industry. 

Coconut oil is not unhealthful, but contains very few PEOs (

Appetite 

• Less Cravings 

• Less Hunger 

• Better Appetite 

Fulfillment 

Heart Health 

• Flexible Arteries 

• Clean Arteries 

• Fast Blood flow 

• Lower Blood Pressure 

• Improves Lipids 

Beauty 

• Healthier Skin 

• Less Dandruff 

• Less Cellulite 

• Healthier Hair 

• Eczema Improved 

Diabetes 

• Less Sweet Cravings 

• Lower Blood Sugar 

• Less Neuropathy/ 

Retinopathy 

PEOs 

SUPPORT 

Anti-inflammation 

• Less Arthritis 

• Less Joint Pain/Swelling 

• Faster Healing 

Hormones/Endocrine 

• Better Sexual Function 

• Smoother Pregnancies 

• Less PMS 

• Fewer Headaches 

Brain Health 

• Better Clarity 

• Better Focus 

• Improved Memory 

• Helps Improve 

ADD & ADHD 

Endurance 

• More Energy 

• Less Fatigue 

• Greater Intensity 

• Faster Recuperation 

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Why “Stuides” Are Misleading—Studies Aren’t Science 

This report was developed to assist physicians and health care professionals 

in their evaluation of treatment protocols. It also serves as a response to the 

following question: 

How Can Professor Peskin Be Right and Everyone Else Wrong? 

I am frequently asked, “How can you be right, and everyone else wrong?” 

This is a valid question. First, everyone else is not “wrong.” There are others 

who understand and report on the pharmaceutical companies’ statistical 

misrepresentations, but they are typically overlooked by the media. I 

am not alone in exposing the fallacies behind many pharmaceutical and 

nutraceutical “successes.” In particular, world-renowned physician, 

mathematician and statistician John P.A. Ioannidis, MD, DSc, is a prominent 

colleague who has been questioning the “massaged” pharmaceutical 

statistics for many years. 

I am right in my scientific conclusions because, like Dr. Ioannidis, I 

follow the science and only use studies to confirm where the sciences of 

human physiology and biochemistry lead. I also understand the science of 

statistics and am not easily fooled by its often-improper use by those more 

interested in finance than accuracy. But physicians and health researchers 

are overworked and have precious little time to do their own research and 

analysis of the latest “breakthrough” study. They need to be able to rely 

upon studies published in the professional journals. 

Sharon Begley’s insightful Newsweek article, “Why Almost Everything 

You Hear About Medicine is Wrong,” which cites Dr. Ioannidis’ findings, 

was published in the January 31, 2011 edition on pages 8-9. Prepared to be 

shocked: 

• “But what if wrong answers aren’t the exception but the rule? More 

and more scholars who scrutinize health research are now making 

that claim. 

• “…[T]he very framework of medical investigation may be offkilter, 

leading time and again to findings that are at best unproved 

and at worst dangerously wrong. 

• “The result is a system that leads patients and physicians astray— 

spurring often costly regimens that won’t help and may even harm 

you. 

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• “As the new chief of Stanford University’s Prevention Research Center, 

Ioannidis is cementing his role as one of medicine’s top mythbusters. 

‘People are being hurt and even dying’ because of false medical 

claims, he says: not quackery, but errors in medical research . 

• “But if Ioannidis is right, most biomedical studies are wrong. [Note: Dr. 

Ioannidis is very right!] 1 

• “In just the last two months, two pillars of preventive medicine fell. 

• “A major study concluded there’s no good evidence that statins 

(drugs like Lipitor and Crestor) help people with no history of 

heart disease. The study, by the Cochrane Collaboration, a global 

consortium of biomedical experts, was based on an evaluation of 

14 individual trials with 34,272 patients. Cost of statins: more than 

$20 billion per year, of which half may be unnecessary. [Note: 

This evaluation did not even consider the negative side-effects 

unnecessarily experienced by the unsuspecting patients.] 

• “‘Negative results sit in a file drawer, or the trial keeps going in 

hopes the results turn positive.’ With billions of dollars on the 

line, companies are loath to declare a new drug ineffective. As a 

result of the lag in publishing negative studies, patients receive a 

treatment that is actually ineffective. That made Ioannidis wonder, 

how many biomedical studies are wrong? 

• “His answer, in a 2005 paper: ‘the majority.’ From clinical trials of 

new drugs to cutting-edge genetics, biomedical research is riddled 

with incorrect findings, he argued. Ioannidis deployed an abstruse 

mathematical argument to prove this, which some critics have 

questioned. [Note: I found his proof unquestionably correct.] 

• “Stanford, the epitome of the establishment, hired him [Dr. Ioannidis] 

in August to run the preventive-medicine center. ‘The core of 

medicine is getting evidence that guides decision making for patients 

and doctors,’ says Ralph Horwitz, chairman of the department of 

medicine at Stanford. ‘John has been the foremost innovative thinker 

about biomedical evidence, so he was a natural for us.’ 

1. When I was working on my undergraduate thesis at M.I.T., I derived a different result than one 

reported in a top science journal. Naturally I thought I was wrong, but I wasn’t wrong. To my 

surprise, my thesis adviser told me that 95% of the published journal articles are WRONG. As a 

young student, I was shocked and appalled! When it comes to the next “miracle” product, you 

should approach the journals with a healthy dose of skepticism 

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“Ioannidis’s first targets were shoddy statistics used in early genome 

studies. [Note: See the report, “Good News: It’s Not Genetic” at www. 

brianpeskin.com.] 

• “‘When you do thousands of tests, statistics says you’ll have some 

false winners,’ says Ioannidis. 

• “Drug companies make a mint on such dicey statistics. By testing 

an approved drug for other uses, they get hits by chance... 

• “Even when a claim is disproved, it hangs around like a deadbeat 

renter you can’t evict.” 

(Emphasis added.) 

I warned you in advance that you’d be shocked to discover this deception. 

Now, I will give you the tools so that you will never be fooled again. 

Deceptive Statistics Mislead Patients… 

• Recently, a physician colleague told me that there were over fifteen 

thousand — that’s correct, 15,000 — studies showing fish oil’s 

effectiveness. My first response was laughter. 

• The next day, a close friend of my wife told her she needed to take 

calcium because it decreased risk of colon cancer by 40%. She went 

on to explain that because she was taking it, and my wife was not, 

that she had a 40% lower risk of contracting colon cancer. Again, I 

started laughing… 

• Later in the week, another physician colleague told me statins 

decrease the chance of a heart attack by over 30%. You’ve likely 

guessed it… more uncontrollable laughter. We shall soon discover 

why, but first let’s explore the reasons for the absurd number of 

repetitive studies. 

Startling Revelation: The number of studies is inversely 

proportional to the effectiveness of what is being studied. 

There should not be a need to keep repeating studies 

unless the substance being studied doesn’t work; if you 

do this, you are trying to get random chance 

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to back up your study, rather than science 

confirming its effectiveness. This is precisely 

the reason why there may be 1,000 studies showing a 

positive result and 950 showing a negative result, yet 

the “positives” are considered to prevail. Physicians will 

actually say this slight preponderance “proves it works.” 

This is dreadfully WRONG and shows an enormous 

lack of scientific reasoning by the health and medical 

professions, because they have no idea of where the 

science is leading them. Experimental results MUST 

CONFIRM science‘s prediction, not be counter to it. 

How we become misled is described below. 

Is Gravity Confirmed on a Weekly Basis? 

How many experiments have been recently done confirming gravity? None. 

It was proven hundreds of years ago, and a small number of scientists 

confirmed its mathematical effects, resulting in proven theorems such as 

that showing the relation between how much distance is traveled versus 

the length of time an object drops when released from the top of a tall 

structure. Case closed. Contrast this to fish oil’s reported 15,000 studies. 

Consider why so many studies need to be done IF it really works. When 

you hear terms like “1,000 studies show…” simply ask, “why so many?” 

You are being deceived. 

When a study or, better yet, an experiment (which has just one highly 

controlled variable), is conducted, the result is either significant in 

EFFECTIVENESS — working very well on the vast majority of patients — 

or it isn’t. Then, if you want to double check, another group performs the 

same experiment ONCE more, to confirm it. That’s it. (As an example of 

both high effectiveness and high significance see www.brianpeskin.com for 

the IOWA Experiment.) 

Before any experiment is conducted, one should have a good idea of what the 

result will be based on established physiology and biochemistry. This was 

conveyed to me while a student at Massachusetts Institute of Technology 

(MIT). The experiment should merely CONFIRM the SCIENCE. 

As a prime example, take fish oil. The simple reason for so many “studies” 

is that it simply doesn’t work as we are led to believe. Fish oil doesn’t work 

because it can’t work. It can’t work because there are no significant metabolic 

pathways that omega-3 EFA derivatives influence that could possibly give 

15

those supposed “extraordinary” results (see www.brianpeskin.com for 

“Fish Oil Fallacies” report). A quick review of physiology (see ”Fish Oil 

Fallacies” at www.brianpeskin.com) tells us why it can’t work — humans 

don’t live in frigid cold waters like most fish do. EPA/DHA oxidize (turn 

rancid and spoil) automatically at room temperature and oxidize even more 

rapidly at body temperature. 

Physicians are in an Unfortunate Situation 

Physicians want to help their patients. As a result, they are often quick 

to dismiss failure or harmful side effects in order to give something to a 

suffering patient. As a recent example, physicians often told patients that 

side effects such as muscle weakness, cognitive impairment, decreased 

sexual desire, etc., did not occur from statin use. After 10 years of steadfastly 

denying that these harmful side effects existed, physicians recently had no 

choice but to acknowledge them. 

Clear thinking is required of today’s medical 

researchers; unfortunately, it doesn’t often occur. 

“The scientists of today think deeply instead of clearly. 

One must be sane to think clearly, but one can think 

deeply and be quite insane.” 

Nicola Tesla 

Finance Masquerades as Science….The Ultimate Tragedy 

To compound the problem, finance often masquerades as science. Nutritional 

companies and pharmaceutical companies often mislead both physicians 

and their patients while chasing profits. Instead of measuring the outcome 

directly, such as fewer heart attacks or less cancer, “surrogates” are used. A 

surrogate is a substitute measure assumed to be associated with the desired 

outcome. This consistent mistake often leads to the tragedy of more failure. 

For example, doctors and researchers concentrate on lowering cholesterol 

rather than studying the ultimate objective of decreased heart attacks. There 

is an assumed relationship. However, this is not backed up by the science: 

while drug companies have done a wonderful job of discovering cholesterollowering 

drugs, this has unfortunately not translated into fewer heart 

16

attacks. Yet this practice is so prevalent that it has become “conventional 

wisdom” that you are supposed to reduce your (LDL) cholesterol! 

Without being overly cynical, this is done because the latest “wonder” drug 

likely has an effect on the surrogate, without regard to its DIRECT impact 

on the problem at hand. Consequently, the drug-company-led studies focus 

on their drug’s ability to alter the surrogate. 

“Effectiveness” is Interpreted Quite Differently Than Any 

True Scientist Would 

If I were told that taking a drug affords me 40% less risk, then I would assume 

that taking that drug would reduce my risk of contracting said disease by 

40% compared to someone not taking the drug. WRONG. You can’t tell the 

size of the effect unless you know the subject population size. This “40% 

reduction” that you think you have achieved would be what is called an 

“absolute” risk, but all the pharmaceutical studies use “relative” risk 

when reporting statistics. The difference is staggering, and it is virtually 

guaranteed that the real difference, the ONLY one that matters, is FAR 

LESS than the reported percentage. This is illustrated in the example below. 

Absolute Risk vs Relative (“Endpoint”) Risk — A Case Study 

in Tortured Logic 

Question: What is the difference between 2 successes in 1,000,000 (drug) 

vs. 1 success in 1,000,000 (placebo)? 

Drug 

Placebo 

2 patient successes out of vs 1 patient success out of 

1,000,000 patients treated 1,000,000 patients treated 

Answer: The absolute result is 0.0002% vs. 0.0001%, or effectively 0% 

success in both cases―ABSOLUTE FAILURE... 

That is, unless you are part of the pharmaceutical or nutraceutical industry, 

whereby 0% success MAGICALLY BECOMES 50% success. 

Here’s how they deceive you: The calculation they will use is this: Ignoring 

the total number of patients tested, they will say that there is a 50% difference 

in effectiveness of the results (2 to 1). They have deleted the sample size of 

1,000,000 patients. This calculation of 50% is termed “relative” risk because 

the sample size was deleted and only the “endpoints”— the successes in each 

group — are used. There is only one “small” problem with this method of 

reporting the drug’s supposed success—it’s absurd! 

17

Absolute Risk MUST Include Sample Size 

No honest scientist or physician would 

claim a 50% improvement with this drug, 

because the SAMPLE SIZE is not included. 

In the following statin example, 1% “magically becomes 36%,” misleading you 

as to the true, accurate measure of difference in heart attack risk. The TRUE 

EFFECTIVENESS is the difference in results in ABSOLUTE MEASURES 

that INCLUDE SAMPLE SIZE: 3% effectiveness of the statin minus 2% 

effectiveness of a placebo equals 1% effectiveness in absolute terms. That’s 

right, a shockingly low 1% is reported as a much more significant 36%! 

The correct effectiveness is NOT calculated as (3% – 2%)/3% = 33%, which 

the drug companies purposely and deceptively use. 

18

Shockingly, there is a one percent (1%) 

difference in effectiveness between the 

results with Lipitor and the results with 

a placebo. If you were given this information, 

would you take this drug? Of course not. That is, 

IF you knew and understood the TRUTH. 

This miniscule 1% difference is termed absolute risk and correctly takes into 

account the sample size. This leads to NNT (number needed to treat) and 

shows why it is critical when evaluating the effectiveness of a protocol. 

NNT (Number Needed to Treat) is Paramount — Not Misleading 

“Endpoint” Statistics 

Many physicians are misled because they have no idea the pharmaceutical 

companies are allowed to manipulate statistics. Pharmaceutical companies 

shockingly, yet legally, get to remove the sample size. Again, when is one 

patient event in a million (drug) compared to two patient events in a million 

(placebo) equal to 50% improvement instead of the statistically correct 1 in 

1,000,000 or 0.0001%? Answer: with the fanciful “pharmaceutical endpoint 

method,”also termed “relative risk,” as Professor of Medicine Stanton Glantz 

so aptly put in his book. (Glantz SA. Primer of Biostatistics. 5th ed. New 

York, NY: McGraw-Hill, 2002, 149-156.) 

You will often see the statement, “Lipitor reduces the risk of heart attack 

by 36% ... in patients with multiple risk factors for heart disease,” quoted 

in drug ads, such as the one on television a few years back featuring Dr. 

Robert Jarvik, inventor of the Jarvik artificial heart. In newspaper ads, the 

36% comes with an asterisk (*) saying, “That means in a large clinical study, 

3% of patients taking a sugar pill or placebo had a heart attack compared 

to 2% of patients taking Lipitor.” The difference between the treated and 

non-treated groups is a miniscule 1%, hardly worth getting excited about 

UNLESS you are a pharmaceutical or nutraceutical company that has 

already invested hundreds of millions of dollars in this drug and must 

ultimately sell this FAILURE to the desperate masses. 

In the case of statins, the NNT is 100 (the reciprocal of the absolute risk, i.e. 

1/1% = 1/.01 = NNT of 100). No, this “100” isn’t a perfect score you aspire 

to on a college exam; quite the contrary, it is an awful score. It means that 

to see a positive effect in just one patient, one hundred patients have to be 

19

treated, and often treated for many years at that. Therefore, 99 out of 100 

patients will see no positive effect — a 99% FAILURE RATE! Many medical 

researchers are convinced that the real NNT for statins in a standard mixed 

population, such as the typical patient a physician treats for CAD, may be 

closer to 250. Even assuming the lower 100 NNT figure, this is even more 

problematic for statins’ performance because 10% to 15% of statin patients 

experience negative side effects, including sexual dysfunction, muscle 

aches – prominently mentioned on Lipitor’s label – and significant cognitive 

problems, including loss of memory. Be aware that neither the NNT nor 

any of the risk statistics looks at negative side effects. This is an entirely 

separate issue. 

