1 Professor Brian Scott Peskin* The Real Science behind Essential Fatty Acids, Cancer, and Heart Disease: An Analysis of the Science behind both the Failure

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Professor Brian Scott Peskin*

The Real Science behind Essential Fatty Acids, Cancer, and Heart Disease: An Analysis of the Science behind both the Failure of Fish Oil, and

the Astounding Success of Plant-Based Oils (PEOs) as confirmed by Photoplethysmography

(IOWA Experiment)

Smart Life Forum March 17th, 2011 Palo Alto, California

*Brian Peskin earned his Bachelor of Science degree in Electrical Engineering from Massachusetts Institute of Technology (M.I.T.) in 1979. He 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 Brian's discoveries: "...His nutritional discoveries and practical applications through Life-Systems Engineering are unprecedented.“ 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.

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“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.”

Richard Feynman, Nobel Prize-winning

physicist

“Belief without understanding is stupidity. Mere generalized statements without sharp, specific conclusions are meaningless.”

Brian Peskin, Life-Systems Engineering Scientist

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REQUIREMENT:

Let’s start to understand without opinion or pre-conceived notions.Follow the science…

“…What should bother you [about incorrect published

results] is that a lot of people read it and couldn’t tell the

difference. There are so many people out there not being

skeptical, or not understanding what they are doing.

“They’re all just following along. That’s what we

have—too many followers and not enough leaders.”

Richard Feynman, Nobel Prize-winning physicist

The Real Science Behind Essential Fatty Acids

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“Why almost everything you hear about medicine is wrong:”a

• “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.

• “The result is a system that leads patients and physicians astray—spurring often costly regimens that won’t help and may even harm you.

• “…[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.

• “As the new chief of Stanford University’s Prevention Research Center, [John P.A.]Ioannidis, MD, DSc, is cementing his role as one of medicine’s top myth busters. ‘People are being hurt and even dying’ because of false medical claims, he says: not quackery, but errors in medical research…. “… most biomedical studies are wrong.

• “In just the last two months, two pillars of preventive medicine fell…. Drug companies make a mint on such dicey statistics. By testing an approved drug for other uses, they get hits by chance…With billions of dollars on the line, companies are loath to declare a new drug ineffective.

• “That made Ioannidis wonder, how many biomedical studies are wrong? His answer, in a 2005 paper: ‘the majority.’

a. Begley, S., “Why Almost Everything You Hear About Medicine is Wrong,” Newsweek, January 31, 2011, pages 8-9.

1) Newsweek, January 2011, pages 8-9. 5

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Deceptive Statistics Mislead Patients…. Studies Aren’t Science!

- continued • “Stanford, 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.’” (Emphasis added.)

• 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.

• Experimental results MUST CONFIRM science‘s prediction, not be counter to it.

• Is Gravity Confirmed on a Weekly Basis? Of course, not. 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?”

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Absolute Risk vs Relative (“Endpoint”) Risk — A Case Studyin Tortured Logic

Question: What is the difference between 2 successes in 1,000,000 (drug) vs. 1 success in 1,000,000 (placebo)?

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Drug2 patients successes out of1,000.000 patients treated

Placebo1 patient successes out of1,000.000 patients treated

-VS-

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!

Never Forget: Absolute Risk MUST Include Sample Size

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Example: Sun Rises at 6am.

• There is little use with mere “associations” found in Epidemiology.

• Cause/Effect Relationships are Mandatory!

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Focus on Physiology

Studies are often open to (mis)interpretation and mistakes in statistical analysis.a “Studies” should be used only to confirm predicted effects of known physiology / biochemistry, metabolic pathways –

Magical “We have no idea how it works…” is ~ not acceptable ~

• Experiment vs “study & mere associations:”

* Experiments count because only 1 variable is changed. * “Associations” are worthless because they do not prove cause/effect relationships at all.

a. 50% of top medical journals used incorrect statistics and therefore reported WRONG CONCLUSIONS. Primer of Biostatistics, Stanton A. Glantz, McGraw-Hill Medical Publishing Division, New York, 2002. Further reference: “How to Detect, Correct, and Prevent Errors in the Medical Literature,” Circulation, 61: 1-7, 1980. 9

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PEOs: Parent Essential Oils(Bio-Identical EFAs)

Parent Essential Oils = Parent Omega-6 +

Parent Omega-3

I coined this term, PEOs, to to clearly delineate between Parent PEOs & Derivative EFAs.

• Parent EFAs − PEOs − are Essential

• Derivative “EFAs” are NOT EFAs because the body makes these derivatives (longer chain) from the parent oils “as needed.” 10


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True EFAs are Bio-Identical PEOs — The Essential Similarity

The Key — PEOs — in particular, parent omega-6 in Esterified Cholesterol

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So close and Yet so Far …..The Key MistakeNot Distinguishing Between Adulterated and Unadulterated, functional PEOs Brown and Goldstein, two 1985 Nobel Prize-winners in physiology and medicine, stated in 2001:a

“How does elevated plasma LDL produce the complex lesions of atherosclerosis…The answer may lie in the unsaturated fatty acids [functional unadulterated PEOs] of the cholesteryl esters and phospholipids of which LDL is composed…. Within the artery wall other unsaturated fatty acids [PEOs] of LDL can undergo oxidation…. “

Life-Systems Engineering Science Analysis: Tragic failure not to distinguish between adulterated and unadulterated essential fatty acids (PEOs) or realize that the two types would produce very different results (disease or health). Brown and Goldstein correctly showed that cholesterol itself has nothing to do with atherosclerosis; it is just a transport vehicle of tremendous amounts of the often adulterated PEOs (LA, parent omega-6 and ALA, parent omega-3).

a. Goldstein JL, Brown MS. Molecular medicine. “The cholesterol quartet.” Science 2001;292:1310-2. [Medline]

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FAILURE 1: Nov. 2010 DHA (also found in krill oil, algae, mussels, etc.) failed to improve cognitive impairment in Alzheimer disease victimsa

a. Quinn, J, et al., “Docosahexaenoic Acid Supplementation and Cognitive Decline in Alzheimer Disease: A Randomized Trial,” Journal of the American Medical Association, November 3, 2010—Vol. 304, No. 17, pages 1903-1911.

In 2010 there were 4 major failures in experiments using DHA, the “active ingredient” in fish oil to either prevent or reverse disease:

2010: Four more fish oil FAILURES: There are NO metabolic pathways leading to “spectacular” results.

To the contrary, they led to expected FAILURE…

• “Conclusion: Supplementation with DHA compared with placebodid not slow the rate of cognitive and functional decline inpatients with mild to moderate Alzheimer Disease.

• “This study was designed to determine of supplementation withDHA would slow the rate of cognitive and functional decline inpatients with mild to moderate Alzheimer Disease. Despiteenrollment of the target population of individuals with lowbaseline DHA…

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Continued… • “The hypothesis that DHA slows the progression of mild tomoderate Alzheimer Disease was not supported, so there is no basis for recommending DHA supplementation for patients with Alzheimer Disease.

• “In summary, these results indicate that DHA supplementationis not useful for the population of individuals with mild tomoderate Alzheimer Disease.”

