The Peskin PrimerUnderstanding Professor* Peskin’s Approach

The Perfect Ten — Ten Years in Ten PagesA decade of work by Prof. Brian Peskin

Pages 1 - 10

Relative Risk — Absolute DeceptionWhy “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,

1

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

2

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 peer-reviewed 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 state-of-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

4

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

5

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)

6

“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 <2% natural conversion of ALA to DHA and less than a mere 0.3% into EPA. Even babies adequately convert PEOs into derivatives. These physiologic facts have been obscured. Parent PEOs are much more significant as compared to derivatives, and no one until now has focused on them. The tables below exemplify key tissue physiology.

With all the focus on omega-3 fatty acids today, it is significant to note that the free fatty acids in human plasma ordinarily are composed of about 15% LA (linoleic acid, parent omega-6) and just 1% of ALA (alpha linolenic acid, parent omega-3), a 15:1 ratio with just 2% DHA (docosahexaenoic acid). Cholesterol esters and plasma phospholipids have ratios of 100:1 in favor of parent omega-6. Physicians need to know these important and critical facts.

7

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 backwards-physiologic 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 (<10%); it is fine to use for cooking, frying, etc.

Why do so many promote krill/fish oil?

They are simply wrong. Also, significant financial interests may be in play. Krill is cheap. Financial benefit is fine, IF and ONLY IF the science is correct. In this case it is tragically incorrect, and the science supports the direct opposite of fish oil’s “opinions and opinionated studies.” Widespread mistakes are nothing new in the fields of science and medicine. As the brilliant Galileo stated back in the 1600’s: “In question of science the authority of a thousand is not worth the humble reasoning of a single individual.”

Also, as Nobel Prize-winning physicist Richard Feynman brilliantly stated, “It does not make any difference how smart you are, who made the guess, or what his name is — if it disagrees with real-life results, it is wrong. That is all there is to it.” The IOWA experiment proves how wrong everyone is concerning fish oil and cardiovascular protection. State-of-the-art physiologic science will prevail.

How long to see results and what objective results can I expect to see in my patients?

Positive results of PEO supplementation often occur very quickly in patients, sometimes within a few days. However, for significant results to manifest, allow patients 3-4 months daily use, as this is the time frame that tissues require to incorporate a significant amount of PEOs. Fully solving PEO deficiency can take 12-18 months. If a patient has been taking fish oil, allow them sufficient time to see and feel improvements of at least 3 months. Examples of physiologic areas of improvement are included below, and also included in the “MacPhail and Sommerfield” testimonials.

10

Heart Health• Flexible Arteries• Clean Arteries• Fast Blood flow• Lower Blood Pressure• Improves Lipids

Brain Health• Better Clarity• Better Focus• Improved Memory• Helps Improve ADD & ADHD

Beauty• Healthier Skin• Less Dandruff• Less Cellulite• Healthier Hair• Eczema Improved

Appetite• Less Cravings• Less Hunger• Better Appetite Fulfillment

Hormones/Endocrine• Better Sexual Function• Smoother Pregnancies• Less PMS• Fewer Headaches

Anti-inflammation• Less Arthritis• Less Joint Pain/Swelling• Faster Healing

Diabetes• Less Sweet Cravings• Lower Blood Sugar• Less Neuropathy/ Retinopathy

Endurance• More Energy• Less Fatigue• Greater Intensity• Faster Recuperation

PEOsSUPPORT

11

Relative Risk — Absolute DeceptionWhy “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 off-kilter, 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.

12

• “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

13

14

“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

15

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

16

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 cholesterol-lowering drugs, this has unfortunately not translated into fewer heart

17

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!

18

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.

19

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

20

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:

21

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.)

22

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…

23

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 sleight-of-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.

24

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

25

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.

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.

Relative Risk — Absolute DeceptionWhy “Studies” are Misleading—Studies Aren’t Science

CambridgeMedScience.org

THE PHYSICIAN’S CONCISE GUIDE TO:THE PHYSICIAN’S CONCISE GUIDE TO:

- 27 -

Copyright 2011

Dedicated to advancing and publicizing breakthrough discoveries in the health sciences

TThere 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 off-kilter, 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 cholesterol-lowering 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

14

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 sleight-of-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

15

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

16

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.

IOWA Study ResultsRemarkable experimental results of

arterial compliance improvement with PEOsProfessor 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.

  1  

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.

  2  

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

  3  

Short-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

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. Comparison to Statins As a comparative example, statins, as reported by the pharmaceutical industry, have NNTs > 80 in preventing a cardiovascular event.