Dr. Nortin M. Hadler, Professor of Medicine at the University of North 

Carolina at Chapel Hill and a long-time drug industry critic, states, 

“Anything over an NNT of 50 is worse than a lottery ticket; there may be no 

winners.” (Carey J., “Lipitor: for many people, cholesterol drugs may not 

do any good,” BusinessWeek. January 17, 2008:52-59.) Even Las Vegas has 

games with a chance of winning greater than 1% or 2%. Shouldn’t drugs or 

nutraceuticals have a higher standard? 

Grasping the Magnitude of the Problem 

Decades old antibiotics commonly have an NNT = 1.1. When 11 people 

are given antibiotics, ten patients are cured of the problem for which the 

antibiotics were prescribed. Contrast this with statins, where 100 patients 

are given the drug and one person is helped; NNT = 100. 

The higher the NNT, the LESS effective the drug. 

If you remember only one point from this report, it should be that the 

intelligence of the answer is directly related to the intelligence of the 

question. Don’t let yourself be misled with shoddy statistics that don’t 

include the critical sample size. 

One Last Critically Important Thought 

When you receive news of the next “miracle” supplement, aside from 

requiring SPECIFIC METABOLIC PATHWAYS and state-of-the-art 

physiologic science supporting these claims, ask yourself: 

20

1. Why is this needed TODAY when it wasn’t needed years ago? 

Take fish oil supplements. People living in 1950 certainly consumed 

significantly less fish oil supplements than we do today; there was only a very 

small market for it. The supposed benefits of fish were not publicized in 

1950, and fish oil supplementation (being highly susceptible to spoilage) 

was simply not as common as it is today. Therefore, we should have seen 

gross pathological disorders due to the deficiency of DHA/EPA found in 

those supplements, which of course we did not. 

• Were there tremendous neurological impairments in the brain, eyes, 

and central nervous system due to low DHA levels? No, and there 

should have been if the supposition were true. 

2. Will taking the supplement stop or reverse conditions it is supposed 

to prevent? 

Regarding fish oil and its huge (supra-physiologic) amount of DHA/EPA, it 

should both prevent Alzheimer’s AND stop the progression of Alzheimer’s 

in patients with low DHA levels. Does it? 

No, in 2010, fish oil FAILED miserably to prevent Alzheimer’s (see www. 

brianpeskin.com, “Fish Oil Fallacy” Special Medical Report). Fish oil 

FAILED to either prevent or to slow the progression of Alzheimer’s. Since 

the same metabolic pathways are used to both prevent and to slow progression 

of any disease, you CANNOT make the absurd claim, as was made in front 

of hundreds of physicians, that fish oil prevents Alzheimer’s, but once you 

have it, fish oil won’t slow its progression. Logic maintains that it is more 

difficult for a substance to prevent a disease (the ultimate “cure”) than for 

a substance to slow progression of that disease. It is illogical to state that it 

will prevent but NOT slow progression. Scientific logic must prevail. 

1. Look at the dosage the supplement provides vs. the amount of food 

that would need to be eaten to provide it. While we are discussing 

fish, do you realize that suggested amounts from the manufacturers 

themselves provide DHA up to 120 times what your body would 

naturally produce on its own, and up to 500 times the amount of EPA 

that your body would naturally produce on its own. Ask what are the 

effects of this tremendous overdosing? 

2. Never rely on mere “associations” from “studies” masquerading as 

experiments (where one controlled variable only is changed). This is 

why one medical and nutritional recommendation after another gets 

REVERSED, like women taking synthetic HRT for its supposed heart 

protection and cancer protection, when in fact the opposite was true. 

(Often you never see the retraction.) 

21

Advanced information for health care professionals (not 

required for the lay public, but included for a more complete 

understanding of this subject) 

What is a “p”-value?” 

Statistics is mathematics and therefore extremely detailed. However, the 

essential concepts you need to know so that you aren’t misled again are 

relatively simple: 

1. The first value looked at by physicians and others (and mistakenly 

too often assumed to be the only important value) is the “p value 

“ or 1 — (p-value), meaning this experimental result occurred by 

chance alone, i.e., the drug doesn’t really work. When the study or 

experiment is repeated many times using the same general group 

of people, this same “successful result” recurs that is entirely due 

to chance alone. The item of interest (drug or nutraceutical) really didn’t 

work at all, but we think it did work. 

2. Typically, the p-value is set to 0.95 (at a 95% confidence level you 

get an inherent 5% allowed possible error rate) for the result to 

be considered “statistically significant.” If p = 0.95 then the study 

would be termed a 95% confidence level study (although a bit more 

information is required). A 0.99 (1% error rate) or 0.995 p-value (0.5% 

error rate) would be even better because there would be much less of 

a random chance effect behaving as though the drug worked when 

it really didn’t, thereby fooling both the physician and patient. With 

p=95%, even if the drug didn’t work, there is a 5% chance that you 

would get these pseudo-positive results 5% of the time, making it 

appear like the drug did work. This 5% means 1 out of 20 times you are 

FOOLED into thinking FAILURE is SUCCESS. 

Once again, a 95% p-value means that if this experiment were carried out 

in the same population sample 100 separate times, then this same result 

would be included at least 95% of the time; this pseudo-positive result 

would occur entirely randomly 5 times, although the drug was a complete 

FAILURE. 

It’s Easy for them to Mislead Everyone… 

22

All a company has to do is to conduct many 

studies and then purposely select only those that 

randomly show a “positive” result. Don’t mention 

the failures, and presto, you have a “successful” 

drug! All you need is lots and lots of money. 

• The p-value is NOT a measure of the size or magnitude of the effect 

of the drug. That is a completely different issue and has to do with 

the means (difference of the averages between both groups). Many 

physicians and patients don’t understand this critical fact and 

mistakenly think that a p-value alone is all that is needed. Wrong. 

• It is true that the MINIMUM p-value should be at least 95%; however, 

even IF the study has a “significant” effect, then one must ask this 

next critical question: 

How Strong is the Effect? A Little or A Lot? 

You need to ask “What is the magnitude of the 

positive effect?” A positive effect can range from a 

very small negligible effect to a tremendous effect. 

What is considered a significant amount or a significant effect? 

If more than 51% (the majority) of a group doesn’t respond IN ABSOLUTE 

NUMBERS (NOT relative measures) to the drug, then I am not impressed, 

and you shouldn’t be, either. Typically today, if just 20% of the treated 

group obtains any positive effect (regardless of how little), it is considered 

a huge success. But this really means 80% FAILURE. 

I am disgusted when substantial failure is transformed, by statistical sleightof-hand, 

into a so-called success. To put this into a real-world perspective, 

an 80% FAILURE rate, whereby buildings collapsed or televisions blew up 

in your face when turned on, would be unacceptable. I hope you would 

concur. 

23

Before I personally would trumpet a drug’s success, at least 80% of the 

subjects IN ABSOLUTE NUMBERS must benefit. Recall that there are 

examples of such high levels of success with drugs: insulin lowers everyone’s 

blood sugars; thyroid hormone decreases everyone’s TSH level; the proper 

antibiotics stop every infection. 

Is the Item Measured Significant, or a Worthless “Surrogate”? 

Low NNT is a necessary, but not an entirely sufficient condition to be 

able to claim victory. Is there a DIRECT cause/effect relationship? This is 

absolutely required or once more, you are being misled. 

To Reiterate: Worthless Surrogates — NOT the Desired Result 

Itself — Are Often Used…The Deception Continues… 

Even though statins lower LDL-cholesterol, heart disease is not significantly 

reduced. The tragic truth was only recently accepted. This still hasn’t 

stopped the pharmaceutical companies and physicians from saying that 

lowered LDL-cholesterol is all that counts. They are WRONG, and patients 

are paying with their lives. 

Therefore, one CANNOT blindly assume that the “disease” is solved when 

a worthless “SURROGATE” is used INSTEAD of measuring the result itself, 

such as how many heart attacks occur with and without statins (the answer is 

the same amount, or even more, occur WITH STATINS). This means that 

statins are ineffective at stopping heart disease. 

A recent example: The JUPITER FAILURE Hailed 

as A Success 

Of course, from the above, it goes without saying that there must first be a 

direct cause/effect relationship to the disease. If you treat 100 patients with 

a drug and all 100 improve, the drug’s number needed to treat (NNT) is 1 

(100 patients/100 successes). If you treat 100 patients and only 1 patient 

responds positively the NNT would be 100 (100 patients treated/1 positive 

response). This is an awful result and equivalent to a 99% failure rate. Dr. 

Nortin M. Hadler, Professor of Medicine at the University of North Carolina 

at Chapel Hill states: “Anything over an NNT of 50 is worse than a lottery 

ticket…” 

Of significant importance is the fact that the 2008 JUPITER study was used to 

try and gloss over the fact that numerous attempts to prove the “cholesterol 

theory” (the lower the patient’s low density cholesterol [LDL-C], the greater 

the prevention of CVD), by attempting to make the case that the real mode 

24

of action of statin drugs was C-reactive protein (CRP) reduction, have 

failed. However, there is one tragic flaw: CRP is not a reliable prognostic 

indicator of cardiovascular events; there are better markers. An article 

entitled Largest-Ever Meta-Analysis Finds CRP Is Unlikely to Be Causal for 

CVD, reports that scientists of the Cambridge-based Emerging Risk Factors 

Collaboration (ERFC) found: 

“[A]lthough CRP concentration was linearly associated with CHD 

(coronary heart disease), stroke, and vascular mortality, as well 

as nonvascular mortality, statistical adjustment for conventional 

cardiovascular risk factors resulted in considerable weakening of 

associations.” 

An Example of How They Fool You 

In the Jupiter Study, the NNT of 240 for 

statins, in preventing any stroke 

(99.58% failure disguised as a hazard 

ratio of 0.52; p = 0.002), was not stated. 

This means that the JUPITER Study had an undisclosed NNT of 240 (99.6% 

FAILURE) for preventing any stroke – instead, a hazard ratio (an estimate 

of relative risk) of 0.52 (appearing as a 52% success) was published, thus 

making the trial appear much more successful than it actually was. 

What appears more impressive? A 0.04 success rate / 99.6% FAILURE rate 

or a 52% success rate / smaller 48% FAILURE rate? Physicians are deceived 

and so are their patients. 

• Always ask for the SAMPLE SIZE, since without it you cannot 

draw any meaningful conclusions. 

• Always ask for the ABSOLUTE RISK DIFFERENCE BETWEEN 

BOTH GROUPS, since without it you cannot draw any meaningful 

conclusions. 

25

CambridgeMedScience.org 

CAMBRIDGE INTERNATIONAL INSTITUTE FOR MEDICAL SCIENCE 

Stephen Cavallino, M.D. - Founder & Chairman (Italy) • Amid Habib, M.D. • David Sim, M.D. • Robert Nemer, D.O. 

THE PHYSICIAN’S CONCISE GUIDE TO: 

- 27 - 


Why “Studies” are Misleading—Studies Aren’t Science 

Copyright 2011 

Dedicated to advancing and publicizing breakthrough discoveries in the health sciences

There is simply no one better in the 21st century at developing 

practical health-related solutions based on the world’s leading medical and 

nutritional science. “Science — Not opinion” is Brian’s trademark. When 

Brian is through explaining a topic it is “case closed!” When he says it, you 

“can take the information to the bank!” 

Unlike most of his peers’ recommendations, Brian’s health and 

nutritional recommendations have stood the test of time. Brian has never 

had to reverse or significantly alter any of his medical reports—reports 

that have tackled everything from the dangers of soy, to the wrongly 

popularized need for fiber in the diet, to his warning about the potential 

harm of supplementing with copious amounts of omega-3. In 1995 he 

published the report “Fiber Fiction” and finally, eleven years later, others in 

research are acknowledging the silliness of recommending fiber in the diet 

of a human being. Brian’s latest crusade is to warn of the dangers of excess 

omega-3 (in particular, fish oil) and how it will lead to increased cases of 

skin cancer. The list goes on and on… 

Brian received an appointment as an Adjunct Professor at Texas Southern 

University in the Department of Pharmacy and Health Sciences (1998-1999). 

The former president of the University said of his discoveries: “...His 

nutritional discoveries and practical applications through Life-Systems 

Engineering are unprecedented.” Brian earned his Bachelor of Science 

degree in Electrical Engineering from Massachusetts Institute of Technology 

(MIT) in 1979. Brian founded the field of Life-Systems Engineering Science in 

1995. This field is defined as The New Science of Maximizing Desired Results 

by Working Cooperatively with the Natural Processes of Living Systems. To 

many, Brian is THE MOST TRUSTED AUTHORITY ON HEALTH AND 

NUTRITION IN THE WORLD. 

Brian continues to be a featured guest on hundreds of radio and 

television shows both nationally and internationally. His sheer number of 

accomplishments during the last decade of the 20th century and into the 21st 

century are unprecedented and uniquely designate him as the #1 authority 

in the world of what really works and why. Forget listening to the popular 

press or most popular so-called health magazines. Their editors simply 

don’t understand the complicated science that they write about — they 

merely “parrot” what everyone else says without independent scientific 

verification. Their recommendations often have no basis in reality of how 

the body works, based on its physiology. 

Brian has dedicated his life to provide the truth — which is almost 

always opposite to what everyone says. Here’s why Brian is the #1 man in 

America to listen to when it comes to your health.

This report was developed to assist physicians and health care professionals 

in their evaluation of treatment protocols. It also serves as a response to the 

following question: 

How Can Professor Peskin Be Right and Everyone Else Wrong? 

I am frequently asked, “How can you be right, and everyone else wrong?” 

This is a valid question. First, everyone else is not “wrong.” There are others 

who understand and report on the pharmaceutical companies’ statistical 

misrepresentations, but they are typically overlooked by the media. I 

am not alone in exposing the fallacies behind many pharmaceutical and 

nutraceutical “successes.” In particular, world-renowned physician, 

mathematician and statistician John P.A. Ioannidis, MD, DSc, is a prominent 

colleague who has been questioning the “massaged” pharmaceutical 

statistics for many years. 

I am right in my scientific conclusions because, like Dr. Ioannidis, I 

follow the science and only use studies to confirm where the sciences of 

human physiology and biochemistry lead. I also understand the science of 

statistics and am not easily fooled by its often-improper use by those more 

interested in finance than accuracy. But physicians and health researchers 

are overworked and have precious little time to do their own research and 

analysis of the latest “breakthrough” study. They need to be able to rely 

upon studies published in the professional journals. 

Sharon Begley’s insightful Newsweek article, “Why Almost Everything 

You Hear About Medicine is Wrong,” which cites Dr. Ioannidis’ findings, 

was published in the January 31, 2011 edition on pages 8-9. Prepared to be 

shocked: 

• “But what if wrong answers aren’t the exception but the rule? More 

and more scholars who scrutinize health research are now making 

that claim. 

• “…[T]he very framework of medical investigation may be offkilter, 

leading time and again to findings that are at best unproved 

and at worst dangerously wrong. 

• “The result is a system that leads patients and physicians astray— 

spurring often costly regimens that won’t help and may even harm 

you. 

1

• “As the new chief of Stanford University’s Prevention Research Center, 

Ioannidis is cementing his role as one of medicine’s top mythbusters. 

‘People are being hurt and even dying’ because of false medical 

claims, he says: not quackery, but errors in medical research . 

• “But if Ioannidis is right, most biomedical studies are wrong. [Note: Dr. 

Ioannidis is very right!] 1 

• “In just the last two months, two pillars of preventive medicine fell. 

• “A major study concluded there’s no good evidence that statins 

(drugs like Lipitor and Crestor) help people with no history of 

heart disease. The study, by the Cochrane Collaboration, a global 

consortium of biomedical experts, was based on an evaluation of 

14 individual trials with 34,272 patients. Cost of statins: more than 

$20 billion per year, of which half may be unnecessary. [Note: 

This evaluation did not even consider the negative side-effects 

unnecessarily experienced by the unsuspecting patients.] 

• “‘Negative results sit in a file drawer, or the trial keeps going in 

hopes the results turn positive.’ With billions of dollars on the 

line, companies are loath to declare a new drug ineffective. As a 

result of the lag in publishing negative studies, patients receive a 

treatment that is actually ineffective. That made Ioannidis wonder, 

how many biomedical studies are wrong? 