• However, “a higher level of α-linolenic acid (ALA; 18:3n-3) [parent omega-3] significantly decreased the risk of mild dementia.... In conclusion, ALA derived from plant sources of n-3 PUFA, butnot eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]from fish, decreased the risk for mild dementia among the Koreanelderly.” [Quinn, J, et al., “Docosahexaenoic Acid Supplementation and Cognitive Decline in Alzheimer Disease: A Randomized Trial, ”Journal of the American Medical Association, November 3, 2010, Vol. 304, No. 17, pages 1903-1911.]

Life-Systems Engineering Science Commentary: Once again, a carefully controlled study FAILS to show that the active ingredient in fish oil has little benefit for a human being. The EFA derivative Docosahexaenoic acid (DHA) is the most abundant long-chain polyunsaturated fatty acid in the brain. If fish oil was beneficial, we should certainly see a positive result in Alzheimer’s patients. The length of time is sufficient to see an improvement. There wasn’t any improvement. This negative result shows that the EFA-derivative DHA offers nothing to “solving the Alzheimer’s problem.” yet parent omega-6 does.

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FAILURE 2: March 2010 Newsflash: Fish Found Worthless in Decreasing Abnormal Heart Rhythm (AF–atrial fibrillation)a

FAILURE AGAIN: Contrary to many report claims, the American Journal of Cardiology reported in 2010 that eating lots of fish did nothing to help an abnormal heartbeat.

However, in contrast to omega-3’s FAILURE, parent omega-6 is effective, as reported in the world’s leading medical journal, Lancet (Riemersma, RA, et al., “Dietary fatty acids and ischemic arrhythmias,” Lancet, 1988;i:285-6). Parent omega-6 did help reverse AF.

a. Berry, J, et al., “Dietary Fish Intake and Incident Atrial Fibrillation (from the Women’s Health Initiative),” The American Journal of Cardiology, Vol. 105, Issue 6, Pages 844-848 (15 March 2010).

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FAILURE 3: June 2010 - “Women With Type 1 Diabetes Receive No Heart Benefit From Omega-3,”a

“Consuming higher amounts of omega-3 fatty acids [derivatives] does not appear to lower heart disease risk for women with type 1 diabetes, according to a University of Pittsburgh Graduate School of Public Health study presented at the 70th Scientific Sessions of the American Diabetes Association.

“Omega-3 fatty acids [omega-3 derivatives], primarily found in fish, [supposedly] promote heart health by preventing the buildup of cholesterol in the arteries. Little is known about the effect of consuming omega-3 in people with type 1 diabetes, who are at much greater risk for heart disease.

“Although omega-3 [derivatives] is typically associated [although not causal] with decreased risk for cardiovascular disease, this may not be the case for women who have type 1 diabetes….”

◗ Life-Systems Engineering Science CommentaryFAILURE AGAIN : We see how fish oil FAILS in preventing heart disease. The population group is Type I diabetic women — a treatment group that needs as much assistance as possible because diabetics have a significantly increased risk of cardiovascular disease. Therefore, this is an ideal population and easierto utilize to see if the fish oil stops heart disease.

Once again, fish oil FAILED miserably. The article mentions fish oil’s supposed metabolic pathway of cholesterol reduction and how fish oil is merely “associated” with a supposed reduction in CVD. Mere “associations” in medicine and medical science are meaningless. True experiments showing direct “cause/ effect” relationships are required and when these are performed, fish oil FAILS time and time again.

a. Medical News Today (Diabetes), Article URL: http://www.medicalnewstoday.com/ articles/193107.php, June 28, 2010.

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a. Woodworth, Hillary, L., et al., “Dietary Fish Oil Alters T Lymphocyte Cell Populations and Exacerbates Disease in a Mouse Model of Inflammatory Colitis," Cancer Res 0008-5472.CAN-10-1396; Published Online First August 26, 2010; doi:10.1158/0008-5472.CAN-10-1396. Cancer Res; 70(20); 7960–9; “Link Between Fish Oil And Increased Risk Of Colon Cancer In Mice,” Medical News Today (Colorectal cancer), Article URL: www.medicalnewstoday.com/ articles/203683.php#post, October 7, 2010.

•“‘We found that mice developed deadly, late-stage colon cancer when given high doses of fish oil,’ [researcher Fenton] said.”

• “More importantly, with the increased inflammation, it only took four weeks for the tumors to develop. “…not only the mice receiving the highest doses of DHA but those receiving lower doses as well.”

• “‘Our findings support a growing body of literature implicating harmful effects of high doses of fish oil consumption in relation to certain diseases, Fenton said.’”

• “We hypothesized that feeding fish oil enriched with DHA to mice would decrease the cancer risk; we actually found the opposite.’”

• “Contrary to expectations, DFO [dietary fish oil] induced severe colitis and adenocarcinoma [epithelial tissue cancer of the colon] formation. DFO consumption was associated with decreased CD8+ cell frequency and diminished CD69 expression on CD4+ and CD8+ T-cell populations. Mice consuming DFO also exhibited higher FoxP3+ CD25+ CD4+ T regulatory cell frequency, FoxP3 expression, and altered L-selectin expression during infection.”

• “[Fenton] said people already receiving enough omega-3 fatty acids through their normal diet and foods have no need for added supplementation.” `

FAILURE 4: Oct. 2010: Warning! Fish Oil Increases Risk of Colon Cancera

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More Fish Oil FAILURES – Continued• Fenton and her fellow researchers fully expected the fish oil to have the opposite and extremely positive effect of reducing cancer risk — not increasing it like it did!

DANGER: This result is directly aligned with the fact that this cancer, adenocarcinoma, occurs in epithelial-based tissue (such as the lining of the colon). There is no omega-3 component to epithelial tissue (just as with skin). Omega-3 supplementation cannot benefit epithelial tissue; a pharmacological overdose of omega-3 derivatives is predicted to harm such tissue, which it does.

• DHA and EPA from fish oil supplements range from a minimum of 20-fold overdoses of DHA to 250-500-fold overdoses of EPA—far more than your body would ever produce on its own. Even so-called “low dose” fish oil supplementation approaches these overdose values.

• It is also significant that Fenton points out that her findings “support a growing body of literature implicating harmful effects of high doses of fish oil consumption in relation to certain diseases.”

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• FAILURE 1995: Fish Oil is completely worthless in preventing or reversing heart disease. (Frank M. Sacks, et al., “Controlled Trial of Fish Oil for Regression of Human Coronary Atherosclerosis,” Journal of the American College of Cardiology Vol. 25, No. 7, June 1995: 1492-8.)

* The daily dose was 6 grams of fish oil vs. 6 grams of olive oil in the control group. *“Fish oil treatment for 2 years DOES NOT promote major favorable changes in diameter of

atherosclerotic coronary arteries.”

• FAILURE 1999: Again, Fish Oil is shown to be completely worthless in preventing heart disease. (“Clemens von Schacky, et al., The Effect of Dietary Omega-3 Fatty Acids on Coronary Atherosclerosis: A Randomized, Double-Blind, Placebo-Controlled Trial, ”Annals of Internal Medicine;130:554-562, 1999.)

* “Ingestion of fish or other sources of omega-3 fatty acids, such as fish oil capsules , has been called a comprehensive strategy toward the prevention of atherosclerosis.”