  4  

This means a minimum of 80 patients would need to be treated to see a single (1) positive outcome. In contrast, the PEOs improve a much more direct physiologic measure, i.e., arterial flexibility, in a profound way resulting in a remarkable 2.3 NNT. Statistics (Highly Significant) — 99% Accuracy

  5  

PEOs versus Fish Oil 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

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.

  6  

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. In contrast, the PEOs improve a much more direct physiologic measure, i.e., arterial flexibility, in a profound way resulting in a remarkable 1.2 NNT. 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

The Missing Link: EFA “Oxygen Magnets”

173

Scientific Studies Show That EFAs Prevent CancerThe 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.

The Hidden Story of Cancer

174

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 cancer-causing 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 metabo-lized 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..

The Missing Link: EFA “Oxygen Magnets”

175

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 inde-pendent 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.

The Hidden Story of Cancer

176

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 giv-en 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 ar-rived 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.

The Missing Link: EFA “Oxygen Magnets”

177

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 indica-tion 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.

The Hidden Story of Cancer

178

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 cancer-protective properties gained by taking parent EFAs in the ratios recommended in this book.

EFAs Provide Many More Health Benefits Above and Beyond Cancer ProtectionThis 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 en-ergy. 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.

What You Should Not Eat: Cancer-Causing Transfats (EFA Imposters)

331

The Power of PEOs (Parent EFAs) to Help Surgeons and Their Patients

Dr. ANDREA RONCARATI FERRARA-Via Montebello 1 tel: 0532/200234Specialista in Chirurgia Plastica RAVENNA-Viale Cilla 20 tel: 0544/456511Ricostruttiva 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 med-icazioni, 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 guari-gione dei pazienti è migliore.

Infine credo fermamente sia giusto continuare su questa interessantis-sima strada intrapresa in particolare sul meccanismo dei tessuti riparativi.

Dr. Andrea Roncarati

The Hidden Story of Cancer

332

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 rec-ommendations, 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 im-proves patient recovery.

This improved recovery included: 1. faster healing2. less inflammation3. less scar tissue and4. less pain to the patient.

I finally believe and feel it is necessary to continue this very interesting tis-sue repair in the near future.

Dr. Roncarati Andrea

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 increasedcellular oxygen increases the effectiveness of both chemotherapy and radiation treatmentsin destroying cancer cells.

It was extremely gratifying to learn of this, since the Peskin Protocol is designed toincrease cellular oxygen throughout the body, including at cancerous sites.

James B. Mitchell, Ph.D., head of the tumor biology (NCI-radiation biology branch) section atthe National Cancer Institute, reported in an article published by Radiological Society ofNorth America (4/23/2008):

· “…‘[T]hey were able to successfully measure oxygen levels in tumors,’ whichcould 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 easilyby making the DNA destruction more difficult.’

· “‘Chemotherapy drugs also don’t work as well when tumors have lessoxygen.’” (emphasis added)

I immediately began searching medical journal articles to see if this critical concept was well-understood. The following comments comprise a (small) representative sample of what Ifound:

RADIATION ADJUNCT THERAPY:

· “A large body of published evidence points to tumor hypoxia as a majorobstacle to effective treatment of tumors using ionizing radiationa,b becausecells exposed to radiation under hypoxic conditions are approximately thrice [3times] more resistant than when treated under aerobic conditions.c (emphasisadded)

· “Despite significant evidence of a role of hypoxia [low cellular oxygen] in cellularresistance to ionizing radiation–induced toxicity, the underlying molecularmechanisms remain unclear. This study focused on the influence of hypoxia onradiation-induced signals in TK6 human lymphoblastoid cells.d (emphasis added)

• OVER •

CHEMOTHERAPY ADJUNCT THERAPY:

· “Solid tumors frequently contain large regions with low oxygenconcentrations (hypoxia). The hypoxic microenvironment induces adaptivechanges to tumor cell metabolism, and this alteration can further distort the localmicroenvironment. The net result of these tumor specific changes is amicroenvironment 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 toionizing radiation and chemotherapy resistance by depriving tumor cells of theoxygen essential for the cytotoxic activities of these agents. Hypoxia may alsoreduce tumor sensitivity to radiation therapy and chemotherapy through one ormore 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: JBLippincott Co.; 1994. p. 133–52.b Samuni, A., et al., “Effects of Hypoxia on Radiation-Responsive Stress-Activated Protein Kinase, p53, andCaspase 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 cytotoxicchemotherapy,” 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 RadiationTherapy and Chemotherapy?,” The Oncologist 2004;9(suppl5):31-40.

• OVER •

80 TOWNSEND LETTER – MAY 2010

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

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 electro-mechanical 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).