• “His answer, in a 2005 paper: ‘the majority.’ From clinical trials of 

new drugs to cutting-edge genetics, biomedical research is riddled 

with incorrect findings, he argued. Ioannidis deployed an abstruse 

mathematical argument to prove this, which some critics have 

questioned. [Note: I found his proof unquestionably correct.] 

• “Stanford, the epitome of the establishment, hired him [Dr. Ioannidis] 

in August to run the preventive-medicine center. ‘The core of 

medicine is getting evidence that guides decision making for patients 

and doctors,’ says Ralph Horwitz, chairman of the department of 

1. When I was working on my undergraduate thesis at M.I.T., I derived a different result than one 

reported in a top science journal. Naturally I thought I was wrong, but I wasn’t wrong. To my 

surprise, my thesis adviser told me that 95% of the published journal articles are WRONG. As a 

young student, I was shocked and appalled! When it comes to the next “miracle” product, you 

should approach the journals with a healthy dose of skepticism 

2

medicine at Stanford. ‘John has been the foremost innovative thinker 

about biomedical evidence, so he was a natural for us.’ 

“Ioannidis’s first targets were shoddy statistics used in early genome 

studies. [Note: See the report, “Good News: It’s Not Genetic” at www. 

brianpeskin.com.] 

• “‘When you do thousands of tests, statistics says you’ll have some 

false winners,’ says Ioannidis. 

• “Drug companies make a mint on such dicey statistics. By testing 

an approved drug for other uses, they get hits by chance... 

• “Even when a claim is disproved, it hangs around like a deadbeat 

renter you can’t evict.” 

(Emphasis added.) 

I warned you in advance that you’d be shocked to discover this deception. 

Now, I will give you the tools so that you will never be fooled again. 

Deceptive Statistics Mislead Patients… 

• Recently, a physician colleague told me that there were over fifteen 

thousand — that’s correct, 15,000 — studies showing fish oil’s 

effectiveness. My first response was laughter. 

• The next day, a close friend of my wife told her she needed to take 

calcium because it decreased risk of colon cancer by 40%. She went 

on to explain that because she was taking it, and my wife was not, 

that she had a 40% lower risk of contracting colon cancer. Again, I 

started laughing… 

• Later in the week, another physician colleague told me statins 

decrease the chance of a heart attack by over 30%. You’ve likely 

guessed it… more uncontrollable laughter. We shall soon discover 

why, but first let’s explore the reasons for the absurd number of 

repetitive studies. 

3

Studies Aren’t Science! 

Startling Revelation: The number of studies is inversely 

proportional to the effectiveness of what is being studied. 

There should not be a need to keep repeating studies 

unless the substance being studied doesn’t work; if you 

do this, you are trying to get random chance 

to back up your study, rather than science 

confirming its effectiveness. This is precisely 

the reason why there may be 1,000 studies showing a 

positive result and 950 showing a negative result, yet 

the “positives” are considered to prevail. Physicians will 

actually say this slight preponderance “proves it works.” 

This is dreadfully WRONG and shows an enormous 

lack of scientific reasoning by the health and medical 

professions, because they have no idea of where the 

science is leading them. Experimental results MUST 

CONFIRM science‘s prediction, not be counter to it. 

How we become misled is described below. 

Is Gravity Confirmed on a Weekly Basis? 

How many experiments have been recently done confirming gravity? None. 

It was proven hundreds of years ago, and a small number of scientists 

confirmed its mathematical effects, resulting in proven theorems such as 

that showing the relation between how much distance is traveled versus 

the length of time an object drops when released from the top of a tall 

structure. Case closed. Contrast this to fish oil’s reported 15,000 studies. 

Consider why so many studies need to be done IF it really works. When 

you hear terms like “1,000 studies show…” simply ask, “why so many?” 

You are being deceived. 

4

When a study or, better yet, an experiment (which has just one highly 

controlled variable), is conducted, the result is either significant in 

EFFECTIVENESS — working very well on the vast majority of patients — 

or it isn’t. Then, if you want to double check, another group performs the 

same experiment ONCE more, to confirm it. That’s it. (As an example of 

both high effectiveness and high significance see www.brianpeskin.com for 

the IOWA Study.) 

Before any experiment is conducted, one should have a good idea of what the 

result will be based on established physiology and biochemistry. This was 

conveyed to me while a student at Massachusetts Institute of Technology 

(MIT). The experiment should merely CONFIRM the SCIENCE. 

As a prime example, take fish oil. The simple reason for so many “studies” 

is that it simply doesn’t work as we are led to believe. Fish oil doesn’t work 

because it can’t work. It can’t work because there are no significant metabolic 

pathways that omega-3 EFA derivatives influence that could possibly give 

those supposed “extraordinary” results (see www.brianpeskin.com for 

“Fish Oil Fallacies” report). A quick review of physiology (see ”Fish Oil 

Fallacies” at www.brianpeskin.com) tells us why it can’t work — humans 

don’t live in frigid cold waters like most fish do. EPA/DHA oxidize (turn 

rancid and spoil) automatically at room temperature and oxidize even more 

rapidly at body temperature. 

Physicians are in an Unfortunate Situation 

Physicians want to help their patients. As a result, they are often quick 

to dismiss failure or harmful side effects in order to give something to a 

suffering patient. As a recent example, physicians often told patients that 

side effects such as muscle weakness, cognitive impairment, decreased 

sexual desire, etc., did not occur from statin use. After 10 years of steadfastly 

denying that these harmful side effects existed, physicians recently had no 

choice but to acknowledge them. 

5

Clear thinking is required of today’s medical 

researchers; unfortunately, it doesn’t often occur. 

“The scientists of today think deeply instead of clearly. 

One must be sane to think clearly, but one can think 

deeply and be quite insane.” 

Nicola Tesla 

Finance Masquerades as Science….The Ultimate Tragedy 

To compound the problem, finance often masquerades as science. Nutritional 

companies and pharmaceutical companies often mislead both physicians 

and their patients while chasing profits. Instead of measuring the outcome 

directly, such as fewer heart attacks or less cancer, “surrogates” are used. A 

surrogate is a substitute measure assumed to be associated with the desired 

outcome. This consistent mistake often leads to the tragedy of more failure. 

For example, doctors and researchers concentrate on lowering cholesterol 

rather than studying the ultimate objective of decreased heart attacks. There 

is an assumed relationship. However, this is not backed up by the science: 

while drug companies have done a wonderful job of discovering cholesterollowering 

drugs, this has unfortunately not translated into fewer heart 

attacks. Yet this practice is so prevalent that it has become “conventional 

wisdom” that you are supposed to reduce your (LDL) cholesterol! 

Without being overly cynical, this is done because the latest “wonder” drug 

likely has an effect on the surrogate, without regard to its DIRECT impact 

on the problem at hand. Consequently, the drug-company-led studies focus 

on their drug’s ability to alter the surrogate. 

“Effectiveness” is Interpreted Quite Differently Than Any 

True Scientist Would 

If I were told that taking a drug affords me 40% less risk, then I would assume 

that taking that drug would reduce my risk of contracting said disease by 

40% compared to someone not taking the drug. WRONG. You can’t tell the 

6

size of the effect unless you know the subject population size. This “40% 

reduction” that you think you have achieved would be what is called an 

“absolute” risk, but all the pharmaceutical studies use “relative” risk 

when reporting statistics. The difference is staggering, and it is virtually 

guaranteed that the real difference, the ONLY one that matters, is FAR 

LESS than the reported percentage. This is illustrated in the example below. 

Absolute Risk vs Relative (“Endpoint”) Risk — A Case Study 

in Tortured Logic 

Question: What is the difference between 2 successes in 1,000,000 (drug) 

vs. 1 success in 1,000,000 (placebo)? 

Drug 

Placebo 

2 patient successes out of vs 1 patient success out of 

1,000,000 patients treated 1,000,000 patients treated 

Answer: The absolute result is 0.0002% vs. 0.0001%, or effectively 0% 

success in both cases―ABSOLUTE FAILURE... 

That is, unless you are part of the pharmaceutical or nutraceutical industry, 

whereby 0% success MAGICALLY BECOMES 50% success. 

Here’s how they deceive you: The calculation they will use is this: Ignoring 

the total number of patients tested, they will say that there is a 50% difference 

in effectiveness of the results (2 to 1). They have deleted the sample size of 

1,000,000 patients. This calculation of 50% is termed “relative” risk because 

the sample size was deleted and only the “endpoints”— the successes in each 

group — are used. There is only one “small” problem with this method of 

reporting the drug’s supposed success—it’s absurd! 

Absolute Risk MUST Include Sample Size 

No honest scientist or physician would 

claim a 50% improvement with this drug, 

because the SAMPLE SIZE is not included. 

7

In the following statin example, 1% “magically becomes 36%,” misleading you 

as to the true, accurate measure of difference in heart attack risk. The TRUE 

EFFECTIVENESS is the difference in results in ABSOLUTE MEASURES 

that INCLUDE SAMPLE SIZE: 3% effectiveness of the statin minus 2% 

effectiveness of a placebo equals 1% effectiveness in absolute terms. That’s 

right, a shockingly low 1% is reported as a much more significant 36%! 

The correct effectiveness is NOT calculated as (3% – 2%)/3% = 33%, which 

the drug companies purposely and deceptively use. 

Shockingly, there is a one percent (1%) 

difference in effectiveness between the 

results with Lipitor and the results with 

a placebo. If you were given this information, 

would you take this drug? Of course not. That is, 

IF you knew and understood the TRUTH. 

8

This miniscule 1% difference is termed absolute risk and correctly takes into 

account the sample size. This leads to NNT (number needed to treat) and 

shows why it is critical when evaluating the effectiveness of a protocol. 

NNT (Number Needed to Treat) is Paramount — Not Misleading 

“Endpoint” Statistics 

Many physicians are misled because they have no idea the pharmaceutical 

companies are allowed to manipulate statistics. Pharmaceutical companies 

shockingly, yet legally, get to remove the sample size. Again, when is one 

patient event in a million (drug) compared to two patient events in a million 

(placebo) equal to 50% improvement instead of the statistically correct 1 in 

1,000,000 or 0.0001%? Answer: with the fanciful “pharmaceutical endpoint 

method,”also termed “relative risk,” as Professor of Medicine Stanton Glantz 

so aptly put in his book. (Glantz SA. Primer of Biostatistics. 5th ed. New 

York, NY: McGraw-Hill, 2002, 149-156.) 

You will often see the statement, “Lipitor reduces the risk of heart attack 

by 36% ... in patients with multiple risk factors for heart disease,” quoted 

in drug ads, such as the one on television a few years back featuring Dr. 

Robert Jarvik, inventor of the Jarvik artificial heart. In newspaper ads, the 

36% comes with an asterisk (*) saying, “That means in a large clinical study, 

3% of patients taking a sugar pill or placebo had a heart attack compared 

to 2% of patients taking Lipitor.” The difference between the treated and 

non-treated groups is a miniscule 1%, hardly worth getting excited about 

UNLESS you are a pharmaceutical or nutraceutical company that has 

already invested hundreds of millions of dollars in this drug and must 

ultimately sell this FAILURE to the desperate masses. 

In the case of statins, the NNT is 100 (the reciprocal of the absolute risk, i.e. 

1/1% = 1/.01 = NNT of 100). No, this “100” isn’t a perfect score you aspire 

to on a college exam; quite the contrary, it is an awful score. It means that 

to see a positive effect in just one patient, one hundred patients have to be 

treated, and often treated for many years at that. Therefore, 99 out of 100 

patients will see no positive effect — a 99% FAILURE RATE! Many medical 

researchers are convinced that the real NNT for statins in a standard mixed 

population, such as the typical patient a physician treats for CAD, may be 

closer to 250. Even assuming the lower 100 NNT figure, this is even more 

problematic for statins’ performance because 10% to 15% of statin patients 

experience negative side effects, including sexual dysfunction, muscle 

9

aches – prominently mentioned on Lipitor’s label – and significant cognitive 

problems, including loss of memory. Be aware that neither the NNT nor 

any of the risk statistics looks at negative side effects. This is an entirely 

separate issue. 

Dr. Nortin M. Hadler, Professor of Medicine at the University of North 

Carolina at Chapel Hill and a long-time drug industry critic, states, 

“Anything over an NNT of 50 is worse than a lottery ticket; there may be no 

winners.” (Carey J., “Lipitor: for many people, cholesterol drugs may not 

do any good,” BusinessWeek. January 17, 2008:52-59.) Even Las Vegas has 

games with a chance of winning greater than 1% or 2%. Shouldn’t drugs or 

nutraceuticals have a higher standard? 

Grasping the Magnitude of the Problem 

Decades old antibiotics commonly have an NNT = 1.1. When 11 people 

are given antibiotics, ten patients are cured of the problem for which the 

antibiotics were prescribed. Contrast this with statins, where 100 patients 

are given the drug and one person is helped; NNT = 100. 

The higher the NNT, the LESS effective the drug. 

If you remember only one point from this report, it should be that the 

intelligence of the answer is directly related to the intelligence of the 

question. Don’t let yourself be misled with shoddy statistics that don’t 

include the critical sample size. 

One Last Critically Important Thought 

When you receive news of the next “miracle” supplement, aside from 

requiring SPECIFIC METABOLIC PATHWAYS and state-of-the-art 

physiologic science supporting these claims, ask yourself: 

1. Why is this needed TODAY when it wasn’t needed years ago? 

10

Take fish oil supplements. People living in 1950 certainly consumed 

significantly less fish oil supplements than we do today; there was only a very 

small market for it. The supposed benefits of fish were not publicized in 

1950, and fish oil supplementation (being highly susceptible to spoilage) 

was simply not as common as it is today. Therefore, we should have seen 

gross pathological disorders due to the deficiency of DHA/EPA found in 

those supplements, which of course we did not. 

• Were there tremendous neurological impairments in the brain, eyes, 

and central nervous system due to low DHA levels? No, and there 

should have been if the supposition were true. 

2. Will taking the supplement stop or reverse conditions it is supposed 

to prevent? 

Regarding fish oil and its huge (supra-physiologic) amount of DHA/EPA, it 

should both prevent Alzheimer’s AND stop the progression of Alzheimer’s 

in patients with low DHA levels. Does it? 

No, in 2010, fish oil FAILED miserably to prevent Alzheimer’s (see www. 

brianpeskin.com, “Fish Oil Fallacy” Special Medical Report). Fish oil 

FAILED to either prevent or to slow the progression of Alzheimer’s. Since 

the same metabolic pathways are used to both prevent and to slow progression 

of any disease, you CANNOT make the absurd claim, as was made in front 

of hundreds of physicians, that fish oil prevents Alzheimer’s, but once you 

have it, fish oil won’t slow its progression. Logic maintains that it is more 

difficult for a substance to prevent a disease (the ultimate “cure”) than for 

a substance to slow progression of that disease. It is illogical to state that it 

will prevent but NOT slow progression. Scientific logic must prevail. 

1. Look at the dosage the supplement provides vs. the amount of food 

that would need to be eaten to provide it. While we are discussing 

fish, do you realize that suggested amounts from the manufacturers 

themselves provide DHA up to 120 times what your body would 

naturally produce on its own, and up to 500 times the amount of EPA 

that your body would naturally produce on its own. Ask what are the 

effects of this tremendous overdosing? 

2. Never rely on mere “associations” from “studies” masquerading as 

experiments (where one controlled variable only is changed). This is 

11

why one medical and nutritional recommendation after another gets 

REVERSED, like women taking synthetic HRT for its supposed heart 

protection and cancer protection, when in fact the opposite was true. 

(Often you never see the retraction.) 

Advanced information for health care professionals (not 

required for the lay public, but included for a more complete 

understanding of this subject) 

What is a “p”-value?” 

Statistics is mathematics and therefore extremely detailed. However, the 

essential concepts you need to know so that you aren’t misled again are 

relatively simple: 

1. The first value looked at by physicians and others (and mistakenly 

too often assumed to be the only important value) is the “p value 

“ or 1 — (p-value), meaning this experimental result occurred by 

chance alone, i.e., the drug doesn’t really work. When the study or 

experiment is repeated many times using the same general group 

of people, this same “successful result” recurs that is entirely due 

to chance alone. The item of interest (drug or nutraceutical) really didn’t 

work at all, but we think it did work. 