* However, at the end of 2 years, BOTH groups had worsened clogging. The same NEGATIVE result as in 1995 above.

MANY MORE Fish Oil FAILURES!

No surprise: There aren’t supporting metabolic pathways

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DHA/Fish Oil FAILURE – a long history of consistent FISH OIL FAILURES as reported in the world’s leading medical journals for over 15 years! …


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• FAILURE 1986: Fish Oil makes existing heart disease WORSE. (Knapp, H, et al., “In vivo indexes of platelet and vascular function during fish-oil administration in patients with atherosclerosis,” The New England Journal of Medicine, Vol. 314, April 10, 1986, No. 15, pages 937-942.)

“...In patients with atherosclerosis, prostacyclin biosynthesis fell by a mean [average] of 42% during the fish-oil period.”

Prostacyclin (PGI2) is the body’s natural blood thinner and keeps platelets apart naturally. The last thing a CVD patient needs is a reduction in this critical substance. CVD patients require more, NOT less PGI2. Decreased PGI2 significantly increases − not decreases − the risk and severity of any heart attack.

Surprise − Fish Oil Makes CVD WORSE! There is a defined metabolic pathway explaining why − fish oil

suppresses PGI2 synthesis!

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• FAILURE 2002: Fish Oil is completely worthless in preventing or reversing heart disease. (Angerer, P., et al., “Effect of dietary supplementation with omega-3 fatty acids on progression of atherosclerosis [plaque buildup in interior of arteries] in carotid [heart to brain] arteries,” Cardiovascular Research; 54:183-190, 2002.)

* The daily dose was 1.65 grams of fish oil vs. 6 grams of olive oil (no DHA-EPA) in the control group.

* “In this group of selected patients with documented coronary artery disease, omega-3 PUFA [fish oil polyunsaturated fatty acids] given for 2 years did not demonstrate an effect on slowing progression of atherosclerosis in carotid arteries as measured by ultrasound.”

• FAILURE 2003 : Fish (oily fish) itself is worthless and fish oil had adverse effects in preventing or reversing heart disease. (Burr, et al., “Lack of benefit of dietary advice to men with angina: results of a controlled trial,” Eur J Clin Nutr 2003, 57:193-200.) This study looked at patients with angina (severe heart pain caused by restricted blood flow) to be divided into two groups; those consuming more fish and those consuming fish oil supplements:

- Those patients eating two servings of fish weekly, had no “protection” benefit from death due to cardiovascular causes. If consuming fish helped heart-related health then one would expect to see fewer deaths from the fish eaters. This did not happen.

- Those patients consuming three (3) fish oil capsules (omega-3-derivatives) daily had an adverse (negative) effect! The fish oil capsules harmed them because this group had more cardiovascular-related deaths.

Fish Oil Fails and Fails and FAILS …

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DHA/Fish Oil FAILURE -- there is a long history of FAILURE to prevent or reverse cardiovascular disease (CVD)


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• FAILURE 2000: Fish Oil decreases immune responsea

• “…[S]tudies indicate that at the levels used, fish oil [omega-3 derivatives] decrease a wide range of immune cell responses (natural killer cell, cytotoxic T lymphocyte activities, lymphocyte proliferation and production of IL-2 and IFN-y (1,2))….

* “…Recent studies have indicated that relatively low levels of

the long chain omega-3 fatty acids (EPA or DHA)…are sufficient to bring about some of the suppressive effects …”

** WARNING: DHA & EPA even in low doses cause these immune suppressive effects. **

Is Fish Oil good for anything positive?

No.

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a. Calder, P., “Omega-3 Polyunsaturated Fatty Acids, Inflammation and Immunity,” Institute of Human Nutrition, University of Southampton, Bassett Crescent End, Southampton, UK. Presented at: The International Society for the Study of Fatty Acids and Lipids (ISSFAL) 4th

Congress, which met on June 4-9, 2000 in Tsukuba, Japan.


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Doesn’t Fish Oil Increase Immunity? No. Fish Oil Lowers Immunity!

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Confirmation of lowered immunity from fish oil:

A drug called Omacor® (Lovaza)* consists of approximately 90% active fish oil(omega-3 derivatives). It is used to reduce high levels of triglycerides.

However, according to the manufacturer’s 2005 medical brochure:

• Under “Adverse Reactions,” there were double the number of people who developed infections (reduced immunity) while taking the drug compared with those not taking the drug!

• Users suffered more flu syndrome, indicating a lowered immune system.

• 4 times more people suffered skin rash while taking the drug.” Note: You will discover why the skin rash result is predicted based on their oil EFA-based formulation.

* © 2005 “Introducing The Body of Evidence,” Reliant Pharmaceuticals, Inc. (September 2005), page 17.


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• FAILURE 2004: Fish Oil worthless in decreasing inflammation (CRP) Mori, T., et al., Current Atherosclerosis Reports; 6:461-467, 2004, “Omega-3 Fatty Acids and Inflammation.”)

*“No evidence for an anti-inflammatory effect as judged by CRP levels…”

• FAILURE 1992, 1990, 1988: Fish Oil creates abnormalities [tissue] in brain.a

• “Feeding of fish oil [omega-3 “derivatives”] to adult rats resulted in a rapid increase in levels of 22:5n-3 and 22:6n-3 as well as 20:5n-3 [omega 3 series] (which is usually present in brain in only trace amounts) with corresponding decreases in 22:5n-6 as well as 20:4n-6 [omega-6 series]...”

• “Nevertheless, the findings may be of relevance to questions concerning the provision of long-chain n-3 FA [from fish oil] in human infant feeding.”

a. Bourre, J.M., et al., Biochim. Biophys. Acta 969, 1988, pages 458-461; Bourre, J.M., et al., Biochim. Biophys. Acta 1043, 1990, pages 149-152;

Carlson S.E., and Salem Jr., N. “Health Effects of ω-3. Polyunsaturated Fatty Acids in Sea Foods,” (edited by Simopoulos, A.P., et al.), Krager, Basel, Switzerland, Vol. 8, 1991, pages 74-86; P.E. Wainwright, et al., “The Effects of Dietary n-3/n-6 Ratio on Brain Development in the Mouse: A Dose Response Study with Long-Chain n-3 Fatty Acids,” Lipids, Vol. 27, no 2 (1992), pages 98-103.

Fish Oil decreases Inflammation doesn’t it? No, but it does cause harmful brain abnormality

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• FAILURE 1988, 1989, 2003:

Fish Oil raises blood sugar levels and blunts insulin response.a

*“The glycemic [blood sugar] control of [all of] the four insulin dependent diabetic patients worsened during the fish oil administration.”

* “Glucose tolerance during the mixed meal profile also deteriorated significantly.”

* “…[T]he insulin dose of the subjects had to be increased throughoutthe six-month period of fish oil administration to maintain constant blood glucose …”

* “Another important finding of our investigation was that consumption of a fish oil-enriched diet worsens glycemic tolerance.”

Fish Oil for diabetics? No. Fish Oil is AWFUL for Diabetics!