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

“[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

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

TOWNSEND LETTER – MAY 2010 81

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

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

➤

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

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

82 TOWNSEND LETTER – MAY 2010

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

Clinical Cardiology

➤

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

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) Reflectedwavefromthesmallartery. 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).

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%).

TOWNSEND LETTER – MAY 2010 83

➤

Clinical CardiologyDetected 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

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 man-age 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.

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

“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

84 TOWNSEND LETTER – MAY 2010

Fortunately, today there is an effective treatment with plant-based, 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.

Clinical Cardiology

➤

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

Important note: The intima is 100% parent omega-6 (LA), not found in fish oil. 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 (angiotensin-converting-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 large-scale epidemiological studies and be used to assess the effects

TOWNSEND LETTER – MAY 2010 85

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 sti�ness; i.e., produce sustained reduction in arterial pressure.

Successful intervention: plant-based, bioidentical PEOs achieve this result naturally via numerous physiologic pathways.

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.

Notes1. 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.

Clinical Cardiology

➤

Prostacyclin (PGI2) production to ensure platelets are free-flowing (natural blood-thinners), production of the body’s most potent anti-inflammatory – PGE1 – 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:

Brian Scott Peskin, BSEE, is available to discuss how you can incorporate 21st-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 a�ectionately 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.

IOWA: Investigating Oils With respect to Arterial BlockageSigni�cant di�erences in biological age compared to physical age

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)

Paired t-test. Median: 24 months PEO use / Mean: 90 months PEO use

Signi�cant di�erences (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 signi�cant with patient CV health 8.8 years better than physical age predicts.

N Minimum Maximum Mean Std Dev Pr > |t|

34 -39.00 22.00 -8.82 14.84 0.0015

Analysis by Alex Kiss, Ph.D. (statistics) — January 21, 2010Analysis Variable : agedi�

Age: 35-75 Median age: 62 22 females, 13 males

TOWNSEND LETTER – MAY 2010

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

Clinical Cardiology➤

TOWNSEND LETTER – AUGUST/SEPTEMBER 2009 87

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.

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 fat-based complex phospholipid found in all mitochondrial membranes, almost exclusively in the inner membrane, and is intimately involved in maintaining mitochondrial function-ality and membrane integrity. It is used for ATP (energy) synthesis, and consists roughly of 20% lipids.2

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

More than 1.5 million Americans will be diagnosed with cancer this year, so effective prevention is vital.

Abnormalities in CL impair mitochondrial function.

In mammals, the main substrate in CL is parent omega-6 (LA) with virtually no parent omega-3 (ALA) or its derivatives.4

Cancer and Mitochondria Defects: New 21st Century Research

by Brian Peskin, BSEE Founder, Life-Systems Engineering Science

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.

This means that humans require plenty of functional omega-6 – the opposite of what many cancer

➤

88 TOWNSEND LETTER – AUGUST/SEPTEMBER 2009

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:

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.

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.

“Breast cancer is not a local problem. It is a systemic [whole body] disease.”9

“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, DirectorCenter for Population Genomics and PharmacogeneticsDuke 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

I’d like to acknowledge the extra-ordinary 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.

TOWNSEND LETTER – AUGUST/SEPTEMBER 2009 89

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 scen-dents 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 oxygen-deficient 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 metas-tasis; 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 bet-ter utilize glycolysis in a hy poxic environment; that is, cancer.13–17

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. 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.

Tragically, we are unknowingly increasing the risk of contracting cancer by eating processed foods.

Mitochondria Defects

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 long-term 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

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

➤

90 TOWNSEND LETTER – AUGUST/SEPTEMBER 2009

Mitochondria Defects

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 deriva-tives. Consequently, practitioners may need to reevaluate their recom-mendations. 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.

Notes1. 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.

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.

u

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.

➤

IOWA Study ResultsRemarkable experimental results of

arterial compliance improvement with PEOsProfessor 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.

  1  

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.

  2  

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

  3  

Short-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

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. Comparison to Statins As a comparative example, statins, as reported by the pharmaceutical industry, have NNTs > 80 in preventing a cardiovascular event.

  4  

This means a minimum of 80 patients would need to be treated to see a single (1) positive outcome. In contrast, the PEOs improve a much more direct physiologic measure, i.e., arterial flexibility, in a profound way resulting in a remarkable 2.3 NNT. Statistics (Highly Significant) — 99% Accuracy

  5  

PEOs versus Fish Oil 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

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.

  6  

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. In contrast, the PEOs improve a much more direct physiologic measure, i.e., arterial flexibility, in a profound way resulting in a remarkable 1.2 NNT. 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