2. Typically, the p-value is set to 0.95 (at a 95% confidence level you 

get an inherent 5% allowed possible error rate) for the result to 

be considered “statistically significant.” If p = 0.95 then the study 

would be termed a 95% confidence level study (although a bit more 

information is required). A 0.99 (1% error rate) or 0.995 p-value (0.5% 

error rate) would be even better because there would be much less of 

a random chance effect behaving as though the drug worked when 

it really didn’t, thereby fooling both the physician and patient. With 

p=95%, even if the drug didn’t work, there is a 5% chance that you 

would get these pseudo-positive results 5% of the time, making it 

appear like the drug did work. This 5% means 1 out of 20 times you are 

FOOLED into thinking FAILURE is SUCCESS. 

Once again, a 95% p-value means that if this experiment were carried out 

in the same population sample 100 separate times, then this same result 

12

would be included at least 95% of the time; this pseudo-positive result 

would occur entirely randomly 5 times, although the drug was a complete 

FAILURE. 

It’s Easy to Mislead Everyone… 

All a company has to do is to conduct many 

studies and then purposely select only those that 

randomly show a “positive” result. Don’t mention 

the failures, and presto, you have a “successful” 

drug! All you need is lots and lots of money. 

• The p-value is NOT a measure of the size or magnitude of the effect 

of the drug. That is a completely different issue and has to do with 

the means (difference of the averages between both groups). Many 

physicians and patients don’t understand this critical fact and 

mistakenly think that a p-value alone is all that is needed. Wrong. 

• It is true that the MINIMUM p-value should be at least 95%; however, 

even IF the study has a “significant” effect, then one must ask this 

next critical question: 

How Strong is the Effect? A Little or A Lot? 

You need to ask “What is the magnitude of the 

positive effect?” A positive effect can range from a 

very small negligible effect to a tremendous effect. 

What is considered a significant amount or a significant effect? 

If more than 51% (the majority) of a group doesn’t respond IN ABSOLUTE 

NUMBERS (NOT relative measures) to the drug, then I am not impressed, 

and you shouldn’t be, either. Typically today, if just 20% of the treated 

13

group obtains any positive effect (regardless of how little), it is considered 

a huge success. But this really means 80% FAILURE. 

I am disgusted when substantial failure is transformed, by statistical sleightof-hand, 

into a so-called success. To put this into a real-world perspective, 

an 80% FAILURE rate, whereby buildings collapsed or televisions blew up 

in your face when turned on, would be unacceptable. I hope you would 

concur. 

Before I personally would trumpet a drug’s success, at least 80% of the 

subjects IN ABSOLUTE NUMBERS must benefit. Recall that there are 

examples of such high levels of success with drugs: insulin lowers everyone’s 

blood sugars; thyroid hormone decreases everyone’s TSH level; the proper 

antibiotics stop every infection. 

Is the Item Measured Significant, or a Worthless “Surrogate”? 

Low NNT is a necessary, but not an entirely sufficient condition to be 

able to claim victory. Is there a DIRECT cause/effect relationship? This is 

absolutely required or once more, you are being misled. 

To Reiterate: Worthless Surrogates — NOT the Desired Result 

Itself — Are Often Used…The Deception Continues… 

Even though statins lower LDL-cholesterol, heart disease is not significantly 

reduced. The tragic truth was only recently accepted. This still hasn’t 

stopped the pharmaceutical companies and physicians from saying that 

lowered LDL-cholesterol is all that counts. They are WRONG, and patients 

are paying with their lives. 

Therefore, one CANNOT blindly assume that the “disease” is solved when 

a worthless “SURROGATE” is used INSTEAD of measuring the result itself, 

such as how many heart attacks occur with and without statins (the answer is 

the same amount, or even more, occur WITH STATINS). This means that 

statins are ineffective at stopping heart disease. 

A recent example: The JUPITER FAILURE Hailed 

as A Success 

Of course, from the above, it goes without saying that there must first be a 

direct cause/effect relationship to the disease. If you treat 100 patients with 

14

a drug and all 100 improve, the drug’s number needed to treat (NNT) is 1 

(100 patients/100 successes). If you treat 100 patients and only 1 patient 

responds positively the NNT would be 100 (100 patients treated/1 positive 

response). This is an awful result and equivalent to a 99% failure rate. Dr. 

Nortin M. Hadler, Professor of Medicine at the University of North Carolina 

at Chapel Hill states: “Anything over an NNT of 50 is worse than a lottery 

ticket…” 

Of significant importance is the fact that the 2008 JUPITER study was used to 

try and gloss over the fact that numerous attempts to prove the “cholesterol 

theory” (the lower the patient’s low density cholesterol [LDL-C], the greater 

the prevention of CVD), by attempting to make the case that the real mode 

of action of statin drugs was C-reactive protein (CRP) reduction, have 

failed. However, there is one tragic flaw: CRP is not a reliable prognostic 

indicator of cardiovascular events; there are better markers. An article 

entitled Largest-Ever Meta-Analysis Finds CRP Is Unlikely to Be Causal for 

CVD, reports that scientists of the Cambridge-based Emerging Risk Factors 

Collaboration (ERFC) found: 

“[A]lthough CRP concentration was linearly associated with CHD 

(coronary heart disease), stroke, and vascular mortality, as well 

as nonvascular mortality, statistical adjustment for conventional 

cardiovascular risk factors resulted in considerable weakening of 

associations.” 

An Example of How They Fool You 

In the Jupiter Study, the NNT of 240 for 

statins, in preventing any stroke 

(99.58% failure disguised as a hazard 

ratio of 0.52; p = 0.002), was not stated. 

This means that the JUPITER Study had an undisclosed NNT of 240 (99.6% 

FAILURE) for preventing any stroke – instead, a hazard ratio (an estimate 

15

of relative risk) of 0.52 (appearing as a 52% success) was published, thus 

making the trial appear much more successful than it actually was. 

What appears more impressive? A 0.04 success rate / 99.6% FAILURE rate 

or a 52% success rate / smaller 48% FAILURE rate? Physicians are deceived 

and so are their patients. 

• Always ask for the SAMPLE SIZE, since without it you cannot 

draw any meaningful conclusions. 

• Always ask for the ABSOLUTE RISK DIFFERENCE BETWEEN 

BOTH GROUPS, since without it you cannot draw any meaningful 

conclusions. 

16

IOWA Study Results 

Remarkable experimental results of 

arterial compliance improvement with PEOs 

Professor Brian S. Peskin* with David Sim, M.D.* 

* Brian Peskin received an appointment as an Adjunct Professor at Texas Southern University in the 

Department of Pharmacy and Health Sciences (1998-1999). 

Dr. Sim is a practicing Interventional Cardiologist.

Long-term Results 

IOWA: Investigating Oils With Respect to Arterial Flexibility 

Significant differences in biological age compared to physical age 

Brian Peskin, BSEE: Founder Life-Systems Engineering Science 

with David Sim, M.D., Interventional Cardiologist 

Long-term Use in Subjects with PEO Formulation 

Long-term (48 month maximum) PEO use 

The effects of long-term PEO supplementation were evaluated in thirty-four (34) 

subjects with a daily dosage of 2,900 mg PEO formulation. The sub-groups were as 

follows: thirteen (13) male subjects and twenty-two (22) female subjects aged 35-75, 

with a median age of 62-years-old, utilizing the formulation a minimum of three (3) 

months to a maximum of forty-eight (48) months. The median duration usage was 

twenty-four (24) months with half of the subjects using the PEO formulation less than 2 

years and the remaining half utilizing the formulation over 2 years but less than 4 years. 

Vascular assessment was made via Photoplethysmography measuring arterial 

flexibility. 

Overall Improvement = 73% Effectiveness – Highly Significant 

Twenty-five (25) subjects of the 34 subjects in the trial improved. This corresponds to a 

seventy-three per cent (73%) effectiveness rating. The average improvement in arterial 

flexibility was 9 years improvement meaning the average subject utilizing the PEO 

formulation had a cardiovascular system with the arterial flexibility of a subject 

representative of nearly a decade younger. 

The best subject measured 39 years less (improvement) than their physical age 

waveforms would suggest. Of the 34 subjects, there was only one (1) subject who 

worsened. 

NNT Effectiveness = 1.4 — A “Remarkable” Result 

The number needed to treat (NNT) is calculated as follows: 34 subjects — 25 improved 

subjects = 1.4. 

NNT quantifies how many patients have to be treated to obtain one successful outcome. 

An NNT of less than 50 is considered effective in the pharmaceutical industry. 

 

1

Comparison to Statins 

As a comparative example, statins, as reported by the pharmaceutical industry, have 

NNTs > 80 in preventing a cardiovascular event. 

This means a minimum of 80 patients would need to be treated to see a single (1) 

positive outcome when using statins. 

In contrast, the PEOs improve a much more direct physiologic measure, i.e., arterial 

flexibility, in a profound way resulting in a remarkable 1.4 NNT. 

Statistics (Highly Significant) — 99.8% Accuracy 

 

2

Short-term Results 





Short-term Improvement in Subjects with PEO Formulation 

Short-term (3-month) PEO use 

The effects of short-term PEO supplementation were evaluated in sixteen (16) subjects 

with a daily dosage of 2,900 mg PEO formulation. The sub-groups were as follows: 

seven (7) male subjects and nine (9) female subjects aged 46-84, with a median age of 64- 

years-old, utilizing the formulation a median of 2.5 months usage (half of the subjects 

with less duration and half of the subjects with more duration) and mean average of 3 

month’s usage. Minimum PEO formulation usage was one (1) month and the maximum 

subject usage was eight (8) months PEO usage. Vascular assessment was made via 

Photoplethysmography measuring arterial flexibility. 

Overall Short-term Improvement = 43% Effectiveness – Highly Significant 

Seven (7) subjects of the sixteen (16) subjects in the trial improved. This corresponds to 

a forty-three per cent (43%) effectiveness rating over a very short period of time. The 

average improvement in arterial flexibility was 7.2 years improvement meaning the 

average subject utilizing the PEO formulation had a cardiovascular system with the 

arterial flexibility of a younger subject. 

NNT Effectiveness = 2.3 – A “Remarkable” Result 

The number needed to treat (NNT) is calculated as follows: 16 subjects / 7 improved 

subjects = 2.3, an outstanding result for such a short period of time. 

NNT quantifies how many patients have to be treated to obtain one successful outcome. 

An NNT of less than 50 is considered effective in the pharmaceutical industry. 




 

3


positive outcome. 



Statistics (Highly Significant) — 99% Accuracy 

 

4

PEOs versus Fish Oil 





Subjects Discontinued Fish Oil Supplementation, replacing it with PEO 

Formulation 

PEOs versus fish oil 

The effects of the PEOs were evaluated in subjects who ceased fish oil supplementation, 

replacing it with a daily dosage of 2,900 mg PEO formulation. The effects of the PEO 

formulation were measured in 15 subjects: seven (7) male subjects and eight (8) female 

subjects aged 46-74, with a mean age of 60-years-old, utilizing the formulation an average 

duration of 3.5 months. Vascular assessment was made via Photoplethysmography 

measuring arterial flexibility. 

Overall Improvement 

Thirteen (13) of the fifteen (15) subjects improved with the PEOs for an 87% 

effectiveness rating and an NNT of 15 / 13 = 1.2. Improvement was 11.1 years as 

measured by standard population samples. 

On average, the PEO formulation quickly improved the cardiovascular system’s arterial 

flexibility by over 11 years (younger) in the subjects. Thirteen (13) subjects improved; 

one (1) subject remained the same, one (1) subject worsened by 1 year. Results were 

highly statistically significant (p=0.0001) — 99.99% accuracy. 

Subjects with “high cholesterol” 

Of the seven (7) subjects previously diagnosed with high cholesterol levels replacing 

fish oil supplements with the PEO formulation instead, six (6) subjects improved their 

cardiovascular biological ages. This translates to an NNT of 7 / 6 = 1.2 for improvement 

in cardiovascular system compliance in subjects with high cholesterol manifestations of 

heart disease. 

Subject with both diabetes and “high cholesterol” 

One (1) subject having both diabetes and high cholesterol diagnosis also improved. 

 

5





positive outcome. 



Statin user improvements 

Two patients are taking statins and both subjects improved their biological age by 

twenty years for an NNT = 1 in those patients taking statins. NNTs of less than 50 are 

considered excellent. Even with the small number of subjects in this sub-group taken 

into account, the results of this trial are exceptional and not due to chance. 

Statistics (Highly Significant) — 99.99% Accuracy 

 

6

The Missing Link: EFA “Oxygen Magnets” 

Scientific Studies Show That EFAs Prevent Cancer 

The great news, presented to the public in a cohesive manner for the 

first time in this book, is that EFAs have been proven in numerous 

studies to prevent cancers from forming in conditions and situations 

where they were expected to form and would have formed had EFAs 

not been administered. Some of these studies also show that EFAs 

can inhibit the growth of cancer already present in the body. The 

results of the most significant of these studies are discussed in detail 

in Chapter 11. 

However, the results of a new study we commissioned to directly 

test the effects of the EFA ratios recommended in this plan were so 

positive that we want to review them here. 

A New EFA Cancer Experiment—Proof That EFAs 

Work 

Starting on page 373, Chapter 11 shows numerous EFA-related studies 

demonstrating how EFAs minimize cancer growth and how distorted 

EFAs (transfats) encourage cancer growth. 

173

The Hidden Story of Cancer 

For example, in 1997, it was shown that an EFA deficiency in 

mice allowed cancer to grow faster. Here is their quote: 

“It may be concluded that, when a tumor initiator injures 

the body as a whole, EFAD [Essential Fatty Acid Deficiency], 

achieved either through a fat-free or an oleic-supplemented 

diet [like olive oil], behaves as a general promoting condition 

for tumorigenesis [cancer].” This finding was published in an 

article titled “Dietary deficiency or enrichment of essential 

fatty acids modulates tumorigenesis in the whole body of 

cobalt-60-irradiated mice.” 8 

That study makes it clear that an EFA deficiency is a cancercausing 

problem. The question that had to be answered was would 

a laboratory experiment under controlled conditions prove that a 

diet sufficient in EFAs either stop or halt cancer in vivo (in the body) 

and not merely in vitro (in a test tube). Too often tests conducted in 

a test tube give a different result than a test in the body in a real-life 

situation. 

I could not find an experiment done on an animal that metabolized 

EFAs in a similar fashion to humans, such as mice, that were 

given an EFA formulation comparable to the one suggested in this 

book (greater parent omega-6 than parent omega-3). 9 Furthermore, 

I could not find any experimenter that used oils from organically 

grown and organically processed sources—guaranteeing that no 

cancer-causing hydrogenated/oxygen deficient oils were used. There 

was only one way to see if the EFA suggestion in The Hidden Story of 

Cancer would work under third-party controls using an independent 

laboratory specializing in oncological (cancer) studies. Furthermore, 

a third-part statistical expert was employed to calculate the validity 

of the results. You will see the undeniably powerful results of this 

8 Prostaglandins Leukot Essent Fatty Acids, 1997 Mar;56(3):239-44. 

9 Unfortunately, tests utilizing cells grown in a test tube often give different results 

than in the body. I hate to see animals harmed if there is another way. It is mandatory 

for an experimenter to be as certain as possible of the outcome based on theoretical 

analysis, as we were, BEFORE needlessly sacrificing animals. We used the minimum 

number of mice (20) so as to obtain a statistically meaningful and valid result. 

. 

174


experiment. Its promise of hope for extending existing cancer patient’s 

lives is nothing short of spectacular. 

In 2004 we commissioned an experiment with mice at an independent 

laboratory experienced in oncological studies. The purpose 

of the experiment was to show whether pretreatment with organic 

raw parent EFA oils in the ratios and amounts comparable to our 

human recommendations, prior to implantation of breast cancer 

tumors in the mice, affected the growth of the cancer cells in any 

way. A breast cancer strain was chosen because breast cancer is the 

Number 1 worldwide cause of death by cancer in women. Mice were 

used because they respond very similarly to humans regarding EFA 

metabolism and because their shorter lifespan allows all effects and 

results to occur more quickly. 10 

One group of mice was pretreated with the EFA oils for four weeks 

prior to tumor implantation (Group 2, showing the greatest inhibition 

of tumor growth at the bottom of the graph in Figure 1), followed by 

a daily dose (five days a week) for 50 days after implantation of the 

cancer tumors. A second group was pretreated with EFA oils for two 

weeks prior to implantation (Group 1, showing less tumor growth at 

the middle of the graph) and then given the daily dose for the rest of 

the 50 days. The third group, the control group (Group 3, showing 

uncontrolled tumor growth at the top of the graph), was not pretreated 

or given any EFAs at all. 