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a. Stacpoole, P, Alig, A., Ammon, L., and Crockett, E., “Dose-Response Effects of Dietary Marine Oil on Carbohydrate and Lipid Metabolism in Normal Subjects and Patients With Hypertriglyceridemia,” Metabolism, Vol. 38, No 10 (October), 1989, pages 946-986; “Adverse Metabolic Effect of Omega-3 Fatty Acids in Non-Insulin Dependent Diabetes Mellitus,” Gluaber, H. et al., Annals of Internal Medicine, 1988; 108:663-668; “Fish-oil supplementation reduces stimulation of plasma glucose fluxes during exercise in untrained males,” British Medical Journal of Nutrition (2003), 90, 777-786.


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“It is concluded that fish oil reduced Rd [rate of glucose disappearance] glucose by 26% by reducing glucose metabolic clearance rate …” “[I]t was observed in healthy human subjects that a 3-week supplementation of the diet with fish oil (6g/day) decreased by 40% the insulin response to an oral glucose challenge without altering either endogenous glucose production or plasma glucose utilization.”

“[N]-3 long-chain fatty acids are incorporated into membranes whose composition remains altered at least 18 weeks after interruption of fish-

oil supplementation…”

Fish Oil? AWFUL for Diabetics! – continueda

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a. Stacpoole, P, Alig, A., Ammon, L., and Crockett, E., “Dose-Response Effects of Dietary Marine Oil on Carbohydrate and Lipid Metabolism in Normal Subjects and Patients With Hypertriglyceridemia,” Metabolism, Vol. 38, No 10 (October), 1989, pages 946-986; “Adverse Metabolic Effect of Omega-3 Fatty Acids in Non-Insulin Dependent Diabetes Mellitus,” Gluaber, H. et al., Annals of Internal Medicine, 1988; 108:663-668; “Fish-oil supplementation reduces stimulation of plasma glucose fluxes during exercise in untrained males,” British Medical Journal of Nutrition (2003), 90, 777-786.


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2011 − Fish oil causes increased cellular oxidative stress leading to decreased life-span:a,b,c

• “Conclusion: These findings suggest that intake of fish oil increases oxidative stress, decreases cellular function, and causes organ dysfunction in SAMP8 mice, thereby promoting aging and shortening the lifespan of the mice.

• “Therefore, fish oil intake may also influence the lifespan of humans. For instance, aging is promoted by an increase of oxidative stress in diabetic patients who have ingested a large amount of EPA and DHA. In the present study, half of the fat intake was substituted with fish oil and the EPA and DHA intake levels were relatively low.…In the second part of the study, we showed that SAMP8 mice fed fish oil had decreased lipid accumulation in the plasma and liver compared with mice fed [parent omega-6] safflower oil.

• “Sardine oil (34% EPA plus DHA) obtained from a local fish meal factory was deodorized by molecular distillation and maintained under a N 2 atmosphere until use. The peroxide value of the oil was less than 2 meq/kg [very low].

a. Tsuduki, T., et al., “Long-term intake of fish oil increases oxidative stress and decreases lifespan in senescence-accelerated mice,” ./ Nutrition 27 (2011) 334-337; Garrido, G., et al., “Ingestion of high doses of fish oil increases the susceptibility of cellular membranes to the induction of oxidative stress,” Lipids, Vol. 24, Issue 9, 1989, pages 833-835; Kaasgaard, SC, et al., “Effects of Dietary Linseed Oil and Marine Oil on Lipid Peroxidation in Monkey Liver in vivo and in vitro,” Lipids , Vol. 27, no 10, (1992), pages 740- 745.

Fish Oil is AWFUL for Everyone!

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• “The present data showed that monkeys were not fully able to compensate for increased peroxidative stress but a four-fold supplement of vitamin E to the diets reduced the oxidation.

• “Lipofuscin [the cause of “age spots” on the hand] content of extractable lipofuscin in liver homogenate was used as an indicator of in vivo lipid peroxidation. The level in the male MO group was threefold higher than in the CO (LA - corn oil) and LO (ALA- linseed oil) groups.

• “The basal TBARS [peroxidation level measurement] level of the MO [fish oil] group was four times higher than that of the [parent] CO and LO groups…”

Life-Systems Engineering Science Analysis: Omega-3 derivative-based fish oil causes significant tissue oxidation issues whereas parent omega-6 and parent omega-3 do not. Precious anti-oxidants are routed to the damaging fish-oil tissue and that leaves other critical tissues unprotected.

WARNING: Just adding more tocopherols (like vitamin E) are insufficient to stop this damage.

Fish Oil? AWFUL for Everyone! – continued

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* There never were significant metabolic pathways that would allow such inflated claims. * Fish oil was “reverse engineered” to deal with and sell lots of waste products, including

spoiled fish, to the “nutritional” supplement market.

Why the Continued Fish Oil Failures?

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a. 3-5% (av.) oil yield; the crude oil requires additional processing.b. Sears B. Q & A with Dr. Barry Sears: Omega-3 ultra-refined fish oil -- http://www.cbn.com/health/NaturalHealth/drsears_qanda.aspx#14.

Capsule Calculation:a,b

1.A fish portion is 4 oz – 113g2.1 g of crude fish oil is equal to eating about one-sixth portion (6% oil content).3.1 g of crude fish oil yields about 250 mg of health-grade fish oil. Consuming 1 g of health-grade fish oil is equal to eating about 70% portion (4:1 factor) – 1/6 th portion x 4 = 2/3rd portion.4.100 g of “health-grade” fish oil yields

1 g of “pharmaceutical grade” fish oil (“super pure” omega 3, EPA, DHA, etc.) then one would need to consume about 71 fish portions = 17 POUNDS of unprocessed FISH per capsule!


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SUCCESS — True Essential EFAs — PEOs

EFA = Essential Fatty Acid = PEO Parent Essential Oils —“EFA” Often Used INCORRECTLY by referring to DERIVATIVES

• Parent omega-6 (LA) – essential• Parent omega-3 (ALA) – essential

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LA and ALA are the only 2 essential (body can’t manufacture) fats

• DHA from fish oil is NOT an EFA – NOT essential – body makes AS NEEDED• EPA from fish oil is NOT an EFA – NOT essential – body makes AS NEEDED

Newsflash: < 5% (approx. 1%) of all PEOs are Converted into Derivativesa,b,c

Contrary to popular belief, your body makes the derivatives AS NEEDED, such as DHA and EPA, with at least 95% staying in parent form.

a. Salem N, Lin Y, Brenna JT, Pawlosky RJ. “Alpha-linolenic acid conversion revisited.” PUFA Newsletter, December 2003. [Link]b.. Pawlosky RJ, Hibbeln JR, Novotny JA, Salem N Jr. “Physiological compartmental analysis of alpha-linolenic acid metabolism in adult humans.” J Lipid Res 2001;42:1257-65. [Medline]c. Goyens PL, Spilker ME, Zock PL, Katan MB, Mensink RP. “Conversion of alpha-linolenic acid in humans is influenced by the absolute amounts of alpha-linolenic acid and linoleic acid in the diet and not by their ratio.” Am J Clin Nutr 2006;84:44-53. [Medline]

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Pharmaceutical Overdose: Fish Oil Can’t & Doesn’t Work

Fish oil is exclusively omega-3 derivatives with enormous supra-physiologic overdose factors of plasma EPA and DHA. Therefore, prophylactic use has no basis in human physiology whatsoever.