Tumors consisting of two million breast cancer cells each were 

implanted in the mice and measurement began. The statistical 

analysis focused on the period from day 26 to 50 to ensure that any 

hormonal changes and other transitory effects that occurred after 

implantation had stabilized (as recommended by Dr. Warburg). An 

independent expert in statistical analysis calculated and reported the 

results. 

10 The metabolism of n-6 and n-3 PUFAs in rats and mice are similar to humans. 

(Lands, W.E.., et al., Lipids, Vol. 25(9), 1990, pages 505-516.) Therefore, studies in 

mice would be predicted to be similar in humans. Regardless, one must be always 

aware that mice are not humans. For this reason, many drugs do not work as well 

in humans as in animals, if at all. Because this EFA formulation was designed 

specifically for humans and their “parent” omega-6/3 tissue ratios, we would 

therefore expect human results to be significantly better than results in mice. 

175


The following statistical analysis doesn’t suffer from mistakes that 

often occur that you learned about on page 58. An F test, opposed to 

multiple t tests, was used to determine the significance. 11 

The experiment showed that although the tumors continued to 

grow in all mice, there was a highly significant 24% smaller tumor size 

(growth) in the longer four-week pretreatment mice than in the control 

mice that received no EFA oils at all. This result occurred consistently 

upon measurements at the day 26 endpoint, the final endpoint (day 

50), and at every intermediate point. This same effect occurred with 

the two-week pretreatment group, although to a lesser extent than 

the four-week pretreatment group, as would be expected. 

Additionally, in the last 10 days of the experiment, there was a 

whopping 42.8% lower growth volume of the tumors in the four-week 

pretreated mice than in the tumors in the untreated mice. 

These results clearly show the EFAs’ value increases with longer 

pretreatment. A logical conclusion from this result would be that the 

EFA oils are modifying the cells’ internal structure, making them 

more cancer resistant. 

A few additional key points should be mentioned: The oils were given 

to the mice only five out of seven days each week. The recommended 

schedule for humans is seven days a week. Although mice use EFAs in 

a similar fashion as humans, this plan’s EFA recommendations were arrived 

at by considering human tissue structure and human biochemistry. 

Therefore, the results should be even better in humans than in the mice 

in the experiment. The dramatic results are present in Figure 1. 

Why Did the Cancer Cells Keep Growing? 

Now, these results sound good, but you might be wondering why 

the tumors in all groups of mice continued to grow, even though the 

pretreated mice’s tumors grew significantly less. Does this negate 

the positive results of the experiment? 

11 F test means the variation between the means (averages) of all the groups divided 

by the variation within the groups. If the groups were the same (no difference) then 

the F value would equal close to 1. In this case it was greater than 4 with 98% 

accuracy. All mice were included in this experiment. Unlike most “studies,” none 

were excluded for any reason. The bottom line; a very significant result. 

176


Figure 1: Tumor volumes between groups from 26 to 50 days 

No, it doesn’t. To be able to complete this kind of experiment 

within a reasonable time, a tumor of sufficient size to be easily 

measurable had to be used. If we started the experiment with one 

or very few cancer cells, we would have a great deal of difficulty 

finding them, much less measuring them, and due to most cancers’ 

slow growth rates, the cells might not have been measurable within 

the mice’s usual lifespan. 

Implanting a tumor consisting of 2 million cancer cells is an 

overwhelming amount for a mouse’s system. We expected this 

avalanche of cancer cells to continue to grow even in the presence 

of EFAs because there is no safe way you can destroy all of it, no 

matter what your defense is. 

But by the same token, when we saw a significant lower tumor 

growth in spite of the initial size of the tumors, it was a telling indication 

that something had acted powerfully against the development of 

the cancer in the mice’s bodies: the EFA oils must have a significant 

cellular modifying capability that made the mice more resistant to 

developing cancer. This was made clear because both the 2-week 

pretreated mice and the 4-week pretreated group were given identical 

EFA doses—only the length of the pretreatment phase differed. 

177


In view of this apparent cellular modifying capability, and the fact 

that naturally occurring cancer begins to develop in the human body 

very slowly, one cell at a time, we must pose this question: Given 

adequate pretreatment with the correct EFAs, would cancer ever 

normally occur in a human? We believe a high degree of probability 

exists that the answer is “no.” 

The results of this experiment clearly demonstrate the cancerprotective 

properties gained by taking parent EFAs in the ratios 

recommended in this book. 

EFAs Provide Many More Health Benefits Above 

and Beyond Cancer Protection 

This book is about the anticancer solution. However, it is important 

that you understand that there are other areas EFAs benefit. 

In addition to EFAs’ cancer-protective properties, EFAs make it 

possible for your cell membranes to operate optimally for a multitude 

of other biochemical functions, such as hormone transfer. This includes 

effective insulin uptake. That’s why these critical EFAs help prevent 

and control diabetes. 

Not least of the benefits of adequate EFA supplementation and 

its resulting increased cellular oxygenation is greatly increased energy. 

Lack of energy is one of Americans’ chief complaints. Proper 

EFA supplementation as given in this book will provide you with a 

marked improvement in your energy level. 

EFAs are the building block of your sexual hormones. With 

sufficient amounts of EFAs you won’t run short because the “raw 

material” was in short supply. EFAs are also the building blocks of 

the endocrine system. This system regulates your levels of anxiety, 

your ability to concentrate and focus, too. Athletes will benefit from 

increased endurance, increased performance, and better immunity 

from fatigue. 

On the next page is a table showing a sampling of the multitude 

of additional areas helped with fully functional EFAs. The medical 

textbooks and medical journals have understood EFAs’ importance 

for years but this information typically is not covered by the popular 

press. 

178

What You Should Not Eat: Cancer-Causing Transfats (EFA Imposters) 

The Power of PEOs (Parent EFAs) to Help 

Surgeons and Their Patients 

Dr. ANDREA RONCARATI FERRARA-Via Montebello 1 tel: 0532/200234 

Specialista in Chirurgia Plastica RAVENNA-Viale Cilla 20 tel: 0544/456511 

Ricostruttiva ed Estetica info@roncaratiandrea.it 

February 25, 2005 

Nella mia attività di Chirurgo Plastico, mi sono trovato ad affrontare 

esiti post-operatori di varia intensità, da quello regolare ( sicuramente in 

numero maggiore ) a quello molto impegnativo per la risoluzione flogistica, 

edematosa,cicatriziale. 

I risultati sono migliorati cambiando le tecniche chirurgiche e delle medicazioni, 

utilizzando coperture antibiotiche e antiflogistiche, ma riconosco 

un vero salto di qualità da quando ho consigliato e prescritto, almeno 15 

giorni prima e 30 giorni dopo l’intervento chirurgico, l’assunzione di ACIDI 

GRASSI ESSENZIALI. 

Il livello di “restituito ad integrum”, da me ricercato in ogni occasione, ma 

soprattutto in cinque pazienti usando la formula dei EFAs di Brian Peskin, ho 

trovato grandissimo giovamento con l’utilizzo di questa semplice ed efficace 

terapia medica che ha dato dei risultati di guarigione quanto segue: 

1. più rapida cicatrizzazione 

2. meno infiammazione 

3. migliore tessuto cicatriziale 

4. meno dolore in fine per il paziente 

Il prolocolo di “Brian Peskin” non causa eccessivo sanguinamento 

come olio di pesce che mi rende la chirurgia più facile ed infine la guarigione 

dei pazienti è migliore. 

Infine credo fermamente sia giusto continuare su questa interessantissima 

strada intrapresa in particolare sul meccanismo dei tessuti riparativi. 

Dr. Andrea Roncarati 

331


Translation 

February 25, 2005 

In my practice as a Plastic Surgeon, I have found myself understanding that 

to obtain good post operative results according to the intensity that varies 

from minor to major operations (the majority are very intense operations) 

the repair flogistic resolution, edema and the scar tissue are all key factors 

to success. 

My results have improved according to the use of new surgical techniques 

as well as the use of antibiotics and antiflogistic drugs. 

However, I must point out a new major factor that improved greatly my 

patients’ surgical results after introducing certain “essential fatty acids” 15 

days prior to 30 days after surgery. 

The level of tissue repair is what I look for especially in my practice and 

having the trial opportunity of five patients using Brian Peskin’s EFA recommendations, 

I found in all five patients an enormously improved result 

with better recovery by just assuming a simple prescribed medical therapy 

with his EFA-based recommendations. 

Unlike fish oil which causes excessive bleeding, Brian Peskin’s Protocol 

does not cause excessive bleeding. In fact, it makes surgery easier and improves 

patient recovery. 

This improved recovery included: 

1. faster healing 

2. less inflammation 

3. less scar tissue and 

4. less pain to the patient. 

I finally believe and feel it is necessary to continue this very interesting tissue 

repair in the near future. 

Dr. Roncarati Andrea 

332

Peskin Protocol: Adjunct Therapy for Use with Chemotherapy and Radiation 

May 2008 it was brought to my attention by the superb radiologist, Robert Kagan, M.D., 

Medical Director of MRI Scan & Imaging Centers in Ft. Lauderdale, Florida, that increased 

cellular oxygen increases the effectiveness of both chemotherapy and radiation treatments 

in destroying cancer cells. 

It was extremely gratifying to learn of this, since the Peskin Protocol is designed to 

increase cellular oxygen throughout the body, including at cancerous sites. 

James B. Mitchell, Ph.D., head of the tumor biology (NCI-radiation biology branch) section at 

the National Cancer Institute, reported in an article published by Radiological Society of 

North America (4/23/2008): 

· “…‘[T]hey were able to successfully measure oxygen levels in tumors,’ which 

could be important because ‘tumors with higher concentrations of oxygen [are] 

more susceptible to radiation.’ 

· “Lower oxygen level ‘in the tumor allows tumor cells to survive more easily 

by making the DNA destruction more difficult.’ 

· “‘Chemotherapy drugs also don’t work as well when tumors have less 

oxygen.’” (emphasis added) 

I immediately began searching medical journal articles to see if this critical concept was wellunderstood. 

The following comments comprise a (small) representative sample of what I 

found: 

RADIATION ADJUNCT THERAPY: 

· “A large body of published evidence points to tumor hypoxia as a major 

obstacle to effective treatment of tumors using ionizing radiation a,b because 

cells exposed to radiation under hypoxic conditions are approximately thrice [3 

times] more resistant than when treated under aerobic conditions. c (emphasis 

added) 

· “Despite significant evidence of a role of hypoxia [low cellular oxygen] in cellular 

resistance to ionizing radiation–induced toxicity, the underlying molecular 

mechanisms remain unclear. This study focused on the influence of hypoxia on 

radiation-induced signals in TK6 human lymphoblastoid cells. d (emphasis added) 

• OVER •

CHEMOTHERAPY ADJUNCT THERAPY: 

· “Solid tumors frequently contain large regions with low oxygen 

concentrations (hypoxia). The hypoxic microenvironment induces adaptive 

changes to tumor cell metabolism, and this alteration can further distort the local 

microenvironment. The net result of these tumor specific changes is a 

microenvironment that inhibits many standard cytotoxic anticancer therapies 

[“chemotherapy”] and predicts for a poor clinical outcome. e (emphasis added) 

· “Hypoxia and anemia (which contributes to tumor hypoxia) can lead to 

ionizing radiation and chemotherapy resistance by depriving tumor cells of the 

oxygen essential for the cytotoxic activities of these agents. Hypoxia may also 

reduce tumor sensitivity to radiation therapy and chemotherapy through one or 

more indirect mechanisms that include proteomic and genomic changes. f 

(emphasis added) 

a Eric, E., “The oxygen effect and reoxygenation.” In: Radiobiology for the radiologist. Philadelphia: JB 

Lippincott Co.; 1994. p. 133–52. 

b Samuni, A., et al., “Effects of Hypoxia on Radiation-Responsive Stress-Activated Protein Kinase, p53, and 

Caspase 3 Signals in TK6 Human Lymphoblastoid Cells,” Cancer Res 2005; 65(2): 579-86. 

c 

Brown, J., “Tumor microenvironment and the response to anticancer therapy,” Cancer Biol Ther; 

2002;1:453–8. 

d Samuni, A., et al., “Effects of Hypoxia on Radiation-Responsive Stress-Activated Protein Kinase, 

p53, and Caspase 3 Signals in TK6 Human Lymphoblastoid Cells,” Cancer Res 2005; 65(2): 579-86. 

e Cairns, R., et al., “Metabolic targeting of hypoxia and HIF1 in solid tumors can enhance cytotoxic 

chemotherapy,” Proceedings of the National Academy of Science, May 29, 2007; vol. 104, no. 22: 

9445–9450. 

f Harrison, L., Blackwell, K., “Hypoxia and Anemia: Factors in Decreased Sensitivity to Radiation 

Therapy and Chemotherapy?,” The Oncologist 2004;9(suppl5):31-40. 

• OVER •

Breakthrough in Clinical 

Cardiology: 

In-Office Assessment with 

Pulse Wave Velocity (PWV) and 

Digital Pulse Analysis (DPA) 

by Brian Scott Peskin, BSEE, with Robert Jay Rowen, MD 

This article explores an exciting, noninvasive, easy-to-use, 

and economical method of assessing patients’ cardiovascular 

physiologic status that is backed by more than 25 years 

of advanced research in medical physics. A 2007 Clinical 

Medicine article points the way to better clinical treatment 

of CVD, stating: “Arterial stiffness measured by pulse wave 

velocity (PWV) is an accepted strong, independent predictor 

of cardiovascular events and mortality.” 1 Anesthesiologists are 

well aware of this technology, used for monitoring purposes. 

While pulse oximetry became standard in the operating room 

and in other critical care areas as a detector of hypoxemia 

– all pulse oximeters are fundamental photoelectric 

plethysmographs – PWV has been largely ignored. This is 

unfortunate, as PWV (plethysmographic) information itself 

may provide important clues regarding the CV condition of 

the patient. 2,3 With this advanced technology, cardiovascular 

science has moved forward, but many physicians have yet to 

appreciate these advances. As stated in the 1993 issue of the 

Journal of Hypertension, “Wave reflection is not a subject with 

which most physicians are familiar and only given mention in 

undergraduate physiology courses.” Little has changed. 

As this article was going to press, however, “Arterial Stiffness 

and Cardiovascular Events: The Framingham Heart Study,” by 

Gary F. Mitchell, MD, et al. (Circulation. 2010;121:505–511) 

was published and featured on Medscape, stating: “In this 

study, we assessed the incremental value of adding pulse 

wave velocity [PWV] ... to a risk model that includes standard 

risk factors for a first cardiovascular event. … Adding pulse 

wave velocity led to significant reclassification of risk and 

improvement in global risk prediction. … [W]e need to focus 

our efforts on identifying and implementing interventions that 

can prevent or reverse abnormal aortic stiffness in order to 

prevent a marked increase in the burden of disease potentially 

attributable to aortic stiffness.” The specific intervention/ 

solution will be given later in this article. 

Known in 1993: Blood pressure alone provides no 

information of the wave itself 

“[T]he fallacy that there is a single ‘systolic’ and a 

single ‘diastolic’ blood pressure that is the same in 

all major arteries and can be measured in the brachial 

or radial artery is quite wrong, but few appreciate this 

fallacy, or its implications.” 4 

In 1996, Murray and Foster observed that pulse oximetry 

brought a major advance to patient monitoring in the 1980s, 

yet some of the most valuable data in the waveform signal 

were being overlooked. 5 Dorlas and Nijboer also make clear 

how this technology surpasses that used in the important (and 

complementary) ECG/EKG: “When displayed continuously 

on an oscilloscope, the plethysmograph indicates electromechanical 

dissociation. The device is noninvasive, and 

can be applied easily and rapidly. However, despite these 

advantages, the method is not applied universally. This may 

be because of unfamiliarity with the method. …” 6 

Cohn et al., writing in 1995, make clear that when waveforms 

are compared between the invasive and noninvasive methods, 

computer analysis allows a very high degree of correlation and 

repeatability for successful use in clinical application across all 

populations (including diabetics): “In hypertensive subjects, 

diabetics, and in the normal aging process – and in asymptotic 

individuals – there was an abnormality in the oscillatory 

component of the diastolic waveform.” 7 They also suggested 

that pulse wave analysis would be useful in screening subjects 

for early evidence of vascular disease and in monitoring the 

response to therapy. 