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Parent to Derivative Ratios–Surprise! The Conversion is Much Less Than Most Physicians Think or Assume.a

Minimum of 95% of PEOs STAY in the Cell’s Membranes ― All 100 Trillion Cells!

** NO delta-6/delta-5 desaturase impairments in general population. **

“…[I]n adult men and women the ‘average estimated conversion of alpha-linoleic acid to n-3 LC-PUFA metabolites and docosa-hexaenoic acid was 17.3 ± 12.8 and 3.6 ± 3.8 percent, respectively (mean + SD).’ This is likely to be an overestimate of the actual overall conversion rates for several reasons. We see even with this excessive estimate of the parent omega-3 derivative conversion that theoretically no more than 37% of them are converted to derivatives.”a

Real-life fact: Only 1% - 5% derivatives from PEOs.

a. British Medical Journal, Oct. 9, 1982, 285-993.

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a. Carnielli, V.P., et al., “The very low birth weight premature infant is capable of synthesizing arachidonic and docosahexaenoic acids from linoleic and linolenic acids,” Pediatric Research, Vol. 40, No. 1, 1996, pages 169-174.

• “…[T]his clearly shows that all infants were capable of actively synthesizing the long chain polyunsaturated FA from their dietary precursors.

• “We report a newly developed approach which enabled us to measure in vivo [in the body] the biosynthesis of LCP with stable isotopes. The study shows that small preterm infants are capable of converting both LA and LNA into LCP [long chain polyunsaturated fatty acid]. We were also able to measure the l3C enrichment of all major metabolites of the essential FA including CI8:3n-6, which is the delta-6 desaturase product of LA and thought to be the limiting step in EFA metabolism.

• “The major finding of this study is that the healthy preterm infant at approximately 1 mo. of age can desaturate and elongate LA and LNA into n-6 and n-3 LCP, respectively.”

**SUPER NEWSFLASH!!!**

FALLACY DESTROYED in 1996— Babies DO PRODUCE AA / DHA (omega-6 derivative / omega-3 derivative):a

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2008 MAJOR NEWSFLASH: CONFIRMED AGAIN (the 3rd time) − EFA Derivatives Made “As Needed”a

“…which shows the effectiveness of ALA conversion [into DHA and EPA] and accretion into erythrocytes. The amounts of ALA required to obtain these effects are amounts that are easily achieved in the general population by dietary modification.

There is independent confirmation from the USDA of conversion amounts, if anyone would care to look…b

“Although an increased intake of dietary ALA might be expected to upregulate ALA conversion, this has . . . not been found…” [Note: These are rate-limited reactions.]

“Overall conversion rates of LA and ALA, calculated from peak [13C] LCP concentrations adjusted for dietary influences on pool sizes of LA and ALA, were low and of similar magnitude overall for AA and EPA (0.18% and 0.26%; Table 2). LA→DGLA and AA formation was significantly lower on the FXO diet in each case, with ALA→EPA and DPA formation on average higher on the FXO diet, although the differences were not significant. Conversion of tracers to DHA was much less.” [Note: We see PEO conversion rates of less than a mere 1%. The same less than 1% conversion rates held for DGLA, DHA, and DPA.]

a. “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,” American Journal of Clinical Nutrition, Vol. 88, No. 3, 801-809, September 2008.b. Hussein, Nahed, et al., “Long-chain conversion of linoleic acid and alpha-linolenic acid in response to marked changes in their dietary intake in men,” Journal of Lipid Research, Volume 46, 2005, pages 269- 280.

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The medical journal article, “Comparison of bolus versus fractionated oral applications of [13C]-linoleic acid in humans,” European Journal of Clinical Investigation, Volume 29 Issue 7, Pages 603 - 609, had this to say regarding over-estimations of derivatives:

“Conclusions: Using areas under the curve [the simple, standard method of analysis] overestimates the conversion, because different residence times are not considered.”

Life-Systems Engineering Science Analysis: PEO derivative supplements are NOT required. They are made from the parent EFAs as needed. Therefore, fish oil is not required for EPA and DHA and often provides harmful pharmacological overdoses:

2,600:1 times more ALA than DHA You need much more ALA. 35


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Simple. There never were any significant metabolic pathways that would allow such claims. Fish oil was initially “reverse engineered” to deal with waste products and fish that was not good enough to be sold to restaurants.

Why Continued Fish Oil Failures?

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What About Fish Oil?No! NOT Bio-Identical

Not Adequate.

• Highly Processed With Chemicals. However, not the most significant problem…

• Not Enough “Parent” EFAs – Mainly Derivatives.a

• High Doses of Derivatives & Not Parents – Body’s JOB is to Make Derivatives AS NEEDED.

a. Peskin, BS, Report: “Scientific Calculation of the Optimum Omega-6/-3 Calculation,” Pinnacle Press, Houston, TX 2008, and the USDA’s website: http://www.nal.usda.gov/fnic/foodcomp/search/.

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• Fish oil contains almost no parent oils — supplements = 20-500-times too many omega-3 derivatives = pharmacologic, physiologic, overdose.

• Fish have no oil glands, so fish oil is essentially “juiced fish.”

• Fish oil does not contain adequate amount of PEOs.

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• Approximately 70% of the cholesterol in the lipoproteins of the plasma is in the form of cholesterol esters attached to apolipoprotein B.a

• Of dietary cholesterol absorbed, 80%–90% is esterified with long-chain fatty acids in the intestinal mucosa.b The majority (about 55%) of the cholesteryl ester component is LA (parent omega-6).c

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Lipids in the Bloodstream

a. Guyton, A., Hall, J., Textbook of Medical Physiology, 9th edition, Philadelphia, Pa: WB Saunders; 1996:872-873.b. Bothem KM, Mayes PA. Cholesterol synthesis, transport, and excretion. In: Murray PK, Granner DK, Mayes PA, Rodwell VW, eds., Harper’s Illustrated Biochemistry, 27th ed., New York, NY: McGraw-Hill;2003;235.c. Sinclair HM. “Essential fatty acids in perspective.” Hum Nutrit 1984;38C:245-260.

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Question: Plasma lipids have preponderance of parent omega-6. What about tissue?Answer: High predominance of tissue parent omega-6 (11:1 conservatively).

Spector, A.A., “Plasma Free Fatty Acids and Lipoproteins as Sources of Polyunsaturated Fatty Acid for the Brain,” Journal of Molecular Neuroscience, Vol. 16, 2001, pages 159-165., “Most of the plasma free fatty acid (EFA) is derived from the triglycerides stored in the adipose tissue [body fat].” Note: Organs, including the brain use these EFAs for structural incorporation. “Metabolism of essential fatty acids by human epidermal enzyme preparations: evidence of chain elongation,“ R.S. Chapkin, et. at., Journal of Lipid Research, Volume 27, pages 954-959, 1986, Markides, M., et al., “Fatty acid composition of brain, retina, and erythrocytes in breast- and formula-fed infants,” The American Journal of Clinical Nutrition, 1994;60:189-94 and Agneta Anderson, et. al., American Journal of Endocrinological Metabolism, 279: E744-E751.

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Warning: With most parent omega-6 being adulterated by food processors, at least 50% is nonfunctional! Therefore, we need lots of FULLY FUNCTIONAL parent omega-6 (11:1 fully functional parent omega-6 to make up for this) +ONLY conservative amounts of parent omega-3(NOT derivatives)

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Physiology: Cholesterol Structure Itself Never Changes

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However, the cholesterol molecule (better termed cholesteryl) is tied to a structure that does change ― EFAs (variable). This is where all of the insight lies.Cholesterol itself can become oxidized, but much more significant is the oxidized esterified component.a,b

Notice the cholesterol ester portion is HUGE compared to free cholesterol or phospholipids.

a. Zhang WB, Addis PB, Krick TP. Quantification of 5α-cholestane-3β,5,6β-triol and other cholesterol oxidation products in fast food French fried potatoes. J Food Sci 1991;56:716-718. [Link]b. Korytowski W, Bachowski GJ, Girotti Aw. Photoperoxidation of cholesterol in homogenous solution, isolated membranes, and cells: comparisons of the 5α- and 6β-hydroperoxides as indicators of singlet oxygen intermediacy. Photochem Photobiol 1992;56:1-8. [Medline] 43

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The Seminal Discovery: Oxidized Cholesterol • World leading biochemist, Dr. Spiteller,a,b concludes that it is oxidized cholesterol esters that are responsible for the initial damage to endothelial cells.

• These products are incorporated into LDL-cholesterol in the liver, and this vehicle, basically a chemical transporter, deposits them on the endothelial cell walls of the vascular system (intima), where they initiate inflammation and familiar arteriosclerotic plaques develop as a result.

The LA (parent omega-6) path is highly relevant for understanding why statins have an NNT of 80-100 — a 99% failure rate. The cholesterol structure in the arterial intima contains significant amounts of oxidized or nonfunctional parent omega-6 attributable largely to ingestion of foods containing LA oxidized or otherwise damaged in the course of routine food processing, before any in vivo oxidation.a. Spiteller G. Is atherosclerosis a multifactorial disease or is it induced by a sequence of lipid peroxidation reactions. Ann NY Acad Sci 2005;1043:355-66. [Medline]

b. Spiteller G. Peroxyl radicals: Inductors of neurodegenerative and other inflammatory diseases. Their origin and how they transform cholesterol, phospholipids, plasmalogens, polyunsaturated fatty acids, sugars, and proteins into deleterious products. Free Radical Biol Med 2006;41:362-87. [Medline] 44

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EFAs = PEOs = Essential

The Key — PEOs —in particular, parent omega-6 in Esterified Cholesterol

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We know that the intima consists of a single layer of endothelial cells containing significant LA, but no ALA.a,b

Consumed, processed LA deposited in arterial intimal cell membranes leads to abnormal oxidation at the vascular injury site, thus causing injurious inflammation. In this case, abnormal oxidation involves formation of a hydroperoxide from LA. What else could cause LA in the endothelial cells to become oxidized? The real culprit is in our food supply, as ubiquitous “processed foods.” Masquerading as harmless, they are the evil villains in this drama.

•Chapkin RS, Ziboh VA, Marcelo CL, Voorhees JJ. Metabolism of essential fatty acids by human epidermal enzyme preparations: evidence of chain elongation. J Lipid Res 1986; 27:945-954.•Andersson A, Sjödin A, Hedman A, Olsson R, Vessby B. Fatty acid profile of skeletal muscle phospholipids in trained and untrained young men. AmJ Physiol Endocrinol Metab 2000;279:E744-E751.

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Success: Major Newsflash 2009: American Heart AssociationChampions Omega-6 PUFAs to Counter Popular Nutrition Advicea

A great deal of discussion in the world of nutrition has given omega-6 fatty acids a bad reputation, which, according to the American Heart Association is unfounded. The debate came about because one of the components of omega-6 fatty acids, called arachidonic acid, is a “building block” for some inflammation-related molecules. This had led to concern that omega-6 consumption would lead to a greater risk of heart disease.

“‛That reflects a rather naive understanding of the biochemistry,’ says William S. Harris, Director of the Metabolism and Nutrition Research Center of the University of South Dakota Sanford School of Medicine and the nutritionist who led the science advisory committee that issued the report in Circulation.”

“‘[O]mega-6 PUFAs also have powerful anti-inflammatory properties that counteract any proinflammatory activity,’ say the advisory authors. ‘It’s incorrect to view the omega-6 fatty acids as “proinflammatory.’”

a. AHA Heartwire 2009, © 2009 Medscape, January 28, 2009 (Dallas, Texas), based on Journal of the American Heart Association, Ref.: AHA Science Advisory, Harris WS, Mozaffarian D, et al., “Omega-6 fatty acids and risk for cardiovascular disease,” downloaded from circ. ahajournals.org on January 29, 2009, to be published in Circulation, February 17, 2009, pages 1-6, and American Academy of Anti-Aging Medicine referenced February 2, 2009 at http://www.worldhealth.net/news/concern_about_omega-6_fatty_acids_leadin.

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All physicians and healthcare professionals need to know…

• 50% of every cell membrane is fat and at least 25% are PEOs with significantly more LA than ALA in every cell membrane.

• PGE1 is the body’s most potent natural anti-inflammatory.

• PGI2, prostacyclin, is the body’s most potent natural anti-aggregatory and prevents platelet adhesion (prevents thrombosis)

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Cancer Prevention Newsflash (2009) of the DECADE!

Nearly a Century Later, New Findings Support Warburg Theory of Cancera (Note: Appropriately, this work was supported by the National Cancer Institute and the National Institute on Aging)

• “Seventy-eight years after Warburg received science’s highest honor [the Nobel Prize in 1931], researchers from Boston College and Washington University School of Medicine [St. Louis] report new [additional] evidence in support of the original Warburg Theory of Cancer.”

• “Major abnormalities in CL [cardiolipin] content or composition were found in all tumors.”

• “Hence, our findings in mouse brain tumors provide evidence linking abnormal CL to irreversible respiratory injury.”

a. Science Daily (January 14, 2009) and 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;49:2545-66.

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L.S.E. Analysis: What is cardiolipin (CL)? It is a fat-based complex phospholipid found in all mitochondrial membranes, almost exclusively in the inner membrane, and it is intimately involved in maintaining mitochondrial functionality and membrane integrity. It is used for ATP synthesis, and consists roughly of 20% lipids.a

In mammals, the main substrate in CL is parent omega-6 with virtually no parent omega-3 or its derivatives.b

a. Krebs JJ, Hauser H, Carafoli E. Asymmetric distribution of phospholipids in the inner membrane of beef heart mitochondria. J Biol Chem 1979;254:5308-16.b. Scottish Crop Research Institute (MRS Lipid Analysis Unit, Invergowrie, Dundee DD2 5DA , Scotland ). Cardiolipin (diphosphatidylglycerol). Structure, occurrence, biology and analysis. Retrieved January 20, 2009 from: http://www.lipidlibrary. co.uk/Lipids/dpg/index.htm.

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Warning: With most parent omega-6 being adulterated by food processors for long shelf-life, at least 50% is nonfunctional! Therefore, we need lots of FULLY FUNCTIONAL parent omega-6 to compensate. +++ONLY conservative amounts of parent omega-3(NOT their derivatives).