The European Society of Hypertension (ESH) and the 

European Society of Cardiology (ESC) have added PWV 

measurement as an early index of large artery stiffening 

in their 2007 Guideline for the Management of Arterial 

Hypertension. 8 

Digital Pulse Analysis (DPA) is the next evolution in pulse 

wave velocity (PWV), and is based on the measurement of 

reflected infrared light (IR). 

Simple, easy-to-use, non-invasive 

finger probe 

There has been an explosion of 

activity in pulse wave analysis, 

and the ability to identify 

premature vascular stiffening 

is of considerable value in the 

prevention of cardiovascular 

disease. “The PWV has been 

established as an important 

biophysical marker of arterial 

ageing, which is independently highly predictive of 

cardiovascular outcome. …” 9,10 

80 TOWNSEND LETTER – MAY 2010

Numerous independent confirma tions show statistically 

significant CV parameters based on age, and how PWV is the 

ideal method for assessing arterial stiffness and central aortic 

pressure. 1,11,12 Measurements are highly reproducible in clinical 

application and apply to both male and female patients. 12,13 

Methodology 

A photodiode detects changes in the amount of light 

absorbed by hemoglobin, and its output waveform is termed 

photoplethysmography, or PTG. PTG has been validated for 

calculating systemic arterial compliance (flexibility). 7 The 

application of this technique in population studies confirms 

the early detection and evidence of vascular disease, as 

well as patients’ response to therapy. 10 The technique is 

underpublicized, and many physicians are not aware of the 

great clinical impact of this technology. 

With advanced computer analysis of the waveforms, 

clinicians can now use this simple, insurance-reimbursable 

procedure to assess the coronary health of their patients, in 

detail – in the office – in less than 5 minutes. Simplicity, ease 

of use, and detailed cardiovascular analysis of the patient 

are key to clinical use. As part of the analysis, the physician 

is also given patients’ CV “biological age” to compare with 

their actual age. This device is extremely responsive and can 

measure patient therapeutic improvement in as little as 3 to 6 

months, if not earlier. 

A New Successful Intervention 

Even though atherosclerosis is a leading cause of CVD, 

age-related arterial stiffening receives little attention 

in everyday clinical practice, because until recently, 

there was no successful intervention that could be 

prescribed. 14 Although no single parameter of arterial 

compliance or stiffness can be expected to describe all 

clinically relevant arterial wall properties, the use of a 

DPA–integrated, multimeasurement approach, coupled 

with an effective protocol to stop and reverse arterial 

stiffening with plant-based, bioidentical parent essential 

oils (PEOs), will change this commonly held belief. This 

approach and the PEO protocol are being investigated 

in the IOWA study – Investigating Oils With Respect 

to Arterial blockages, which commenced in December 

2009 (results reported later in article). 

2010/2009 IOWA (Investigation Oils with Respect to 

Arterial Blockage) Study 

IOWA’s goal is to assess the intervention of plant-based, 

bio identical PEOs and measure their effectiveness in both 

stopping progression of and reversing existing atherosclerosis; 

that is, reversing “hardening of the arteries” as evidenced not 

by hopeful but ineffective “surrogates,” but by detailed DPA 

patient profiles, which are a much more direct measure of the 

physiologic CV state. 15 The study ultimately will include over 

200 participants. 

Many commonly used CVD surrogates are not indicative 

of the true state of the cardiovascular system; that is, patient 

markers may improve but the patient still ultimately suffers 

from CVD. Even coronary calcification (CA), once considered 

a possible “gold standard” in cardiovascular diagnostic 

measurement, has recently been called into question as an 

accurate diagnostic risk indicator. 15–17 Another deficiency 

of CA is that patients’ soft plaque is not measured at all – a 

significant issue. 

LDL-C Therapy Fails to Prevent CVD (an ineffective 

surrogate) 

C-Reactive Protein Marker ‘Called into Question’ 

There is now significant doubt that C-reactive protein is a 

dependable CVD surrogate. 19 Current DPA technology provides 

a much better way to both prevent and treat CV disease in 

the 21st century than merely “controlling cholesterol” via 

statins (with their ineffective NNT of 100), or hoping that CRP 

reductions will help. 15 

Aging and Decreased Arterial Flexibility 

It is well known that aging is accompanied by increased 

stiffness of large elastic arteries, leading to an increase in 

PWV. Premature arterial aging, as determined by an elevated 

aortic PWV, is now recognized as a major risk factor for 

ischemic heart disease. 20–24 An influence of vascular aging on 

the contour of the peripheral pressure and volume pulse in the 

upper limb is also well recognized, and the aortic pulse wave 

velocity more than doubles between ages 17 and 70. 25,4 

Aortic / Large Artery Stiffness Measurements: 

Millasseau et al. report: “the stiffness of the aorta can be 

determined by measuring carotid-femoral pulse wave velocity 

(PWVcf). PWV may also influence the contour of the peripheral 

pulse, suggesting that contour analysis might be used to assess 

large artery stiffness.” 10 Because of difficulty in computing 

individual patient path lengths of these pulses, large artery 

stiffness (SI) cannot be considered a direct measure of the pulse 

wave velocity; however, SI is a definitive index of the stiffness 

of both the aorta and large arteries throughout the body. The 

systolic component arises from the pressure wave from the 

left ventricle to the finger; the diastolic pressure component 

arises from the reflected wave’s traveling backward. Increased 

cardiovascular events are strongly correlated to arterial 

stiffness. 10 

Note: Healthy CV patients have a well defined “dicrotic 

wave” in the diastolic phase at D, whereas 98% of overt 

arteriosclerotic patients had significant decrease or 

disappearance of the wave. 26 

➤ 

TOWNSEND LETTER – MAY 2010 81

Clinical Cardiology 

➤ 

Elements of PTG (Systolic Phase) 

1. S (Starting Point) 

Starting point of systolic phase of arterial pulse-wave. 

Aortic valve opens and the blood of the LV is ejected into aorta. 

2. P (Percussion Wave) 

Wave caused from LV ejection that increases the blood volume within 

artery. 

Higher point means stronger LV ejection and higher compliance of 

larger artery. 

3. T (Tidal Wave) 

Reflected wave from the small artery. 

Higher point means contraction and stiffness of small artery. 

4. C (Incisura) 

End-point of systolic phase, then aortic valve is closed. 

Less drop from pulse height (PH) means larger resistance (arterial 

contraction & tension). 

Note: A sophisticated approach to contour analysis of 

the PTG utilizes its second derivative, often referred to as 

the acceleration photoplethysmograph. This facilitates the 

distinction of 5 sequential waves, called a, b, c, d, and e waves. 

The relative heights of these waves (b/a, c/a, d/a, and e/a ratios) 

have been related to age, arterial blood pressure, large artery 

stiffness, and effects of vasoactive drugs. The b/a ratio has been 

related to aging and carotid distensibility. Following analysis 

of the correlation of the b/a, c/a, d/a, and e/a ratios with age, 

a more complex “aging index” was defined as [(b–c–d–e)/a]. 

In a study to assess arterial distensibility in adolescents, the 

d/a ratio identified individuals at increased risk of developing 

atherosclerosis. The second-derivative approach has also 

recently been applied to the study of the peripheral pressure 

pulse. 9,27 

With the PTG wave as a basis, its second derivative, termed 

the APG wave, provides an extremely useful measurement of 

the “biological age” of the patient’s cardiovascular system. 9,27 

A Short Summary of Operation 

A short description of operation of the photoelectric 

plethysmograph has been provided by Challoner and 

Ramsay. 28 The fact that the absorption spectrum of the skin 

varies with oxygen content was known in 1943. Photoelectric 

plethysmography dates back to 1936, with the research 

conducted by Molitor and Kniazuk. 29 It was important that 

detection of oxygen content alone could not be the basis of 

measurement based on frequency; and it was found that at 

a frequency of 805 nm, both oxygenated and deoxygenated 

blood have the same absorption, thereby ensuring accuracy 

based on blood flow alone. 

Blood has a light absorption coefficient that is higher than 

surrounding tissue. This is a consequence of the Lambert-Beer 

law relating light absorption to optical density. Therefore, 

increases in the amount of blood give rise to decreased 

detected light. Erythrocytes and vessel walls also reflect light. 

However, reflection heavily dominates, and arterial pulses 

produce merely small reductions in detected light (1%–2%). 


Detected light variation is amplified and converted to a voltage 

signal. 6 There are many factors involved in the attenuation of 

light, including absorption, multiple scattering, and reflection. 

But all technical issues have been resolved, and small changes 

in patient profile are easily detectable. 

Blood Pressure Measurement Is Not Enough 

For many reasons, blood pressure measurement, even 

measuring the central aortic systolic, is highly problematic 

and is not definitive in diagnosing CVD because patient blood 

pressure varies significantly throughout the day, depending 

on stress level and physical activity. O’Shea and Murphy 

make it clear: “Thus, inconsistency in the selection of arms 

for BP measurement, by different techniques, may confound 

estimation of patients’ cardiovascular morbidity risk.” 31 Also, 

as Izzo and Shykoff comment, BP is a late-stage diagnostic: 

“Because wide pulse pressure and systolic hypertension are 

late manifestations of arteriosclerosis, they are only crude 

indicators of arterial wall disease.” 14 

Early DPA Detection in Diabetics – BP Measurement Failure 

Increased large artery stiffness contributes directly to 

the observed age-related increase in systolic pressure as the 

following illustration details. 14 

As this article was going to press, papers presented 

at the 2010 annual meeting of the American College of 

Cardiology (details published online at www.sciencedaily. 

com/releases/2010/03/100314091130.htm) and scheduled 

to be published in the New England Journal of Medicine 

(April 29, 2010) made clear that “hopeful” CVD interventions 

for type 2 diabetics aren’t effective: “ACCORD: Intensive 

BP, combined lipid therapies do not help adults with 

diabetes. Our results also showed a higher risk of serious 

adverse events with more intensive blood pressure control.” 

Shockingly, pharmacologically lowering blood pressure to 

normal levels – below currently recommended levels – did 

not significantly reduce the combined risk of fatal or nonfatal 

cardiovascular disease events in adults with type 2 diabetes 


who were at especially high risk for cardiovascular disease 

events, according to new results from the landmark Action to 

Control Cardiovascular Risk in Diabetes (ACCORD) clinical 

trial. (Note: Lowering blood pressure to below the standard 

level significantly cut the risk of stroke by about 40% (relative 

risk). The researchers caution, however, that participants in 

the intensive blood pressure group were more likely to have 

complications such as abnormally low blood pressure or high 

levels of blood potassium.) “Our results provide no conclusive 

evidence that targeting a normal systolic blood pressure 

compared with targeting a systolic blood pressure of less than 

140 mmHg lowers the overall risk of major cardiovascular 

events in high risk adults with type 2 diabetes.” Clinician 

Dr Roger Blumenthal, referring to triglyceride-lowering 

fenofribrate, states in Medscape’s Heartwire: 

But a lot of us in the cardiology community who manage 

high-risk diabetic patients thought we were doing 

patients a favor, thinking we were decreasing events at 

five years. So it was a bit of a surprise [pharma cologically 

lowering patient triglycerides failed]. 

The online CV News Digest for the American College 

of Cardiology stated: “According to studies presented at the 

American College of Cardiology meeting and to be published 

online March 18 by the New England Journal of Medicine: 

[A]ggressive treatment strategies doctors had expected 

would prevent heart attacks among people with type 

2 diabetes and some who are the verge of developing 

it have proved to be ineffective or even harmful. … 

Moreover, researchers found that Abbott’s drug TriCor 

(fenofibrate), even though it did lower triglyceride 

levels, did not stop patients from having strokes and 

heart attacks. 

If high-risk patients show no positive effect, it is unlikely 

that any patient will benefit with these interventions. 

Pharmacologic (artificial) – not physiologic lowering of BP 

may sound good, but doesn’t work. If you have followed my 

work you will understand why. For several years, I have been 

advocating an effective intervention to make patient arteries 

more compliant, which also positively affects lipid profiles 

without complications. 

Unlike other surrogates, a critically important aspect of the 

PWV is that “diastolic variability [arterial flexibility/compliance] 

in the plethysmograph is independent of arterial pressure.” 3 

Furthermore, plethysmography is extremely sensitive to small 

amounts of pulsatile blood flow, and most importantly, the 

amplitude of the plethysmograph signal is directly proportional 

to the vascular distensibility or flexibility. 3 Therefore, DPA is 

significantly superior to mere blood pressure measurement. 

➤ 

“Yet the adverse consequences of age-related 

arterial stiffening still receive little attention in 

everyday clinical practice, perhaps because 

clinicians assume that nothing can be done 

about the process.” 14 



➤ 

Fortunately, today there is an effective treatment with plantbased, 

bioidentical PEOs, as DPA measurement confirms. 

PWV Analysis with DPA Bests Ultrasound 

Ultrasound is insufficient to measure arterial compliance 

because arterial volume and the associated pressure cannot 

be simultaneously measured, and only a particular segment is 

scanned; DPA is significantly superior because it is a systemic 

measurement. The best method to estimate the distensibility 

and stiffness of the aorta and large arteries is PWV, because 

PWV is directly related to the stiffness of the large arteries. 

PWV directly correlates with aging, hypertension, renal failure, 

and other disorders affecting the cardiovascular system. To 

eliminate the need for central catheterization when measuring 

the central pulse contour, a transfer function was devised that 

reconstructs the central waveform from the peripheral. 33 

Aortic Stiffness (AI) Measurement 

An extremely useful parameter from this technique is termed 

the (systolic) augmentation index (AI), relating the magnitude 

of the reflected peak to the magnitude of the incident systolic 

pressure surge from the left ventricle contraction. The 

amplitude of the pulsatile component of the DVP is influenced 

by respiration, sympathetic nervous system activity, and other 

factors that influence local perfusion. The shape or contour of 

the pulse, however, remains approximately constant. 9 This is a 

significant reason for the reliability of this measurement of the 

system circulation – it is uninfluenced by transitory conditions 

such as patient stress level. 

efficiency is decreased by just 16% from arterial stiffness, 

then for the heart to sustain the same systemic blood flow 

(stroke volume), myocardial oxygen consumption increases 

significantly by 30% to 50%. 4 

Arterial Stiffness: Arteriosclerosis and Atheromatosis 

The physiology of the artery necessitates two separate 

pathologies, although they are typically combined into 

the single term atherosclerosis, which is nonspecific. 

Arteriosclerosis is typically referred to as a generalized 

thickening and stiffening of the media (see illustration below). 

Atheromatosis refers to the inflammatory occlusion response of 

the endothelial tissue (intima) in the lumen from oxidized lipid 

deposits, etc. These two processes often coexist. Over time, 

chronic inflammation makes vascular alterations irreversible. 

Therefore, early intervention is critical. In atheromatosis, lumen 

diameter is maintained until the final stage of the disorder. The 

process can be considered originating from the “inside out,” 

whereas arteriosclerosis is best defined as an “outside-in” 

process. Wall thickness and the outer arterial diameter both 

increase. Unfortunately, there are often no clinical symptoms 

until sudden death, an outcome cardiologists know too well. 

The pathologic hallmark of arteriosclerosis is thickening 

of the adventitia and media (see illustration) leading to excess 

arterial wall stiffness and systolic hypertension. There is also 

loss of and degradation of elastin fibers. 

DPA Diagnoses Hypertrophy 

It is important to note that “muscular arteries” are not equally 

affected by arterial hypertension, so “normal appearance” may 

be misleading, whereas DPA outputs are comprehensive and 

detect otherwise hidden arterial concerns. 

Important note: The intima is 100% parent omega-6 (LA), not 

found in fish oil. 

Diabetic Implications 

Endothelial dysfunction and increased arterial stiffness 

are associated with type 1 diabetes mellitus, both of which 

contribute to excess cardiovascular mortality in these kinds of 

patients. 