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Food processors never use omega-3 fats, as they are far too oxygen-reactive. Most parent omega-3 in foods is not adulterated.

The problem lies exclusively in the adulterated parent omega-6 fats. This key issue is never properly addressed.

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We know that the intima consists of a single layer of endothelial cells containing significant LA, but no ALA.c,d Consumed, processed (nonfunctional) LA deposited in arterial intimal cell membranes leads to abnormal oxidation at the vascular injury site, thus causing injurious inflammation. (Note: In this case, abnormal oxidation involves formation of a hydroperoxide from LA.) **The real culprit is in our food supply, as ubiquitous “processed foods.” Masquerading as harmless, they are the villains in this drama.**

c. Chapkin RS, Ziboh VA, Marcelo CL, Voorhees JJ. Metabolism of essential fatty acids by human epidermal enzyme preparations: evidence of chain elongation. J Lipid Res 1986; 27:945-954.d. Andersson A, Sjödin A, Hedman A, Olsson R, Vessby B. Fatty acid profile of skeletal muscle phospholipids in trained and untrained young men. AmJ Physiol Endocrinol Metab 2000;279:E744-E751.

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When these precious PEOs become oxidized, oxygen transfer stops and cardiovascular disease starts

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Arterial Tissue

Important Note: The intima is 100% parent omega-6 (LA) not found in fish oil.

DPA note: 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.

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Cause of Thrombosis (Blood Clots): The LDL Connection

• “Cholesterol esters are the predominant lipid fraction in all plaque types…• “Intimal [innermost arterial lining] macrophages contain substantial amounts of cholesterol esters, which are rich in PUFAs [PEOs].”Note: The intima is all parent omega-6 – with virtually no parent omega-3.a

More Confirmation It’s the Unadulterated Parent Omega-6…

German physician Clause Weiss, MD, et al. states:• “In summary, infusion therapy with PGE1 in patients with peripheral arterial occlusive disease (PAOD) reduces thrombin formation and results in a decrease of fibrin degradation. PGE1 may thus reduce fibrin (thrombosis) deposition involved in the pathogenesis of atherosclerosis.”b

Solution: Unadulterated PEOs with a predominant LA (Parent Omega-6) component.a. Felton CV, Crook D, et al., “Relation of plaque lipid composition and morphology to the stability of human aortic plaque,” Artherioscler Thromb Vasc Biol, 1997;17:1337-1345.b. Prostaglandins, Leukotrienes and Essential Fatty Acids, Nov. 2000; 63(5):271-277.

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SUCCESS: Prostaglandins REVERSE Thrombosis

• 1987 ― prostaglandins are capable of limiting thrombosis (clogged arteries)a

• 1988 ― prostaglandins can reverse thrombosisb

How:c

– PGE1, a parent omega-6 derivative, is the body’s most powerful natural anti-inflammatory and

– PGI2, a parent omega-6 derivative, is the body’s “natural blood thinner.”When human experiments cause blood vessels to be made hypoxic by decreasing the cellular oxygen, PGI2 (prostacyclin) decreases significantly:

• Prostacyclin (PGI2) is the most potent anti-aggretory (“helps blood thinning”)

agent known! • Prostacyclin acts as a protective to the heart. Irritation and inflammation zap your

important cellular oxygen supply. • Unadulterated parent omega-6 in the phospholipids of your body’s 100 trillion cells

comes to the rescue (IF you have enough) ― being utilized as substrates in both the cyclooxygenase and lipoxygenase pathways.

Decrease PGE1 and PGI2 and you have a heart attack in the making.

a. Witt & Müller, 1987: Prostaglandins in the Cardiovascular System, edited by HF Sinzinger, MD and K Schrör, MD, Birkhäuser Verlag, Basel, Switzerland, 1992.

b. Witt & Baldus,1988: ibid.c. Also see: “Pathophysiology of critical leg ischaemia and mode of action of prostaglandins,” Bertele’, V., et al., “Role of prostacyclin in normal

and arteriosclerotic human coronary arteries during hypoxia,” Siegel, G., et al.; “Effects of 9, 12, 15-octadecatrien-6-ynoic acid on the metabolism of arachidonic acid in platelets and on the platelet aggregation,” Guichardant, M., et al.; and “Endogenous prostacyclin preserves myocardial function and endothelial-derived nitric oxide formation in myocardial ischemia,” Schrör, K. and Woditsch, I.in Prostaglandins in the Cardiovascular System (1992) 57

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Eicosanoids: Critical prostaglandins, etc. from parent omega-6 AND omega-3: Cell-by-cell hormone analogy (PGE1 – PGE4, etc.) - very short half-life.

Very Significant in Vascular Function

PATHWAY SUMMARY

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• PGE1 is body’s most potent anti-inflammatory.

• Prostacyclin is body’s natural “blood thinner.”* * S. Bunting, S. Moncada, and J.R. Vane, “Prostacyclin—Thromboxane A2 Balance: Pathophysiological and Therapeutic Implications,” British Medical Journal, (1983), Vol. 39, No. 3, pages 271-276.

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Clinical Analytic Solution:

Pulse Wave Velocity with Digital Pulse Analysis

•New, Noninvasive, easy to use, insurance reimbursable, economical method to assess patient’s cardiovascular physiologic status backed by more than 25 years of advanced research in medical physics termed photoelectric plethysmographs (PTG) — similar to pulse oximeter.

•“Arterial stiffness measured by pulse wave velocity (PWV) is an accepted strong, independent predictor of cardiovascular events and mortality.”a Anesthesiologists are well aware of this technology, used for monitoring purposes, but most other medical disciplines are not aware.

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a. 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.

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The technique is underpublicized and many physicians are not aware of the great clinical impact of this technology.

• “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…”a

• Very high degree of correlation and repeatability for successful use in clinical application across all populations (including diabetics)b

Detects early evidence of vascular disease and monitors the response to therapy.b

a. Dorlas JC, Nijboer JA. “Photo-electric plethysmography as a monitoring device in anaesthesia.” Br J Anaesth 1985;57:524-30.b. Cohn J, Finkelstein S, McVeigh G, et al. “Noninvasive pulse wave analysis for the early detection of vascular disease.” Hypertension 1995;26:503-

508.

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• This device is extremely responsive and can measure patient therapeutic improvement in as little as 3-6 months, if not earlier.

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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.a

a. Izzo JL Jr, Shykoff BE. “Arterial stiffness: clinical relevance, measurement and treatment.” Rev Cardiovasc Med. 2001;2:29-34, 37-40.

1. 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. 2. Simplicity, ease of use, and detailed cardiovascular analysis of the patient are key to clinical use. 3. As part of the analysis, the physician is also given patients’ CV “biological age” to compare to their actual age.

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a. 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;32:565-9.b. 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;33:1111-7.c. 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;14:91-7.d. 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;99:2434-9.e. 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;37:1236-41.f. Kelly RP, Hayward C, Avolio A, O’Rourke M. “Noninvasive determination of age related changes in the human arterial pulse.” Circulation 1989;80:1652-9.g. O’Rourke MF, Kelly RP. “Wave reflection in the systemic circulation and its implications in ventricular function.” J Hypertens 1993;11:327-37.