2010 Newsflash: AI Diagnoses Diabetic Arterial Stiffness 

Increased Aortic Stiffness = Excess Oxygen Consumption = 

Increased Risk for Heart Attack 

Increased aortic stiffness causes decreased cardiac efficiency 

(ratio of stroke work to oxygen consumption). If cardiac 

Treatment of CVD with PEOs 

O’Rourke and Kelly commented: “Delay or reduction in 

wave reflection is a logical strategy to apply in the management 

of hypertension. Priority is given to ACE inhibitors (angiotensinconverting-enzyme 

inhibitors) and beta-blockers which 

reduce cardiac output, or to drugs which decrease arteriolar 

resistance.” 4 While these drugs have garnered the spotlight, 

there is a new therapy that has direct physiologic and etiologic 

effect for arterial compliance – PEOs. 

Because of its simplicity, DPA can be employed in largescale 

epidemiological studies and be used to assess the effects 


of these new interventions. 9 Both the aorta and large arteries 

have slow turnover of both cells and matrix proteins. A main 

therapeutic aim in preventing and reversing CVD is to reduce 

arterial stiffness; i.e., produce sustained reduction in arterial 

pressure. 

Successful intervention: plant-based, bioidentical PEOs 

achieve this result naturally via numerous physiologic 

pathways. 

Prostacyclin (PGI 2 

) production to ensure platelets are 

free-flowing (natural blood-thinners), production of the 

body’s most potent anti-inflammatory – PGE 1 

– that 

both prevents and reverses thrombosis, incorporation 

of parent omega-6 into the epithelial tissue (intima) 

itself, along with incorporation directly into the media 

and adventitia, allowing maximum flexibility. PEOs, 

parent essential oils (plant-based) – not fish oils – 

in a ratio 1:1-2.5:1 LA/ALA, with more parent omega-6 

than parent omega-3, provide profound cardiovascular 

protection as evidenced by IOWA with 34 subjects, and 

the results are unprecedented: 

IOWA: Investigating Oils With respect to Arterial Blockage 


Brian Peskin, BSEE: Founder: Life-Systems Engineering Science with David Sim, M.D., Interventional Cardiologist 

(Based on 34 patients using the PEOs over 3 month and as long as 144 months) 

Age: 35-75 Median age: 62 22 females, 13 males 

Paired t-test. Median: 24 months PEO use / Mean: 90 months PEO use 

Significant differences (p 0.0015) with standard error of the mean +-5 years. 

Subject’s biological age being (average of) 8.8 years lower than their actual physical age. 

Note: This experiment has a 99.85% accuracy—30 times more accurate than the 5% standard error 

used in most clinical trials. Therefore, this result is not due to possible error and is highly significant 

with patient CV health 8.8 years better than physical age predicts. 

Analysis by Alex Kiss, Ph.D. (statistics) — January 21, 2010 

Analysis Variable : agediff 

N Minimum Maximum Mean Std Dev Pr > |t| 

34 -39.00 22.00 -8.82 14.84 0.0015 


Study Summary 

The above numbers, based on APG, mean as follows: 

There were 34 people who completed the study, using PEOs 

from 3 to 144 months. There was no baseline (the weakness 

of the study). Half were under two-year users, and half were 

over two years, double females to males. The subjects had 

their arteries studied and compared with accepted waveforms 

for age. The best subject was 39 years less than chronological 

age. The worst was 22 years over, and the only subject greater 

than chronological age. Overall, the mean age of arteries 

(flexibility) was 8.82 years less than chronological age. The 

p value (chance of this being chance only) was 15 in 1,000, 

indicating extremely significant results. 

Special thanks to renowned interventional cardiologist David 

Sim, MD, for his invaluable technical expertise, and to 

Michael Czajka (Australia) for introducing us to PWV and DPA 

technology. 

Notes 

1. Khoshdel AR, Carney SL, Nair BR, Gillies A. Better management of cardiovascular 

diseases by pulse wave velocity: combining clinical practice with clinical 

research using evidence-based medicine. Clin Med Res . 2007;5:45–52. 

2. Nijboer JA, Dorlas JC, Mahieu HF. Photoelectric plethysmography – some 

fundamental aspects of the reflection and transmission method. Clin Phys 

Physiol Meas. 1981;2:205–215. 

3. Shelley KH, Dickstein M, Shulman SM. The detection of peripheral venous 

pulsation using the pulse oximeter as a plethysmograph. J Clin Monit. 

1993;9:283–287. 

4. O’Rourke MF, Kelly RP. Wave reflection in the systemic circulation and its 

implications in ventricular function. J Hypertens. 1993;11:327–337. 

5. Murray WB, Foster PA. The peripheral pulse wave: information overlooked. 

J Clin Monit . 1996;12:365–377. 

6. Dorlas JC, Nijboer JA. Photo-electric plethysmography as a monitoring device in 

anaesthesia. Br J Anaesth . 1985;57:524–530. 

7. Cohn J, Finkelstein S, McVeigh G, et al. Noninvasive pulse wave analysis for the 

early detection of vascular disease. Hypertension. 1995;26:503–508. 

8. Mancia G, De Backer G, Dominiczak A, et al. 2007 Guidelines for the 

management of arterial hypertension: the Task Force for the Management of 

Arterial Hypertension of the European Society of Hypertension (ESH) and of the 

European Society of Cardiology (ESC). J Hypertens. 2007;25:1105–1187. 

➤ 

Brian Scott Peskin, BSEE, is available to discuss how you can incorporate 21 st -century DPA, anti-CVD technology 

into your practice. Brian 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, and was appointed 

adjunct professor at Texas Southern University in the Department of Pharmacy and Health Science from 1998 to 1999. 

He is chief research scientist at Cambridge International Institute for Medical Science ( www.CambridgeMedScience. 

org). Peskin integrates theory into practical applications – enhancing and extending the quality of life. He readily 

acknowledges his role as the messenger of critically important but overlooked information published in leading medical 

textbooks and medical journals. His medical insights and often-unique ability to “connect the dots” have given him an 

international following of leading physicians demanding state-of-the-art medical science in treating their patients. For 

more information, visit www.peskinpharma.com or contact prof-peskin@peskinpharma.com . 

Robert Jay Rowen, MD, is editor-in-chief of Second Opinion Newsletter (www.secondopinionnewsletter.co m). He is 

affectionately known as the “father of medical freedom” and was instrumental as an Alaskan physician in drafting legislation 

making Alaska the first state to provide statutory protection to alternative physicians (medical freedom law). While he 

continues to treat patients for conditions like heart disease and cancer, Dr. Rowen’s greatest desire is to help people avoid 

these diseases in the first place. He has nearly 30 years’ experience practicing alternative medicine, and is considered one of 

America’s foremost physicians practicing state-of-the-art, evidence-based medicine. 



➤ 

9. Millasseau SC, Ritter JM, Takazawa K, Chowienczyk PJ. Contour analysis of the 

photoplethysmographic pulse measured at the finger. J Hypertens. 2006;24:1449– 

1456. 

10. Millasseau SC, Kelly RP, Ritter JM, Chowienczyk PJ. Determination of age-related 

increases in large artery stiffness by digital pulse contour analysis. Clin Sci (Lond). 

2002;103:371–377. 

11. Hlimonenko I, Meigas K, Vahisalu R. Waveform analysis of peripheral pulse 

wave detected in the fingertip with photoplethysmograph. Measure Sci Rev. 

2003;3:49–52. 

12. Wilkinson IB, Cockcroft JR, Webb DJ. Pulse wave analysis and arterial stiffness. J 

Cardiovasc Pharmacol. 1998;32:S33–S37. 

13. Sherebrin MH, Sherebrin RZ. Frequency analysis of the peripheral pulse wave 

detected in the finger with the photoplethysmograph. IEEE Trans Biomed Eng. 

1990;37:313–317. 

14. Izzo JL Jr, Shykoff BE. Arterial stiffness: clinical relevance, measurement and 

treatment. Rev Cardiovasc Med. 2001;2:29–34,37–40. 

15. Peskin BS, Sim D. Vytorin failure explained – a new view of LDL. Townsend Lett. 

2008;299:101–112. 

16. McCullough PA, Chinnaiyan KM. Annual progression of coronary calcification 

in trials of preventative therapies: a systematic review. Arch Intern Med. 

2009;169:2064–2070. 

17. O’Malley P. A double take on serial measurement of coronary artery calcification. 

Arch Intern Med. 2009;169:2051–2052. 

18. Ridker P, Danielson E, Fonseca FA, et al. Rosuvastatin to prevent vascular 

events in men and women with elevated C-reactive protein. N Engl J Med. 

2008;359:2195–2207. 

19. Nazmi A, Victora CG. Socioeconomic and racial/ethnic differentials of C-reactive 

protein levels: a systematic review of population-based studies. BMC Public 

Health. 2007;7:212. 

20. Lehmann ED, Hopkins KD, Rawesh A, et al. 

Relation between number of cardiovascular risk 

factors/events and noninvasive Doppler ultrasound 

assessments of aortic compliance. Hypertension. 

1998;32:565–569. 

21. Blacher J, Asmar R, Djane S, London GM, Safar 

ME. Aortic pulse wave velocity as a marker of 

cardiovascular risk in hypertensive patients. 

Hypertension. 1999;33:1111–1117. 

22. Asmar R, Rudnichi A, Blacher J, London GM, Safar 

ME. Pulse pressure and aortic pulse wave velocity 

are markers of cardiovascular risk in hypertensive 

populations. Am J Hypertens. 2001;14:91–97. 

23. Blacher J, Guerin AP, Pannier B, Marchais SJ, 

Safar ME, London GM. Impact of aortic stiffness 

on survival in end-stage renal disease. Circulation. 

1999;99:2434–2439. 

24. Laurent S, Boutouyrie P, Asmar R, et al. Aortic 

stiffness is an independent predictor of all-cause 

and cardiovascular mortality in hypertensive 

patients. Hypertension. 2001;37:1236–1241. 

25. Kelly RP, Hayward C, Avolio A, O’Rourke 

M. Noninvasive determination of age related 

changes in the human arterial pulse. Circulation. 

1989;80:1652–1659. 

26. Lax H, Feinberg AW, Cohen BM. Studies of the 

arterial pulse wave and its modification in the 

presence of human arteriosclerosis. J Chronic Dis. 

1956;3:618–631. 

27. Hashimoto J, Chonan K, Aoki Y, et al. Pulse wave 

velocity and the second derivative of the finger 

photoplethysmogram in treated hypertensive 

patients: their relationship and associating factors. J 

Hypertens. 2002;20:2415–2422. 

28. Challoner AV, Ramsay CA. A photoelectric 

plethysmograph for the measurement of cutaneous 

blood flow. Phys Med Biol. 1974;19:317–328. 

29. Molitor H, Kniazuk M. A new bloodless method 

for continuous recording of peripheral circulatory 

changes. J Pharmacol Exp Ther. 1936;57:6–18. 

30. Jago JR, Murray A. Repeatability of peripheral 

pulse measurements on ears, fingers and toes using 

photoelectric plethysmography. Clin Phys Physiol 

Measure. 1988;9:319–329. 

31. O’Shea JC, Murphy MB. Ambulatory blood 

pressure monitoring: which arm? J Hum Hypertens. 

2000;14:227–230. 

32. Wilkinson IB, MacCallum H, Rooijmans DF, et al. 

Increased augmentation index and systolic stress in 

type 1 diabetes mellitus. QJM. 2000;93:441–448. 

33. Karamanoglu M, O’Rourke MF, Avolio AP, Kelly 

RP. An analysis of the relationship between central 

aortic and peripheral upper limb pressure waves in 

man. Eur Heart J. 1993;14:160–167. 

34. Davies JE, Baksi J, Francis DP, et al. The arterial 

reservoir pressure increases with aging and is the 

major determinant of the aortic augmentation 

index. Am J Physiol Heart Circ Physiol. 

2010;298:H580–H586. 

35. Levy D, Larson MG, Vasan RS, Kannel WB, Ho KK. 

The progression from hypertension to congestive 

heart failure. JAMA. 1996;275:1557–1562. 

©2010 Brian Scott Peskin 

TOWNSEND LETTER – MAY 2010

Cancer and Mitochondria Defects: 

New 21st Century Research 

by Brian Peskin, BSEE 

Founder, Life-Systems Engineering Science 

I recently presented at the 17th 

Annual World Congress on Anti- 

Aging Medicine in Orlando, Florida 

(April 2009), utilizing new research 

from 2007–2009 to identify the prime 

cause of cancer. Predictably, these 

findings caused quite a sensation. 

Numerous physicians met with me 

afterwards to applaud the presentation 

and discuss direct patient application 

in their practices. This article addresses 

the major points of my presentation, 

with a focus on clinical application. 

While environmental pollution and 

other factors certainly play a role in 

the cancer causing process, they are 

a topic unto themselves. “Connecting 

the dots” with this new information 

leads to a startling conclusion that we 

will now explore. 

What Cancer Isn’t 

First, let me state what cancer is not. 

Cancer is not an invader in our bodies 

like a virus or bacterial infection, nor 

is it a genetic distortion determined 

to kill us. Cancer is the body, at the 

cellular level, attempting to allow 

the injured tissue or organ to survive 

by reverting to a primitive survival 

mechanism. This definition is the 

result of embracing the latest research 

from a variety of disciplines whose 

practitioners include epidemiologists, 

geneticists, and oncologists in the 

forefront of their fields. 

More than 1.5 million 

Americans will be 

diagnosed with cancer 

this year, so effective 

prevention is vital. 

2008/2009 Cancer Research 

Breakthrough 

In remarkable research sponsored 

by the National Cancer Institute 

published in 2008 and 2009, 

researchers found major abnormalities 

in content or composition in a complex 

lipid called cardiolipin (CL). These 

abnormalities are “found in all tumors, 

linking abnormal CL to irreversible 

respiratory injury.” 1 Cardiolipin is a fatbased 

complex phospholipid found in 

all mitochondrial membranes, almost 

exclusively in the inner membrane, 

and is intimately involved in 

maintaining mitochondrial functionality 

and membrane integrity. It is 

used for ATP (energy) synthesis, and 

consists roughly of 20% lipids. 2 

Abnormalities in CL 

impair mitochondrial 

function. 

CL serves as an insulator and 

stabilizes the activity of protein 

complexes important to the electron 

transport chain. It also “glues” these 

protein complexes together. 3 While 

most lipids are linked together in the 

endoplasmic reticulum, cardiolipin is 

synthesized in the mitochondria. 

In mammals, the main 

substrate in CL is 

parent omega-6 (LA) 

with virtually no parent 

omega-3 (ALA) or its 

derivatives. 4 

This means that humans require 

plenty of functional omega-6 – 

the opposite of what many cancer 

researchers and physicians believe; 

they think it is cancer-causing (which 

it is if adulterated). 

Breakthrough research in 2006 

by Valeria Fantin and colleagues 

at Harvard University showed that 

although mitochondria may be intact 

in cancerous cells, they don’t function 

properly because their membranes 

have a high potential, not a low 

potential as they should. 4 Why does 

this physiologic change occur? The 

key is unadulterated, fully functional 

parent omega-6. 

Major American Heart Association 

Reversal: Omega-6 Is Good 

For over a decade, virtually all 

cancer researchers and physicians 

have scorned omega-6; however, in 

2009 the American Heart Association 

started championing parent omega-6 

because: “[O]mega-6 PUFAs also have 

powerful anti-inflammatory properties 

that counteract any pro-inflammatory 

activity.” 5 

The Cancer/Inflammation 

Connection 

Inflammation plays a large part in 

the development of cancer. This is 

exactly the condition that renowned 

cancer researcher Dr. Robert 

Weinberg of the Massachusetts 

Institute of Technology (MIT) spoke 

of in 2007: “The connection between 

inflammation and cancer has moved 

to center stage in the research arena.” 6 

It is fortunate that a cancer researcher 

of Weinberg’s stature has been 

influential in refocusing the research 

community’s attention. What does 

chronic inflammation cause? Massive 

➤ 

TOWNSEND LETTER – AUGUST/SEPTEMBER 2009 87

amounts of oxygen deployment to the 

inflamed tissue, if enough oxygen is 

available. 