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 pulse wave velocity (PWV). • Premature arterial aging, as determined by an elevated aortic PWV, is now recognized as a major risk factor for ischaemic heart disease.a-e

An influence of vascular aging on the contour of the peripheral pressure and volume pulse in the upper limb is also well recognizedf and the aortic PWV more than doubles between ages 17 and 70 years of age.g

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a. Millasseau SC, Ritter JM, Takazawa K, Chowienczyk PJ. “Contour analysis of the photoplethysmographic pulse measured at the finger.” J Hypertens 2006;24:1449-56. b. 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;20:2415-22. 64

Elements of PTG (Systolic Phase)

1.S (Starting Point)• Starting point of systolic phase of arterial pulse-wave. • Aortic valve opens and the blood of the LV is ejected into aorta.

2. P (Percussion Wave)• Wave caused from LV ejection that increases the blood volume within artery.• Higher point means stronger LV ejection and higher compliance of larger artery.

3. T (Tidal Wave)• Reflected wave from the small artery.• Higher point means contraction and stiffness of small artery.

4. C (Incisura)• End-point of systolic phase, then aortic valve is closed.• Less drop from pulse height (PH) means larger resistance (arterial contraction & tension).

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.a,b

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WARNING: BP is late-stage diagnostic

“Because wide pulse pressure and systolic hypertension are late manifestations of arteriosclerosis, they are only crude indicators of arterial wall disease.”a


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Fortunately, today there is an effective treatment with plant-based, bio-identical, PEOs, as DPA measurement confirms (IOWA* Experiment).

* Note: IOWA Experiment is not open to interpretation – the device outputs a number – just like a scale outputs your weight, period.

SUCCESS: A New Protocol

“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.”a


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“A.C.C.O.R.D.: Intensive BP / combined lipid therapies do not help adults with diabetes prevent CVD.”a

a. 2010 annual meeting of the American College of Cardiology (published on-line at www.sciencedaily.com/releases/2010/03/100314091130.htm) and scheduled to be published in the New England Journal of Medicine (April 29, 2010).

FAILURE: Just Released March 2010…

• “Hopeful” CVD interventions for Type II Diabetes aren’t effective: “Our results also showed a higher risk of serious adverse events with more intensive blood pressure control.”

• “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.”

• Shocking, pharmacologically lowering blood pressure to normal levels did not significantly reduce the combined risk of fatal or nonfatal CVD…

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SUCCESS: “The Answer” — Plant-based, bio-identical, PEOs achieve SUCCESS via numerous physiologic pathways:

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 landmark IOWA Experiment; the results are unprecedented.

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* 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.

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SUCCESS — Short-term ResultsIOWA: Investigating Oils With Respect to Arterial Flexibility

Significant differences in biological age compared to physical ageBrian Peskin, BSEE: Founder Life-Systems Engineering Science

with David Sim, M.D., Interventional Cardiologist

Short-term Improvement in Subjects with PEO Formulation

Significant differences (p 0.0099) with an experimental error of the mean +-5 years. Subjects’ cardiovascular biological age (average of)

7.2 years lower than their actual physical age.

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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.

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Note: This experiment has a 99.00% accuracy—5 times more accurate than the 5% standard error used in most clinical trials. Therefore, this result is not due to possible error, and is highly significant, with patient CV health 7.2 years better than physical age predicts.

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

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N Mean Std Dev Pr>|t|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||16 -7.24 10.19 0.0099||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||

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MAJOR SUCCESS—PEOs versus Fish OilIOWA: Investigating Oils With Respect to Arterial Flexibility

Significant differences in biological age compared to physical ageBrian Peskin, BSEE: Founder Life-Systems Engineering Science

with David Sim, M.D., Interventional Cardiologist

Subjects Discontinued Fish Oil Supplementation, replacing it with PEO Formulation

Significant differences (p 0.0001) with an experimental error of the mean +-5 years. Subjects’ cardiovascular biological age (average of) 11.1 years lower

than their actual physical age. NOTE: Taking fish oil leads to a greater improvement than taking nothing. Conclusion: fish oil makes patient

cardiovascular systems WORSE!

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.

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Statistics (Highly Significant) — 99.99% Accuracy

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SUCCESS — Wonderful Life-Extension withPEO Supplementation Preventing Cancerand CVD deaths(a) – see next slide

Age % Lives Saved Expected value*

60 years old 61% of lives SAVED at least 20 more years of life70 years old 64% of lives SAVED at least 13 more years of life80 years old 59% of lives SAVED at least 8 more years of life + + many more years

* These are general approximate expected values (means) for the general population.

• Given that PEOs improve oxygenation and are fundamental to so many life-processes, expected values will be greater.

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a) Analysis based on data from the following sources: MR/LE from Heron MP et al. Deaths: preliminary data for 2006. National Vital Statistics Reports 2008;56; Data (2004) calculated from: U.S. Cancer Statistics Working Group. United States Cancer Statistics: 2004 Incidence and Mortality. Atlanta: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention and National Cancer Institute; 2007; Data from Ford ES, Capewell S. Coronary heart disease mortality among young adults in the U.S. from 1980 through 2002: concealed leveling of mortality rates. J Am Coll Cardiol 2007;50:2128-32; Data (2002) calculated from Disparities in deaths from stroke among persons aged < 75 years—United States, 2002. MMWR 2005;54:477-481 and Jamal A, et al. Trends in the leading causes of death in the United States, 1970-2002. JAMA 2005;294:1255-59; ACS: (http://www.cancer.org/downloads/STT/2008CAFFfinalsecured.pdf)AHA: (http://www.americanheart.org/presenter.jhtml?identifier=3054076); data from 2000 census.

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What PEO Ratio is Best for you and your patient? A Balanced Blend of Significantly “Parent” PEOs (Bio-Identical) that Allows the

Body to Make Derivatives AS NEEDED.

• Flax is Great for Parent Omega-3 ― NOT Parent Omega-6.• Sunflower & Safflower are Fine for Parent Omega-6.

• Parent Omega-6/-3 Ratio MUST BE 2.5:1 – 1:1 NO fish oil and few derivative EFAs (only GLA is recommended).a

• High linoleic (LA) MUST be used with minimum oleic content. • Not high oleic variety (omega-9 used for baking and frying).

Don’t we get too much omega 6 in our food? True, but most (>50%) is adulterated. Therefore, a substantial portion

must be counted as zero because it is nonfunctional.

Isn’t it true LA promotes tumors! WRONG, in vitro (not unadulterated in vivo) misunderstanding!b

a. Fatty Acids and Lipids – New Findings, International Society for the Study of Fatty Acids and Lipids, 4th Congress, June 4-9, 2000, Tsukuba, Japan,” Effects of n-6 and n-3 fatty acid supplementation on rat tissue lipid peroxidation,” pages 28-34, published by: Karger, Switzerland, 2001.

b. “Omega-3 Fatty Acids and Inflammation,” Mori, T., et al., Current Atherosclerosis Reports; 6:461-467, 2004. 79

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Documents

1 Professor Brian Scott Peskin* The Real Science behind Essential Fatty Acids, Cancer, and Heart Disease: An Analysis of the Science behind both the Failure