Respiration vs. Glycolysis 

(Fermentation) 

Over 80 years ago, medical 

physicist, physiologist, and Nobel 

Prize-winner Otto Warburg, MD, 

PhD, proved that a 35% reduction in 

oxygen causes any cell to either die or 

turn cancerous. Meticulous (American) 

experiments performed by renowned 

researchers from 1953 to 1955 also 

confirmed the result. While it is 

understood that heart attacks can stem 

from lack of oxygen, this is also true of 

cancer. Most normal, healthy cells get 

the majority of their energy by using 

oxygen – in a process called cellular 

respiration (oxidative phosphorylation) 

that takes place in the mitochondria. 

However, cells can also utilize energy 

without oxygen, and this metabolic 

process is termed glycolysis. This 

energy method is useful for short-term 

energy expenditure, such as lifting a 

weight, but not for long-term energy 

requirements like running a marathon 

– it is too energy inefficient. Cancers 

live and ultimately thrive on the energy 

from glycolysis, and that is why they 

need such large vascular networks 

providing tremendous amounts of 

carbohydrates. Glycolysis is also a 

much simpler biochemical process, 

compared with cellular respiration 

(oxidative phosphorylation). In the 

presence of oxygen deficiency, cells 

that can’t obtain enough energy 

through glycolysis perish. But the cells 

that succeed in utilizing glycolysis 

exhibit their innate will to survive; 

these are the ones that don’t die from 

the oxygen deficiency. 

But there is a huge price to be paid 

for lack of oxygen: lack of cellular 

intelligence – these cells have the 

intelligence of “dumb yeast.” In 

essence, cancer is the “idiot cell” that 

can survive but do little more than 

reproduce more “idiot cells” with no 

fully functional mitochondria. 

Recently Released Research 

Changing Minds 

Most members of the medical and 

research professions, including those 

physicians who treat cancer, still 

mistakenly believe that the answer 

to the cancer puzzle will be found in 

oncogenes – genes that predispose 

the individual toward cancer. The 

following 2009 statement should give 

you pause: 

Nature provides a means to escape quick organ 

death caused by lack of oxygen by allowing 

anaerobic glycolysis, but at a price – that is, if the 

problem isn’t fixed, the benign tissue becomes 

malignant (cancerous) and ultimately destroys its 

host. 

concept has been advocated in the 

past, the most recent noteworthy 

research suggests that the cancerous 

tissue is the most oxygen-deprived 

tissue; that’s why that particular tissue 

became cancerous. 8 Once the cell 

is chronically oxygen deprived, the 

genetic material does change, but that 

is solely a consequence, not a cause. 

You’ve got much more to worry 

about than one cancerous area, since 

many tissues are oxygen deprived 

along with the cancerous ones. They 

just haven’t reached the critical 35% 

cellular oxygen deficiency threshold 

yet. 

“There is very little reason to be encouraged that 

prevention strategies can be revolutionized with 

what we’ve discovered so far [on the genetic basis 

of common diseases].” 

David Goldstein, Director 

Center for Population Genomics and Pharmacogenetics 

Duke University, Durham, North Carolina 

Geneticists Misled … 

In 2008, Scientific American 

published an article describing how 

cancer researchers had been led astray 

by renowned geneticist Lawrence 

Loeb’s claims of cancer’s 10,000 

to 100,000 mutations per cell. The 

reality was that there were only 65 to 

475 mutations per cell – not enough 

mutations to cause cancer! 7 That is 

why “more research” in this area 

often yields little, except to motivate 

the well meaning to contribute more 

money to finance those researchers’ 

wrong path. 

Cancer is a Systemic Problem – Not 

Just a Local One 

Many physicians approach cancer 

as a localized issue, meaning that 

they focus only on the affected tissue 

as the problem because the genes 

have been ruined there. While this 

“Breast cancer is not 

a local problem. It is a 

systemic [whole body] 

disease.” 9 

I’d like to acknowledge the extraordinary 

insight of the above 2009 

statement by Homer Macapintac, 

MD, chair and professor of nuclear 

medicine at the University of Texas 

M. D. Anderson Cancer Center. The 

proof of his statement follows. 

In 2007 it was reported that 

tumor-free breast tissue manifests 

precancerous epigenetic changes: “A 

new study using mastectomy tissue 

shows that precancerous changes 

can occur in normal-appearing areas 

of the breast as distant as two inches 

from a tumor’s edge.” 10,11 

Relying solely on genetics to 

explain this is difficult at best. 

With the wealth of new scientific 

information that has become available 

over the last two and a half years, it is 

reasonable to conclude that there has 

to be a physiologic (epigenetic) cause 

changing the distant tissue, not vice 

versa. 

88 TOWNSEND LETTER – AUGUST/SEPTEMBER 2009

Major News Flash in 2007: 

Physiologic Environment Triggers 

Cancer 

Genetic factors may be less 

important than initially thought. 

In 2007 it was also reported that 

scientists discovered a new type of 

cell that plays a significant role in 

the development of cancer – a highly 

volatile, precancerous stem cell 

(pCSC) that can either remain benign 

or become malignant, depending 

upon environmental cues. “[I]t 

appears that pCSCs require some sort 

of signal, or cue, from their immediate 

environment that directs them to 

become benign or malignant.” 12 

These cancer researchers are on the 

right path, and by now “connecting 

the dots” we understand that this 

environmental cue is lack of oxygen 

(hypoxia). 

Why Cancers Are Highly Resistant to 

Treatment Once They Return 

Oncologists already know that 

when cancer returns, chemotherapy 

often won’t work again. The reason 

for the returning cancer’s virulence 

requires understanding the following 

three key points: 

1. Chemotherapy and radiation 

kill both respiring (normal) and 

cancerous (fermenting) cells. If 

respiration (oxygen transfer) falls 

below a specific minimum, even 

for a cancer cell, that cell will die. 

Normal cells survive chemo and 

radiation better than cancer cells, 

because they start with a better 

respiration; therefore they have 

stronger residual respiration after 

chemo/radiation treatments. 

2. Oncologists understand that after 

chemo and radiation treatments, 

many normal cells are killed and 

many new cancerous cells are 

created in which glycolysis takes 

the place of the cells’ ruined 

respiration. These surviving de scendents 

of normal cells com pensate 

for decreased respiration with 

increased glycolytic capability. 

Therefore, the cells that live and 

haven’t been killed are now prime 

candidates for a continued oxygendeficient 

environment. Hypoxia 

won’t kill these cells, because they 

already thrive in a deoxygenated 

environment, making them harder 

to treat. 

3. Therefore, over time, these 

concentrated groups of functional 

hypoxic cells can easily become 

fully cancerous, capable of metastasis; 

they possess the exact 

conditions needed to cause more 

cancer in the future. Chemo and 

radiation will be much less effective 

the next time around because we 

have created (through “treatment”) 

a more efficient cell with decreased 

respiration capability that can better 

utilize glycolysis in a hy poxic 

environment; that is, cancer. 13–17 

Our cells are struggling 

to stay alive to keep 

the oxygen-deprived 

hypoxic organ alive, but 

they have a handicap 

and can’t get the 

necessary oxygen for 

respiration. 

2009 Revelation: Number One 

Cancer in Men Depends on Oxygen 

Level 

Very recently, a group of 

investigators studying prostate cancer 

reported: “Hypoxia, or reduced 

oxygen levels, in prostate tumors 

significantly predicts a poor longterm 

biochemical outcome, regardless 

of other prognostic factors…. We 

have followed the patients now for 8 

years and it turns out that the patients 

who had low prostate tumor oxygen 

levels had much worse outcomes and 

much more biochemical failures than 

patients who had normal or higher 

levels of oxygen in their tumors.” 18 

This is a problem because oxygen 

delivered to a tumor is critical to 

the treatment for many cancers. For 

example, radiation therapy creates free 

radicals that damage DNA in tumors, 

and oxygen acts as the mediator 

Mitochondria Defects 

that perpetuates the free radicals. 

This finding, along with many other 

medical journal reports concerning 

the hypoxia/cancer connection in 

nonprostate cancers, confirms that 

the greater the oxygen deficiency, the 

more virulent the cancer. 

A Possible Cause of Widespread 

Cellular Oxygen Deficiency 

Cellular oxygen deficiency occurs 

with long-term consumption of 

adulterated oils and fats courtesy of 

the food processing industry, crossing 

all socioeconomic barriers. Normal 

but harmful processing and refining 

ruin omega-6-containing oils, such as 

canola, safflower, and sunflower oils, 

and even many olive oils found in 

supermarkets. 

Tragically, we are 

unknowingly increasing 

the risk of contracting 

cancer by eating 

processed foods. 

The creation of trans fats by 

stopping the oxygenation capability 

of vital oxygenating fats is only one 

method used by food processors to 

obtain long shelf life. All commercial 

cooking oils have significantly 

impaired oxygen transferability. 8 

Nature in her wisdom has also 

provided us with an opportunity to 

fix this problem. Because full-blown 

cancer takes years to develop, often 

decades, we have the opportunity to 

remedy the cells’ oxygen deficiency. 

The great news is that it has already 

been proven that these precancerous 

cells can be kept in check so that 

they either stay benign or are killed 

as a result of the resupply of cellular 

oxygen. 

Identifying the Appropriate 

Omega-6:-3 Ratio 

My research emphasis over the 

past 15 years has been on deducing 

the appropriate supplemental ratio of 

➤ 

TOWNSEND LETTER – AUGUST/SEPTEMBER 2009 89

Mitochondria Defects 

➤ 

Figure 1: Group 2 (bottom) was pretreated with PEO formulation for 4 weeks prior 

to tumor implantation. Group 1 (middle) was pretreated for 2 weeks prior to tumor 

implantation. Group 3 (top) is the control. 

physiologic omega-6:-3 to maximally 

oxygenate cells and keep their 

mitochondria optimal. Parent omega-3 

(not fish oil derivatives, such as EPA) 

is required in each cell, although we 

require much more unadulterated 

parent omega-6. 19 Most physicians 

think that the majority of “parents” 

automatically become transformed 

into “derivatives,” so fish oil makes 

an appropriate supplement. This is 

questionable at best when referring 

to the most current research. It was 

published in 2008 that EFA derivatives 

(including DHA and EPA) are made “as 

needed” by the body and a maximum 

of only 1% to 5% of parents become 

derivatives; the majority, over 95%, 

remain as parents in the cell. 20 Other 

journal articles report less than 1% 

normal conversion amounts. 21 In view 

of these new findings, fish oils give 

a phar ma cologic overload of derivatives. 

Consequently, practitioners 

may need to reevaluate their recommendations. 

In my research, I commissioned and 

directed an experiment with mice to 

study the relationship between cancer 

growth rates and supplementation 

with Peskin Protocol PEOs. 22 Mice 

metabolize EFAs as humans do, so 

these experimental results are directly 

applicable to humans. This seminal 

experiment showed that, in spite of 

tumor implantation with 2 million 

cancer cells at once, there was a 

statistically significant 24% reduction 

in tumor size (growth) in the longer 

4-week pretreated mice compared 

with the control mice that received 

no PEO supplementation. In the last 

10 days of the experiment, there was 

a 42.8% lower growth volume of the 

tumors in the 4-week pretreated mice 

compared to the untreated mice. These 

results clearly show the increasing 

value of a longer pretreatment period 

of PEOs, and that PEO-based oils are 

modifying the cells’ internal structure 

in an epigenetic fashion, making them 

more cancer resistant. 

Notes 

1. Kiebish MA, Han X, Cheng H, Chuang JH, Seyfried TN. 

Cardiolipin and electron transport chain abnormalities 

in mouse brain tumor mitochondria: lipidomic evidence 

supporting the Warburg theory of cancer. J Lipid Res. 

2008;49:2545–2566. 

2. Krebs JJ, Hauser H, Carafoli E. Asymmetric distribution 

of phospholipids in the inner membrane of beef heart 

mitochondria. J Biol Chem. 1979;254:5308–5316. 

3. Zhang M, Mileykovskaya E, Dowhan W. Gluing the 

respiratory chain together: cardiolipin is required for 

supercomplex formation in the inner mitochondrial/ 

membrane. J Biol Chem. 2002;277:43553–43556. 

4. Fantin VR, St-Pierre J, Leder P. Attenuation of LDH-A 

expression uncovers a link between glycolysis, 

mitochondrial physiology, and tumor maintenance. 

Cancer Cell 2006;9:425–434. 

5. Harris WS, Mozaffarian D, Rimm E, et al. Omega-6 

fatty acids and risk for cardiovascular disease: a science 

advisory from the American Heart Association Nutrition 

Subcommittee of the Council on Nutrition, Physical 

Activity, and Metabolism; Council on Cardiovascular 

Nursing; and Council on Epidemiology and Prevention. 

Circulation. 2009;119:902–907. 

6. Stix G. A Malignant Flame. Sci Am. July 2007:60–67. 

7. The Special Edition of Scientific American (Vol. 18, No. 

3, August/September 2008) devoted the entire issue to 

cancer. 

8. Peskin BS, Carter MJ. 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? Med 

Hypotheses. 2008;70:298–304. 

9. Tumor-free breast tissue can have precancerous changes. 

Medical News Today, Jan 15, 2007. 

10. Singer E. Interpreting the genome. Technol Rev. January/ 

February 2009:48–53. 

11. Yan PS, Venkataramu C, Ibrahim A, et al. Mapping 

geographic zones of cancer risk with epigenetic biomarkers 

in normal breast tissue. Clin Cancer Res. 2006;12:6626– 

6636. 

12. Chen L, Shen R, Ye Y, et al. Precancerous stem cells have 

the potential for both benign and malignant differentiation. 

PLoS One. 2007;2:e293. 

13. Matsumoto S, Hyodo F, Subramanian S, et al. Low-field 

paramagnetic resonance imaging of tumor oxygenation and 

glycolytic activity in mice. J Clin Invest. 2008;118:1965– 

1973. 

14. Samuni AM, Kasid U, Chuang EY, et al. Effects of hypoxia 

on radiation-responsive stress-activated protein kinase, 

p53, and caspase 3 signals in TK6 human lymphoblastoid 

cells. Cancer Res. 2005;65:579–586 

15. Brown J. Tumor microenvironment and the response to 

anticancer therapy. Cancer Biol Ther. 2002;1:453–458. 

16. Hockel M, Schlenger K, Aral B, Mitze M, Schaffer U, 

Vaupel P. Association between tumor hypoxia and 

malignant progression in advanced cancer of the uterine 

cervix. Cancer Res. 1996;56:4509–4515. 

17. Hall EJ, Giaccia AJ, Giaccia AJ. Radiobiology for the 

Radiologist. Philadelphia: Lippincott; 1994:133–152. 

18. Turaka A, et al. Hypoxic prostate/muscle pO2 (P/M pO2) 

ratio predicts for biochemical failure in patients with 

localized prostate cancer: long-term result [abstract 5136]. 

Paper presented at: Annual meeting American Society of 

Clinical Oncology; May 31, 2009; Orlando, FL. 

19. Peskin BS. The scientific calculation of the optimum PEO 

ratio. Available at: www.brianpeskin.com. Accessed May 

23, 2009. 

20. Barceló-Coblijn G, Murphy EJ, Othman R, Moghadasian 

MH, Kashour T, Friel JK. Flaxseed oil and fish-oil capsule 

consumption alters human red blood cell n–3 fatty acid 

composition: a multiple-dosing trial comparing 2 sources 

of n–3 fatty acid. Am J Clin Nutr. 2008;88:801–809. 

21. Hussein N, Ah-Sing E, Wilkinson P, Leach C, Griffin BA, 

Millward DJ. Long-chain conversion of linolenic acid and 

alpha-linolenic acid in response to marked changes in 

their dietary intake in men. J Lipid Res. 2005;46:269–280. 

22. Perry Scientific Pre-clinical Oncology Group, San Diego, 

CA, 2004. 

Brian Scott Peskin earned his bachelor of 

science degree in electrical engineering from the 

Massachusetts Institute of Technology (MIT) in 1979. 

He founded the field of Life-Systems Engineering 

Science in 1995. Brian was appointed adjunct 

professor at Texas Southern 

University in the Department 

of Pharmacy and Health 

Science from 1998 to 

1999. He is chief research 

scientist at the Cambridge 

International Institute for 

Medical Science (www. 

CambridgeMedScience. 

org), exclusively devoting 

the last 5 years to the cause 

and solution of cancer. 

E-mail: prof-nutrition@ 

sbcglobal.net; www. 

BrianPeskin.com. 

u 

90 TOWNSEND LETTER – AUGUST/SEPTEMBER 2009

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